Chest Physiotherapy in Mechanical Ventilated Patients

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EFFECT OF MULTIMODALITY CHEST PHYSIOTHERAPY

ON THE RATE OF RECOVERY AND PREVENTION OF
COMPLICATIONS IN PATIENTS WITH MECHANICAL
VENTILATION-A PROSPECTIVE STUDY IN MEDICAL AND
SURGICAL INTENSIVE CARE UNITS
Thesis submitted to
THE KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,
BELGAUM
(KLE DEEMED UNIVERSITY)
[Declared as Deemed-to-be-University u/s 3 of the UGC Act, 1956 vide Govt. of India Notification No.F.9-19/2000-U.3 (A)]
(Accredited A Grade by NAAC)
For the award of the degree of
Doctor of Philosophy
In the Faculty of Medicine
Discipline: Physiotherapy
By
Renu B. Pattanshetty M.P.T

(Registration No: KLEU/Ph.D/07-08/DOUNO7047)
Under the Guidance of
Prof. Dr. Gajanan. S. Gaude M.D.,DNB, F.C.C.P.

K.L.E. Universitys JN Medical College, Belgaum 590010
Karnataka, India
APRIL 2011
I
KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,


BELGAUM
Declaration
I hereby declare that the thesis entitled EFFECT OF MULTIMODALITY
CHEST PHYSIOTHERAPY ON THE RATE OF RECOVERY AND PREVENTION OF
COMPLICATIONS
IN
PATIENTS
WITH
MECHANICAL
VENTILATION
PROSPECTIVE STUDY IN MEDICAL AND SURGICAL INTENSIVE CARE UNITS
is
a bonafide and original research carried out by me under the guidance of

DR.GAJANAN .S. GAUDE,
Professor, Department of Pulmonary Medicine,
K.L.E Universitys JN Medical College, Belgaum. The thesis or any part

thereof has not formed the basis for the award of any degree/fellowship or
similar title to any candidate of any University.
Place: Belgaum
Renu B. Pattanshetty M. P.T.
Date:
KLEU Institute of Physiotherapy,

Belgaum.
II


BELGAUM
Certificate
This is to certify that the thesis
entitled EFFECT OF MULTIMODALITY

COMPLICATIONS
IN
PATIENTS
WITH
MECHANICAL
VENTILATION
is
a bonafide and genuine research carried out by Renu B. Pattanshetty under

my guidance.
DR. GAJANAN.S.GAUDE
Place: Belgaum
M.D.,DNB, F.C.C.P.
Date:
Prof. & Head,

Dept. of Pulmonary Medicine,
K.L.E. U. JN Medical College,
Belgaum -590010. Karnataka
III


BELGAUM
Certificate

COMPLICATIONS
IN
PATIENTS
WITH
MECHANICAL
VENTILATION
is

the guidance of Dr. Gajanan. S. Gaude, Professor & Head, Department
of Pulmonary Medicine, K.L.E Universitys JN Medical College, Belgaum.
Prof. Dr. Sanjiv Kumar
Place: Belgaum
MPT
Date:
Principal,
K.L.E. U. Institute of Physiotherapy,
Belgaum -590010. Karnataka.
IV


BELGAUM
Certificate

COMPLICATIONS
IN
PATIENTS
WITH
MECHANICAL
VENTILATION
is

the guidance of Dr. Gajanan. S. Gaude, Professor & Head, Department
of Pulmonary Medicine, K.L.E Universitys JN Medical College, Belgaum.
Prof. Dr. V.D. Patil
Place: Belgaum
M.D. DCH
Date:
Dean, Faculty of Medicine,

Principal,
K.L.E. U. JN Medical College,
Belgaum -590010. Karnataka


BELGAUM
Copyright Declaration
We hereby declare that KLE ACADEMY OF HIGHER
EDUCATION AND RESEARCH, BELGAUM,
KARNATAKA,
shall have the rights to preserve, use and disseminate this thesis in print or
electronic format for academic/research purpose.
DR. GAJANAN S. GAUDE M.D.,DNB, FCCP
RENU B. PATTANSHETTY
Place: Belgaum
Date:

BELGAUM.
VI
M.P.T.
TABLE OF CONTENTS
SNO
PARTICULARS
PAGE NOS
Declarations
ii
Acknowledgement
iii
Operational definitions
iv
List of abbreviations
XIII
List of tables
XV
vi
List of figures
XVII
vii
List of photographs
XIX
viii
Abstract
XX
1.
INTRODUCTION
2.
OBJECTIVES
3.
HYPOTHESIS
4.
REVIEW OF LITERATURE
5.
MATERIAL AND METHODS
40
6.
RESULTS
56
7.
DISCUSSION
115
8.
CONCLUSION
149
SUMMARY
151
10.
BIBLIOGRAPHY
153
11.
ANNEXURE I- Ethical clearance certificate
186
12.
ANNEXURE II Informed consent form
187
13.
ANNEXURE III Photographs
191
14.
ANNEXURE IV - Proforma
197
15.
ANNEXURE V- Master chart
199
16.
PUBLICATIONS
VIII
VII
XI
ACKNOWLEDGEMENT
This dissertation would not have been possible without the guidance and
the help of several individuals who in one way or another contributed and
extended their valuable assistance in the preparation and completion of this study.
I consider myself blessed and lucky and would like to take this opportunity
to heartily thank Hon. Chancellor Dr. Prabhakar Kore and Hon. Vice Chancellor
Dr. C.K. Kokate without whose motivation , it would have been impossible to
pursue this PhD Research programme.
My utmost gratitude and heartfelt thanks to my teacher and guide
Dr. Gajanan .S Gaude, Prof and Head, Dept. of Pulmonary Medicine, whose
encouragement, supervision, useful suggestions and support from the preliminary
to the concluding level enabled me development interest, motivation and
enthusiasm to work for the study.
I would also like to express my deepest gratitude to Dr. V. D. Patil, Dean,
Faculty of Medicine and Principal of JN Medical College, Belgaum for allowing
me to conduct the study.
I am thankful to Dr. M.V. Jali, Medical Director, KLES Dr. Prabhakar
Kore Hospital and Medical Research Centre, Belgaum for allowing me to carry
out this research work in the ICUs.
VIII
I am grateful to Mr. M.D. Mallapur, Assistant Professor, Dept. of

preventive and community medicine for his relentless help with the statistical
analysis of the research data.
I offer my regards and gratitude to my Principal Dr. Sanjiv Kumar and all
my colleagues for their support and encouragement. My special thanks to
Dr.Arati, Dr.Deepa, Dr.Snehal, Dr.Chitra, Dr.Peeyoosha, Dr.Vijay, Dr. Anil and
Dr. Chandu for their time, useful and critical comments and insightful questions
during my mock presentations for open house seminars.
My heartfelt thanks to all my patients and their relatives without whose
participation and cooperation, this study would have been incomplete and
impossible.
This work would not have been possible without the help of the ICU staff. I
am thankful to all the ICU medical staff and nursing staff for all their help that
they have rendered during the period of my study.
I would like to thank my family for all their love and encouragement. For
my parents who raised me with a love of medical science and supported me in all
my pursuits, for my brother and sister for their constant love and best wishes in all
my endeavors. For my two lovely and naughty nephews, Akshaj and Amogh whos
ever smiling faces were a continuous source of motivation. And most of all, for my
loving, supporting, encouraging, and patient husband, Mr. Murigendra M. Kori
IX
whos never- ending support especially during the final stages of this Ph.D work
will always be cherished.
I thank Miss. Veena & Mr. Deepak of SAI D.T.P. & Xerox Centre, for
formatting, printing & binding of this dissertation work.
Lastly, I offer my heartfelt thanks and gratitude to all those who supported
me in any respect during the completion of my project.
Date:
Renu B. Pattanshetty M.P.T
Place:
Faculty of Medicine,
Discipline: Physiotherapy,
KLE University, Belgaum.
OPERATIONAL DEFINITIONS
VAP- A type of nosocomial pneumonia that affected the lung parenchyma after
48 hours of mechanical ventilation
VAP > 5 days- defined as VAP that occurred after 5 days after intubation and
mechanical ventilation. Also referred to as delayed onset of Ventilator associated
pneumonia.
VAP < 5 days defined as VAP that occurred within 5 days of the intubation and
mechanical ventilation. Also referred to as early onset Ventilator associated
pneumonia
Adverse event Was defined as any undesired event that could deteriorate or
worsen the patients current medical status during and after 30 minutes of chest
physiotherapy intervention.
Discharge against medical advice-
Was defined as an outcome that was
considered as failure since patients relative opted for patients discharge from
ICU
when he/she was still intubated and ventilated against the treating
physicians and/or surgeons advice due to what so ever reasons.
Discontinuation of the treatment was defined as abrupt stopping of the chest

physiotherapy treatment as per the patients relative(s) since they believed that the
chest physiotherapy was not helping the patient.
Unsuccessful weaning: Was defined as the patients who fulfilled the weaning
criterion and underwent the weaning process as per the treating physiciansand /or
surgeon instructions but failed during the CPAP or the T-Piece trial and could not
proceed with spontaneous breathing and were re-intubated.
XI
Successful outcome - Was defined as the patients who fulfilled the weaning
criterion and underwent the weaning process as per the treating physicians and
/or surgeon instructions and tolerated the CPAP or the T-piece trial and proceeded
with the extubation and spontaneous breathing.
XII
LIST OF ABBREVIATIONS
ARDS
Acute respiratory distress syndrome
APACHE II
Acute physiology and chronic health evaluation system II
AE
adverse events
ALI
Acute lung injury
APRV
Assist pressure release ventilation
ABG
Arterial blood gas analysis
CPIS
Clinical pulmonary infection score
CABG
Coronary artery by - pass graft
CLdyn
Dynamic lung compliance
DBP
Diastolic blood pressure
D/C AMA
Discharge against medical advice
EELV
End expiratory lung volume
EPAP
Expiratory positive airway pressure
FG
French gauge
Failure
FiO2
Fraction of inspired oxygen
GCS
Glasgow coma score
GBS
Guillian Barre Syndrome
ICU
Intensive care unit
ICCU
Intensive coronary care unit
XIII
MH
Manual hyperinflation
MM chest PT
Multimodality chest physiotherapy
MV
Mechanical ventilation
MAWP
Mean airway pressure
MICU
Medical intensive care unit
NSICU
Neuro-surgical intensive care unit
PaO2
Partial pressure of arterial oxygen tension
PaCO2
Partial pressure of arterial carbon dioxide tension
PAP
Peak airway pressure
PEEP
Positive end expiratory pressure
P&A
Pneumonia and atelectasis
PS
Pressure support ventilation
RR
Respiratory rate
RSBI
Rapid shallow breathing index
SO
Successful outcome
SIMV+PS
SCI
Synchronized intermittent mandatory ventilation + Pressure

support
Spinal cord injury
SBP
Systolic blood pressure
SICU
Surgical intensive care unit
VAP
Ventilator associated pneumonia
Vt
Tidal volume
XIV
LIST OF TABLES
SNO
TABLE LEGEND
PAGE
NOS
1.1
Age and sex distribution of patients
59
1.2
ICU profile of patients in both the groups
61
1.3
Underlying predisposing conditions of patients
63
1.4
Mode of intubation and initial ventilator mode at baseline
65
1.5
Components of RSBI in both the groups
67
1.6
Baseline CPIS and GCS scores in both the groups
69
1.7
Duration of intubation, ICU stay, hospital stay and ventilation

weaning in both the groups
71
1.8
Baseline oxygenation parameters before chest physiotherapy

in both the groups
73
1.9
Baseline ventilatory parameters before chest physiotherapy in

both the groups
75
1.10
Baseline vital signs parameters before chest physiotherapy in

both the groups
77
1.11
Global outcome in both the groups
79
1.12
Distribution of patients according to chest radiological

evidence of diseases of diseases in both the groups
81
2.1
Mean values of oxygenation status parameters after chest

physiotherapy in both the groups
83
2.2
Mean values of ventilatory parameters after chest

85
2.3
Mean values of vital signs parameters after chest

87
SNO
TABLE LEGEND
XV
PAGE
NOS
2.4
Mean values of CPIS and GCS scores after chest

89
3.1
Complications rates in both the groups
91
3.2
Incidence of VAP in both the groups
93
3.3
Complications other than VAP in both the groups
95
4.1
Mean differences between oxygenation parameters before and

after chest physiotherapy among both the groups
97
4.2
Mean differences between ventilatory parameters before and

99
4.3
Mean differences between vital signs parameters before and

101
4.4
Mean differences between CPIS and GCS scores before and

103
5.
Risk factors for ventilator associated pneumonia in both the

groups
105
6.
Risk factors for mortality in both the groups
106
7.1
Patients outcome with relation to PEEP in both the groups
107
7.2
Patients outcome with relation to age in both the groups
109
7.3
Patients outcome according to nature of ICUs in both the

groups
111
7.4
Overall outcome of patients in both the groups
113
XVI
LIST OF FIGURES
Fig No
FIGURE LEGEND
PAGE
NOS
1.1
Age and sex distribution of the patients
60
1.2
ICU profile of the patients
62
1.3
Underlying predisposing conditions of the patients
64
1.4
Percentage wise distribution of various diseases in both the groups
64
1.5
Mode of intubation and initial ventilator mode at baseline
66
1.6
Components of RSBI in both the groups
68
1.7
Baseline CPIS and GCS scores in both the groups
70
1.8
Duration of intubation, ICU stay, hospital stay and duration of

weaning in both the groups
72
1.9
Baseline oxygenation status parameters values before chest

74
1.10
Baseline ventilatory parameters values before chest physiotherapy

in both the groups
76
1.11
Baseline vital signs parameters before chest physiotherapy in both

the groups
78
1.12
Global outcome in both the groups
80
1.13
Distribution of patients according to chest radiological evidence of

diseases of diseases in both the groups
82
2.1
Mean values of oxygenation status parameters after chest

84
2.2
Mean values of ventilatory parameters after chest physiotherapy in

both the groups
86
2.3
Mean values of vital signs parameters after chest physiotherapy in

both the groups
88
2.4
Mean values of CPIS and GCS scores after chest physiotherapy in

both the groups
90
XVII
Fig No
FIGURE LEGEND
PAGE
NOS
3.1
Complications rates in both the groups
92
3.2
Incidence of VAP in both the groups
94
3.3
Complications other than VAP in both the groups
96
4.1
Mean differences between oxygenation status parameters before

and after chest physiotherapy among both the groups
98
4.2
Mean differences between ventilatory parameters before and after

chest physiotherapy among both the groups
100
4.3
Mean differences between vital signs parameters before and after

102
4.4
Mean differences between CPIS and GCS scores before and after
104
5.1
Patients outcome with relation to PEEP in both the groups
108
5.2
Patients outcome with relation to age in both the groups
110
6.1
Patients outcome in relation to nature of ICUs in both the groups
112
6.2
Overall outcome of patients in both the groups
114
XVIII
LIST OF PHOTOGRAPHS
PHOTO NO
DESCRIPTION
PAGE
NO
1.
Servo 300 C and Servo 900 ventilator systems
191
2.
Patient in an ICU set up
192
3.
Routine pharmacological therapy
192
4.
Procedure of suctioning
193
5.
Romsons suctioning catheters
194
6.
Head of bed end elevation to 30-45 degrees
194
7.
Manual hyperinflation bag
195
8.
Procedure of manual hyperinflation
195
9.
Procedure of chest vibrations
196
XIX
ABSTRACT
Background: Patients receiving mechanical ventilation have an increased risk of
complications besides an increased risk of sputum retentions leading to ventilation
weaning more difficult and resulting in excess morbidity and mortality. Various chest
physiotherapy techniques play an important role in management of ventilated patients.
The chest physiotherapy techniques adopted have been studied on patients as a single
entity or with combination of two techniques.
Objectives: The present study was designed to evaluate the effect of multimodality chest
physiotherapy on rate of recovery and prevention of complications in ventilated patients.
Material and methods: A total of 220 patients were referred for chest physiotherapy,
out of which 20 patients were excluded since they did not meet the inclusion criteria. 200
patients were randomly allocated to each of the two groups with 100 patients in study
group and 100 in control group respectively. MH and suctioning was administered to 86
patients in the control group and suctioning + MH + chest vibrations and positioning to
87 patients in the study group, respectively, till they were extubated. Both the groups
received chest physiotherapy treatment twice daily. Standard care in the form of routine
nursing care, pharmacological therapy as advised by concerned physician/surgeon was
strictly implemented throughout the intervention period. 13 patients from the study group
and 14 from the control group withdrew from the study during the study period. All the
patients were followed up for the global outcomes in terms of successful weaning,
recovery and discharge from hospital, death, total length of stay on ventilation and
complications encountered during mechanical ventilation
XX
Results: Data of 173 adult intubated and ventilated patients who participated in the study
were subjected to statistical analysis using SPSS windows version 13.0. The study
demonstrated significant improvements with multimodality chest physiotherapy
treatment in terms of rate of recovery with 66.7% patients in study group compared to
32.6% of patients in control group (p=0.000). Complication rates were higher with 61.6%
in the control group as compared to 26.4% complications in the study group. VAP was
observed in 32 patients in the study group as compared to 38 patients in the control
group. The physiotherapist based protocol was helpful in significant reduction of
complications. Only 26.4% of patients suffered from complications in the study group as
compared to 61.6% in the control group (p=0.000). Duration of hospitalization was
longer in the study group (169.40 days) as compared to the control group (12.86.12
days). Successful weaning from mechanical ventilation was noted in 58 patients in study
and 24 patients in control group.
Conclusion: Multi modality chest physiotherapy protocol has shown to prevent ventilator
associated pneumonia and enhance the clinical outcome in adult ventilated patients and
may be recommended as a treatment option in ICU. This therapist based protocol has also
enhanced the weaning process and has proved to be safe with no advent of adverse events
and may be used as a routine chest physiotherapy treatment in adult intubated and
ventilated patients.
Key words: multimodality chest physiotherapy, ICU, mechanical ventilation, suctioning,

manual hyperinflation, chest vibrations, positioning, complications, outcome.
XXI
Introduction
INTRODUCTION
Patients needing mechanical ventilation represent an important subset of all
individuals admitted to an ICU due to the intensity of medical service they receive and
their associated costs. Additionally, approximately one third of all patients who enter an
ICU require mechanical ventilation for the management of hypoxemia and hypercapnea,
making this one of the most common indications for admission in ICU. Mechanical
ventilation is indicated in acute reversible respiratory failure. However, patients receiving
mechanical ventilation may have an increased risk of ventilator associated pneumonia
(VAP) and atelectasis, besides an increased risk of sputum retentions leading to
ventilation weaning more difficult and resulting in excess morbidity and mortality. The
cost of maintaining patients on prolonged ventilation in ICUs of acute care hospitals are
high. Thus, every effort should be made to determine which patient can be rapidly
extubated so as to keep the weaning period minimum1.
In most hospital in developing countries, chest physiotherapy is seen as an
integral part of the management of patients in ICUs. The precise role of the chest
physiotherapists varies considerably from one unit to the next, depending on factors such
as the country in which the ICU is located ,local tradition, staffing levels, training, skill
and expertise. The most common techniques use by chest physiotherapists in the ICU are
positioning, mobilization, manual hyperinflation (MH), percussion, chest vibrations,
suction , cough techniques and various breathing exercises.2-8 Some physiotherapists
routinely treat , if not all, ICU patients with combination of these techniques regardless of
the patients underlying
patho-physiological condition, with intention of preventing
Introduction
complications, whereas other physiotherapists use such techniques selectively when they
believe they are specifically indicated.
Physiological benefits of all the techniques have been well documented like
improvements in V/Q matching, clearing airways, improving lung collapse, preventing
pulmonary collapse, re-expanding the collapsed alveoli and improving oxygenation.9-23
Limb exercises may be performed with ICU patients with the aim of maintaining or
improving joint range of motion, soft tissue length, muscle length, muscle strength and
function and of decreasing the risk of thrombo-embolism.3, 10, 24
Chest physiotherapy plays an important role in day to day management of patients
on mechanical ventilation. Several measures hold promise in helping to prevent VAP and
atelectasis. Chest physiotherapy has shown to reduce occurrence of VAP and
atelectasis in patients intubated for more than seven days with APACHE score > 15. 25
Manual
hyperinflation
&
suctioning
are
commonly
adopted
techniques
by
physiotherapists during the management of mechanically ventilated patients which aim to

improve lung volume, promote ventilation and mobilize secretions.26
In spite of the short term benefits of the chest physiotherapy techniques in ICUs,
there has been hardly any documentation regarding the effectiveness of multimodality
chest physiotherapy (combination of suctioning + MH + chest vibrations + positioning)
on the rate of recovery , prevention of complications and length of stay in ICU. There are
no data concerning its effectiveness in preventing or treating other pulmonary conditions
common to ICU patients, and there is only limited evidence concerning which individual
physiotherapy techniques are effective. The ability of physiotherapy to facilitate weaning
Introduction
and to improve function and outcomes of intubated ICU patients receiving mechanical
ventilation is unknown. As the cost associated with the management of ICU patients is
very high, the requirement for all those who work in ICUs including physiotherapists to
provide evidence based practice is mandatory.
Also the chest physiotherapy techniques and combination of the chest physiotherapy
techniques which have shown to reduce the occurrence and prevention of VAP and
atelectasis and other such complications in intubated and ventilated patients have been
least studied. Hence the present study needed to answer the following questions:
1. Does multimodality physiotherapy have any effect on the rate of recovery,
prevention of complications reducing the stay in ICU?
2. Should multimodality physiotherapy be incorporated in management of all
patients with mechanical ventilation along with manual hyperinflation and
suctioning in medical and intensive care?
Objectives of the Study

OBJECTIVES OF THE STUDY
1. To evaluate the effect of multimodality chest physiotherapy on the rate of

recovery in mechanical ventilated patients in MICUs and SICUs.
2. To assess the effect of multimodality chest physiotherapy in reducing
complications in mechanically ventilated patients in MICUs and SICUs.
3. To analyze the effect of multimodality chest physiotherapy in decreasing the
duration of stay in patients admitted to MICUs and SICUs.
Hypothesis
HYPOTHESIS
NULL HYPOTHESIS
The present study hypothesized that multimodality chest physiotherapy will not enhance
rate of recovery, prevent complications, and decrease the duration of hospital stay in
adult mechanically ventilated patients admitted in MICUs and SICUs.
ALTERNATE HYPOTHESIS
Alternate hypothesis stated that multimodality chest physiotherapy will enhance rate of
recovery, prevent complications, and decrease the duration of hospital stay in adult
mechanically ventilated patients admitted in MICUs and SICUs.
Review of Literature
REVIEW OF LITERATURE
HISTORICAL ASPECTS OF MECHANICAL VENTILATION
As far back in the 5th century B.C., Hippocrates widely regarded as the Father of
Modern medicine described a technique for the emergency intubation of persons to
prevent asphyxiation. In his work Treatise on Air, Hippocrates states One should
introduce a cannula into the trachea along the jaw bone so that air can be drawn into the
lungs. Hippocrates thus provided what is possibly the first description of endotracheal
intubation (ET).27 Ventilators have evolved from simple mechanical devices into highly
complex micro-processor controlled systems which make for smoother patient-ventilator
interaction.
Modern critical care may date its origin to the landmark article published by
Drinker and Mckhann describing iron lung for the treatment of the neuromuscular
weakness induced respiratory failure of poliomyelitis. Others might date the modern era
of critical care to the early 1960s, with the description of closed chest cardiac massage
and the use of a synchronized capacitor discharge for defibrillation in the treatment of
cardiac arrhythmias. Regardless of when the modern advent of critical care began, it has
been quite clear that the database of this new discipline has increased exponentially over
the two decades. Despite the best efforts put up by all health professionals in critical care
the mortality rate continues to be high especially from hospital acquired infections like
pneumonia along with length of hospital stay and hospital costs. 28
Although the concept of artificial respiration was recognized in the 16th century
by Vesalius, it was not until the 20th century that the mechanical ventilation became
widely used therapeutic modality. Over the past thirty years and especially over the past
decade, there has been an explosion of new ventilatory techniques that present a
bewildering array of alternatives for the treatment of patients with respiratory disorders.28
Mechanical ventilation entails the use of sophisticated life support technology
aimed at maintaining tissue oxygenation and removal of carbon dioxide. At its most basic
level, mechanical ventilation supports or replaces the normal ventilator pump in moving
air into and out of the lungs. In other words, the primary function of a mechanical
ventilator is to ventilate. It follows that the main indications for mechanical ventilation is
inadequate or absent spontaneous breathing.29
INDICATIONS FOR MECHANICAL VENTILATOR SUPPORT 29
The most common reason for initiation of mechanical ventilator support is
respiratory failure which is defined as a sudden decrease in the arterial blood oxygen
levels (PaO2 < 60 mm Hg, SaO2 < 90%) with or without carbon dioxide retention (PaCO2
> 45 mm Hg) may be further classified by primary disorder present. Acute respiratory
failure may be further classified as Hypoxaemic respiratory failure or Lung failure is
present when the primary problem is oxygenation of the arterial blood. Hypercapneic
respiratory failure or Ventilatory or Pump failure is when the primary defect is in the
ventilation.
Disease states/ conditions that predispose patients to the development of respiratory
failure are as follows: 29
1) Acute lung injury
2) ARDS
3) Pneumonia
4) Pulmonary edema
5) Pulmonary embolism
6) Heart failure
7) Shock
8) Sepsis
9) Trauma
10) Smokes or chemical inhalation
11) Aspiration and near drowning
Decreased Ventilatory drive may be caused by: 29
1) Excessive sedation
2) General anesthesia/ abdominal & cardio thoracic surgeries
3) Narcotic or sedative drug overdose
4) Head trauma
5) Stroke
Respiratory muscle fatigue & increased work of breathing are associated with: 29
1) Acute exacerbation of chronic obstructive pulmonary disease
2) Acute severe asthma
3) Obesity
4) Severe burns
5) Upper airway obstruction
6) Thoracic deformities
Neuromuscular diseases associated with respiratory failure include:29
1) Guillian Barre syndrome
2) Amyotrophic lateral sclerosis
3) Myaesthenia gravis
4) Poliomyetitis
5) Spinal cord injury
6) Botulism
7) Tetanus
Though the above conditions are indicative of the mechanical ventilatory support,
however the decision to begin mechanical ventilator support should be made with sound
clinical judgment and based on multiple factors including diagnosis, clinical status,
physiological values (ABGS) and expected progression of the patients disease or
condition.
Thus the primary indications for mechanical ventilation are simplified as BIG FOUR:
a) Apnea
b) Acute ventilatory failure
c) Impending ventilatory failure
d) Severe oxygenation problems
THE OBJECTIVES OF MECHANICAL VENTILATION MAY BE CLASSIFIED

AS FOLLOWS: 28
1) Physiological objectives and
2) Clinical objectives.
Physiological objectives include:

1) To support or otherwise manipulate pulmonary gas exchange
2) To increase lung volume
3) To reduce or otherwise manipulate the work of breathing
Clinical objectives include:

1) To reverse hypoxaemia
2) To reverse acute respiratory acidosis
3) To relieve respiratory distress
4) To prevent or reverse atelectasis
5) To reverse ventilatory muscle fatigue
6) To permit sedation and/ or neuro-muscular blockade
10
7) To decrease systemic or myocardial oxygen consumption
8) To reduce the intracranial pressure
9) To stabilize the chest wall
MODES OF VENTILATION
The act of breathing is a complex process. During mechanical ventilation, the
respiratory system is under the influence of two, the ventilator pump and the patients
own respiratory muscles. Depending on the mode of mechanical ventilatory support,
ventilation may be totally controlled by the ventilator or may be determined by the
interaction between patients respiratory effort and ventilatory function. In either case,
compared to the spontaneous breathing; the breathing pattern is altered and this may
influence:
1. Force length and force velocity relationships of the respiratory muscles
(mechanical feedback)
2. Chemical stimuli (chemical feedback)
3. The activity of various receptors located in the respiratory tract, lung and chest
wall (reflex feedback) &
4. Behavior response (behavior feedback)
Changes in these feedback systems may modify the function of the ventilator that
is dependent on the mode of mechanical ventilatory support ,ventilatory settings,
mechanics of the respiratory system and the sleep- awake stage.30
11
In controlled mandatory ventilation or control mode, the ventilator delivers the
preset tidal volume at a set time interval (time triggered respiratory time).In this mode,
the patient will not be able to change the ventilatory respiratory rate or breath
spontaneously. It should be used only when the patient is adequately sedated. it is usually
indicated in patients suffering from tetanus, seizures, head injuries or patients who
require s complete rest typically for 24 hours, Chest injury or flail chest. Patient is totally
blunted with spontaneous respiratory drive and is totally dependent on ventilator for
ventilation and oxygenation. The primary hazard in this mode is apnea and hypoxia
which may occur due to accidental disconnection or if ventilator fails to operate.31
SIMV is a mode in which ventilator delivers control (mandatory) breaths to the
patient at or near the time of a spontaneous breath to the patient at or near the time of a
spontaneous breath. The mandatory breaths are synchronized with the patients
spontaneous breathing efforts so as to avoid breath stacking. The primary indication for
SIMV is to provide partial ventilatory support as against CMV. 31
SIMV mode helps to maintain respiratory muscle strength, decrease ventilation to
perfusion mismatch; decreases mean airway pressure and also facilitate weaning.
However, the primary disadvantage of SIMV is the desire to wean the patients too rapidly
leading to first high work of spontaneous breathing and ultimately to muscle fatigue and
failure.32
Besides these modes, various ventilatory strategies like the use of smaller Vt,
careful use of PEEP, lung open strategies, volume and pressure limited ventilation,
turning the patient to prone position, use of alternate modes, adjunctive therapies have
12
been recommended in various studies to improve the outcome in ARDS,VAP and
minimize ventilator induced lung injury (VILI) 33- 36
In recent times, a lot of different modes of ventilation are available. Unlike the
other therapies used in the ICU, such as pharmacological therapies, the incorporation of a
new mode of ventilation does not require the demonstration (in a clinical trial) that it is
similar or better than previously established modes of ventilation as long as the ventilator
itself is not a completely new device. Synchronized intermittent mandatory ventilation
itself is not a completely new device. SIMV became available on ventilators in 1970 but
the first study assessing its efficacy was not until 1973 and similarly pressure support
(PS) appeared in 1980 and yet the first publications related to its use are from 1985.31
VOLUME CONTROLLED VERSUS PRESSURE CONTROLLED
VENTILATION
The arguments for using pressure controlled ventilation (PCV) over volume
controlled ventilation (VCV) are the potential decrease in the need for fro high
inspiratory pressures and improvement s in the gas exchange. Three studies37,
38, 39
in
critically ill patients have shown that ventilation with a decelerating inspiratory flow
pattern is associated with a significant reduction in the peak inspiratory pressure and in
the total inspiratory resistance. In addition, oxygenation was improved in these patients.
One of the theoretical advantages of pressure limited ventilation may be that flow
is adapted to both the patients demand as well as the mechanical properties of the lung.40
In a study of 18 patients with acute lung injury or acute respiratory syndrome (ARDS), it
was found that the higher inspiratory peak flow was obtained with PCV than with VCV
13
(103.2 L/min vs. 44 L/min) that produced a decrease in the work of breathing (WOB).41
This flow pattern has also been seen to improve gas distribution.42
Beneficial effects of PCV on oxygenation may arise because the decelerating flow
pattern could increase the alveolar recruitment.The results of the reported studies are
however contradictory.43,44,45 The disagreement between the studies regarding
oxygenation could be due to the fact that a main determinant of oxygenation and
haemodynamics is the mean airway pressure generated rather than the actual mode of
ventilation .46
CLINICAL OUTCOMES WITH VCV vs. PCV
One of the randomized clinical trials have reported no significant differences in
the mortality of 27 patients receiving care in medical ICU for acute , severe hypoxic
respiratory failure (PaO2/FiO2 <150) randomized to VCV(64%) or PVC (56%).38 To
estimate the effect of these modes of ventilation on mortality , the Spanish Lung Failure
Collaborative Group performed a randomized clinical trial clinical trial involving 79
patients who met criteria for ARDS, randomized into two groups: PCV (n=42) and VCV
(n=37). Mortality in the PCV group was 51% vs. mortality in VCV group of 78%.47
However research indicates that at the present time there is no strong evidence
suggesting that one mode of ventilation should be chosen over another. This applies not
only to patient centered outcomes such as mortality, but also to physiological variables
like gas exchange and the work of breathing.
14
WEANING FROM MECHANICAL VENTILATION
Weaning is the process of withdrawing mechanical ventilator support and
transferring the work of breathing from ventilator to the patient. This approach is
sometimes referred to as taking the patient off the ventilator as discontinuing the
ventilator. Weaning success is defined as effective spontaneous breathing without any
mechanical assistance for 24 hours or more.48
Not all patients can be weaned from mechanical ventilation successfully on first
attempt. Also the duration needed to wean the patient from mechanical ventilation may
also vary greatly. One of the studies reported that 15% of the ventilator patients required
more than 7 days to be weaned successfully.49 The success rate of weaning attempts is
partly dependent on the patient population. It is generally more difficult to predict
weaning outcome in medical in medical patients. Since medical patients often have coexisting problems, they usually take more time to complete to wean in process than
surgical patients. 49
Weaning failure is harder to define than weaning success because whenever the
patient s placed back on the ventilator, weaning attempt has failed in one form or the
other. Weaning process depends on the therapist, intensivist or the physicians skill and
experience and also the aggressiveness and the criteria of the weaning may differ from
one health professional to another though many weaning indices and approaches are
there. Weaning failure may be defined as weaning failure has occurred when the patient
is returned back to mechanical ventilation after any length of weaning trial.48
15
T tube weaning is a technique of weaning by alternating the patient between
spontaneous aerosol T- tube breathing (5min) and full ventilatory support of 30-60
minutes. 48
CPAP is the treatment of choice with obstructive sleep apnea and acute
ventilatory failure. CPAP provides positive airway pressure during the entire spontaneous
breath and it does not include any mechanical breaths. The work of breathing is entirely
assumed by the patient. CPAP should be used with care and also close monitoring of the
patient since it is not effective in apnea due to neuromuscular diseases, progressive
hypoventilation and fatigue in respiratory muscles.48
In the early 1990s, some of the independent weaning criteria were combined to
make up accumulative index of weaning. Among the indices developed, Rapid shallow
breathing index (RSBI) is one which is simple to use, calculate and highly predictable in
weaning success. RSBI or f/Vt ratio i.e. respiratory frequency to Vt ratio quantifies rapid
shallow spontaneous breathing. Absence of rapid shallow breathing as f/Vt ratio less than
100 cycles/ liter is very accurate predictor of weaning success.50 To measure the f/Vt
ratio, the patient is taken off the ventilator and allowed to breath spontaneously for 3
minutes or until a stable breathing pattern is established. The minute expired volume
(VE) and respiratory frequency (f) are measured.
16
COMPLICATIONS DUE TO MECHANICAL VENTILATION
Mechanical ventilation is not without risk and the complications and hazards can
be life threatening. Hence, the decisions to initiate mechanical ventilator support is a
serious one that requires sound clinical judgment and clear understanding of the
indications and associated clinical goals and objectives.27
Apart from its supportive role in patients while undergoing operative procedures,
mechanical ventilator support is indicated in critically ill patients whose spontaneous
ventilation is inadequate for sustenance of life. The word Support bears emphasis, for
mechanical ventilation is not a cure for the disease for which it is instituted; it is at best a
form of support, offering time and rest to the patient until the underlying disease
processes are resolved. 27
Results with mechanically ventilator support are initiated early and electively
rather than in a crash situation.27 Mechanical ventilation though potentially life saving,
i.e. capable of producing variety of complications, some of which may in themselves be
life threatening. Critically ill patients are often immuno - suppressed and are susceptible
to nosocomial pneumonia for a number of reasons. Endotracheal intubation may
predispose these patients to ventilator associated pneumonia (VAP), a form of
nosocomial pneumonia. A large number of complications are a direct result of generation
of positive pressure inside the thorax (e.g. barotrauma & hypotension).31
It is important to realize that complications with ventilated patients are relatively
common and meticulous monitoring is vital for their prevention. Prompt corrective action
may be life saving should ascertain of these complications (such as pneumothorax or
sudden blockage of the endotracheal tube) occur. Complications cannot occur only at the
17
time of initiating mechanical ventilator support but also at any time during the course of
ventilator support.
The complications may be classified as: 31
i) Peri-intubation complications which may be caused due to hurried or difficult
intubations in technically demanding sedation.
ii) Complications that occur acutely at any stage during mechanical ventilation &
iii) Delayed Complications.
PERI- INTUBATION COMPLICATIONS31
1) Laryngeal injury
2) Pharyngeal lacerations
3) Tracheal rupture
4) Pneumothorax
5) Mediastinal emphysema
6) Epistaxis
7) Dental Trauma
8) Cervical spine injury
9) Esophageal intubation
10) Right main stem intubation
11) Cardiac arrhythmias
12) Aspiration
13) Bronchospasm
18
ACUTE COMPLICATION THAT CAN OCCUR AT ANY TIME OF M. V. 31
1) Endotracheal/ Tracheostomy tube obstruction
2) Endotracheal tube migration
3) Self Extubation
4) Cuff leak
5) Barotrauma & volutrauma:
i.
Sub-pleural air cysts
ii.
Pneumothorax
iii.
Pneumo-mediastineum
iv.
Pneumo-peritoneum
v.
Subcutaneous emphysema.
DELAYED COMPLICATIONS DUE TO MECHANICAL VENTILATION31

1) Peri- oral pressure sores
2) Nasal Necrosis
3) Sinusitis
4) Serous or purulent otitis media
5) Pneumonia
6) Tracheomalacia
7) Tracheo-oesophageal fistula
8) Tracheo innominate artery fistula
9) Tracheo Cuntaneous fistula
10) Oxygen toxicity
19
VENTILATOR ASSOCIATED PNEUMONIA (VAP)
Ventilator associated pneumonia is a health care associated infection that
commonly causes morbidity and mortality in mechanically ventilated patients.51 VAP is
associated with an increased duration of mechanical ventilation with crude death rates
from 5% to 65% and increased health costs. 52-55
Ventilator associated pneumonia is a common complication in intensive care units
occurring in 9% to 24% of patients intubated for longer than 48 hours. Because of this
large disease burden and the resultant attributable morbidity and mortality there is great
interest in accurately diagnosing treating and preventing this complication. More severely
ill patients tend to develop VAP and identified risk factors include prolonged mechanical
ventilation, re-intubation after failed extubation and a few other clinical variables.56 VAP
is defined as parenchymal lung infection occurring lore than 48 hours after the initiation
of mechanical ventilation which servers to differentiate this disorder from community
acquired pneumonia and highlights pathogenic features peculiar to mechanically
ventilated patients.57
The pathogenesis of VAP usually requires two processes:1.
Bacterial colonization of aero-digestive tract and 2. the aspiration of contaminated

secretions into the lower airway. Hence, the strategies aimed at prevent VAP usually
focus on reducing the burden of bacterial
colonization in the aero-digestive tract
decreasing the incidence of aspiration or both.58

Development of late onset ventilator associated pneumonia is due to certain high
risk micro-organisms which has shown to be an independent risk factor for hospital
mortality among patients requiring prolonged ventilation.59 Studies also suggest that
20
nosocomial pneumonia in medical and surgical intensive care units at the most frequent
infection sites.(blood stream, urinary and respiratory tract) are almost always associated
with use of invasive devices. Also the infection rates are different in different ICU set
ups. But the other risk factors for infections in MICUs included previous surgery,
underlying disease, etc.60 Respiratory failure, coma on admission (GCS <9) depressed
consciousness enteral feeding and length of stay are also suggested as independent risk
factors for VAP is approximately 5 fold higher than non infected patients.60 Although
risk factors for nosocomial pneumonia in ICUs have been assessed in various studies,
results are frequently controversial mainly due to the methodological differences.61
Health Care associated infections are also clearly a huge threat and largely
unrecognized threat and largely unrecognized threat to patient safety in the developing
world like India as compared to the developed world which include device associated
infections, active infection control programs that perform surveillance of infection and
implement guidelines for prevention can improve patient safety and must become and
must priority in every country.62
Host related risk factors for VAP include pre-existing conditions such as immunosuppressions, chronic obstructive lung disease, acute respiratory distress syndrome,
patients body positioning, levels of consciousness, number of intubations, and
medications. Besides the device related risk factors like endotracheal tubes, ventilator
circuit, nasogastric or orogastric tube, there are number of personnel related risk factors
including improper hand washing, failure to change gloves between contacts with
patients, and not wearing personnel protective equipment when antibiotic resistant
bacteria have been identified.63, 64 In an attempt to find out the modifiable risk factors,
21
one of the studies concluded
that the epidemiological profile of VAP in terms of
incidence, length of stay and clinical course resembles the general pattern described
everywhere. However, surprisingly the authors could not identify any potential
modifiable risk factors for VAP and suggested comprehensive multicenter studies about
the specific micro-biological, genetic and clinical features of VAP.65
In a recent study in an Indian tertiary hospital, risk factors associated with VAP
were observed to be impaired consciousness, tracheostomy, re-intubation, emergency
intubation, and nasogastric tube. Emergency intubation, and intra-venous sedatives were
found to be specific risk factors for early onset VAP while tracheostomy and reintubation were the independent predictors of late onset VAP. Hence, knowledge of these
risk factors may be useful in implementing simple and preventive measure including non
invasive ventilation, precaution during emergency intubation minimizing the occurrence
or re-intubation, avoidance of tracheostomy, as far as possible and minimal sedation may
prove beneficial for more effective implementation as preventive strategies for VAP.66
VAP leads to excessive morbidity, mortality and costs in critically ill patients.
While many preventive strategies have proven successful in decreasing the incidence of
VAP by small amount, significant reduction requires a multimodal approach
encompassing positioning, equipment, nutritional support, infection control, sedation
minimization and ventilator weaning. Adjunctive therapies such as stress ulcer
prophylaxis, glycemic control, and blood transfusion also play a role because of their
support on the immune system.64 In one of the reviews from the clinical trials strategies
for prevention of VAP suggested education of practitioners about VAP prevention,
timing of antibiotic treatment, appropriate regimen, proper identification of patients
22
requiring therapy and counseling against the overuse of antibiotics may help in reduction
of burden of VAP.65 Preventing colonization by following protocol for hand washing,
using oral decontamination, stress ulcer prophylaxis, avoiding saline lavage, with
suctioning, turning the patients every 2 hours and changing ventilator circuits not more
than every 24 hours and preventing aspiration by positioning the head end of bed >30
degrees ,minimal use of narcotic and sedative agents, thorough suctioning of oropharynx,
using endotracheal tubes that have subglottic suction ports, monitoring gastric residual
volumes for over distension and maintaining endotracheal cuff pressures of at 20 cms
H2O are some of the important preventive strategies of VAP.67
Evidence based clinical guidelines for the prevention of VAP developed by
Canadian critical Care Society orotracheal route of intubation, change of ventilatory
circuits only for each new patient and if the circuits are soiled, use of closed endotracheal
suction systems that are changes for each patients and as clinically indicated, heat and
moisture exchangers in the absence of contraindications and its weekly changes and
semi-recumbent positioning in the absence of contraindications which when effectively
implemented may decrease the morbidity, mortality and cots of VAP in mechanically
ventilated patients .68
It is also suggested that maintaining the intra cuff pressure between 25-30cms of
H2O is mandatory to guarantee the effective drainage of secretions and safety. 69
Vigorous airway management and respiratory care strategies have been greatly
emphasized.61,57 but studies have also suggested that VAP is still common in ventilated
patients and increase in its incidence and have suggested that this is mainly due to non
23
adherence of evidence based guidelines for preventing VAP.70 Questionnaires and
pneumonics have been developed as preventive strategy as a part of educational programs
for the paramedics and other health professionals which may be adopted in all ICUs to
reduce the incidence and prevention of VAP.71, 72
Many studies have shown risk factors associated with VAP include presence of
chronic obstructive airway disease, airway intubation reduced conscious state, intracranial pressure monitoring, airway re-intubation, mechanical ventilation greater than 7
days, use of positive end expiratory pressure and supine patient positioning .73 , 74
Fact that airway intubation and mechanical ventilation reduce the normal
clearance of airway secretions, increasing risk of VAP.75 Chest physiotherapy including
gravity assisted drainage, chest wall percussion, chest wall vibrations and manual lung
hyperinflation (or bagging) are commonly used techniques. 75
Studies have shown than twice daily chest physiotherapy comprising gravity
assisted drainage, patient positioning in side lying or head down, chest wall vibrations
and airway suctioning via endo-tracheal tube was independently associated with a
reduction in the occurrence of VAP.76
CLINICAL PULMONARY INFECTION SCORE
The diagnosis of a pneumonia which occurs in critically ill patients undergoing
positive pressure ventilation (ventilator associated pneumonia or VAP) in often a
problem. This is mainly due to the lack of sensitivity and specificity of clinical and
radiographic signs of pneumonia in this patient population. Many studies have
investigated some clinical variables (fever, tracheal aspirates, blood leukocytosis and
24
radiographic criteria) but none of these individually considered resulted predicted enough
to be useful for the bedside diagnosis of VAP.77 The Clinical Pulmonary infection Score
(CPIS) was developed in 1991and was based on 6 variables (fever, leukocytosis, tracheal
aspirates ,oxygenation, radiographic infiltrates and semi-quantitative culture of tracheal
aspirates with gram stain) and was found to be more sensitive to diagnose VAP.78
Compared with other associations of clinical variables, this one allows for the signs not to
be present at the same time.78 In one of the studies79 it was reported that found that the
CPIS of more than 6 was associated with high likelihood of pneumonia with a sensitivity
of 93% and specificity of 100%. Another study80 suggested that though there are study
bias regarding the entry criteria, the diagnostic sensitivity of a radiographic infiltrate and
one clinical feature (fever, leukocytosis, or purulent tracheal secretions) is high for VAP
but specificity is found to be low and the author suggested that the only way to increase
the specificity of the clinical criteria is to require all the 4 criteria but may result in an
unacceptable low sensitivity(<50%).In an attempt to diagnose VAP by comparing
histologic, microbiologic and clinical criteria. Other investigators81 have reported that
none of the quantitative bacteriology specimens used were predictive of the histologic
presence of pneumonia nor did they correlate with specific clinical symptoms. The
Clinical Pulmonary infection Score (CPIS) original or modified has been proposed for
the clinical diagnosis and management of ventilator associated pneumonia.80 Studies have
also shown that incorporating the gram stain results of either directed or blind protected
sampling increased the diagnostic accuracy (sensitivity and specificity of 85% and 49%
and 78% and 56% respectively) of the clinical score and increases the likelihood ration
for pneumonia of a score of more than 6 from 1.46 to 1.67 and 1.77. The study also
25
suggested that CPIS had a low diagnostic accuracy, however incorporating gram stain
results into the score may help in the clinical decision making in patients with clinically
suspected pneumonia correlate with the absence of histologic pneumonia.82
Though many criteria may used to diagnose VAP, one study reported82 that
independently of the diagnostic value of the procedure and ICU population, the choice of
the best technique of diagnosis depends on many factors such as costs, the easiness of the
technical procedure ,adverse side effects and the swiftness of available results. However,
the direct examination of BAL (bronchoscopic aspirate lavage) and PSB (protected
specimen brush) appeared to be the best available, recovering 80%of the microorganisms for a 96% sensitivity and 84% specificity.
In spite several studies, the diagnosis of infection in the ICU patient is often
difficult as typical features such as fever, tachycardia, tachypnoea, raised WBC counts,
are non specific indicators of an inflammatory response. Also patchy alveolar infiltrates
on chest X-ray are typical of pneumonia but also occur in pulmonary edema, infarction or
atelectasis. Positive cultures from bacterial aspirates may be relevant but could represent
colonization without infection.83
But, CPIS score has been able to fulfill these criteria where pre-test probability
has been measured using all the variables. The score also established the likelihood that
he patient has VAP. Modification of CPIS has been used to treat low risk patients (CPIS
<6) with suspected VAP may be treated with 3 days of antibiotic and had better clinical
outcomes.83
26
SECRETION MANAGEMENT IN VENTILATED PATIENTS
Mechanically ventilated patients are at risk for retained secretions from a myriad
of causes leading to ventilator associated pneumonia. Endotracheal intubation disrupts
the muco-ciliary escalator and predisposes to infection. which increases the volume and
tenacity of mucus.84,85 Relative immobility of the mechanically ventilated patient
confined to bed can lead to atelectasis, impaired cough and retained secretions.86 Upper
abdominal surgeries and thoracic surgeries frequently lead to post operative atelectasis,
weak cough and secretion retention.87 Muscle weakness associated with prolonged ICU
stay may also contribute to secretion retention.88
Secretion management in the mechanically ventilated patients includes routine
methods for maintaining muco-ciliary function as well as techniques for secretion
removal. Humidification, mobilization of the patient, airway suctioning, aerosol /
inhalation therapy are all routine procedures for managing secretions in the ventilated
patients.89 Inhalation therapy/aerosol therapy was used in the present study too as a part
of routine bronchial hygiene care. Both pressurized metered inhalers and nebulizers were
given to deliver bronchodilator or mucolytic drug (as prescribed by the physician) via the
ventilatory circuit as per the feasibility of the patient to afford the drug. 89
Studies have demonstrated that with careful attention to administration technique,
drugs administered via metered dose inhaler or nebulizer are safe and effective in
mechanically ventilated patients.90, 91, 92 It has been established now that there is a firm
scientific base for inhalation therapy in ICU and improved inhalation devices and
27
surfactant formulations can be employed for several indications in mechanically
ventilated patients.93
Aerosol antibiotics have seen increased used in an effort to reduce systemic
effects, reduce VAP and direct high drug concentrations at the side of infection. Drug
resistant pneumonia has also been effectively treated with aerosolized antibiotics.93
CHEST PHYSIOTHERAPY MANAGEMENT IN VENTILATED PATIENTS
Chest physiotherapy is one of the most frequently performed interventions in the
intensive care units. There are many physiological reasons that a patient in ICU may
benefit from physiotherapy treatment. These include mucociliary dysfunction, altered
lung volumes when patients are mechanically ventilated, increased pulmonary shunt, the
effects of neuromuscular weakness on respiratory flows, increased risk of nosocomial
pneumonia. So far, chest physiotherapy has been recognized as an important aspect to
achieve successful weaning from ventilator.94
Indeed, lack of reduction of the cough
reflex in an intubated patient may be associated with retention of bronchial secretions and
the risk of pulmonary infection. Several physiotherapy techniques are used to facilitate an
adequate bronchial drainage in these patients, mainly depending on the patients
compliance and staff expertise.95, 96
Evidence also suggests that earlier physical therapy rehabilitation can begin, the
greater the potential to reverse the effects of immobility and prolonged bed rest.97 Studies
also suggest that the incidence of adverse effects during physiotherapy intervention are
low in ICUs demonstrating the physiotherapy intervention as safe.98
28
MANUAL HYPERINFLATION IN VENTILATED PATIENTS
Manual hyperinflation is one of the techniques which are employed by the
physiotherapists in the critical care telling the technique was first described in
physiotherapy 30 years ago and commonly involves slow deep inspiration, inspiratory
pause and fast obstructed expiration.99
The use of MH varies between and within
countries. It is commonly employed by the physiotherapists to assist in the removal of

secretions and re-expand areas of atelectasis. Despite the popularity of the technique,
research examining its efficacy is conflicting especially with the effect of MH on
cardiovascular parameters. 99
Manual hyperinflation was originally defined as inflating the lungs with oxygen
and manual compression to a tidal volume of 1.0L requiring a peak inspiratory pressure
between 20-30 cms of H2O.100 More recent definitions include providing a larger Vt
than the base Vt to the patient and using Vt which is 50%greate than that delivered by the
ventilator.1, 101
Indications for MH have been well established in various conditions including
mechanically ventilated patients with chronic obstructive pulmonary disease.102
There is evidence that MH performed in a stable patient with atelectasis
associated with mechanical ventilation can improve spontaneous Vt and chest radiograph
signs, however suggesting further investigations similar kind with larger sample size,
evaluation of effects of manual hyperinflation in different techniques of MH in different
patient groups and determine the long term outcomes of MH.103 When used in isolation,
MH in medically stable ventilated patients has shown significant improvements in lung
29
compliance, PaO2/FiO2 ratio, and alveolar arterial oxygen tension difference (Aa)PO2.104, 105
Hyperinflation may be delivered by the therapist (MHI) or by the ventilator (VHI)
depending upon the respiratory, cardio-vascular status of the patients. Both methods of
hyperinflation improve static pulmonary compliance, clear similar volume of pulmonary
secretions.106 However, some studies suggest VHI promotes greater improvements in
respiratory mechanics with less metabolic disturbance as compared to MHI. Sputum
production, haemodynamics and oxygenation are similarly affected by both
techniques.107
Though studies have demonstrated improvements with manual hyperinflation in
lung mechanics and in gas exchange in patients there was no impairments in cardiovascular status.108 However, lung model studies suggest that Laerdal resuscitation bag
may not be generate peak expiratory flow that would theoretically clear pulmonary
secretions when PEEP levels are of 10-15 cms of H2O and needs to be confirmed when
used in the critically ill patients.108
Head down tilt involving elevating the foot of the bed to 35-45 degrees from the
horizontal plane along with manual hyperinflation and endotracheal suctioning in patients
who were intubated and ventilated increased sputum production and improved peak
expiratory flow.109 Atelectasis and other pulmonary changes including pleural effusion
and pneumonia are common complications in post operated patients in CABGs. Effect of
manual hyperinflation associated with PEEP in patients with CABGs has shown to
30
promote increased lung volumes and static compliance and recommend use of MHI in
critical care setting with further confirmation of the results.110
Though manual (bag) ventilation is believed to achieve better oxygenation than
mechanical ventilation, clinicians believe the very high airway pressure generated during
manual hyperinflation may help in alveolar recruitment but this high pressure in some
patients may injure the alveoli in some patients causing barotrauma.111 It is also
suggested that lung hyperinflation is frequently not achieved by MHI in normovolemia
and stable circulatory status critically ill patients. Further, significant fall in the cardiac
output with increase in the tidal volume are noted and these changes may occur
independent of the status of lung compliance or the vaso-active drugs during support.104
Though the role of manual hyperinflation in airway clearance is unclear,
combined with suctioning techniques, it has shown to improve oxygenation status, static
lung compliance, decrease in the post pulmonary complications, shorter mechanical
ventilation duration and in various patients population.112 MH in conjunction with
suctioning has also shown to have improved respiratory mechanics in terms of decreasing
airway resistance and improving lung compliance in patients with VAP in intubated
patients.1
However, though MHI is widely employed as an airway clearance technique, the
mechanisms by which this treatment may enhance muco-ciliary clearance are
undoubtedly multifactorial.99
31
SUCTIONING IN VENTILATED PATIENTS
Intubated patients need regular endotracheal suctioning to remove pulmonary
secretions and maintain patent airway. There are basically 2 types of suctioning systems
i.e. open suctioning system and closed suctioning system. Though suctioning is generally
considered safe, but it is said to cause arterial hypoxemia, altered mean arterial pressure,
and cardiac arrhythmias and even cardiac arrest.113
Though closed suctioning systems are used more frequently these days because
adverse effects on the cardio-pulmonary function are thought to be less common evidence
is lacking.114 but closed suctioning systems have shown not to cause mechanical and
upon the removal of the suction catheter , the ventilator s have shown to reduce resume
their pre suctioning procedure gas delivery within two breaths but it has shown to
decrease end expiratory pressure during suctioning.115 Continuous sub glottis suctioning
via endotracheal tube has demonstrated to be safe and useful in prevention of VAP in
patients admitted to the ICU and also during the post operative period of a major heart
surgery.116, 117
Various policies and studies for endotracheal suctioning of patients receiving
mechanical ventilation have been developed with recommendations such as changing of
inline catheters every 48 hours118 and elimination of routine inline catheters changes
estimated as safe and also help in reduction of costs associated with providing
mechanical ventilation.119 Research findings indicate that there are variations in
suctioning techniques and airway management practice patterns. Consistent performance
of practice such as suctioning patients mouth, oral care practices, maintaining the
32
pressure in the cuff of the endotracheal tube at a set level which should be evaluated for
effectiveness in reduction of VAP.120
Since lung collapse is a contributing factor in the hypoxaemia that is observed
after open endotracheal suctioning, in patients with acute lung, studies suggest lung
recruitment maneuvers are effective in regaining lung volume and oxygenation after open
endotracheal suctions in ARDS.121 Also, if the respiratory and hemodynamic effects of
open suctioning versus closed suctioning during pressure control and volume control.
Volume control ventilation were compared in animal studies, it was observed that
PaO2/FiO2 (oxygenation index)was better maintained during closed suctioning with both
VC and PC modes during lung protective ventilation for ARDS compared to open
suctioning.122 However, there is insufficient evidence to support performing recruitment
maneuvers after suctioning in pediatric populations.123 Also the study has demonstrated
that suctioning does not increase dynamic compliance in ventilated pediatric patients
during the recruitment maneuver.123 However, the same authors in another study have
demonstrated that endotracheal suctioning caused immediate drop in the dynamic
compliance and expired tidal volume in ventilated children with different lung
pathologies with small endotracheal tubes, indicating loss of lung volume caused by
suctioning procedure with no evidence of reduction of airway resistance due to
suctioning.124
However, animal studies have suggested that endotracheal suction (both OSS and
CSS) causes lung collapse leading to impaired gas exchange which is more severe and
persistent in pressure control ventilation and volume control ventilation.125
Normal
saline instillation is defined as delivery of 2 to 10 cc of normal saline solution (09%) into

33
an artificial airway prior to suctioning for either tracheal toileting or as a component of
physiotherapy intervention. It can be included during both open and closed suction
methods. This technique is utilized by many health practitioners126 and is believed to
increase sputum yield by diluting and loosening secretions, stimulating cough and
lubricating the suction catheter.120
One of the published Evidence Based Guideline Practices suggested that 0.9%
NaCl should not be instilled prior to suctioning adult ventilated patients with artificial
airway.127 However, evidence suggests that normal saline may be indicated in situations
where it is necessary to elicit cough and normal saline may be useful for clearing
secretions after suctioning to avoid re-introduction of pathogens into the airway. Multisite
studies have recommended instillation of normal saline for thicker secretions.127, 128
CHEST VIBRATIONS IN VENTILATED PATIENTS
Chest vibration is a therapy widely used to assist the removal of secretions from
lungs of people with airway disease. It is defined as the manual application of fine
oscillatory movement combined with compression of patients, chest wall.129, 130 These
fine oscillations are given by the therapist hands which are directed inward against the
chest and is performed after deep inhalation. Studies have suggested that physiotherapists
should encourage a much slower inspiratory flow rate prior to vibration so that expiratory
flow rates generated by vibration would be greater than the inspiratory flow rates.131, 132
During vibration, the chest behaves as highly linear system. Changes in the intra-pleural
pressure occurring during vibration appear to be the sum of changes in the pressure due
34
to lung recoil and the compressive and oscillatory components of the technique
suggesting all the three components are needed to optimize expiratory flow.132
POSITIONING IN VENTILATED PATIENTS
Positioning also plays an important role in clearing secretions in ventilated
patients. Studies have suggested improvements in static compliance and sputum
clearance with MHI along with side lying positioning and suctioning without
compromise in the cardio-vascular stability or gas exchange.133
Pulmonary physical therapy has focused largely on improving ventilation.
Bronchial techniques have incorporated body positioning to affect gravity assisted
mucous clearance and to enhance air entry. Body positions directly affect ventilation
perfusion matching and arterial oxygen levels.133 Studies have suggested that in the
supine position ,44 years was critical age was the critical age when the closing capacity
exceeded FRC and significant impairment of ventilation distribution to the dependent
lung zones.134 This may be further deteriorated in mechanically ventilated patients.133 It
is also suggested that seated position is a therapeutic adjunct for improving gas exchange
compared with conventional supine position.135 Effects of changes in position on gas
exchanges in post thoracotomy subjects, have general limited magnitude and needs
further evaluation.135
Prone position has shown to improve oxygenation in ARDS.136-140 It has shown
to augment recruitment and prevent alveolar overinflation in acute lung injury and also in
hypoxaemia but does not seem to reduce mortality or duration of ventilation despite
improved oxygenation and a decreased risk of pneumonia.141
35
However, though
beneficial effects of prone positioning of prone positioning have been documented in
ventilation ARDS patients, evidence also suggests that prone position doesnt improve
the survival of the patients.142 Also the definite mechanism of the arterial oxygenation
improvement with prone positions remains to be clarified.143 Studies have shown that
there is no benefit of prone positioning on gas exchange in patients with idiopathic
pulmonary alveolar proteineosis who breathe spontaneously but requires further
invenstigations.144
Different therapeutic positioning using therapeutic beds have been used
extensively in ICUs. Therapies that can be delivered using therapeutic bed are many and
will continue to increase. The therapies include thermoregulation, pressure related wound
care support, patients positioning techniques including continuous rotation, prone lying,
semi-recumbent positioning turn assist options, physiotherapy techniques including
vibration and percussion and patient comfort improvement.145
The early use of continuous lateral rotation therapy in comatosed and immobile
patients decreases the incidence of lower respiratory tract infection including pneumonia
over the first 7 to 14 days of ICU care. While kinematic bed therapy has been purported
to reduce the incidence of nosocomial pneumonia in mechanically ventilated patients, the
overall body of evidence a sufficient to support this view.146 It is estimated that though
even after factors such as back rest elevation, supine positioning and use of paralytic
agents were accounted for pneumonia, it was more likely to develop in patients who were
turned less often.147 Evidence suggests that semi-recumbent positioning is one of the best
preventive strategies in all eligible patients on mechanical ventilation to reduce the
incidence of ventilator associated pneumonia, which may prevent prevention aspiration
36
of sub-glottic secretions.148 Another evidence suggests that semirecumbent position
should be used routinely, rotational therapy should be considered in selected patients and
prone position should not be used as a technique to reduce the risk of VAP.149 Backrest
elevation of about >30 degrees has shown to decrease the incidence of early onset VAP150
Since the mortality rate in onset VAP is higher investigation to whether backrest
elevation and decrease incidence of late onset VAP can decrease incidence of late onset
VAP is equally important. Nursing practices also suggests head of bed end elevation
should be at 30-45 degrees elevated in mechanically ventilated patients at high risk of
aspiration prevents ventilator associated pneumonia unless medically contraindicated.151
Semi recumbent positioning for giving positioning to mechanical ventilated
patient is defined as an angle between the torso and the floor/bed of 30 degrees or
greater.152 A Cochrane protocol suggested this position as a preventive measure for VAP
and stated that adoption of this theoretical feasible intervention was sporadic and cited
reasons like of knowledge, concerns about detrimental effects such as hemodynamic
instability, development of decubitus ulcers, safety concerns like increased falls out of
bed and lack patient comfort as reasons for lack of adherence.153
COMBINED CHEST PHYSIOTHERAPY IN VENTILATED PATIENTS
Airway intubation and mechanical ventilation reduce the normal clearance of
airway secretions increasing the risk of developing VAP.154 There is some evidence that
aggressive preventive measures may reduce the high rates of morbidity associated with
VAP in the critically ill.155 Chest physiotherapy including gravity assisted drainage, chest
wall percussions, chest wall vibrations and manual lung hyperinflation (bagging) are
37
commonly used intensive care procedures.156 There is supportive evidence that various
combinations of chest physiotherapy assist in ere-expansion of lungs.
short term improvements in total lung/thorax compliance
157,161
157-160
and confer
and expiratory flow
rates.162 However, till date there is no clear evidence that chest physiotherapy aimed at
enhancing secretion clearance and assists in prevention or treatment of VAP and rated of
recovery in mechanically ventilated patients.163
THERAPIST DRIVEN PROTOCOLS
Therapists driven protocols (TDPs) are consensus of medical knowledge and
opinion that is summarized into a care plan or algorithm with changes in therapy directed
by changes in objectively measurable patients variables.164 The daily plan of a TDP
consists of recording functional activities: initial evaluation will include assessment of
the patient and ventilator status and patient ventilator synchrony. This evaluation is
usually performed routinely every day and at each ventilator setting change.
Despite conflicting results exist regarding the application of a fixed protocol
based strategy to discontinue mechanical ventilation165-168 the use of TDPs has proven to
be effective when applied to the weaning process in the critical care area. In one of the
studies, the investigators prospectively studied 51 patients weaned by affixed protocol
and compared them with 50 retrospective controls. The implementation of the protocol
decreased the duration of mechanical ventilation and ICU stay by increasing the number
of safe directed extubations.167 Similar results were found in another study where the
investigators have observed that the daily screening of the respiratory function of
38
ventilated patients which was followed by trials of spontaneous breathing helped in the
reducing the length of ventilation, the cost of intensive cares and complications.165
However, whatever method of weaning is used, it is important to stress the point
that the technique employed in the weaning process is less important than the confidence
and familiarity with the protocol adopted, or the underlying pathologies.169, 170
39
Material & Methods

MATERIAL AND METHODS
Based on the results of the previous studies, assuming complications and
decreased rate of recovery proportion of 40% in the control group, to detect the 20%
absolute reduction (40 % to 20%) in complications and enhanced rate of recovery in the
study group, the sample size was derived 100 in each group with type I error () p= 0.05,
power of 80% and dropout rate of 20% .
STUDY DESIGN: Experimental design
TYPE OF STUDY: Prospective randomized clinical trial
BLINDING: Single blinded (All patients in the study were blinded to the
treatment )
STUDY PERIOD: March 2008 November 2010
SOURCE OF DATA: KLES Dr. Prabhakar Kore Hospital & Medical Research
Centre, Belgaum, Karnataka.
SETTING : Critical care setting (MICUs & SICUs)
STUDY POPULATION: All admitted and referred both
male and female
intubated and mechanically ventilated patients
SAMPLE SIZE : 200 (100-Study group, 100- Control group, )
SAMPLING DESIGN: Non probability sampling.
SAMPLING METHOD:
ALLOCATION: Concealed random allocation (envelope method)
Convenience sampling.
40
Material & Methods

INCLUSION CRITERIA
1. Both male and female patients who were mechanically ventilated from
adult MICUs and SICUs.
2. Referred by the concerned physician, surgeon or the intensivist.
3. 18 years and above.
EXCLUSION CRITERIA
1. Haemo-dynamic instability
2. CABG patients
3. Bed side dialysis
4. Untreated pneumothorax
5. Conditions where head of bed end elevation contraindicated.
6. Any clinical condition where chest physiotherapy was contraindicated.
41
Material & Methods

FLOW CHART OF THE METHODOLOGY
Ethical approval by UERC
Consent form & Baseline data
Random allocation by envelope method
STUDY GROUP
CONTROL GROUP
Multimodality chest physiotherapy
Suctioning & manual hyperinflation
Treated twice a day till their stay in ICU
Primary outcomes
Secondary outcomes
Analysis
Multimodality chest physiotherapy protocol

Suctioning + manual hyperinflation + suctioning + chest vibrations +suctioning + positioning
(Head of bed elevation 30-45 degrees)
42
Material & Methods

METHODOLOGY:
Ethical approval was obtained from the KLE Universitys Ethical Review
Committee (UERC) before the commencement of the study. The patients were recruited
into the study after the fulfilling the exclusion and the inclusion criteria. Written consent
was obtained from the patients relatives. The objectives, procedures of the physiotherapy
treatment, and benefits of the intervention were explained to the patients relatives. All
patients recruited to the study were ventilated by Servo Ventilator-900C or Servo
ventilator-300C ventilation systems. The operational self check system (designed to
ensure optimal function) of the ventilator was performed before use by each patient.
Baseline data including age, gender, admission diagnosis, ventilatory mode, type of
intubation(s), radiological features suggesting pneumonia , staging of atelectasis and
other conditions, and clinical parameters (CPIS score and GCS score) of all the patients
prior to the chest physiotherapy was noted.
After obtaining the baseline data, the patients were categorized either of two
groups i.e. the study group or control group by concealed envelope method.
Chest physiotherapy treatment in the study group was administered with
multimodality chest physiotherapy protocol of suctioning + chest vibrations +
suctioning+ manual hyperinflation +suctioning+ positioning (head of bed elevation 30-45
degrees).
Chest Physiotherapy treatment in the control group were given the standard form
of chest physiotherapy treatment which included manual hyperinflation (MH) and
suctioning.
43
Material & Methods

Standard care in the form of pharmacological therapy, inhalation (aerosol)
therapy, as advised by the concerned physician, surgeon or the intensivist and the routine
nursing care was given throughout the intervention period.
The changes in ventilatory parameters were adjusted by the intensivist according
to the clinical condition of the patient. The blood for ABG analysis was drawn by the
nursing staff after the physiotherapy intervention or as per the advice of the intensivist,
physician or surgeon respectively.
Oxygenation status (PaO2, PaCO2, PaO2/FiO2), ventilator parameters (mean
airway pressure, PEEP, peak airway pressure, static lung compliance, FiO2), were noted
daily. The respiratory system parameters (rapid shallow breathing index, respiratory rate
(RR) spontaneous VT score) were noted and used as one of the weaning criterion.
CPIS score was used to assess presence of ventilator associated pneumonia. GCS
score was used to assess conscious levels of all patients daily till the patients were
intubated.
All the patients in both the groups were treated twice a day (9.30 am and 3.30 pm)
till patients were weaned off from the ventilator. All the patients were followed up for the
global outcomes in terms of successful weaning, recovery and discharge from hospital,
death, total length of stay on ventilation, discharge against medical advice or any other
complications.
44
Material & Methods

OUTCOME MEASURES
1. Sex distribution( M/F)

2. Age(years)
3. Admission of patients to different ICUs (MICU,SICU,NSICU, ICCU)
4. Mode of intubation( Endotracheal, tracheostomy)
5. Initial ventilator mode (PSV, VCV)
6. RSBI (rapid shallow breathing index: ratio of tidal volume to respiratory rate
Vt/RR)
7. Duration of intubation(MV) in days
8. Duration of ICU stay in days
9. Duration of hospital stay in days
10. CPIS (clinical pulmonary infection score)
11. GCS (Glasgow coma score)
12. Oxygenation status parameters :
PaO2
PaCO2
PaO2/FiO2
13. Ventilator parameters:
Vt (tidal volume)
Mean airway pressure (MAWP)
Peak airway pressure (PAP)

45
Material & Methods
Positive end expiratory pressure (PEEP)
Dynamic lung compliance (CL Dyn ) :calculated by Vt/PAP-PEEP
Fraction of inspiratory oxygen (FiO2)
14. Radiological evidence of respiratory condition(s)

15. Vital signs parameters:
Pulse rate (PR)
Systolic blood pressure
Diastolic blood pressure
16. Global outcome
Successful outcome
Death
Discharge against medical advice (D/C AMA)
Chest physiotherapy discontinued
17. Weaning mode (CPAP , T-piece trial/ spontaneous breathing)

18. Weaning duration (in hours)
46
Material & Methods

CLINICAL PULMONARY INFECTION SCORE 78
Temperature(c)
>or equal to 36.5 & <or equal to 38.4=0 point
> or equal to 38.5 & <or equal to 38.9=0 point
> or equal to 39 & <or equal to 36=0 point
Blood leukocytes (mm3)

> or equal to 4000 & <or equal to 11,000 =0 point
< 4000 or > 11,000 = 1 point + band forms >equal to 50% = add 1 point
Tracheal secretions
Absence of tracheal secretions = 0 point
Presence of non-purulent tracheal secretions = 1 point
Presence of purulent tracheal secretions = 2 points
Oxygenation: PaO2 /FIO2, mmHg

>240 or ARDS (ARDS defined as PaO2 /FIO2, < or equal to 200, Pulmonary arterial
wedge pressure < or equal to 18 mm Hg and acute bilateral infiltrates) = 0 point
< or equal to 240 and no ARDS = 2 points
47
Material & Methods

Pulmonary radiography
No infiltrate = 0 point
Diffuse (or patchy) infiltrate = 1 point
Localized infiltrate = 2 points
Progression of pulmonary infiltrate

No radiographic progression = 0 point
Radiographic progression (after CHF and ARDS excluded) = 2 points
Culture of tracheal aspirate

Pathogenic bacteria cultured in rare or light quantity orgrowth = 0 point
Pathogenic bacteria cultured in moderate or heavy quantity = 1 point
Same pathogenic bacteria seen on Gram stain, add 1 Point.
ARDS = acute respiratory distress syndrome
CHF = congestive heart failure
PaO2 /FIO2 = ratio of arterial oxygen pressure to fraction of

inspired oxygen.
A score > 6 is considered suggestive of pneumonia.
48
Material & Methods
GLASGOW COMA SCORE171
Sl. No.
1
Activity
score
EYE OPENING
spontaneous
To speech
To pain
To response
BEST MOTOR RESPONSE

Follows motor commands
Localizes
Withdraws
Abnormal flexion
Extensor response
No response
VERBAL RESPONSE
Oriented
Confused conversion
Inappropriate words
Incompressible sounds
No response
Total score (out of 15)
49
Material & Methods
QUANTIFICATION OF ATELECTASIS ON CHEST RADIOGRAPHY172
SCORE
DESCRIPTION
no identifiable atelectasis
plate like or sub segmental
multiple plate- like or sub segmental
Segmental
multiple segmental
Lobar
multiple lobar
50
Material & Methods

PROCEDURE OF THE CHEST PHYSIOTHERAPY TECHNIQUES
1. SUCTIONING1
Endotracheal and tracheostomy suctioning was done as per the intubation of the
patient. Duration of suctioning was limited to 15 seconds. To standardize the suctioning
procedure and to enhance aspiration of dry secretions in some patients one ml of normal
saline via the tracheal tube before manual hyperinflation was done. The suctioning
session involved instillation of one ml of normal saline in the tracheal tube, followed by
suctioning once every minute for four minutes. The size of the suctioning catheters used
was FG14, and FG 16 (Romsons 53 cms in length).The catheter was inserted fully up to
the carina and then withdrawn for one cm prior to the application of negative pressure.
During suctioning, the specimen from the lower respiratory tract was collected in a sterile
container after instillation of one ml of normal saline for culture and sensitivity testing
which was also used for assessing VAP using CPIS score.
2.
MANUAL HYPERINFLATION (MH) 25:

To ensure that uniform and correct technique was employed, MH was employed
by the principal investigator to all the patients. A 2.0 L reusable manual resuscitator
(Hudson RCI-non disposable and autoclavable (silicone)) was used to deliver the MH
breaths. It was connected to a flow of 100% oxygen at 15L/min. Patients received MH to
a peak airway pressure of 20cms of H2O by the use of resuscitator. The resuscitator was
slowly compressed with both hands and an inspiratory breath was maintained for 3 to 5
seconds at end of pressing half of the resuscitator, and then completely pressing the
resuscitator. Expiration was passive and unobstructed to facilitate expiratory flow with no
positive end expiratory pressure applied. Sufficient time was allowed for the resuscitator
51
Material & Methods

to fill completely prior to next breath. The MH procedure was carried out at rate of 8 to
13 breaths /min for a period of 20 min at each session twice a day( 9.30 am and 3.30 pm)
daily till the resolution of atelectasis and pneumonia as per the radiological and clinical
findings.
3. CHEST VIBRATIONS130
Vibration is defined as the manual application of a fine oscillatory movement
combined with compression to the patients chest wall. It helps to loosen and mobilize
the secretions and is given prior to suctioning. The patient was positioned in supine and
then randomly positioned right and left side lying in the bed. Therapist placed her hands
anteriorly and laterally on the patients chest with fingers placed in the inter rib space.
The therapist then applied vibration in the expiratory phase of breathing. The technique
was repeated thrice in each of the three zones i.e. upper zone, mid zone and lower zone of
the chest.
4. POSITIONING133
All the above explained procedures were carried out in supine lying .i.e. lying flat.
At the end of the treatment session i.e. after suctioning, the head end was elevated to
about 30 -45 degrees (as measured by goniometer) and maintained for minimum of 30
minutes for improving ventilation in all patients. Change in positions from supine lying to
lateral positions by turning the patients was done by nursing staff every 2 hourly. The
manual hyperinflation and vibrations was given by the principal investigator to ensure the
uniformity in the technique and suctioning and positioning was assisted by the trained
intern or a trained nursing staff.
52
Material & Methods

During the chest physiotherapy, care was taken to secure the endotracheal tube to
prevent from the dislodgement.
All the patients were observed for occurrence of any adverse event during and
after thirty (30) minutes of chest physiotherapy treatment in both the groups.
53
Material & Methods

WEANING CRITERIA48
Ventilator criteria:
Spontaneous Vt > 58 mL/kg
Spontaneous RR (f) < 30/min
PaO2 > 50 mmHg with normal pH
Oxygenation criteria:
PaO2 with PEEP >100 mmHg at FiO2 up to 0.4.
SaO2 > 90% , FiO2 up to 0.4
PaO2/FiO2 > 200 mmHg
PaO2 > 60 mmHg.
RSBI < 80
54
Material & Methods

FLOW CHART OF WEANING PROCESS
ICU admission with intubation
Mechanical ventilator with A/CMV or SIMV + PSV
With recovery
Change mode to PSV with CPAP and

decrease to PSV 5 cms H2O +CPAP 5 cms H2O
Re-intubation
weaning failure
T-piece for 60 min
Weaning success
Weaning success but

Extubation failure
Extubation
Weaning
and extubation success
55
Results
RESULTS
A total of 220 intubated and mechanically ventilated patients were referred for
chest physiotherapy by the treating physician and/or surgeon during the two years and
eight month study (from March 2008 to November 2010) out of who twenty (20) were
excluded as ineligible. Major reasons for exclusion were age not above 18 years, patients
with haemodynamic instability, patients with haemo-dialysis, and conditions where head
of bed end elevation was contraindicated. Other reasons for exclusion were CABG
patients and patients in whom chest physiotherapy was contraindicated. Overall, 200
patients fulfilled all the inclusion criteria and were randomly allocated to either of the two
groups with 100 patients in each group.
Thirteen patients (13) from the study group and fourteen (14) patients from the
control group withdrew during the study period due to various reasons (D/C AMA,
shifting to other ICUs at other places, not interested in continuing to participate in the
study or could not afford the ICU treatment costs).
Finally, data consisting of all the primary and the secondary variables of eighty
seven (87) patients in the study group and eighty six (86) patients in control group were
successfully subjected to statistical analysis.
56
Results
TRIAL PROFILE: CONSORT FLOWCHART
220 MV adult patients referred for chest physiotherapy in ICU
Exclusioncriteria:
10Didnotcomplete18
yearsofage
200MVadultpatientsscreenedandeligibleforenrollment
04Haemodynamically
unstable
03Advisedheadlow
position
RANDOM ALLOCATION
Studygroup(n=100)
03Bedsidedialysis
Controlgroup(n=100)
13 Dropouts
14dropouts
N= 87 patients with Multimodality

chest physiotherapy
N= 86 patients treated with Suctioning &

manual hyperinflation
Assessed for primary outcomes & secondary outcomes
Statistical analysis
57
Results
STATISTICAL ANALYSIS
Statistical analysis of the data was done using SPSS windows version 13.0.
1. Student paired t test was used to compare the results within the groups.
2. Student unpaired t test was used to compare the results between the groups.
3. Wilcoxon Test was used depending on the nature of the data.
4. Comparison of the results obtained in both the groups was done using Student
unpaired t test or Mann Whitney U test depending on the normal distribution of
the data.
5.
Chi Square Test was used in finding the independence (association) of the
qualitative variables.
6. Logistic regression was used to analyze risk factors for mortality and ventilator
associated pneumonia
58
Results
Table 1.1: Age and sex distribution of patients
S
No
Variables
1.
Sex Distribution
2.
Study
Group
N=87)
Control
Group
N=86
Statistical
test used
D F
p
value
Males
64 (73.6%)
67 (77.9%)
X2 test
0.505
Females
23(26.4%)
19(22.1%)
Age
49.416.13
49.716.21
Student t
test
171
0.949
The above table shows that sex and age distribution were well matched in both the
groups with 64 and 67 male patients in the study and control group respectively. A total
of 23 and 19 female patients participated in the study and control group respectively.
59
Results
Figure 1.1 Age and sex distribution of patients
60
Results
Table 1.2: ICU profiles in both the groups
S
No
Variables
Study
Group
N=87)
Control
Group
N=86
Statistical
test used
DF
p
value
Admission to ICU
1.
NSICU
13(14.9%)
24(27.9%)
2.
MICU
48 (55.2%)
43 (50%)
} X2
test=9.528
3.
SICU
9 (10.3%)
13 (15.1%)
4.
ICCU
17 (19.5%)
06(7%)
03
0.023
Table 1.2 shows admission of patients to different ICUs among both the groups
showed statistical significance of p= 0.02 with highest number of patients in the MICU in
both the groups(48-study group,43-control group) followed by 24 patients in NSICU in
control group compared to 13 patients in study group. 9 patients were admitted to SICU
in study group compared to 13 patients in the control group followed by 17 patients
admitted to ICCU in study group compared to 6 patients in control group.
61
Results
Figure 1.2 ICU profile of patients
62
Results
Table 1.3: Underlying predisposing conditions of patients

S. No.
Condition
Study group
Control
group
Total
1.
Respiratory diseases
17
16
33 (19.07%)
2.
Neurological diseases
28
38
66 (38.15%)
3.
Musculoskeletal/ trauma
00
04
04 (2.31%)
4.
Cardiac diseases
16
06
22 (12.71%)
5.
Other medical conditions
17
15
32 (18.49%)
6.
Surgical conditions
09
07
16 (9.24%)
Total
87
86
173
According to table 1.3, it was observed that the patients distribution according to
the conditions in both the groups was not equally distributed. Highest number of patients
in the study suffered from neurological diseases (38.15%), followed by respiratory
diseases (19.07%), other medical conditions (18.49%), cardiac diseases (12.71%),
surgical
conditions
(9.24%)
and
musculoskeletal
respectively.
63
conditions/trauma
(2.31%),
Results
Figure 1.3: Underlying predisposing conditions of patients
Figure 1.4: Percentage wise distribution of various conditions in both the groups
64
Results
Table 1.4: Mode of intubation and initial ventilator mode at baseline
S
NO
Mode of
intubation
Study
Group
N=87)
Control
Group
N=86
1.
Endotracheal
85(97.7%)
84(97.7%)
2.
Tracheostomy
2(2.3%)
2(2.3%)
Statistical
test used
DF
p
value
X2 test =0
X2 test
=10.909
0.001
Initial ventilatory
mode
1.
Volume Control
38(43.7%)
49(56.3%)
2.
SIMV+ PS
59(68.6%)
27(31.4%)
65
Results
Table 1.4 shows most of patients in the study were intubated with endotracheal
tubes in both groups with 85 in study group and 84 in control group. Tracheostomy was
another form of intubation which was found in 2 patients in both of the groups
respectively with no statistical significance (p=1).Initial ventilator mode showed
statistical significance (p=0.001) with 38 patients in study group and 49 patients in
control group with Volume Control and 59 patients in study group and 27 patients in
control group with SIMV and PS.
66
Results
Figure1.5: Mode of intubation and initial ventilator mode at baseline
67
Results
Table 1.5: Components of RSBI in both the groups
S
No.
Variables
Study
Group
(n=58)
Control
Group
(n=24)
Statistical
test used
DF
p
value
1.
RR/Vt
75.64.49
76.43.22
t test=.784
80
0.099
2.
RR
32.91.30
33.21.64
t test=.982
80
0.329
3.
Spontaneou
s Vt score
0.43.02
0.43.02
t test= .845
80
0.921
The above table shows rapid shallow breathing index (RSBI) which was one of
the weaning criteria showed no statistical significance among both the groups.
(p > 0.05)
68
Results
Figure 1.6: Components of RSBI in both the groups
69
Results
Table 1.6: Baseline CPIS and GCS scores in both the groups
S No
Variables
Study
Group
(N=87)
Control
Group
N=86
Statistical
test used
DF
p
value
CPIS
3.81.16
3.6.65
Mann Whitney U
test, z=1.666
171
0.09
GCS
6.81.70
4.761.76
Mann Whitney U
test, z = 6.765
171
0.000
The above table shows that among the CPIS and GCS scores prior to chest
physiotherapy, GCS values showed statistical significance (p=0.000) with higher values
of 6.81.70 in study group compared to 4.761.76 in the control group respectively.
70
Results
Figure 1.7: Baseline CPIS and GCS scores in both the groups
71
Results
Table 1.7: Duration of intubation, ICU stay, hospital stay and ventilation weaning in
both the groups
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
1.
Duration of
intubation
(days)
7.63.97
6.84.46
t test= 1.274
171
0.201
2.
Duration in
ICU(days)
11.49.75
9.35.92
t test=1.699
171
0.091
3.
Hospital stay
(days)
169.40
12.86.12
t test= 2.685
171
0.008
N=58
N=24
1.980.73
2.10.78
t test=0.632
80
0.529
4.
Duration of
weaning
Table 1.7 shows that duration of hospital stay was higher with 169.4 in study
group compared to 12.86.12 in control group which demonstrated statistical significance
(p=0.008). However, successful weaning was noted in 58 patients in study group and 24
patients in control group. The duration of weaning (in hours) in both the groups was not
statistically significant. (p=0.52)
72
Results
Figure 1.8: Duration of intubation, ICU stay, hospital stay and ventilation weaning
in both the groups
73
Results
Table 1.8: Baseline oxygenation parameters before chest physiotherapy in both the
groups
S No
Variables
Study
Control
Group
Group
Statistical
DF
test used
p
value
(N=86)
(N=87)
Oxygenation
Status
Parameters
1.
PaO2
60.66.95
68.77.86
t test=7.22
171
0.000
2.
PaCO2
51.63.41
50.83.66
t test=1.388
171
0.167
3.
PaO2/FiO2
94.825.44
99.628.88
t test=1.149
171
0.252
Among the oxygenation status parameters as shown in the above table 1.8, only
values of PaO2 showed statistical significance (p=0.000) with higher baseline values in
control group with 68.77.86 compared to 60.66.95 study group. Other parameters i.e
PaCO2 and ratio of PaO2 to FiO2 did not demonstrate any statistical significance.
74
Results
Figure 1.9: Baseline oxygenation parameter values before chest physiotherapy in

both the groups
75
Results
Table 1.9: Baseline ventilatory parameters before chest physiotherapy in both the
groups
S
No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
Ventilatory
parameters
1.
Vt
3.529.44
320.187.44
t test=31.887
171
0.000
2.
PAP
33.95.65
25.33.79
t test=11.760
171
0.000
3.
PEEP
9.43.91
9.7 2.68
t test=0.714
171
0.476
4.
Vt/ PAP
PEEP
13.94.76
21.77.78
t test=8.001
171
.000
5.
MAWP
21.652.907
21.6522.104
t test=0.005
171
0.99
6.
FiO2
0.67.15
0.72.14
t test=2.272
171
0.024
Among the ventilator parameters prior to giving chest physiotherapy as shown in

table 1.9, Vt (p=0.000), PAP (p=0.000), dynamic compliance (p=0.000) and FiO2
(p=0.02) showed statistical significance compared to both the groups .PEEP and MAWP
values did not demonstrate any statistical significance in both the groups.
76
Results
Figure 1.10: Baseline ventilatory parameter values before chest physiotherapy in

both the groups
77
Results
Table 1.10: Baseline vital signs' parameters before chest physiotherapy in both the
groups
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
Vital signs
1.
PR
10813.74
120.911.87
t test=6.372
171
0.000
2.
SBP
117.918.04
107.39.90
t test=4.720
171
0.000
3.
DBP
6010.58
64.96.27
t test=3.720
171
0.000
From the above table 1.10 it was noted that all the values of vital signs prior to
chest physiotherapy demonstrated statistical significance compared to both the groups.
Values of PR were higher in the control group ( 120.911.87) compared to study group
(10813.74) which was statistically significant (p=0.000).SBP demonstrated higher
values in the study group(117 18.04) as compared to the control group (107 9.90)
which was statistically significant.(p=0.000). DBP values were more in the control group
(p=64.96.27) as compared to study group (p=6010.58) which was statistically
significant (p=0.000)
78
Results
Figure 1.11: Baseline vital signs' parameters before chest physiotherapy in both the
groups
79
Results
Table 1.11: Global outcome in both the groups
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
X2 = 22.577
0.000
X2 =22.198
0.000
Global outcome
1.
Successful outcome
58(66.7%)
28 (32.6%)
2.
Death
24(27.6%)
39(45.3%)
3.
AMA
5(5.7%)
17(19.8%)
4.
Discontinued
02(2.3%)
Table 1.11 shows successful weaning and outcome of patients were noted in more
patients in study group (58) compared to the control group (28) which was statistically
significant.(p=0.000). Patients who took discharge against medical advice were few in the
study group (05) compared to the control group (17) which was statistically
significant.(p=0.000). Only 2 patients in the control group discontinued the treatment.
80
Results
Figure 1.12: Global outcome in both the groups
81
Results
Table 1.12: Distribution of patients according to radiological evidence of diseases in

both the groups
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
46(53.5%)
Statistical
test used
D
of F
p
value
X2= 5.906
0.05
Radiological
parameters
1.
No evidence of
any disease
55(63.2%)
2.
Pneumonia
32(36.8%)
3.
Atelectasis
2(2.3%)
4.
Pneumonia &
Atelectasis
5 (5.8%)
5.
Others
33(38.4%)
Among the radiological evidence of diseases in both the groups as shown in the
above table 1.12, 55 patients in the study group and 46 patients in the control group
showed no evidence of any diseases on radiography which was statistically significant
(p=0.05).Pneumonia was evident in 32 patients in study group and 33 patients in control
group. Atelectasis and pneumonia with atelectasis was found in 2 and 5 patients
respectively in control group which was statistically significant. (p= 0.05). Two patients
had grade 3 atelectasis which was resolved within two days.
82
Results
Figure 1.13: Distribution of patients according to radiological evidence of diseases

in both the groups
83
Results
Table 2.1: Mean values of oxygenation parameters after Chest physiotherapy in

both the groups
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
Oxygenation
Status
Parameters
1.
PaO2
80.95.66
78.95.91
t =2.225
171
0.027
2.
PaCO2
44.83.35
47.13.86
t = 4.282
171
0.000
3.
PaO2/FiO2
204.170.41
152.162.98
t = 5.105
171
0.000
It was observed from the above table 2.1 that oxygenation status parameter values
after chest physiotherapy in both the groups were statistically significant with PaO2
values more in the study group (80.95.66) compared to control group (78.95.91).
PaCO2 values were more in the control group (47.13.86) compared to the study
group(44.83.35) which were highly significant(p=0.000). PaO2/FiO2 improved in the
study group with 20470.41 compared to 152.170.41 in the control group which was
statistically significant.
84
Results
Figure 2.1: Mean values of oxygenation parameters after Chest physiotherapy in

both the groups
85
Results
Table 2.2: Mean values of ventilator parameters after chest physiotherapy in both
the groups
S
No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
D F
p
value
Ventilatory
parameters
1.
Vt
320.944.71
322.583.49
t =0.161
171
0.872
2.
PAP
33.64.16
25.83.79
t =12.744
171
0.000
3.
PEEP
9.62.08
9.12.39
t =1.589
171
0.112
4.
Vt/ PAP PEEP
13.93.60
20.66.69
t = 7.462
171
0.000
5.
FiO2
0.42.17
0.59.17
t = 6.202
171
0.000
6.
MAWP
21.952.74
21.622.218
t =0.870
171
0.385
Table 2.2 shows that among the ventilator parameters, mean PAP value in the
study group was higher in the study group (33.64.16) post chest physiotherapy
compared to value in the control group (25.83.79) which was statistically significant
(p=0.000).dynamic compliance demonstrated higher values in the control group with
20.66.69 compared to 13.93.60 in the study group with statistically significance
(p=0.000). Requirement of FiO2 decreased post chest physiotherapy in the study group
(0.42) compared to the value in the control group (0.59) which was statistically
86
Results
significant.(p=0.000). However, Vt, PEEP and MAWP showed no significant changes
among both the groups post chest physiotherapy.
Figure 2.2: Mean values of ventilatory parameters after chest physiotherapy

in both the groups
87
Results
S No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
Vital signs
1.
PR
110.312.21
120.711.65
t = 5.721
171
0.000
2.
SBP
116.520.41
107.69.51
t =3.665
171
0.000
3.
DBP
60.517.84
64.110.73
t =2.554
171
0.012
Table 2.3: Mean values of vital signs after chest physiotherapy in both the groups
From the above table 2.3, it was observed that vital signs showed significant
changes post chest physiotherapy in PR, SBP and DBP (p=0.000,p=0.000 and p=0.01
respectively) with no adverse events.
88
Results
Table 2.3: Mean values of vital signs parameters after chest physiotherapy in both
the groups
89
Results
Table 2.4: Mean values of CPIS and GCS scores after chest physiotherapy
in both the groups
S
No
Variables
Study
Group
(N=87)
Control
Group
(N=86)
Statistical
test used
DF
p
value
1.
CPIS
4.21.32
4.40.98
z = 1.936
171
0.000
2.
GCS
7.31.97
5.31.81
z = 6.146
171
0.053
Table 2.4 shows that CPIS scores decreased in the study group (4.21.32)
compared to the control group (4.40.98) which was highly significant (p=0.000).GCS
scores also demonstrated marginal significance (p=0.053) with 7.31.97 in the study
group compared to 5.31.81in the control group.
90
Results
Figure 2.4: Mean values of CPIS and GCS scores after chest physiotherapy
in both the groups
91
Results
Table 3.1: Complications rates in both the groups
S No
1.
2.
Variables
No complications
With complications
Study
Group
(n=87)
Control
Group
(n=86)
64 (73.6%)
33(38.4%)
23 (26.4%)
Statistical
test used
DF
p
value
2 =21.74
0.000
53 (61.6%)
Table 3.1 shows that thirty three(33) patients in control group demonstrated no
complications as compared to sixty four (64) patients in study groups which was
statistically significant(p=0.000). twenty three patients (23) demonstrated complications
in the study group compared to fifty three (53) patients in the control group which was
statistically significant.(p=0.000).
92
Results
Figure 3.1 Complications rates in both the groups
93
Results
Table 3.2: Incidence of VAP among both the groups
S
No
Variables
Study
Group
(n=87)
Control
Group
(n=86)
1.
No VAP
55(63.2%)
48(55.8%)
2.
VAP< 5 days
23 (26.4%)
29 (33.7%)
3.
VAP>5 days
9(10.3%)
09(10.5%)
Statistical
test used
DF
p
value
X2= 1.162
0.559
Table 3.2 shows ventilator associated pneumonia was observed in thirty two
patients in study group compared to thirty eight in the control group. Among the 32
patients in the study group,23 patients had VAP< 5 days and 9 patients had VAP> 5 days
compared to 29 patients in the control group with VAP<5 days and 09 patients with
VAP> 5 days with no statistical significance.
94
Results
Figure 3.2: Incidence of VAP among both the groups
95
Results
Table 3.3: Complications other than VAP in both the groups
S No
Variables
Study
Group
(n=87)
Control
Group
(n=86)
Statistical
test used
DF
----
12 (14%)
X2=9.108
1.
Septicemia
2.
UTI
3.
Hypokalemia
-----
6 (7%)
4.
Hyperkalemia
------
---------
5.
Hyponatremia
02(2.3%)
01(1.2%)
6.
Hypernatremia
-------
01(1.2%)
Renal failure
01(1.1%)
07(8.1%)
8.
Seizures
02(2.3%)
05(5.8%)
9.
Paralytic Ileus
- -----
03(3.57%)
10.
Cardiac arrest
03(3.4%)
------
15(17.2%)
p
value
0.011
18 (20.9%)
It was observed from table 3.3 that presence of septicemia (control group- 12) and
UTI (control group-18 and study group -15) were the other complications among others
which demonstrated statistical significance of p=0.01. Other complications like
hypokalemia, hyponatremia, hypernatremia, renal failure, seizures, paralytic ileus, and
cardiac arrest were observed but demonstrated no statistical significance. None of the
patients from both the groups demonstrated hyperkalemia as a complication.
96
Results
Figure 3.3: Complications other than VAP in both the groups
97
Results
Table 4.1: Mean differences between oxygenation status parameters before

and after chest physiotherapy among both the groups
PaO2
PaCO2
PaO2/FiO2
Study group
20.38.01
-6.8 5.13
109.269.42
Control group
10.28.93
-3.74.06
52.570.30
7.837
4.403
5.331
DF
171
171
171
0.000
0.000
0.000
p value
It was observed from the above table that there were mean differences between
the values of oxygenation status parameters before and after chest physiotherapy between
both the groups that showed improvement which was statistically significant (p<0.05) in
all the three parameters i.e. PaO2, PaCO2, PaO2 /FiO2 respectively.
98
Results
Figure 4.1: Mean differences between oxygenation status values before and
99
Results
Table 4.2 : Mean differences between ventilatory parameters before and after chest
Physiotherapy among both the groups
Vt
PAP
PEEP
Vt/PAPPEEP
FiO2
317.456.74
-0.33.70
0.22.82
0.063.72
-0.20 .20
2.511.61
0.52.61
0.61.88
-1.74.44
-0.1 0.23
50.442
1.847
2.495
2.817
3.456
DF
171
171
171
171
171
0.000
0.066
0.014
0.005
0.001
Study group
Control group
p value
From the table 4.2 it was observed that among the ventilatory parameters, except
for PAP, all parameters showed improvements before and after chest physiotherapy in Vt,
PEEP, dynamic compliance and FiO2 which was statistically significant.(p=0.000,
p=0.01,p= 0.005, p=0.001)
100
Results
Figure 4.2: Mean differences between ventilatory parameters before and after chest
101
Results
Table 4.3: Mean Differences between vital signs parameters before and after chest
PR
Systolic BP
Diastolic BP
Study group
1.810.47
-0.1.410.84
0.46.49
Control group
-0.32.92
0.33.56
-0.810.24
1.760
1.411
0.985
DF
171
171
171
p value
0.80
0.160
0.326
Table 4.3 shows that there were significant changes in vital signs post chest
physiotherapy in PR, SBP and DBP (p=0.000,p=0.000 and p=0.01 respectively).
102
Results
Figure 4.3 Differences between vital signs parameters before and after chest
103
Results
Table 4.4: Mean differences between CPIS and GCS before and after chest
physiotherapy among both the groups
GCS
CPIS
Baseline
values
Mean
values
Baseline values
Mean values
Z= 6.705
Z=6.146
Z= 1.666
Z= 1.936
0.000
0.000
0.09
0.05
Study group
Control group
p value
From table 4.4, it was observed that CPIS scores decreased in the study group
(4.21.32) compared to the control group (4.40.98) which was highly significant
(p=0.000). GCS scores also demonstrated marginal significance (p=0.053) with 7.31.97
in the study group compared to 5.31.81in the control group.
104
Results
Figure 4.4: Mean differences between CPIS and GCS scores before and after chest
105
Results
Table 5: Risk factors for ventilator associated pneumonia in both the groups
Unadjusted OR
S No Risk Factors
OR
95% CI
Adjusted OR
OR
95% CI
value
p
value
1.
Age > 40 years
4.09
1.02-16.38
0.047
3.99
1.03-15.55
0.046
2.
Vt
.97
.95-.99
0.007
.97
.95-.99
0.008
3.
PAP
1.35
1.03-1.77
0.028
1.33
1.02-1.73
0.034
4.
PEEP> 10 cms
H2O
6.24
1.23-31.55
0.027
6.24
1.25-31.07
0.025
1.65
1.17-2.32
0.004
1.59
1.16-2.18
0.004
.009
.002-.049
0.000
.01
.002-.049
0.000
5.
6.
Vt /PAP-PEEP
CPIS
From table 5, it was observed that age >40 years (OR-3.99,95% CI-1.0315.55,p=0.04),Vt
1.73,p=0.03),
(OR-.97,95%
PEEP>10cms
CI-.95-.99,p=0.008),
H2O
PAP(OR-1.33,95%CI-
1.02-
(OR-1.59, 95%CI-1.25-31.07,p=0.002),dynamic
compliance (OR- 1.59, 95% CI-1.16-2.18, p= 0.004) and CPIS score OR- .01,95% CI.002-.049, p= 0.000) were demonstrated as independent risk factors for ventilator
associated pneumonia.
106
Results
Table 6: Risk factors for Mortality in both the groups
S No Risk Factors
Unadjusted OR
Adjusted OR
(univariate analysis)
(multivariate analysis)
OR
95% CI
OR
95% CI
value
p
value
1.
Age > 40 years
.37
.15-.92
0.032
.39
.16-.94
0.035
2.
PEEP > 10 cms

HO
3.10
1.09-8.83
0.034
4.29
1.88-9.79
0.001
3.
FiO
.02
.002-.29
0.004
.04
.004-.42
0.007
4.
GCS
1.58
1.24-2.03
0.000
1.47
1.18-1.83
0.001
5.
CPIS
.80
.56-1.16
0.242
Table 6 shows that independent risk factors for mortality included age >40 years
(OR-.39, 95%CI-.16-.94, p=0.03), PEEP >10cms of H2O (OR-4.29, 95%CI- 1.889.79,p=0.001),FiO2 (OR-.04, 95%CI-.004-.42, p=0.007) and GCS scores (OR-1.47, 95%
CI- 1.18-1.83, p=0.001). However, CPIS score did not demonstrate risk factor for
mortality.(p = 0.24)
107
Results
Table 7.1: Patients outcome with relation to PEEP in both the groups
S.No
Variables
PEEP
PEEP
Statistical
>10cms of H2O
< 10cms of
H2O
test used
Successful outcome
19 (23.5%)
67(72.85%)
2.
Death
47 (585%)
16(17.4%)
X2 =
43.019
3.
AMA
15(18.5%)
07(7.65)
4.
Discontinuation of
MV & treatment
2(2.2%)
5.
Total
81
92
DF
p
value
0.000
It was observed from Table7.1 that more successful outcome was observed in
patients who were ventilated with PEEP <10 cms H20 with 67 patients as compared to 19
patients who were ventilated with PEEP > 10cms of H2O which was statistically
significant (p=0.000). Death was noted in 47 patients who were ventilated with PEEP
>10 cms H2O as compared to 16 patients with PEEP <10 cms H20 which showed
statistical significance (p= 0.000)
108
Results
Figure 5.1: Patients outcome in relation to PEEP in both the groups
109
Results
Table 7.2: Patients outcome with relation to age in both the groups
S.No
Variables
> 40 years
< 40 years
Successful outcome
62(51.7%)
24 (45.3%)
2.
Death
39(32.5%)
24 (45.3%)
3.
Discharge against
medical advice
18(15%)
4(7.5%)
4.
Discontinuation of the
Mechanical ventilation
and treatment
1(0.8%)
1(1.95)
5.
Total
120
53
Statistical
test used
Df
p
value
X2 =
3.036
0.219
Table 7.2 shows that patients age > 40 years or age < 40 years was not related to
overall outcome among patients in both the groups and did not demonstrate statistical
significance.
110
Results
Figure 5.2: Patients' outcome with relation to age in both the groups
111
Results
Table 7.3: Patients outcome according to nature of ICUs in both the groups
NSICU
Successful
outcome
Death
09
19
(24.3%)
MICU
SICU
Total
Dis
(51.4%) (18.9%)
32
10
(53.8%)
(35.2%)
(11%)
09
10
03
Total Test used
continued
07
49
(40.9%)
ICCU
D/C
AMA
02
DF p
value
37
(5.4%)
00
91
00
22
00
23
02
173
X2=22.017
0.001
(54.5%) (13.6%)
19
02
02
(82.6%)
(8.7%)
(8.7%)
86
63
22
Table 7.3 shows that according to patients admission to various intensive care
units, a total of 86 patients had successful outcome with 82.6% of patients successfully
weaned off in ICCU followed by 53.8% in MICU, 40.9% in SICU and 24.3% in NSICU
which was statistically significant (p=0.001). Total number of deaths noted at the end of
the study was 63 with 54.5% in SICU followed by 51.4% in NSICU, 35.2% in MICU and
8% in ICCU which demonstrated statistical significance. A total of 22 patients opted
discharge against medical advice among which 18.9% of the patients belonged to
NSICU, followed by 13.6% of SICU, 11% from MICU and 8.7% from ICCU which
showed statistical significance(p=0.001). Only 2 patients discontinued the chest
physiotherapy treatment from NSICU.
112
Results
Figure 6.1: Patients' outcome with relation to nature of ICUs in both the groups
113
Results
Table 7.4: Overall outcome of patients in both the groups
Type of
Successful
Failure
Total
ICU
outcome
NSICU
09
28
37
MICU
49
42
91
SICU
09
13
22
ICCU
19
04
23
Total
86
87
173
Statistical
DF
Test used
X2=20.800
p
value
0.0001
It was observed from the above table 7.4, highest number of patients were
admitted in MICU with 91(SO- 49,F-42), followed by 37 patients in NSICU (SO-09,F28), 23 patients in ICCU (SO-19,F-04) followed by 22 patients in SICU(SO-9,F- 13) .
114
Results
Figure 6.2: Overall outcome of patients in both the groups
115
Discussion
DISCUSSION
A total of 220 intubated and mechanically ventilated patients who were referred
for chest physiotherapy by the treating physician and/or surgeon were included in the
study over a period of 2years and 8 months (March 2008 to November 2010). Twenty
(20) were excluded from the final analysis due to various reasons. Major reasons for
exclusion were age not above 18 years, patients with haemodynamic instability, patients
with haemo-dialysis, and conditions where head of bed end elevation was
contraindicated. Other reasons for exclusion were CABG patients and patients in whom
chest physiotherapy was contraindicated. Overall, 200 patients fulfilled all the inclusion
criteria and were randomly allocated to either of the two groups with 100 patients in each
group. The critically ill patients who were intubated and mechanically ventilated in the
study group were treated with multimodality chest physiotherapy (suctioning +MH
+chest vibrations +positioning) and patients in the control group were treated with
standard form of chest physiotherapy in the form of manual hyperinflation and suctioning
twice daily till the patients were extubated. Thirteen patients (13) from the study group
and fourteen (14) patients from the control group withdrew during the study period.
Finally, raw data consisting of all the primary and the secondary variables of eighty seven
(87) patients in the study group and eighty six (86) patients in control group were
successfully subjected to statistical analysis.
In the present study age and sex distribution were well matched in both the
groups. The mean age of patients in both the groups ranged between 49.4 16.13 years
in the study group and 49.716.21 years in the control group which were lower compared
to the other studies. conducted by Estabaan et al173, 174 in their two international studies
116
Discussion
observed that the age of the patients receiving mechanical ventilation was similar with
medians (inter quartile range) of 61years (44-71) and in the second study it was 63years
(48-73).In both the above studies, 25% of the patients were more than 75 years of age.
The distribution of gender in both studies with male : female ratio to be 2:1, a finding
similar to observations made in populations with sepsis ,ARDS and myocardial
infarction.
The present study has demonstrated better recovery rates in 58 (66.7%) patients
from mechanical ventilation with multimodality chest physiotherapy in the study group
as compared to 28 (32.6 %) patients in the control group. Death rates were low with 24
(27.6 %) patients in the study group than 39 (45.3%) patients in the control group,
suggesting that multimodality chest physiotherapy has shown better results in terms of
recovery in the study group. In one of the first studies that examined the initial results and
outcomes following the introduction of mechanical ventilation Rogers et al175 reported on
212 patients who were ventilated during their first 5 years in their ICU. These patients
had extremely high mortality rate of 63%. Jimenez and co- investigators176 evaluated the
outcome of 118 patients, 76 being ventilated for more than 72 h. thirty three (28%) of
these patients died. In the population studied by the authors in the above mentioned study
, the best predictors of outcome the number of associated complications and the degree of
severity of the disease as assessed by simplified acute physiology score (SAPS), the
degree of hypoxaemia, and the age of the patients. A logistic regression analysis revealed
that the exclusion of oxygenation index and the age did not reduce the prognostic
assessment indicting that degree of global impairment was a major determinant of
outcome. However, the authors in the above study did not mention whether the patients
117
Discussion
received routine chest physiotherapy or MM chest PT. It should be emphasized that the
study by Jimenez et al176 included a mixture of underlying diseases, thus the prognosis
and the mortality for each of the patients may be different. Mortality rates in the present
study especially in the control group with 39(45.3%) patients are similar to the mortality
rates of around 50 % as observed in different studies conducted by Gillepsie et al177,
Elpern et al178 and Spicher et al179 respectively.
In a retrospective cohort study by Papdikis and co-workers180 to find out the
predictors of in-hospital mortality and 1 year mortality of 612 mechanically ventilated
patients from 6 medical intensive care units, observed that 975 of patients ventilated were
men with mean age 6311 years and the hospital mortality was 64 %. The authors
concluded that the patients age, APACHE II score, serum albumin levels or the use of
cardio-pulmonary resuscitation may identify a subset of mechanical ventilated veterans
for whom mechanical ventilation provides little or no benefit.
In the present study, mean age of patients in both groups was well matched with
no difference. Also the sex distribution in both the groups was well matched. However,
age >40 years for both for both the sexes was identified as one of the risk factors for
mortality in mechanically ventilated patients. Meinders et al181 studied the outcome of
prolonged (>3 days) mechanical ventilation in 181 patients aged over 70 years and the
risk factors associated with in hospital mortality. They observed that the overall in
hospital mortality was 57.5% and the previous medical history did not influence the final
outcome predictor, but co-existing chronic diseases ,the functional status and the severity
of the acute illness may play
an important role in predicting the mortality in
mechanically ventilated patients. Though the present study has concluded that age >40
118
Discussion
years as one of the risk factors for mortality, the other factors related to ventilatory
parameters like PEEP >10cms H2O ,increased FiO2 values and low GCS scores also
demonstrated to be the risk factors for in hospital mortality in ventilated patients
receiving either conventional or multimodality chest physiotherapy.
Factors like the types of respiratory failure (type I), use of ionotropes, APACHE
II scores at admission have demonstrated as independent predictors of mortality in
patients on mechanical ventilation. In a cohort study by Friedrich et al182 the long term
outcomes and clinical predictors of hospital mortality were studied in a very long stay (at
least 30 days) in intensive care units patients. They observed that patients with very long
stays in ICU appear to have a reasonable chance of survival. In the present study, the
duration of ICU stay (days) and hospital stay (days) was comparable to the control group.
However, this may explain the long term survival in the study group. It was observed in
the above study, that mean age of 63 years, prolonged requirement of life support
therapies like mechanical ventilation,
182
vasoactive agents or acute dialysis and pre-
existing co-morbid conditions were predictors of patients mortality. Though risk factors
like vasoactive agents, immunosuppressant therapy were not included in the study, they
may play a role in the clinical decision making for ICU patients.
Gajic et al183 conducted a study in 17 academic centers to study the prediction of
death and prolonged mechanical ventilation in acute lung injury patients and developed
an ALI-specific prediction model. They concluded that a model based on age and cardiopulmonary function three days after the intubation is able to predict death and /or
prolonged mechanical ventilation with acute lung injury.
119
Discussion
In a primarily surgical critically ill patients population, acute or chronic multiple
organ dysfunction syndrome or unexpected cardiac arrest may also be cause of death in
the intensive care units. Mayr et al184 concluded that malignant tumor disease and
exacerbations of chronic cardio-vascular disease were the most frequent causes of death
in the hospital in a study conducted in 3700 adult patients admitted to ICU irrespective of
whether they were ventilated or non ventilated.
The present study population included mixed population including all types of
patients admitted to different ICUs with maximum number of patients being admitted to
medical intensive care units(MICU) followed by neuro-surgical intensive care units..The
neurological cases included patients with traumatic head injury, spinal cord injuries
(SCI), neurological conditions like stroke, Guillian Barre Syndrome, etc. The care of
patients high level SCI is made more complex by the need for mechanical ventilation.
Although most of the patients are ventilated with tracheostomy tube, Bach and colleagues
in many of their studies185-188 found that patients with neuromuscular disorders can be
successfully decanulated and treated with non invasive ventilation. Patients with
neurological disorders prefer more of non invasive ventilation than the invasive one for
the reasons of appearance, comfort, swallowing and speech with other advantages like
reduction in secretions because of tracheostomy tube is not present to irritate the trachea,
fewer hospitalizations and lower cost of care.
189, 190
Hence it is suggested that more
attention should be paid in the option of non invasive ventilation.

Mechanically ventilated patients typically prefer larger tidal volume (Vt). The
reason is not established but it may be related to relieve dyspnoea that is associated with
small tidal breaths. Large breaths also have the benefit of preventing small airway
120
Discussion
narrowing or closure by stretching airway smooth muscle and by reducing surface tension
by expanding the surface area of pulmonary surfactant. Breath sizes as large as 1.0L often
with PEEP levels of 5 cms of H2O are common and do not cause ventilator associated
lung damage in the absence of acute lung injury from other causes.191
However, in the present study PEEP>10 cms of H2O was one of the risk factors
for mortality in both the groups and PEEP>10 cms of H2O may be one of factors for
ventilator associated lung damage leading to mortality resulting in low PaO2. Also FiO2
> 0.4 (40%) in both groups was a risk factor for mortality which may also be cause for
ventilator associated pneumonia. Brown and co- authors observed that diabetes mellitus,
heart disease, cigarette smoking, and percentage of predictive FEV1 to be the independent
predictors of all cause mortality. They also suggested airway clearance techniques
including chest physiotherapy which may help in reducing the mortality.192
In the present study, initial ventilation modes used were Controlled mandatory
ventilation (volume control), and intermittent mandatory ventilation (synchronized
intermittent mandatory ventilation SIMV +Pressure support). Fifty nine (59) patients
were initiated with SIMV+PS higher than the number compared in the control group (27)
which also showed statistical significance. Recently few studies have been done that
allows insight into the way in which ventilator modes are used in daily practice outside
the realm of the clinical trials. Unfortunately, the number of trials comparing the use of
different ventilator modes and examining important patient related outcomes such as
mortality or rate of recovery from mechanical ventilation is even fewer. Venus and coworkers193 published the results of a survey conducted by mail in United States which
concluded that in the respiratory care departments that responded, 72 % indicated that
121
Discussion
SIMV was their mode of first choice. The results of this study were similar in the present
study with 59(68.6%) patients in the study group initiated with SIMV + PS. However,
contradictory to these reports, Estaban et al194 stated that it was better to examine the
actual patient data rather than self reported practices and concluded that assist control
mode (also known as volume control mode) was most commonly used mode of
ventilation. Assist control mode was used in 55% and 47 % of the patients in a Spanish
study conducted by Estaban et al194 in another similar study in international point
prevalence study respectively. The results of the present study where 49 (56.3%) of the
patients in the control group were initiated with volume control mode of ventilation, were
similar to the other studies and the possible explanations to these variations may be
attributed to regional practice variations, severity of different diseases in different
countries.
In an international study conducted by Estabaan et al
174
where 5,183 patients
were studied, the median duration of mechanical ventilation was 3 days (inter quartile
range 2-7) and only a small percentage (3%) were ventilated for longer than 3 weeks.
When the different pathologies that necessitated the initiation for mechanical ventilation
were analysed. It was observed that significant differences were present in the duration of
mechanical ventilation. Though the present study did not consider the reason for
mechanical ventilation since the patients were referred, however, the results of mean
duration of mechanical ventilation in the present study were almost similar to the results
of the above mentioned study. The mean duration of mechanical ventilation in the study
group was 7.63.97 days and 6.84.46 days in the control group. There have been
various studies that have compared the duration of mechanical ventilation for different
122
Discussion
indications. One study conducted by Troche and Moine195 to find if duration of
mechanical ventilation could be predictable concluded that patients with acute lung injury
had a duration of ventilation of 15 days compared to a mean of only 2 days in patients
with post operative respiratory failure. Stauffer et al196 conducted a study to assess the
survival rates in men following mechanical ventilation and observed that patients with
pneumonia had longer durations of ventilation than those patients who were without
pneumonia (11 vs 3.7 days)
The mortality rates among different studies of mechanically ventilated patients
vary according to the composition of the groups in the observation studies. However,
these rates may not be similar in control groups of the clinical trials. However, it is
important to note that though they may satisfy number of inclusion and exclusion criteria
in order to be included in the trial they may not represent a typical ICU population. In one
of the studies by Papadakis et al180 where outcome in 612 patients were studied, the
mortality was 64%. Another Spanish international study conducted by Estabaan et al194
290 patients reportedly died in the ICU representing 34% of all mechanically ventilated
patients. Doughlas et al197 conducted a study in small population of 57 patients who were
undergoing prolonged ventilation and observed 44% mortality. In the present clinical
trial, mortality rate was 45.3% (39) in the control group which was certainly higher than
27.6% (24) in the study group. Decrease in the mortality rate in the study group may be
attributed to the fact that the group received MM chest PT in additional to the routine
care.
Among the complications that were encountered by the patients in the present
trial, VAP emerged as the major complication in both the groups with 32 (37.7%)
123
Discussion
patients in the study group and 38 (44.2%) patients in the control group respectively.
However, 55 (63.2%) patients in study group and 48 (55.8%) patients in the control
group did not have VAP. Needless to say that probably multimodality may have helped
in prevention of VAP and may have also played a role in decreasing mortality in the
study group.
VAP is defined as parenchymal lung infection occurring more than 48 h after
initiation of mechanical ventilation and the immediate administration of treatment is
crucial in VAP and inappropriate treatment is associated with an increased risk of death
due to pneumonia.57 In addition to antimicrobial treatment, several risk factor for VAP
can be minimized by simple and inexpensive preventive strategies. Studies have
suggested that chest physiotherapy is one such preventive strategy where chest
physiotherapists routinely treat most of the ICU patients with various physiotherapy
techniques such as MH, suctioning, patients positioning ,chest vibrations chest
percussions
various coughing techniques in combination or individually to prevent
pulmonary complications like VAP and atelectasis in the ICUs. Mackenzie et al157 and
MacLean et al163
have conducted different studies to find the effect of chest
physiotherapy on various parameters like arterial oxygenation, hemodynamic ventilatory

effects and changes in total lung/ thorax compliance and have observed improvements in
these parameters post chest physiotherapy. However, Ntoumenopuolos et al76 stated that
though many studies have investigated the short term effects of chest physiotherapy on
pulmonary functions of intubated ICU patients receiving mechanical ventilation , there
have been very few studies to study the effects of multimodality chest physiotherapy in
prevention of VAP and decrease in the mortality rates in ICU patients. There is only one
124
Discussion
study to find out the effect of multimodality chest physiotherapy in reduction of VAP
which was conducted by Ntoumenopuolos et al.76 They administered MM chest PT
(gravity assisted drainage or positioning, chest vibrations and suctioning) was
administered in 60 patients receiving mechanical ventilation and concluded that chest
physiotherapy was independently associated with a reduction of VAP similar to the
finding of the present study. The authors also concluded that there has been a lack of
systematic review or meta- analysis for chest physiotherapy for pneumonia and no study
has been published yet. The use of chest physical therapy for patients with variety of
pulmonary problems is well entrenched in medical care. The evidence in support of these
techniques is inconsistent and variable and the literature on this account seems to bound
with confusion and conflicts. The clinical effectiveness of chest physiotherapy for
pneumonia is controversial and according to Kirilloff et al198, chest physiotherapy does
not seem to play a role in resolution of pneumonia.
Intubation and mechanical ventilation may impair muco-ciliary clearance leading
to sputum retention, airway occlusion, atelectasis and VAP. Patients in the ICU have a
tendency to retain secretions particularly while receiving long term ventilation and,
further
they are at risk of contracting pneumonia.154 Pryor
95
has highlighted the
importance of chest physiotherapy as part of intensive care teams care to optimally

manage the clearance of the trachea-bronchial airway. Choi et al25 have demonstrated that
manual hyperinflation in conjunction with suctioning has shown to have beneficial
changes in respiratory mechanics in patients receiving mechanical ventilation with VAP
although they did not study the effects of MH plus suctioning on the prevention of VAP.
125
Discussion
Weisse et al118 in a study obseved that effective suctioning is an essential aspect
of airway management and has an important role to play in the prevention of VAP
especially early onset VAP. In the present study the suctioning to both groups was given
by open suctioning system (OSS). Seymour et al113 have effectively studied the
physiological impact of closed sytem endotracheal suctioning (CSS) in spontaneously
breathing patients receiving mechanical ventilation and they observed significant and
sustained alterations in cardiac variables, respiratory pattern an lung volumes after using
CSS method. However the clinical importance of such findings remains unknown.
Endotracheal suctioning may also have side effects or complications which may lead to
partial lung collapse which may further lead to desaturation. Almgren et al125 investigated
the effects of endotracheal suctioning in volume controlled ventilation(VCV) and
pressure controlled ventilation(PSV) with OSS or CSS and they observed that PCV
caused more lung collapse leading to impaired gas exchange which was more severe and
persistent than VCV. In the present study 38(43.7%) patients were initiated with VCV in
the study group versus 49 (56.3%) patients in the control group. SIMV+PS was initiated
in 59 (68.6%) patients in the study group versus 27 (31.4%) patients in the control group.
Mortality rate was lower in the study group as compared to the control group. However,
correlation between the modes of ventilation and mortality was not studied since it was
not the objective of the study but may be suggested as future scope of research.
Vibrations are a manual technique which is being used widely by the
physiotherapists for removal of pulmonary secretions129 Kim et al199 has explained the
theoretical effects of vibrations on secretion clearance. The expiratory flow rates
generated during vibrations do not adequately augment secretion clearance by annular
126
Discussion
flow. In vitro studies conducted by Kim et al199 suggested that annular flow can assist
removal of secretions when there is an expiratory bias to airflow which results in a mass
movement of secretions by annular flow towards the mouth if critical volume and
thickness of secretions are present. Effectiveness of vibrations have also been evaluated
in two different studies conducted by Stiller et al
atelectasis. Besides VAP that emerged as a
159, 160
major
in prevention of acute lobar
complication, atelectasis was
observed as a radiological finding in 2 (2.3%) patients in the control group and 05 (5.8%)
patients in the study group with pneumonia and atelectasis which demonstrated marginal
statistical significance.(p=0.05). These results may explain the fact that MM chest PT
may have prevented the occurrence of atelectasis in the study group since the treatment
protocol included chest vibrations besides OSS method, patient positioning and manual
hyperinflation. Eales et al
200
studied 37 patients receiving mechanical ventilation after
cardiac surgery and found that arterial blood gas analyses (ABG) n=values and lung
compliance did not significantly change during the treatment course with MH and suction
with or without the chest vibrations. Hence the authors have suggested more future trials
in similar studies so that effect of vibrations in prevention of VAP may be established.
Another simplest means and the least expensive measures in preventing VAP is
maintaining the patients head end of the bed in an elevated position. Eales et al200
suggested that increasing the angle of the head of the bed is effective because it decreases
the risk of aspiration of both gastric contents and secretions from the upper aerodigestive tract. It is also observed that these secretions are often colonized with potential
pathogenic bacteria and generally colonization precedes infection. Hess150 has proposed
various procedures such as use of rotational beds, and semi-recumbent positions as
127
Discussion
procedures to prevent VAP. The use of semi- recent positioning has been addressed in the
evidence based guidelines put up by Grap et al.151
In the absence of medical
contraindications, elevation of the head end of the bed of patients at angle of 30-45
degrees may help in decreasing the VAP. In the present study, head end of bed elevation
was maintained from 30-45 degrees as tolerated by the patients in the study group.
The clinical pulmonary infection score (CPIS) original or modified has been
proposed for the clinical diagnosis and management of VAP by Pugin.78 Any values > 6
was considered as diagnosis of VAP. In the present study, baseline CPIS scores prior to
chest physiotherapy was lower in the in study group (3.81.16) compared to higher
values in the control group (3.66.5). Post chest physiotherapy, the mean values of CPIS
showed a decrease in the control group(4.40.98) compared to the study group (4.21.32)
which was statistically significant (p=0.000). These results suggests that administration
of chest physiotherapy ib both the groups has been able to prevent VAP. Though CPIS
scores were not a risk factor for mortality in mechanically ventilated patients in both the
groups, however, CPIS > 6 has demonstrated as an independent risk factor for VAP.
Kollef et al57 reported in one of his studies that development of late onset VAP
was due to certain high risk microorganisms which showed to an independent risk factor
for hospital mortality among patients requiring prolonged ventilation. Richards et al63 in
one of their studies suggested that nosocomial pneumonia in medical and surgical
intensive care units at the most frequent infection sites (blood stream, urinary and
respiratory tract) were always associated with use of invasive devices. In a case control
study conducted by Erbay et al201 in a Turkish university hospital, reported respiratory
failure, coma on admission (GCS < 9), depressed consciousness, enteral feeding and
128
Discussion
length of stay were independent risk factors for VAP and was found 5 fold to be higher
than non infected patients. Rosenthal et al202 suggested that results regarding risk factors
for VAP were controversial and this was mainly due to the methodological differences.
In the present study, age >40 years, ventilator parameters like mean value of Vt of
9.5 ml/kg ,peak airway pressure, PEEP >10cms H2O ,CLdyn and CPIS scores > 6 have
been noted as risk factors for VAP in mechanically ventilated patients receiving chest
physiotherapy. Augustine67 observed that mechanical ventilation, H2 receptor blocker
usage, prophylactic anti-microbial therapy, depressed consciousness, massive gastric
aspiration, length of stay in ICU, duration of mechanical ventilation, trauma, severity of
illness, and underlying disease, male gender, transfer from another hospital ward, reintubation after weaning, supine body position, enteral nutrition and Glasgow coma score
<9 to be the independent risk factors for developing nosocomial pneumonia in ICU
patients.
Jaimes et al62 in an observational study reported that health care associated
infections were clearly a huge threat and largely an unrecognized threat to patient safety
in the developing world like India as compared to the developed world which included
device associated infections. They suggested that active infection control programs that
perform surveillance of infection and implement guidelines for prevention could help in
the improvement of patient safety and emphasized that such programs should become a
priority in every country. Joseph et al reported risk factors for the development of VAP
such as impaired consciousness, tracheostomy, re-intubation, emergency intubation, and
nasogastric tube. Emergency intubation, and intra-venous sedatives were found to be
129
Discussion
specific risk factors for early onset VAP while tracheostomy and re-intubation were the
independent predictors of late onset VAP.66
Various host related risk factors for VAP has also been reported This includes
pre-existing patients conditions such as immunosuppressions, chronic obstructive lung
disease, acute respiratory distress syndrome, patients body positioning, levels of
consciousness, number of intubations, and use of medications. The author also
highlighted device related risk factors like endotracheal tubes, ventilator circuit,
nasogastric or orogastric tube. It has been suggested personnel related risk factors which
included improper hand washing, failure to change gloves between contacts with patients,
and not wearing personnel protective equipment when antibiotic resistant bacteria have
been identified to be responsible for development of VAP. Jaimes et al
62
observed that
the epidemiological profile of VAP in terms of incidence, length of stay and clinical
course resembled the general pattern described everywhere.
There are hardly any studies to suggest risk factors associated related with
ventilatory parameters for VAP. In the present study, factors like Vt, Peak airway
pressures, PEEP >10 cms H2O,CLdyn, have been studied and may be attributed as a new
and an important finding of risk factors for VAP. However, more number of clinical trials
of similar type is needed to confirm such findings. In the present study one of the
component of multimodality chest physiotherapy was maintaining head end elevation
between 30- 45 degrees to improve oxygenation and prevention of aspiration may have
proved beneficial and improving the patients over all outcome in the study group.
130
Discussion
It is also suggested that greatest benefit is derived by patients requiring fewer than
10 days of mechanical ventilation and not exposed to antibiotic therapy. 65 However, in
the present study, though the mean duration of intubation was similar in both groups. The
incidence of VAP and other complications were more in control group that may be
attributed to the conventional from of chest physiotherapy which included only manual
hyperinflation and endotracheal suctioning. Though ventilatory parameters were found as
a risk factor for VAP in the present study, Diaz et al69 suggested that maintaining the
intra-cuff pressure between 25-30 cms of H2O was mandatory to guarantee the effective
drainage of secretions and safety.
An evidence based study conducted by Dodek et al68
to formulate clinical
guidelines for the prevention of VAP developed by Canadian critical Care Society,
suggested orotracheal route of intubation; change of ventilatory circuits only for each
new patient and if the circuits are soiled, use of closed endotracheal suction systems that
are changed for each patients and as clinically indicated; heat and moisture exchangers in
the absence of contraindications and its weekly changes and semi-recumbent positioning
in the absence of contraindications which when effectively implemented would help to
decrease the morbidity, mortality and costs of VAP in mechanically ventilated patients.
Although invasive ventilation has beneficial effects on acute respiratory failure
pathophysiology, in most instances it principally provides support while the respiratory
system recovers.203 Invasive mechanical ventilation is associated with significant time
dependent risks and complications including VAP, sinusitis, airway injury, thromboembolism
and
gastro-intestinal
bleeding.
Therefore,
once
significant
clinical
improvement occurs, efforts shift to rapidly removing the patient from the mechanical
131
Discussion
ventilator Fortunately 75% of the patients satisfying weaning readiness criteria tolerate
their initial spontaneous breathing trial (SBT) conducted with no or minimal ventilator
assistance , indicating that mechanical ventilator is no longer required. 203
Assessment of readiness commences within hours for intubation related to rapidly
reversible processes (eg drug overdose, cardiogenic pulmonary edema, etc)while for
other processes , 24 48 hours of full ventilatory support may be required .Estabaan et
al204 and Brochard et al205 in two different studies compared different methods of
weaning which mainly consisted of subjective readiness criteria and was later replaced
by the objective clinical assessment criteria as suggested by Ely et al166 and Kollef et al167
which includes evidence of clinical improvement, PaO2/FiO2 250 on PEEP 5 ,and
adequate haemodynamics which may serve as surrogate markers of recovery. In the
present study, weaning criteria included both oxygenation and ventilator criteria which
were more objective in nature marking as better markers of recovery.
In the present study, success rate of weaning as noted as 66.6% (58 ) in the study
group and 29.1% (24) in the control group which was found to be statistically significant
.However, in the present study population included mixed population involving all types
of patients in all different patterns of ICUs ,what contributed to successful weaning may
be difficult question to answer and was not the objective of the study but may be
attributed
to the initial mode of ventilation in the study group which was SIMV+PS.
However, this reason may need confirmation with further future trials and treating
patients with multimodality chest physiotherapy also may have contributed to successful
weaning and successful outcome. No weaning trial was attempted in 29(33.3%)of
patients in study group and 62 (70.9%) in control group. This may be attributed to either
132
Discussion
due to patients underlying condition or patients not fulfilling the weaning criteria. T
piece trial, CPAP and RSBI (rapid shallow breathing index was used as weaning strategy.
T tube weaning is a technique of weaning by alternating the patient between
spontaneous aerosol T- tube breathing (5min) and full ventilatory support of 30-60
minutes. The duration of the T tube use is gradually increased as tolerated by the patients.
CPAP is another mode available in Servo 300 and Servo 900 ventilators which may be
used as weaning trial mode. In the present study, 21.8% of patients in the study group and
5.8% patients in the control group were give CPAP as weaning which showed statistical
significance.
Among the weaning indices developed, rapid shallow breathing index (RSBI) is
one which is simple to use, calculate and highly predictable in weaning success. RSBI or
f/Vt ratio i.e. respiratory frequency to Vt ratio quantifies rapid shallow spontaneous
breathing. Absence of rapid shallow breathing as f/Vt ratio less than 100 cycles/ liter is
very accurate predictor of weaning success as suggested by Chang et al .48 In the present
study, RSBI was calculated in 58 patients in study group and 28 patients in control group
and these patients were successfully weaned off and successfully discharged from the
hospital. Krieger et al206 studied role of RSBI in weaning by conducting serial
measurements of RSBI in medically elderly patients during the period of spontaneously
breathing and have shown to accurately predict the to be successfully weaned from
mechanically ventilated patients. Another study by Heffner207 suggested that besides
RSBI, PaO2/FiO2 ratio (oxygenation index), ASA class (American class of
Anesthesiologists) and emergency status should be considered for successful weaning
and extubation in post-operative ICU patients on mechanical ventilator support. Timing
133
Discussion
of tracheostomy has shown to promote weaning from mechanical ventilation but not in
all ventilator dependent patients. Heffner207 suggested that patients who require long term
ventilation because of marginal respiratory mechanics may be weaned more rapidly from
mechanical ventilation with conversion to a tracheostomy because of enhanced
psychological well being provided by the ability to eat orally ,to communicate by
articulated speech and to experience enhanced mobility. Enhanced mobility also may
assist physical therapy and more rapid recovery of ventilatory strength. Besides RSBI,
which is very widely and commonly used in ICUs all over the world for its high
predictability, sometimes these indices may be inaccurate. Recently, Nemer et al208
suggested use of a new integrative weaning index using three essential parameters i.e.
CLstat, SaO2, and
f/Vt ratio and this index has
shown to be the best predictive
performance index of weaning outcome and suggested that this index may be used in the
intensive care settings. In a study
conducted by Estaban et al204 who compared 4
weaning modes suggested that compared to intermittent mandatory ventilation and

pressure support ventilation , once daily trial of spontaneous breathing lead to extubation
about 3 times more quickly than intermittent mandatory ventilation and about twice as
quickly as pressure support ventilation. Other methods of weaning as suggested by
Capdevila et al209 are airway occlusion pressure and ratio of airway occlusion pressure to
maximum inspiratory pressure and these have shown to be predicting extubation success.
Arterial blood gas analyses (ABG) values are also important factor and also affect
the decision making of the physicians to extubate the patient from ventilator. A Study
done by Salam et al210 has shown that ABG values did not affect the clinical decision
making of weaning from mecahnnical venitlation. Meyers et al211 conducted a study to
134
Discussion
find the effect of assist pressure release ventilation (APRV) in the weaning process and
have shown to improve ventilation/perfusion mis-matching, cardiac filling and comfort
of the patient and suggested APRV as alternate weaning strategy. However, investigators
suggested carrying out more clinical trials to prove the usefulness of this weaning
strategy. Studies about mechanical ventilation including operating and weaning strategies
are difficult to implement, protocols to be operationalized continuously and entails the
daily detailed data collection. For the first time, pilot WEAN study was carried out in
Canada by Burns et al212 in multicenter ICUs to determine the feasibility of conducting
large scale future weaning trials and to establish a collaborative network of ICU
clinicians dedicated for advancing the science of weaning. In various studies conducted
by Imaculada et al213, Soo Hoo et al214 and Koch et al215 concluded that though there are
variations in the measurements of weaning parameters, use of various protocols, different
weaning strategies, and determinants of weaning, comparative studies using various
modes for predicting weaning success from mechanical ventilation have to be widely
published all over the world. It becomes difficult to implement the established protocols
because of different ICU settings in various countries with different patient population.
Though there are many ongoing studies regarding predicting success of weaning,
evidence based guidelines are available for
weaning and discontinuing ventilatory
support as suggested by various authors.216-226
Ultimately, the decision making of
weaning and weaning criteria is left at the discretion of the physician/surgeon or the
intensivist based on his skill, experience and understanding the patho-physiology of the
disease. However, in the present study, duration of mechanical ventilation (i.e. duration
of intubation) was not significant between the two groups but weaning trials were carried
135
Discussion
in larger number of patients and were successfully extubated in the study group than in
the control group suggesting the effectiveness of multimodality chest physiotherapy in
terms of recovery and decreasing mortality.
Positive end expiratory pressure (PEEP) is an essential component of mechanical
ventilation for all ventilated patients and especially for patients with ARDS that should
be utilized to increase the proportion of non aerated lung resulting in improved
oxygenation.227
The administration of PEEP is mainly aimed at preventing the end
expiratory collapse of diseased pulmonary areas in order to reverse severe hypoxemia

resulting from pulmonary shunting. Despite its first introduction in the late sixties, it is
not easy to establish practical recommendation for setting the right level of PEEP. 228
In the present study, high levels of PEEP (>10cms of H2O) has shown to be a risk
factor for VAP. Though there are no studies to show that high levels of PEEP is a risk
factor for VAP, but a study by Cereda et al229 has shown that higher levels of PEEP
(15cms of H2O) was required to prevent the respiratory system compliance. Estabaan et
al174 in a large study of mechanical ventilation International study group who studied the
characteristics and outcomes in more than 14,000 patients recovering from mechanical
ventilation in mechanically ventilated patients and they reported that higher levels of
PEEP may decrease the lung compliance during mechanical ventilation that may allow
the development of atelectasis.
Higher levels of PEEP (>10cms H2O) have also shown to be a risk factor for
mortality in the present study. Mercat et al230 demonstrated that a lung recruitment
strategy of increasing levels of PEEP to maintain plateau pressures of 28 to 30 cms H2O
136
Discussion
did not improve mortality in adults with acute lung injury but suggested that morbidity
status may be improved. The present study demonstrated a better outcome with lower
levels of PEEP (<10cms H2O) compared to higher levels of PEEP (>10cms H2O). The
results are similar to another study by Grasso et al231 who suggested that higher level of
PEEP may critically affect the venous return and their data suggested the standardization
of higher PEEP and lower FiO2 for better outcome. A protocol proposed by ARDS NET
work in the same study stated that such standardization lacked a physiological basis and
frequently failed to induce the alveolar recruitment increasing the risk of alveolar
hyperinflation. However, the authors suggested physiological variables like increase in
oxygenation, reduction in static lung elastance and the shape of the volume pressure
curve may be used in predicting alveolar recruitment when applying higher than
traditional PEEP levels.
Though the present study did not intend to study the type of lung injury or its
severity caused by mechanical ventilation, a study conducted by Halter et al232 to evaluate
the effects of PEEP and Vt on lung injury induced by alveolar instability in animal
model, concluded that a ventilator strategy employing high Vt and low PEEP causes
alveolar synergistic stabilization of alveoli although increased PEEP is more effective at
stabilizing alveoli than reduced Vt. The study also suggested that the mechanism of lung
injury in the animal model of high Vt/low PEEP group that was used in the study was
more mechanical in nature and not inflammatory. Though the present study did not intend
to study the typer of lung injury since the study consisted of a mixed population with
various diseases, it may be concluded that the patients receiving low PEEP had a better
outcome and had lower risk of mortality irrespective of the amount of Vt they received.
137
Discussion
In four different studies conducted by Bonfim et al233 , Sugarman et al234, Mutoh
et al235 and Malbrain et al236 have emphasized that the occurrence of intra-abdominal
hypertension in ICU can lead to decrease in blood flow to the intra-abdominal organs,
resulting in tissue hypoxia, interstitial edema and multiple organ failure and increasing
the morbidity and mortality of critically ill patients. Torquato et al237 studied the
interaction between intra-abdominal pressure and PEEP by placing a 5 kg weight on the
abdomen of patients under mechanical ventilation with a PEEP of 10 cms of H2O. They
concluded that there was significant increase in the intra abdominal pressure but no
corresponding increase in the airway plateau pressure , thus suggesting that PEEP levels
>10cms H2O may increase the risk of mortality and morbidity in critically ill patients
with a significant increase in the intra-abdominal pressure.
A study by Leuke and Pelosi238 suggested that in patients with mechanical
ventilation, high levels of PEEP may be necessary to maintain or restore oxygenation,
despite the fact that aggressive mechanical ventilation can markedly affect cardiac
function in a complex and often unpredictable fashion. As the heart rate usually doesnt
change with PEEP, the entire fall in the cardiac output is a consequence of a reduction in
left ventricular stroke volume. Mechanical ventilation with PEEP like any other active or
passive ventilatory maneuver, primarily affects cardiac function by changing lung
volume and intra- thoracic pressure. However, in the present study, the PR which is a
variable of heart rate did not show much difference in the baseline or the in the mean
values. (pre and post physiotherapy). The SBP and DBP values demonstrated slightly on
the lower side probably justifying the above explanation.
138
Discussion
A study conducted by Kirby et al239 cautioned the treating physicians and other
health professionals that PEEP should be utilized in the same fashion as any potent drug
i.e. the dose should be tailored to each patient according to his needs and response. Since,
the degree of parenchymal injury varies from patient to patient, the requirement for a
specific level of PEEP may be expected to vary. Arbitrary selection of an upper limit
prevents optimal utilization of this potentially life saving techniques.
Another study conducted by ARDS Clinical Trials Network by NHLB240 which
compared the effects of higher and lower PEEP in patients with ARDS found that
patients with acute lung and ARDs who received mechanical ventilation with low Vt and
an end inspiratory plateau pressure limit of 30 cms H2O, the clinical outcomes in terms
of mortality was 26 % and were similar irrespective of higher or lower levels of PEEP
suggesting the use of lower tidal volume and inspiratory pressures.
Clinical and experimental research on the effects of positive end expiratory
pressure has produces a plethora of information during the last two decades. How PEEP
improves the pulmonary function is still a matter of research. The application of PEEP is
expected to increase PaO2. However, it is generally agreed that simply using increased
PaO2 as the end point is inappropriate. Villar et al241 explained four mechanisms to
explain the improved pulmonary function and gas exchange with PEEP.1. Increased
functional residual capacity, 2.Alveolar recruitment, 3. Redistribution of extravascular
lung water and 4. Improved ventilation and
matching.
139
4. Improved ventilation perfusion
Discussion
However, the optimal method of PEEP application is controversial till date. The
main effect of augmenting PEEP is to maintain recruitment of alveolar units that were
previously collapsed. 241 Since Vt is distributed to more alveoli, peak airway pressure is
reduced and compliance is increased. During acute lung injury due to any lung disease,
PEEP can markedly alter the compliance of the lung by alveolar recruitment. 241 Though
the present study did not aim to study the effect of PEEP or FiO2 but low levels PEEP i.e
<10cms H2O had better results in terms of overall outcome in patients compared to higher
levels of PEEP >10 cmsH2O with MM chest PT.
Reider et al242 suggested that there is ample experimental and clinical evidence to
that there is a wide variability in the adequate levels of PEEP in each patient. Since the
present study had a mixed adult population with mechanical ventilation suffering from
various disorders, admitted to the different ICUs, it was difficult to set the same levels of
PEEP for all patients. Also the PEEP levels were adjusted by the intensivists or treating
physician and not by the physiotherapist, hence correlation of PEEP with FiO2 and / or
PaO2 was not studied. However, this study was preliminary study to observe the effect of
multimodality chest physiotherapy with low or high levels of PEEP (as set by the
intensivists) on overall outcome in ventilated patients and we have concluded that there
was better outcome in patients with low levels of PEEP. These results also suggests that
high level of PEEP did not offer any additional survival benefits since in those patients
there was no need to apply an average PEEP level above 10cms H2O.
In a study conducted by Reider et al242 to study the short term effects of PEEP in
40 elderly male patients were being weaned from mechanical ventilation, it was observed
140
Discussion
that PEEP at 7 cms H2O during 30 min period demonstrated that during weaning from
mechanical ventilation , the use of fixed level of EPAP caused an increased work of
breathing that was not accompanied by any other significant cardio-respiratory changes.
The authors suggested to be cautious when using EPAP as a physiotherapeutic tool
during weaning from mechanical ventilation.242 However, in the present study though
physiotherapist was not involved in the setting or selection of PEEP, weaning was done
considering the opinion of the treating physiotherapist.
The weaning decision in the present study was entirely left to the discretion of the
intensivists, and treating physician. However, it was noted that weaning in 8 patients in
study group and 13 patients in the control group was not successful. Though the reasons
for unsuccessful weaning were not known, some of the important mechanisms as
suggested by Mc Intyre243 that may lead to unsuccessful weaning include alterations in
respiratory drive, oxygenation and excessive load being imposed on respiratory muscles.
In an editorial reply, Tobin et al244 have suggested that certain studies suggest that the
application of external positive expiratory pressure (PEP), during mechanical ventilation
minimizes hyperinflation effects and reduce the work of breathing, which may be helpful
during the weaning process.
In an NIH ARDS clinical Trials Network study by
suggested that
Kallet and Branson245
PEEP and FiO2 are the primary means of improving PaO2 during
mechanical ventilation. Based on extensive literature review of PEEP and respiratory

system mechanics in ARDS, they concluded that firstly for most patients, the therapeutic
range of PEEP is relatively narrow, so the ARDS Network PEEP/FiO2 strategy was
141
Discussion
reasonable with high level evidence. Secondly, how best to adjust PEEP to prevent
ventilator induced lung injury(VILI )is unknown and thirdly, in a small subset of patients
with severe lung injury and / or abnormal chest wall compliance, highly individualized
titration of PEEP based upon respiratory system pressure volume curve is necessary.
Though there is no universal level of PEEP for all patients with any acute lung injury or
ARDS, the ARDS Net investigators have suggested PEEP levels according to a series of
tables with predetermined combinations of PEEP and FiO2 instead of applying PEEP
based on the information of the lung mechanics in individual patients as in the Amato et
al246 or Ranieri et al247 studies.
The present study decreased mean values of PaO2 and PaO2/FiO2 values in the
control group with statistical differences. Pugin78 stated that oxygenation status is one of
the important components to define ARDS which is defined as PaO2/FiO2 < or equal to
200. According to Zilberg and Shorr,248 of all the components of CPIS scores, the
measures of oxygenation provides the most information as a time dependent factor during
early VAP for predicting its outcome. Hence, the authors concluded that though CPIS
may have a limited role both clinically and as a research tool, ratio of PaO2/FiO2 may be
informative in predicting the response to the VAP treatment. However, in the present
study PaO2/FiO2 was used only as an assessment parameter of the oxygenation status, it
was not used as a parameter for antibiotic therapy. PaO2/FiO2 ratio did not suggest as a
risk factor for VAP or for patients mortality. It is suggested that this ratio may be used to
diagnose ARDS.
High FiO2 values has also been found to be a risk factor for mortality in the
present study in mechanically ventilated patients receiving chest physiotherapy. These
142
Discussion
results are similar to the study conducted by Jonge et al249 who studied to find out the
association between administered oxygen, arterial partial oxygen pressure and mortality
in mechanically ventilated intensive care unit patients. They observed that high FiO2 and
low FiO2 values in the first 24 hours after admission are independently associated with in
hospital mortality in ICU patients. It was also observed also suggested that PaO2/FiO2
ratio is not only influenced by pulmonary dysfunction but also by ventilatory settings
such as PEEP levels.249
In another retrospective study by Karbing et al250 data of 35 mechanically
ventilated patients and 57 spontaneously breathing patients was used to find out the
variation in PaO2/FiO2 with FiO2.The authors opined that PaO2/FiO2 is dependent on both
the FiO2 levels and the arterial oxygen saturation levels. As a minimum, the FiO2 level at
which the PaO2/FiO2 ratio is measured should be defined when quantifying the effects of
therapeutic interventions or when specifying diagnostic criteria for acute lung injury and
ARDS. Alternately, they suggested that oxygenation problems could be described using
parameters describing shunt and ventilation /perfusion mismatch.
However, research suggests that FiO2 60% is without major adverse effects and
that
an individual
at risk of developing arterial hypoxemia can be protected by
administering high FiO2 and routine administration of supplementary oxygen is useful,

harmless and clinically indicated. Downs et al251 suggested that there is now substantial
evidence that none of the above mentioned suppositions are correct and on the contrary,
supplementary oxygen is actually detrimental to many of the patients who receive it. The
mean values of FiO2 in the study group and control group in the present study were one
of the major risk factors for mortality in mechanically ventilated patients receiving chest
143
Discussion
physiotherapy. However, though FiO260% was a risk factor, administration is a matter
of concern and may be studied as future research topic.
Berry and Pinard reviewed various ways to assess tissue oxygenation providing
in depth knowledge about diffusion of gases and interpretation of Hb concentration,
oxygen saturation cardiac output and acid base balance which are important variables to
be assessed as baseline data.252 Accurate assessment, prompt recognition and proper
management of adverse changes are vital components in all the heath care settings
dealing with patient with compromised functioning.253 Though the present study took into
consideration the oxygenation index (PaO2/FiO2) as an assessment parameter, it may also
be used in as weaning criteria in mechanically ventilated patients. Though tissue
oxygenation saturation was not taken as an assessment parameter, it may be suggested to
consider this as an assessment parameter in future trials, since study by Lima et al253
studies have shown that patients who consistently exhibited low stO2 (tissue oxygenation
saturation) levels following initial resuscitation significantly worsens the organ failure
than in patients with normal stO2 values. It was also observed that stO2 changes had no
relationship with global hemodynamic variables.
Artucio et al254 opined that while it is important to attempt to predict HDI
(hemodynamic instability) it should be appreciated that 78% of intensive care patients are
likely to experience arrhythmias spontaneously. Other important findings include anxiety
fear, and inability to communicate and were rated higher than suctioning as perceived
causes of distress in people who have experienced intensive care treatment. A study by
Berghom et al255 concluded that sedation and /or analgesia have also shown to alleviate
the adverse response to physiotherapy.
144
Discussion
Though in the present study vital signs including PR,BP (systolic blood pressure
and diastolic blood pressure) were statistically significant at both baseline and mean
values however, no adverse event was noted during the delivery of chest physiotherapy.
The investigator did not find any hemodynamic instability during chest physiotherapy or
after 30 minutes later proving the techniques of chest physiotherapy as safe. However,
this needs further investigation in terms of immediate changes post chest physiotherapy
and influence of underlying disease, patho-physiology of the disease and other patient
related factors .
According to Klein et al256 the present state of research of hemodynamic stability
during respiratory physiotherapy in intensive care patients is inconclusive. The treatment
techniques may vary in their effect according to the actual patho-physiology of the
patients and with a heterogeneous sample. A study by Paratz et al257 suggested there was
need for widespread multi-center documentation of hemodynamic events during
physiotherapy and also to find out correlations between the chest physiotherapy
techniques and the hemodynamic parameters.
Lung compliance is the volume change (lung expansion) per unit pressure change
(work of breathing).Abnormally low or high lung compliance impairs the patients ability
to maintain efficient gas exchange. Low compliance typically makes the lung compliance
induces incomplete exhalation and CO2 elimination. These abnormalities are often
contributing factors to the need for mechanical ventilation. Lung compliance is usually
studied in terms of static lung compliance and dynamic lung compliance. In the present
study, CLdyn (dynamic lung compliance) was taken as one of the assessment parameters.
It was observed in the present study, that the baseline and mean values of CLdyn were
145
Discussion
lesser as compared to the normal values of 30-40 ml/cms H2O,which was statistically
significant. Also the overall results indicated that the decrease in the CLdyn was an
independent risk factor for ventilator associated pneumonia but not for mortality, which
is a significant observation in the present study. There are hardly any studies to suggest
that CLdyn is a risk factor for VAP and this variable may be considered as an additional
risk factor for VAP. Abnormal compliance impairs gas exchange mechanism. When an
abnormally low or high compliance is uncorrected and prolonged muscle fatigue may
occur and this may lead to the development of ventilatory and oxygenation failure.258
Study by Gattinoni et al259 and Woo et al 260 found that the increased chest wall elastance
is important in pathogenesis of ventilatory induced lung injury(VILI) due to excessive
and unphysiological strain on the lung structures and VILI worsens with an open chest or
artificial respiration. Patients with heart failure have shown that thoraco-pulmonary
compliance remains low at all PEEP levels (0-20 cms H2O) and this justifies the findings
in our study where
CLdyn showed lower values than the normal which
may be
attributed to the PEEP values and patho-physiology of various conditions as suggested by

Kotunidou et al.261
Glasgow coma Scale is probably the most common grading scale especially in
neuro-traumatology all over the world. Moskopp et al262 studied the problems for
assessing GCS in mechanically ventilated patients and concluded that since most of the
patients on mechanical ventilation are comatosed or either sedated as per their agitation
levels ,GCS may not always represent a satisfying ranking scale in the modern ranking
system. In the present study, baseline values of GCS scores were less in the control group
compared to the study group (p=0.000) There was slight improvement in the mean scores
146
Discussion
after chest physiotherapy in both the groups which was statistically significant. Though
there was improvement in GCS scores in the mixed population admitted to different ICUs
in the present study, however, GCS<5.31.81 may demonstrate poor prognosis in
patients receiving chest physiotherapy or multimodality chest physiotherapy in mixed
population in adult mechanically ventilated patients.
Khilnani et al263 conducted a study in 82 patients with acute respiratory failure
secondary to COPD admitted to MICU, hospital mortality was 36.6%(in 30 patients)with
high incidence of requirement for mechanical ventilation. The mean GCS scores were
higher in the survivors (12.82.1) as compared to the non survivors (10.83.7). However,
there were other reasons for mortality noted, notably serum albumin, and high APACHE
II scores as independent risk factors within 24 hours of admission. GCS scores in the
present study demonstrated that GCS scores of 5.3 1.81 to be an independent risk factor
for mortality. The authors also suggested that GCS scores may be used as baseline data to
design prognostic models in identification of high risk subgroups in very elderly (i.e. 80
years and older) to predict in hospital mortality.
A study by Wayne M et al
264
has shown that a very accurate GCS score can be
derived in the absence of the verbal component which is important in intubated patients.
Contradictory to the results of the present study, where the GCS score of 5.3 1.81 was a
risk factor for mortality, pre-hospital endotracheal intubation in trauma patients with
blunt injury and scene GCS of 8 or less had improved survival in severe head injuries
patients and this broadens the indications for intubations by paramedical personnel to
have great potential to improve outcome in patients with severe head injury and this has
been substantiated by a study by Winchell et al.265 However, in the present study, pre147
Discussion
hospital intubation was not an inclusion criteria and all patients in the study were referred
by the treating physician /surgeon.
In patients with complicated myocardial infarction requiring mechanical
ventilation in ICUs, Lesage et al
266
concluded that the demographics, medical history
and the GCS scores were similar in survivor and non survivor groups. However, main
risk factors for high mortality rates were high APACHE II scores, early development of
acute renal failure, low resting left ventricular function and PaO2/FiO2 ratio <200 at
admission. In a prospective cohort study done by Tormicic et al267 conducted in Chilean
critical care units where various characteristics like demographic data, severity of illness,
reason for initiating mechanical ventilation, ventilatory modes and settings, weaning
strategies, hospital stay and hospital mortality were studied, the authors concluded that
magnitude of multi-organ dysfunction and high plateau pressure were important factors
associated with mortality.
Plateau pressure is the pressure to maintain lung inflation in the absence of air
flow and is obtained by applying inspiratory hold or occluding the exhalation port at the
end inspiration and is one of the determinants of the static compliance of the lung which
may be severely affected in clinical conditions like atelectasis, ARDS, tension
pneumothorax, obesity and retained secretions. However, in the present study, dynamic
compliance was taken into consideration that demonstrated as a risk factor for mortality
which is an important finding.
According to Raooij et al268 in a recent ARDS network randomized controlled
trial conducted in patients with acute lung injury and ARDS, it was observed that low Vt
mechanical ventilation (6 ml/kg) reduced mortality by 22% as compared with traditional
148
Discussion
mechanical ventilation (12ml/kg). The clinical risk factors were reclassified as pulmonary
versus non pulmonary predisposing conditions and infections related versus non infection
related conditions and found no evidence that the efficacy of low Vt ventilation differed
among clinical risk factors subgroups. However, the present study included a mixed
population besides ARDS and low Vt strategy as low as 9.5 ml/kg was a risk factor for
VAP .However, low Vt strategy was not a risk factor for mortality This difference may
be due to various heterogeneous clinical conditions in various ICUs which included
medical, surgical, coronary care and neurological intensive care units and may have
different effects in patients with lower lung compliance.
In patients with ARDS, prognosis of ARDS and hospital survival after the onset
of ARDS can be made by taking into account a general severity score, underlying
diseases, the mechanism of lung injury, oxygenation index and the presence or right
ventricular dysfunction.269 Rocca et al concluded that in ARDS ventilated patients for
more than 48 hours, significant risk factors for mortality are high peak inspiratory
pressures, increasing PEEP levels and Vt. However, non ventilated risk factors for
mortality in ARDS included sepsis, low pH, elevated lactate, low albumin, transfusion of
red blood cells, and transfusion of plasma, high net fluid balance and low respiratory
compliance. To prevent ventilator induced lung injury, transpulmonary pressure has been
suggested to be taken into consideration and should be kept within the physiological
range. It has also been suggested not to give prone positioning since prone position may
attenuate ventilator associated lung injury by increasing the homogeneity of
transpulmonary pressure distribution. PEEP may also prevent VILI by keeping open lung
thus reducing the regional stress/strain maldistribution. 269
149
Conclusion
CONCLUSION
The present clinical trial has demonstrated significant improvements with
multimodality chest physiotherapy treatment in terms of rate of recovery from
mechanical ventilation with 58 (66.7%) patients in study group compared to 28 (32.6% )
patients
in control group which was statistically significant (p=0.000)..The
physiotherapist based protocol was helpful in significant reduction of complications.

VAP emerged as a major complication in both the groups Only 26.4% of patients
suffered from complications in the study group as compared to 61.6% in the control
group which was statistically significant.(p=0.000) . Duration of hospital was longer in
the study group (169.40 days) as compared to the control group (12.86.12
days).Successful weaning was done in 58 patients in the study group as compared to 24
patients in the control group.
Though the study constituted only referred cases with a heterogeneous population
of mechanically ventilated adult patients with various disorders admitted in different
ICUs, multimodality chest physiotherapy has demonstrated significant improvements in
the oxygenation status and ventilator parameters between both the groups irrespective of
the above differences. The results of the present study suggests that multimodality chest
physiotherapy, a first time physiotherapist based protocol may be used as a regular chest
physiotherapy treatment option in ICUs in the routine management of mechanically
ventilated adult patients. The study was one of the largest chest physiotherapy clinical
trials conducted in a critical care setting with a sample size of 200 patients with a first
time use of a physiotherapist based protocol of multimodality chest physiotherapy. The
150
Conclusion
protocol has also demonstrated to be safe irrespective of the clinical condition with no
advent of adverse events. The above study may help in the referral attitudes of the
physicians / surgeons which may help in reducing the morbidity and mortality of
mechanically ventilated patients.
Similar clinical trials may be conducted in single ICU set up with a single
condition like GBS, ARDS, SCI, etc. Prevention of other ICU related complications like
Critical illness myopathy and critically illness polyneuropathy may be also studied from
physiotherapy perspectives.
151
Summary
SUMMARY
Patients needing mechanical ventilation represent an important subset of all
individuals admitted to an ICU due to the intensity of medical service they receive and
their associated costs. They may also have an increased risk of Ventilator associated
pneumonia (VAP) and atelectasis, besides an increased risk of sputum retentions leading
to ventilation weaning more difficult and resulting in excess morbidity & mortality.
Hence, every effort should be made to determine which patient can be rapidly extubated
so as to keep the weaning period minimum1.
Chest physiotherapy plays an important role in management of patients on
mechanical ventilation. This study was designed to evaluate the effect of multimodality
chest physiotherapy on rate of recovery and prevention of complications in ventilated
patients. A total of 200 adult intubated and ventilated patients were included in the study
out of which 13 in the study group and 14 in the control group withdrew from the study
due to various reasons. MH and suctioning was administered to 86 patients in the control
group and suctioning + MH + chest vibrations and positioning to 87 patients in the study
group, respectively till they were extubated. Both the groups were treatment twice daily.
Standard care in the form of routine nursing care, pharmacological therapy as advised by
concerned physician/surgeon was strictly implemented throughout the intervention
period. Data of 173 patients were finally subjected for statistical analysis.
The results of the present clinical trial demonstrated significant improvements
with multimodality chest physiotherapy treatment in terms of rate of recovery with
58(66.7%) patients in study group compared to 28 patients (32.6%) in control group
152
Summary
which was statistically significant (p=0.000). The physiotherapist based protocol was
helpful in significant reduction of complications. Only 23 (26.4%) patients suffered from
complications in the study group as compared to 53(61.6%) in the control group which
was statistically significant.(p=0.000). VAP emerged as the largest complication in both
the groups with no statistical significance. Duration of hospital was longer in the study
group (169.40 days) as compared to the control group (12.86.12 days). However,
weaning was successful in 58 patients in study group and 24 in the control group with
statistical significance.
Multimodality chest physiotherapy also demonstrated significant improvements in
the oxygenation status and ventilator parameters between both the groups. The results of
the present study suggests that multimodality chest physiotherapy, a first time
physiotherapist based protocol may be used as a regular treatment option in ICUs in
mechanically adult ventilated patients.
The protocol has also demonstrated to be safe irrespective of the clinical condition
with no advent of adverse events. The above study may help in the referral attitudes of
the physicians / surgeons which may help in reducing the morbidity and mortality of
Similar clinical trials may be conducted in single ICU set up with a single
condition like GBS, ARDS, SCI, etc. Prevention of other ICU related complications like
critical illness myopathy and critically illness polyneuropathy may be also studied from
physiotherapy perspectives.
153
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Complicated acute myocardial infarction requiring mechanical ventilation in the
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Characteristics and factors associated with mortality in patients receiving
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186
Annexures
ANNEXURE I: ETHICAL CLEARANCE CERTIFICATE
187
Annexures
ANNEXURE II: INFORMED CONSENT FORM
TITLE OF THE STUDY:
EFECT OF MULTIMODALITY CHEST PHYSIOTHERAPY ON THE RATE OF
RECOVERY AND PREVENTION OF COMPLICATIONS IN PATIENTS WITH
MECHANICAL VENTILATION - A PROSPECTIVE STUDY IN MEDICAL AND
SURGICAL INTENSIVE CARE UNITS.
OBJECTIVES OF THE STUDY
To study the effect of multimodality physiotherapy among mechanical ventilated
patients in MICUs and SICUs.
To evaluate the effect of multimodality physiotherapy on the rate of recovery in
mechanical ventilated patients in MICUs and SICUs.
To assess the effect of multimodality physiotherapy in reducing complications in
To analyze the effect of multimodality physiotherapy in decreasing the duration
of stay in MICU and SICU.
There is no funding required for study or for the participation.
PROCEDURES INVOLVED:
The adult participants who are on mechanical ventilator shall be recruited in the
study.
The procedures involved are therapeutic body positioning, suctioning, manual
hyperinflation and chest vibrations. Based on inclusion and exclusion criteria you
188
Annexures
will be allocated to the experimental group or to the control group. The total
number of participants are approx 170 (one hundred and seventy). The treatment
in the experimental group will of chest vibrations, therapeutic positioning,
suctioning, manual hyperinflation. The treatment in the control group will consist
of the standard form of chest physiotherapy in the form of manual hyperinflation
and suctioning. Respiratory parameters, Oxygenation status, ventilatory
parameters, Radiological parameters and Clinical parameters will be noted.
Treatment to both the groups will be taken twice a day during the entire study
period.
RISKS AND BENEFITS:
There are no potential risks involved in the above mentioned chest physiotherapy
procedures to the participants.
This research will study the rate of recovery and also whether it will help in
reducing complications like ventilator associated pneumonia and atelectasis, and
also the decrease the duration of stay in ICUs with help of chest physiotherapy.
ALTERNATIVES:
The participant will not be denied routine nursing care and pharmacological
therapy as decided by the treating physician/surgeon and aerosol therapy during
the entire study period.
The participant will be told about the recent developments and new information
regarding the treatment.
189
Annexures
PRIVACY AND CONFIDENTIALITY:
Confidentiality of the information you provide will be safeguarded for subject to

any legal requirements.
INSTITUTIONAL/SPONSERS:
The KLE University will provide, within the limitation of the laws of the State of
Karnataka, facilities and medical attention to subjects who suffer injuries as a
result of participating in this study, you may contact the principal investigator.
Dr. Renu B. Pattanshetty (919448482564) or Dr. Gajanan S. Gaude
(919448143994), Professor and HOD, Dept. of Pulmonary Medicine, JN Medical
College, Belgaum. The Institute is the sponsor of this study project in which you
are participating.
FINANCIAL INCENTIVES FOR PARTICIPATION:
You will not receive any payment for participating in this study.
AUTHORIZATION TO PUBLISH RESULTS:
Results of this study may be published for scientific purpose and/or presented to
scientific groups: however you will not be identified.
VOLUNTARY PARTICIPATION:
Your participation in this study is voluntary. Your decision whether or not to

participate and continue in the study will not affect care during your hospital
admission. You are free to discontinue participation in this study at any time and
190
Annexures
for any reason. In case, you need any further information regarding your rights as
study participant, you may please contact Dr. V. D. Patil, Dean, Faculty of
Medicine, Principal, JN Medical College, Belgaum and
Chairman of
J.N.M.C Institutional Ethical Committee on Human Subject Research,

Telephone(office) 0831 2473777 ,Ext. 1554.
CONSENT STATEMENT:
I volunteer and consent to participate in this study. I have read the consent or it
has been read and explained to me in my own vernacular language. The study has
been fully explained to me and I may raise question at any time and withdraw
from the study.
Participants name/ relatives name:

Participants/ relatives signature / thumb impression:
Investigators name:
Investigators signature:
Witness name:
Witness signature:
Date:
191
Annexures
ANNEXURE III: PHOTOGRAPHS
SERVO 300 VENTILATOR SYSTEM
SERVO 900 VENTILATOR SYSTEM
192
Annexures
2. PATIENT IN ICU SET UP
3. ROUTINE PHARMACOLOGICAL THERAPY ADMINISTERED THROUGH

INFUSION PUMP
193
Annexures
4. PROCEDURES OF SUCTIONING
194
Annexures
5. ROMSON SUCTION CATHETERS
6. HEAD END OF BED ELEVATION TO 30-45 DEGREES
195
Annexures
7. MANUAL HYPERINFLATION BAG
8. PROCEDURE OF MANUAL HYPERINFLATION

196
Annexures
9. PROCEDURES OF CHEST VIBRATIONS AT THE DIFFERENT AREAS OF THE CHEST

197
Annexures
ANNEXURE IV: PROFORMA SHEET

CONTROL /STUDY GROUP
Patients Name:
IP No:
MH + suctioning / MM chest PT
SNo.
OUTCOME MEASURES
Sex
Age
Admission of patient to different ICU
4
5
Admission Diagnosis
Initial Ventilatory Mode
Duration of Intubation
RESPIRATORY PARAMETERS
i) Rapid shallow breathing index

ii) Respiratory rate
iii) Spontaneous VT score
8
OXYGENATION STATUS
i) PaO2
ii) PaCO2
iii) PaO2/ FiO2
9
VENTILATORY PARAMETERS
i) Mean airway pressure (MAWP)

ii) PEEP
iii) Peak airway pressure (PAP)
iv) Dyn lung compliance ( VT/ PAPPEEP)
v) FiO2
10
RADIOLOGICAL FEATURES
i) Pneumonia
198
Day
1
Day
2
Day
3
Day
4
Day
5
Day
6
Annexures
ii) Scoring of atelectasis
11
CLINICAL PARAMETERS
i) CPIS
ii) GCS
12.
Duration of ICU stay(days)
13.
Duration of hospital stay(days)
14
VITAL SIGNS
i.PR
ii SBP
iii DBP
15.
GLOBAL OUTCOME
i successful outcome
ii death
iii. D/C AMA
16
iv. chest physiotherapy

discontinued
Duration of weaning (hrs)
17.
Weaning mode
199
Annexures
KEY TO THE MASTER CHART
1.
SEX
6.
VAP (Ventilator Associated Pneumonia)

NO VAP 0
VAP < 5 days 1
VAP > 5 days - 2
7.
Weaning Mode
Male (M) : 1
Female (F) : 2
2.
WARD
NSICU - 1
MICU -2
SICU - 3
ICCU - 4
3.
Type of Intubation
Non Weaned
T-Piece Trial CPAP
8.
ET1
Tracheostomy - 2
4.
Initial Ventilation mode
Radiological Parameters
No radiological evidence of any
complications - 0 Pneumonia - 1
Atelectasis - 2
Pneumonia+ Atelectasis- 3
Others 4
Other complications
No Complications - 0
Septicemia 1
UTI
2
Hypokalemia - 3
Hperkalemia 4
Hyponatremia- 5
Hypernatremia - 6
Renal failure 7
Seizures 8
Paralytic Ileus - 9
Cardiac arrest- 10
9.
GLOBAL OUTCOME
10
Successful outcome
1
Death 2
Discharge Against medical advice 3
Discontinued 4
RSBI (rapid shallow breathing index)
VC
1
SIMV + PS - 2
5.
RR/Vt , RR and Vt score

0 = non weaned
11
Weaning duration
0 = non weaned
200
-0
1
2
263123
21
599860
62
266606
35
267335
75
268202
58
269922
49
272982
10
264091
11
AMI with
pacemakker
OP Poisoning
SAH c obs.
Hydrocephalus
Septicemia
74.5
48.5
106.42
72.5
47.7
120.83
2.25
30
10
11.25
0.7
21.50
2.25
27.26 10.8
13.66
0.6
22.24
80
92
60
85.33
93.86
60.66
3.86
7.26
15
20
25
72.5
49.5
120.83
71.9
49.0
89.87
3.25
25
19.11
0.6
21.80
3.25
28.25
10
17.80
0.80
23.70
120
90
60
111.3
91
67
4.5
10
15
70.5
50.5
100.71
85
45.5
212.5
2.50
35
9.25
0.7
22.50
2.5
35
9.25
0.40
22.50
80
32
0.400
110
98
60
106
98
61.33
1.33
15
17
78.2
52.5
97.75
86
44.5
215
2.75
28
13.75
0.8
17.80
2.75
26
5.5
13.41
0.40
17.80
71.4
30
0.420
98
100
60
95.66
105
64.33
5.35
12
15
2.5
70.2
53.4
78.01
75.9
48.1
108.42
2.50
25
14.7
0.9
17.90
2.68
27.95 9.33
14.44
0.70
19.16
130
110
60
113.5 109.16
60.33
3.74
5.08
24
42
45
69.4
47.4
86.76
85.5
46.2
244.28
2.25
30
0.8
17.80
2.27
30.33 8.33
10.35
0.35
18.41
113
107
62
115.8
109
61.11
3.77
5.44
12
15
65.4
48.5
81.76
75.9
45.4
151.8
2.25
25
13.23
0.8
21.50
2.35
26
13.05
0.50
21.50
120
108
62
122.7
108
62.66
2.33
11.89
0.30
22.80
115
118
70
115
119
70
3.75
3.5
10
15
OXYGEN STATUS PARAMETERS
VITAL SIGNS
RSBI
Baseline
Baseline
Mean
Pa02 PaC02
Pa02/
Fi02
Pa02
PaC02
Pa02/
Fi02
Vt
(ml/kg)
PAP
PEEP
Vt/
Vt
Fi02 MAWP
PAP-PEEP
(ml/kg)
PAP PEEP
Mean
Baseline
Mean
Vt/
Fi02 MAWP RR/ Vt RR
PAP-PEEP
75.55
34
Spont Vt
score
0.450
PR
BP
SBP DBP
PR
BP
71.4
52.5
89.25
85.25
51.9
284.16
2.50
30
10.41
0.8
22.80
2.58
27.75
65
coronary artery
diease
Hemiplegia
60.4
48.5
86.35
72.95
46.1
145.9
2.25
25
10
15
0.7
25.30
2.27
28.11 10.9
13.20
0.50
26.00
119
108
70
119.1 108.90
54
ALD c Asciitis
61.2
46.5
87.42
75.95
45.1
86.27
2.58
25
12
19.84
0.7
27.40
2.87
27.36 10.84
17.37
0.90
26.97
135
96
60
131.7
282451
64
65.8
49
94
72.95
48.2
145.9
2.25
28
10
12.5
0.7
23.20
2.67
26.4
11.6
18.07
0.50
14.92
121
98
70
12
274083
64
Septicemia c
Dengue
ARDS
62.8
48
104.66
69.59
47.1
115.98
2.30
25
12
17.69
0.6
22.90
2.35
27.4
11.6
14.87
0.60
22.90
110
100
13
276980
64
79.4
49
158.8
78.1
49.1
111.57
2.25
28
10
12.5
0.5
16.00
2.37
29
11.65
13.68
0.70
16.95
119
14
268190
24
15
281990
16
292009
17
Glasgow
ComaScore
(GCS)
Baseline Mean
Score Score
Clinical Pulmonary
Infection Score
(CPIS)
Baseline
Score
Mean
Score
Weaning duration
(Days )
GLOBAL OUTCOME
23
DBP
Other Complications
WEANING MODE
248830
SBP
Length of hospital Stay

(Days)
RTA with sub

acute
acute liver
disease
OP Poisoning
Total duration in ICU

(days)
50
Total duration of
Intubation (days)
Ventilator associated
Pneumonia (VAP)
258731
RADIOLOGICAL
PARAMETERS
Admission
diagnosis
Initial ventilation mode
Sex
Type of Intubation
IP No
Ward
Sl.
No.
Age (yrs)
CONTROL GROUP
3.5
1.5
70
3.63
4.27
11
11
15
97.89
61.89
3.84
5.21
19
21
25
121.4
99.2
70
3.2
5.2
10
11
15
60
110
104
60
3.4
5.2
10
2,5
110
60
118
112.5
61.6
3.5
5.4
20
25
30
121
110
60
121
110
61.33
3.33
10
96
110
60
96
110
61.5
8.75
10
79.5
48
198.75
77.5
45.5
96.87
2.34
25
10
15.6
0.4
18.50
2.44
25
10
16.31
0.80
18.50
34
VBI-Basilar
stroke
Traumatic
Quadriplegia
Laprotomy
78.5
49.5
157
87.25
48.2
218.12
2.50
22
14.7
0.5
19.80
2.73
26.75
12.58
0.40
19.80
22
OP Poisoning
72.5
50.1
120.83
72.5
45.5
103.57
2.25
35
10
0.6
20.50
2.33
35
8.04
0.70
20.50
77.08
37
0.480
135
114
60
135
114
62.66
3.66
231421
32
ARDS
76.5
52.1
127.5
88.1
44.5
220.25
2.50
30
10
0.6
20.90
2.42
30
9.68
0.40
20.90
70.21
33
0.470
114
110
60
114
110
61.2
7.4
4.8
10
1.5
18
291427
45
ARDS
77.4
53.1
129
89.15
44.5
222.87
2.25
22
10
18.75
0.6
20.50
2.52
24.8
13.40
0.40
20.98
121
107
60
121
107
60
10
1.5
19
274310
28
Trauma
75.4
54.2
107.71
72.15
44.5
90.18
2.50
25
10
16.66
0.7
21.80
2.36
23.66
10
17.32
0.80
21.80
120
108
60
115.7
108
60
3.33
8,3
20
286451
42
ARDS
76.4
55.5
109.14
75.15
50.5
93.93
2.50
22
10
20.83
0.7
20.50
2.5
23
10
19.23
0.80
20.50
110
110
60
110
110
60
10
21
285432
38
Dangue
68.5
56.5
97.85
76.61
50.4
95.96
2.30
22
16.42
0.7
20.50
2.3
23
16.42
0.80
20.50
107
90
62
108
90
62
3.5
1.5
10
22
291863
75
66.4
58.5
83
79.1
47.5
87.88
2.20
24
10
15.71
0.8
21.20
2.38
24
11.6
19.25
0.90
21.85
106
90
64
116.5
92.8
64.75
3.7
6.5
20
20
25
23
244892
39
chronic renal
failure
GBS
69.4
58.2
86.75
86.25
50.5
215.62
2.35
25
11.75
0.8
25.20
2.4
25
12
0.40
25.20
106
98
62
106
98
62
8.5
5.5
10
24
290007
39
Trauma c Rib#
66.5
54.2
83.12
79.1
51.7
158.2
2.30
24
10
16.42
0.8
23.50
2.11
23.5
9.5
15.13
0.50
24.15
117
99
64
113.5
99.5
64
1,3
4.25
4.87
10
25
288570
62
67.4
55.5
74.88
78.25
51.0
111.78
2.30
28
10
12.77
0.9
22.50
2.27
25
10.5
15.68
0.70
22.50
117
100
70
112.3
105
70
3.5
10
26
287126
59
sub-Dural
Haemorrhage
laparotomy
69.39
54.5
86.73
78.25
48.1
97.81
2.25
24
14.06
0.8
21.30
2.25
31.33
10.01
0.80
21.30
117
100
70
116.8
108
70
12
27
288911
61
HIV with TB
60.15
51
75.18
79.21
49.5
113.15
2.95
28
10
16.38
0.8
19.50
2.99
26.42 11.92
20.64
0.70
19.90
122
100
70
121.1 108.85
70.42
3.28
5.07
14
16
20
28
289012
52
GBS
66.17
52.5
94.52
88.15
43.5
251.83
2.92
30
13.27
0.7
19.20
2.91
32
9.2
12.77
0.35
19.20
120
100
70
120.4
100
70
5.2
10
29
292764
51
Stroke
64.45
54.5
92.07
77.91
48.5
97.38
4.02
22
10
33.5
0.7
19.80
4.02
24.5
12.5
33.5
0.80
19.80
132
100
72
134.5
100
72
3.5
4.75
10
30
290007
48
Septicemia
66.72
55.5
83.4
77.81
47.1
111.3
4.25
22
10
35.41
0.8
19.20
3.85
23
11
32.08
0.70
19.65
135
98
62
137.5
98
63.2
3.5
5.5
10
10
15
31
250141
58
Stroke
50.12
56.6
55.68
75.9
46.5
126.5
4.10
22
10
34.16
0.9
20.30
4.07
23.5
11.5
33.95
0.60
21.35
128
98
62
129
98
62
3.25
4.75
12
32
293022
38
Trauma
65.25
57.6
72.5
77.1
46.2
154.2
2.35
22
16.82
0.9
20.10
2.15
22.8
12.2
20.87
0.50
20.85
127
98
62
124.5
98
62
4.7
4.8
10
10
15
33
291863
42
stroke
50.2
52.1
50.2
76.95
48.1
109.92
2.50
23
16.66
21.60
2.62
23.66 6.83
15.59
0.70
22.15
123
90
62
122.5
90
62
4.83
10
34
302113
32
GBS
68.21
50.1
75.78
78.65
47.1
98.31
2.25
22
12
22.5
0.9
24.20
2.41
23
9.5
17.87
0.80
24.20
125
90
62
125
90
62
5.25
3.5
12
35
222141
48
68.2
52.1
75.77
77.95
44.9
97.43
2.70
22
12
27
0.9
25.20
2.62
22.8
10.8
21.87
0.80
24.70
127
90
62
124.5
90.4
62
4.8
4.4
10
18
36
298330
38
GBS c Bulbar
Dydfunction
Head injury
67.2
53.4
74.66
78.15
52.1
87.72
2.40
22
10
20
0.9
22.50
2.42
23.14 11.14
20.23
0.90
16.32
135
90
62
137.1
90.85
62
5.14
37
256450
40
17.30
0.35
22.50
135
100
64
135
100
64
8.75
2.5
38
301492
130
110
64
128.7
110
65.33
5.55
39
236110
127
110
70
125.2
110
70
7.66
40
297966
130
110
70
129
113
70
6.16
78.2
55.1
97.75
89.12
45.1
254.62
2.20
22
15.71
0.8
22.50
2.25
22.5
30
Pyopneumothor
ax
GBS
9.5
77.4
55.1
96.81
77.95
60.1
155.9
2.62
22
18.71
0.8
21.30
2.8
23.77 10.44
21.57
0.50
22.18
18
OP Poisoning
78.1
47.8
86.77
88
45.2
293.33
2.75
24
16.17
0.9
27.20
2.78
27.76
12.25
0.30
27.13
72
VBI-Basilar
stroke
77.2
49.8
85.83
78.5
47.1
130.83
3.10
28
10
17.22
0.9
24.30
3.17
23
22.67
0.60
24.30
76.59
78.72
70.83
78.52
77.16
36
37
34
34
32
0.470
0.470
0.480
0.4330
0.4120
2
2.5
1
1
1.5
2
1.5
1.5
21
10
14
15
5.11
12
5.46
13
14
16
4.33
10
12
2
1
1
2
3.5
1
3
41
304256
84
72.3
50.8
80.33
77.9
48.1
111.28
4.10
22
10
34.16
0.8
22.10
4.1
22
10
34.16
0.70
22.25
140
110
70
138.5
54
forner's
gangrene
gastromal tumor
42
302910
43
294413
44
69.5
50.4
86.88
78.5
49.1
112.14
4.20
22
12
21
0.7
23.10
4.2
23
10.28
33.01
0.70
21.98
137
112
60
135.9 110.57
42
post op glioma
68.2
55.4
97.42
77.5
50.1
129.16
4.25
24
26.56
0.7
18.50
4.23
22.66
28.87
0.60
18.50
138
110
60
138
110
60
298038
83
65.4
54.4
110.66
76.5
52.1
153
4.41
22
27.56
0.6
19.50
4.22
25.71 5.85
21.25
0.50
19.50
121
110
60
122.7
110
60
45
297707
81
parkinson's
disease
ARDS
66.4
52.2
137.8
78.21
54.1
130.35
4.20
24
26.25
0.5
20.10
4.25
26.59
0.60
20.10
122
112
60
123
112
60
46
297339
55
polytrauma
68.9
56.2
156.8
77.65
56.1
110.92
2.12
22
12
13.25
0.5
20.90
2.28
23.28 10.28
17.55
0.70
20.90
128
98
60
128.9
98
47
305449
76
78.4
56.2
154.8
88.25
45.2
220.62
4.05
24
25.31
0.5
20.50
4.07
22.8
6.8
25.48
0.40
20.50
128
98
62
128
48
311923
68
IHD with
cardiogenic
meningioma
77.4
50.1
199.75
69.95
50.4
99.92
4.20
24
12
35
0.4
20.10
4.25
24
10.5
31.5
0.70
20.10
125
96
62
49
250953
32
GBS
79.9
55.1
150.25
89.45
44.5
279.53
4.75
25
23.75
0.4
20.10
4.59
12.64 3.21
23.63
0.32
20.21
125
96
50
255368
42
60.1
49.2
130.5
69.95
45.9
99.92
2.76
25
12
21.23
0.5
20.50
3.03
25
10.25
20.54
0.70
20.85
125
51
293247
22
65.2
47.2
132.5
69.75
45.6
99.64
4.10
22
29.28
0.5
24.20
4.1
23.5
26.45
0.70
23.35
52
300128
49
66.2
49.5
139
69.71
46.1
87.13
4.20
22
30
0.5
22.50
4.2
23.5
27.09
0.80
22.25
53
296107
42
anemia with
evere alcoholism
cervico dorsal
myelitis
diffused axonal
injury
Head injury
69.5
50.3
119.83
86.15
42.6
246.14
3.75
30
15
0.6
23.50
3.57
24.4
18.40
0.35
23.50
72.84
33
54
309002
40
75.29
32
55
309161
56
309101
57
24
80
73.33
34
33
70
6.5
4.75
12
60
4.71
5.14
12
15
5.33
3.33
10
12
60.85
3.71
10
98
62
8.6
3.8
10
124
96
62
5.25
3.5
12
62
126.4
98.85
63 .85
7.35
2.71
14
20
23
98
64
127.5
99
64
6.25
4.87
10
12
128
125
72
128.2
124
72
6.4
4.5
10
18
22
127
127
72
127
127
72
10
0.453
128
128
72
128
128
72
7.2
12
2.5
0.425
128
130
70
128
130
70
7.25
4.75
1.5
0.425
0.450
110
2.5
1
3
3.5
1
2
8
4
3
71.9
52.5
111.57
86.16
39.4
287.2
3.30
22
19.41
0.7
18.50
3.3
23.5
17.83
0.30
18.50
60
Intra-Cranial
Haemorrhage
Pneumonia
78.1
54.5
100.28
79.5
50.9
113.57
3.30
20
10
33
0.7
19.20
3.2
20
10
32
0.70
19.20
128
120
70
120.5
120
70
3.5
57
IHD
70.2
56.6
110.28
79.16
51.9
98.95
4.10
24
25.62
0.7
19.20
4.1
24
25.62
0.80
19.20
128
110
72
128
110
72
305766
45
77.2
55.7
77.42
74.59
49.1
93.23
4.25
22
30.35
0.7
20.50
4.21
31
6.6
17.25
0.80
20.50
110
110
72
110
110
72
4.4
3.6
58
305670
34
Intracranial
Bleed
OP Poisoning
54.2
46.7
84.57
86.15
42.9
246.14
4.11
22
24.17
0.7
18.50
4.11
23.5
4.66
21.81
0.35
18.50
72.84
33
0.453
115
112
72
115
111
72
7.33
4.66
10
1.5
59
296743
65
59.2
45.6
75.12
86.15
51.5
287.2
4.28
22
25.17
0.8
21.50
4.28
23.28 4.57
22.87
0.30
21.80
75.29
32
0.425
115
110
68
114.1 113.42
69.14
7.85
4.42
12
1.5
60
334216
48
60.1
49.5
77.75
77.15
52.5
110.21
4.10
24
27.62
0.8
21.20
4.16
23.4
7.6
26.32
0.70
21.20
116
100
68
116.4
100
68
4.4
4.6
10
61
335660
72
10
31.11
0.70
22.50
116
100
69
116
100
69
4.25
12
62
340812
117
110
60
117
110
61
5.5
12
63
340994
102.5
61
5.25
10
12
64
60.92
7.84
4.61
13
17
20
aorto-femoral
grafting
ARDS
62.2
49.5
80.31
78.12
46.5
111.6
4.20
24
10
30
0.8
22.50
4.2
23.5
58
Intra Cranial
Bleeding
Myeloma
64.2
42.5
97.81
78.12
40.9
97.65
4.40
25
12
33.84
0.8
22.50
4.4
24.5 10.33
31.05
0.80
22.20
60
GBS
78.2
45.9
97.75
85.5
38.9
213.04
4.21
24
26.31
0.8
22.50
4.2
23.5
6.87
25.28
0.40
22.55
75.22
34
0.452
117
110
60
118.5
288570
53
78.2
45.9
97.55
85.5
37.5
244.28
3.75
22
12
37.5
0.9
20.90
3.83
22.46 7.15
25.02
0.35
20.94
76
32
0.421
118
110
60
118.2 104.69
65
288117
42
S.D
Haemorrhage
Cellulitis
59.9
46.6
66.55
72.52
46.1
145.04
3.00
30
15
20
0.8
21.50
3.09
31.2
11.8
15.92
0.50
21.50
120
110
60
120.8
110
60
4.2
12
66
287126
47
laparotomy
54.4
45.8
68.06
77.68
46.9
129.46
3.15
35
12
13.69
0.7
22.50
3.11
33.33 10.66
13.74
0.60
22.50
125
110
82
127.7
120
82
67
286789
29
Septicemia
55.5
45.9
79.28
77.89
38.7
111.27
4.27
32
15
26.29
0.7
24.50
4.29
32.33
24.63
0.70
24.50
128
120
82
128.7
124
82
4.66
68
287495
35
laparotomy
69.7
45.9
99.57
88.5
46.7
252.85
2.21
22
15
31.57
0.6
22.50
2.21
22.75 10.25
17.68
0.35
22.50
127
124
80
127
125
80
9.33
5.25
69
288859
36
65.4
48.1
109
69.59
47.1
99.41
4.20
32
10
19.09
0.5
21.20
4.23
32.83 9.33
18.02
0.50
21.20
125
125
60
125
110
80
6.5
4.66
10
70
287884
60
B/L Pleural
Effusion
Craniotomy
66.5
49.4
133
69.5
44.5
86.87
4.28
28
10
23.77
0.5
22.50
4.24
28.5
22.91
0.60
22.50
112
110
60
112
110
60
3.5
71
287484
48
Head Injury
65.5
49.4
131
77.5
45.9
96.87
4.40
30
12
24.44
0.6
21.10
4.4
27.28 11.42
22.91
0.70
21.70
121
110
62
4.57
5.28
10
72
285980
67
78.1
49.5
130.16
78.5
45.3
130.83
4.19
32
12
20.95
0.7
25.20
4.24
30.16
22.15
0.80
25.20
122
110
60
60
5.66
3.5
11
73
357884
27
79.2
50.5
113.14
75.49
47.2
150.98
4.40
30
12
24.44
0.8
22.50
4.22
30.16 10.28
21.27
0.80
22.50
98
110
50
54.57
6.28
12
74
298330
38
Parkinson
disease
strangulation
with C1and C2 #
Head injury
77.2
42.5
96.5
75.1
48.3
152.2
4.10
33
12
19.52
0.9
21.50
4.1
34.12 10.25
17.18
0.60
22.00
98
110
50
50
6.12
3.37
10
12
75
357343
42
OP Poisoning
50.1
44.5
55.66
78.1
44.5
156.2
4.40
32
12
22
0.8
22.50
4.33
31.88 11.55
21.32
0.50
23.94
97
124
54
55.11
6.66
3.88
12
15
76
333173
35
B/L pneumonia
59.6
44.3
74.5
88.8
45.3
222
4.05
20
33.75
0.8
21.20
4.05
24
22.5
0.40
21.20
96
126
68
96
127
68
6.6
77
358149
35
B/L pneumonia
77.7
47.5
97.12
79.2
45.3
113.14
2.25
24
12
18.75
0.8
22.50
2.25
25.5
13.63
0.70
22.50
95
127
80
95
117.75
80
3.25
3.25
12
78
356897
62
78.5
48.5
98.12
76.2
45.3
108.85
2.51
22
12
20.91
0.8
21.60
2.6
27.5
7.25
12.88
0.70
21.75
117
117
60
117.2 108.33
60.33
3.33
4.83
12
16
18
79
332997
62
bronchopneumonia
ARDS
76.5
49.2
95.62
85.5
44.5
244.28
2.92
22
12
29.2
0.8
22.50
2.92
25.64 9.35
17.97
0.35
22.21
120
110
70
123.4
105
70.57
7.71
4.21
14
17
21
80
300244
52
129
110
70
129
104
70
3.4
5.4
10
81
310932
134
110
70
131.8
110
70
3.75
4.87
10
15
82
299416
141.1 119.14
83
15
10
11
79.90
80.76
79.01
33
34
32
0.413
0.421
0.405
121.4 112.85
122
98.85 105.71
99
72.5
50.1
90.6
69.49
43.5
115.81
2.30
30
15
15.33
0.8
22.80
2.34
30.4
12.6
13.14
0.60
22.80
43
74.5
51.1
93.12
85.5
44.5
244.28
2.40
22
15
34.28
0.8
25.70
2.47
22.62 9.87
19.41
0.35
25.25
70
GI bleeding
72.5
52.5
90.62
65.49
44.5
93.55
2.90
30
15
19.33
0.8
24.50
3.09
32.55 11.66
14.81
0.70
25.05
140
110
70
300255
72
COPD
50.45
50.5
63.06
76.6
46.5
127.66
2.10
22
15
30
0.8
23.10
2.1
12.2
19.44
0.60
23.10
141
118
72
141
84
357597
75
60.25
50.5
66.94
85.7
45.5
244.85
4.20
24
12
35
0.9
21.50
4.2
22.66 6.66
26.25
0.35
21.50
79.01
32
0.405
130
110
70
85
358167
23
haemorhagic
strke
B/L pneumonia
61.9
52.1
68.77
88.9
48.5
222.25
4.21
24
12
35
0.9
22.10
4.21
25
11
30.07
0.40
22.10
79.6
32
0.402
135
110
86
300401
62
dengue
60.9
52.1
67.66
76.5
60.1
127.5
4.20
24
12
35
0.9
22.50
4.2
24
12
35
0.60
22.50
140
110
23
33
0.412
117
97.77 123.33
myocardial
infarction
OP Poisoning
80.09
113
62
1.5
1
1
2.5
2.5
70
4.66
4.55
13
15
118
72
3.8
5.2
10
130
110
70
7.33
5.33
2.5
70
134
110
70
15
2.5
70
140
110
70
PAP
PEEP
Vt/
Fi02
PAP-PEEP
MAWP
Vt
(ml/kg)
PAP
PEEP
Vt/
PAPPEEP
Fi02
MAWP
0.5
20.50
2.84
28.6
9.4
14.79
0.6
20.42
60.45
48.0
100.75
72.25
49.5
103.21
2.30
30.5
10
11.21
0.6
18.50
2.93
32.62
10.25
13.5
0.7
19.27
60.25
49.9
86.07
69.1
46.9
98.71
4.20
35
15
21
0.7
20.50
3.16
32
11.4
15.33
0.6
19.74
meningitis
59.75
48.3
74.68
79.1
45.9
131.83
2.30
28.5
15
17.03
0.8
20.50
2.78
27.41
11.66
17.67
0.3
16.88
54
ARDS
59.4
49.7
66
81.5
45.5
271.66
4.20
30
16.8
0.9
20.50
3.48
29.68
14.73
0.6
21.72
44
OP poisoning
60.1
49.8
75.12
75.5
49.4
125.83
4.35
25
10
29
0.8
21.50
3.31
26.28
14.14
27.29
0.5
25.30
262003
62
laparotomy
60.4
46.5
75.5
79.1
46.00
158.2
4.40
30
20
0.8
21.80
3.28
27.5
11.12
20.03
0.8
21.70
268046
48
laparotomy
54.2
45.6
77.42
78.2
47.1
97.75
2.30
30
10
11.5
0.7
22.50
3.17
27.22
11.22
19.82
0.3
23.00
270408
85
IHH
52.4
48.5
74.85
82.4
46.6
274.66
2.40
30
10.9
0.7
22.50
2.72
34.25
8.5
10.56
0.8
22.45
10
264091
54
pleural effusion
with ALD
55.5
49.5
92.5
78.1
49
97.75
2.50
30.5
10
12.19
0.6
25.80
3.32
29.75
13.1
19.93
0.4
22.83
11
273214
65
cholecystectomy
54.5
48.2
90.66
88.1
40.1
220.25
2.75
25
13.75
0.6
22.50
3.08
29.45
7.1
13.78
0.3
22.50
12
273280
35
GBS
63.5
49.7
127
82.5
40.2
275.00
2.85
30
12.95
0.5
21.50
2.91
30.83
6.6
12.03
0.8
22.81
13
267450
36
GBS
77.2
46.5
85.77
76.78
46.1
95.97
2.75
25
15
27.5
0.9
22.80
3.2
29
11.58
18.41
0.7
22.95
14
268280
23
OP poisoning
55.4
48.5
61.55
77.81
46.2
111.15
2.85
25.5
15
27.14
0.9
24.50
3.29
30.62
11.75
17.45
0.6
23.65
15
248130
21
OP poisoning
55.4
50.5
61.55
78.1
45.8
130.16
3.90
30
15
26
0.9
22.00
2.97
28.7
11
16.82
0.4
27.72
16
258013
38
GBS
55.4
44.5
110.8
82.99
43.5
206.75
2.95
25.5
14.39
0.5
28.50
3.38
31.55
7.7
14.2
0.4
26.38
17
298453
42
laparotomy
55.2
48.6
110.4
88.1
44.7
220.25
2.90
30
11.6
0.5
28.00
2.51
30.00
8.6
11.72
0.3
26.66
18
299413
39
GBS
60.25
49.5
120.5
84.3
45.1
281.00
2.30
25.5
11.21
0.5
23.70
2.55
31.68
7.6
10.31
0.3
23.24
19
27418
24
GBS
62.25
50.4
103.75
88.4
45.2
294.66
2.40
30
9.6
0.6
23.70
2.76
32.00
7.6
11.31
0.3
23.15
20
228196
52
asthma
63.23
51.4
105.38
88.1
42.3
293.66
3.15
25
15.75
0.6
22.10
3.06
32.25
7.1
12.2
0.4
22.30
21
292764
40
GBS
60.1
48.5
85.85
84.3
44.7
210.75
2.18
40
6.22
0.7
22.50
2.45
36.37
7.1
8.39
0.4
22.72
22
290241
42
B/L pneumonia
60.2
46.4
75.25
83.1
42.2
207.75
2.15
40
6.14
0.8
22.80
2.51
34.00
7.7
9.56
0.4
23.21
23
250188
65
40.5
45.5
50.62
69.1
45.2
86.37
3.05
40
15
12.2
0.8
23.90
3.4
34.63
12.45
15.32
0.8
24.09
24
282280
22
50.4
49.5
56
68.59
48.2
76.211
3.15
40
10
10.5
0.9
27.80
3.4
36.75
12.25
13.9
0.9
26.61
25
288117
43
cellulitis
50.25
50.5
55.83
72.9
47.2
91.125
3.05
40
10
10.16
0.9
25.30
3.23
37.3
12.1
12.81
0.8
25.40
26
286789
39
septicemia
57.25
52.5
63.61
71.9
49.2
89.875
3.15
40
9.84
0.9
22.50
3.16
37.62
9.87
11.38
0.80
22.76
27
272418
52
laparotomy
58.2
54.6
72.75
84.1
45.5
280.33
3.15
40
0.8
22.50
3.36
37.57
7.7
11.27
0.30
22.67
28
338867
55
RHD
59.2
52.5
65.77
85.3
40.5
284.33
3.50
40
10.93
0.9
22.50
3.33
38.33
7.6
10.87
0.30
22.60
29
339712
84
IHD
60.2
52.6
75.25
84.1
45.6
280.33
3.35
35
12.4
0.8
22.50
3.27
37.5
11.49
0.30
22.90
30
339315
25
CVA
61.2
55.6
76.5
69.75
45.5
99.642
3.05
42
10
9.53
0.8
21.10
3.23
39.14
10.39
0.20
21.70
31
338870
42
GBS
62.5
52.7
89.28
85.1
45.6
212.75
3.30
40
10.31
0.7
20.90
3.14
37.1
9.1
11.23
0.40
21.11
32
339986
59
GBS
63.7
52.1
91
87.1
48.6
290.33
3.50
40
10.93
0.7
21.20
3.64
38.33
6.8
11.54
0.30
19.70
33
339019
41
GBS
64.9
54.1
108.16
88.1
47.7
251.71
3.35
42
10.46
0.6
18.20
3.34
35.77
10.4
13.18
0.35
18.36
34
338533
62
ILD
65.9
55.5
131.8
72.15
48.8
120.25
3.20
40
10
10
0.5
17.20
36.5
9.1
10.98
0.40
25.20
35
339777
60
Diffused axonal
injury
60.0
52.1
120
81.1
44.5
202.5
3.20
42
8.64
0.5
17.50
3.57
39.2
8.2
11.53
0.40
20.70
36
337769
31
HIV with TB
70.1
56.1
175.25
72.91
49.6
104.15
3.15
40
12
11.25
0.4
18.90
3.36
35.9
10.9
13.47
0.70
19.31
37
337076
45
IHD
49.2
50.1
70.28
85.2
44.5
284
3.30
40
9.42
0.7
18.50
3.41
38.66
7.6
11
0.30
18.50
38
335554
60
IHD with MI
58.4
55.1
146
85.12
46.1
283.73
2.75
40
7.85
0.4
19.50
3.18
33.33
7.6
12.37
0.30
19.50
39
339714
36
Pneumonia
58.3
50.5
83.28
72.59
49.1
90.73
2.85
38
12
14.8
0.7
18.50
3.71
37.3
9.38
9.71
0.80
19.46
40
255394
61
ALD
54.5
48.5
77.85
88.42
45.1
294.73
2.75
40
8.59
0.7
17.50
2.65
38.25
8.7
8.96
0.30
18.20
264210
19
254230
267088
COPD with renal

failure
Diffused axonal
injury
OTHER COMPLICATIONS
Vt
(ml/kg)
17.3
WEANING Mode
Pa02/
Fi02
12
62
WEANING Duration (Days)
PaC02
25
Length of hospital Stay (Days)
Pa02
2.25
263230
Total duration in ICU (days)
Pa02/
Fi02
125.75
Total duration of Intubation (days)
PaC02
86
135
60
98.6
135.2
60.8
6.2
5.42
30
35
35
87
140
60
99.25
131.5
67.5
3.25
6.16
12
12
97
145
60
108.2
137.8
65.4
4.9
11
11
100
135
40
106.33
115.5
45.83
4.5
77.64
33
0.425
110
150
45
115.87
151.3
61
7.5
2.61
13
13
2.5
110
148
60
98.14
146.9
53.42
3.71
10
98
150
45
101.25
161.8
55.62
3.5
2.37
10
98
148
60
104.66
156.7
68.33
3.77
2.08
12
15
77.85
32
0.411
98
150
72
108.75
157
66.5
4.5
10
1.5
98
120
65
111
131.4
63.3
4.7
3.22
10
18
18
80.95
34
0.420
88
124
72
96.5
133.3
69.9
8.8
6.76
10
13
17
2.5
75.98
31
0.408
130
140
65
116.83
114
65
9.16
4.62
13
2.00
130
140
70
94.66
134.7
60.91
3.87
12
70
70
88
120
72
82.5
140.5
64.12
4.5
5.72
11
15
72
135
70
77
146.6
65.8
3.4
1.66
12
15
73.17
33
0.451
130
150
78
117.77
156.7
69.88
7.55
4.5
10
15
78.04
32
0.410
130
158
70
131.66
152
72.33
3.4
79.13
33
0.417
120
168
78
101.72
148
75.45
7.45
5.7
11
15
20
77.09
34
0.441
110
116
78
120.5
115.4
75.8
8.5
3.91
10
12
15
73.68
35
0.475
110
150
79
101.62
136.4
65.25
7.37
10
12
73.37
35
0.477
110
138
80
103.12
156.3
77.12
7.37
4.16
12
17
74.46
35
0.470
110
120
60
94.88
149.6
63.83
5.5
3.6
18
20
24
110
141
78
112.18
121.5
66.63
5.45
5.65
11
23
25
10
109
130
60
90.5
145.8
63.16
6.58
7.17
12
63
70
101
120
78
88
112.3
66.2
3.8
3.37
10
15
2,7
110
110
70
111.87
106.6
66.5
3.25
4.85
10
73.75
34
0.416
108
121
60
104.14
113.1
59.14
2.07
14
18
74.82
33
0.441
110
110
70
105.33
112.7
65
8.66
3.33
20
78.08
32
0.410
110
110
50
109
105
45
8.5
3.5
20
88
110
50
89.28
99.28
53.42
5.71
3.5
15
2
Hrs
0
78.19
33
0.422
110
110
60
106.86
114.9
69.4
3.05
15
17
20
74.94
32
0.427
130
100
50
118.5
108.3
56.5
7.58
4.28
12
74.3
35
0.471
113
100
60
104.11
95.66
67.22
9.44
5.81
11
15
99
100
62
106
91.8
57.9
4.2
10
10
2,7
80.95
34
0.420
110
109
64
105.8
116
61.3
6.6
6.63
10
11
16
98
109
64
101.72
104.6
58.09
3.63
4.77
11
11
73.17
30
0.410
127
100
64
129
103.3
58.66
8.66
3.75
10
78.75
33
0.419
110
110
60
120
109.7
58
8.66
3.6
13
130
110
50
117..69 123.8
60.38
3.76
2.2
13
10
77.3
31
0.401
80
130
50
120.87
53.12
8.72
4.2
10
16
Baseline
49.2
60
Mean Score
Pa02
Mean
75.45
Baseline Score
Baseline
110.9
264231
Mean Score
Mean
51.0
Baseline Score
Baseline
55.45
24
RSBI
VITAL SIGNS
258703
Ventilator associated Pneumonia

(VAP)
Initial ventilation mode
OXYGEN STATUS PARAMETERS
RADIOLOGICAL PARAMETERS
sub acute
haemorrhage
acute renal
failure
COPD with renal
failure
Type of Intubation
Admission
diagnosis
Ward
IP No
Age (yrs)
Sl.
No.
Sex
STUDY GROUP
RR/ Vt RR
Mean
Spont Vt
score
PR
BP
SBP DBP
PR
BP
SBP DBP
138.3
Glasgow
ComaScore
(GCS)
Clinical
Pulmonary
Infection Score
(CPIS)
41
311950
67
Pleural effusion
with ALD
55.6
49.6
69.5
88.52
45.4
295.06
3.85
35
14.25
0.8
20.50
3.53
35.75
9.5
13.46
0.30
20.92
42
302284
60
hemiplegia
55.6
45.5
69.5
81.17
44.3
202.92
3.50
38
10.60
0.8
22.50
3.36
38.66
8.5
11.16
0.40
22.60
43
297141
47
POST. OP. CA.

CAELUM
66.6
51.6
74
87.12
45.5
290.4
2.95
40
9.21
0.9
20.50
2.97
38.08
10.05
10.62
0.30
21.80
44
297204
48
pyothorax
60.6
52.5
67.33
82.45
44.9
274.83
3.05
38
9.24
0.9
22.50
2.61
24.12
10.25
18.85
0.30
23.75
45
300244
52
IHD WITH AWMI
61.6
53.5
77
80.12
45.1
267.06
3.15
25
18.52
0.8
24.50
2.9
32.66
11.77
0.30
25.60
46
307067
55
IHD
66.6
56.5
95.14
80
44.1
200
2.69
40
7.68
0.7
28.90
2.91
34.07
9.14
11.66
0.40
28.10
47
314465
19
brain abcess
67.2
55.5
96
87.12
43.2
290.4
2.85
25
19.25
0.7
24.50
3.12
28.13
10.18
17.42
0.30
24.73
48
331729
57
pneumonia
68.2
54.7
97.42
87
42.1
217.5
3.15
25
15.75
0.7
23.20
26
7.66
16.72
0.40
23.43
49
294617
63
post. Op.
GLIOMA
68.2
51.7
97.42
80.1
41.7
200.25
3.15
35
10.5
0.7
24.50
2.8
29.61
8.8
13.46
0.40
25.11
50
312280
48
LVD with IHD
69.2
52.1
98.85
80.4
36.2
201.00
4.00
25
23.52
0.7
22.90
4.06
33.6
15.86
0.40
22.88
51
330410
49
asthma
69.2
58.1
98.85
89
38.2
222.5
4.15
25.5
20.24
0.7
22.50
3.93
21.75
26.69
0.40
22.57
52
316241
59
IHD
70.12
56.1
116.86
80.2
39.1
200.5
4.25
28
18.47
0.6
23.50
29.16
6.6
17.73
0.40
23.50
53
306451
62
IHD
54.25
44.5
90.41
80.4
40.2
201
4.17
29.5
17.02
0.6
22.60
4.12
29.83
7.6
18.54
0.40
22.60
54
346780
43
laparotomy
54.25
48.5
90.41
79.9
44.9
266.33
4.20
32.5
15.27
0.6
23.60
3.6
26.77
7.7
19.6
0.30
23.20
55
337485
52
55.4
49.6
92.33
78.25
44.6
260.83
4.75
28
20.65
0.6
24.80
4.22
29.4
9.4
21.14
0.30
24.52
56
345210
41
40.5
49.5
67.5
72.15
47.4
90.187
4.50
38.5
12
16.98
0.6
20.90
4.3
39.62
12.75
16
0.80
20.90
57
346638
48
54.5
45.5
90.83
77.12
44.9
257.06
4.25
38
12.87
0.6
21.50
3.57
29
9.1
18.71
0.30
21.50
58
396233
78
74.5
56.4
124.16
78.12
42.4
260.4
4.20
38
12.72
0.6
18.70
3.53
34.33
9.3
14.12
0.30
18.70
59
346391
74
MENINGITIS
46.1
52.1
76.83
78.1
47.5
130.16
2.80
25.5
12
20.74
0.6
18.50
2.65
29.1
9.2
13.33
0.60
18.66
60
346798
70
Lt. HEMIPLEGIA
60.2
55.1
86
77.21
42.9
257.36
2.75
28
13.75
0.7
18.50
2.65
29.6
9.4
18.06
0.30
18.50
61
347095
63
B/L PNEUMONIA
65.5
54.5
93.57
89.1
44.5
222.75
2.80
28.5
13.65
0.7
17.50
2.87
30
10
14.37
0.40
17.50
62
347037
72
66.6
56.6
95.14
80.1
45.1
267
2.85
28.5
13.9
0.7
17.80
2.96
32.31
9.62
13.12
0.30
18.20
63
358017
65
66.7
54.6
83.37
69.45
48.9
120.15
3.05
38.5
10
10.70
0.8
16.50
3.23
35.68
11.5
13.36
0.30
17.65
64
326145
45
69.9
54.4
77.66
68.1
46.1
125.25
2.20
25
15
22
0.9
19.50
3.28
32.61
10.11
14.61
0.30
20.05
65
360101
61
70.1
56.9
77.88
85.15
40.9
207.15
3.15
35.5
12
13.40
0.9
20.50
3.19
35.15
10.7
13.04
0.30
23.15
66
358830
56
74.2
52.4
74.2
86.15
42.1
287.25
3.20
38.5
15
13.61
23.50
3.23
37.45
9.63
11.61
0.40
24.09
67
351784
40
62.1
55.4
69
80.25
36.5
221.7
3.15
35.5
12
13.40
0.9
23.40
3.08
36.5
9.71
11.51
0.40
23.48
68
313945
40
56.1
52.1
62.33
79.1
50.9
131.7
2.75
40.5
15
10.78
0.9
22.80
2.74
39
11.66
10.04
0.30
23.35
69
331412
42
MT with ARF
MI with
PULMONARY
EDEMA
alcoholism
Head Injury with
Rt. Frontal
Contusion
MI
54.2
48.2
67.75
78.1
50.1
138.9
2.70
38.5
15
11.48
0.8
18.50
37
13
12.5
0.60
18.50
70
357295
71
COPD
66.6
49.5
83.25
82.35
44.1
202.45
2.70
35
18
15.88
0.8
19.80
2.3
34.25
13
10.82
0.60
19.80
71
328115
62
CAD
67.2
50.2
96.71
84.25
39.8
224.45
2.80
30
15
18.66
0.7
17.90
3.08
30.12
14.5
19.76
0.70
17.90
72
323980
37
B/L pneumonia
68.2
54.5
113.66
85.4
39.8
204.45
2.15
30.5
18
17.2
0.6
17.50
2.24
30.8
12.6
12.32
0.50
17.50
73
320190
48
GBS
69.1
56.5
115.16
85.2
48.1
96.12
2.20
35.5
18
12.57
0.6
19.80
2.41
36.1
12.2
10.08
0.30
19.80
74
377401
18
Closed Head
Injury SDH
54.5
54.5
109
86.5
42.5
200.45
2.50
30
15
16.66
0.5
20.80
3.3
33.25
13.33
16.56
0.30
20.80
75
330568
74
IHD with MI
62.5
52.1
125
85.5
43.9
227.7
3.30
35.5
12
14.04
0.5
20.50
3.65
37.33
12.33
14.6
0.40
21.00
76
346690
45
GBS
62.1
53.4
124.2
86.15
40.9
205.45
3.50
35.5
15
17.07
0.5
21.50
2.79
36.14
10.85
11.04
0.30
22.24
77
372508
30
GBS
54.2
50.1
108.4
84.12
45.1
225.45
3.30
37.5
16
11
0.5
17.80
3.56
37.5
12.75
14.41
0.30
17.15
78
313820
60
AWMI with HTN
59.4
54.1
118.4
83.25
44.5
207.15
3.15
37.94
15
12.35
0.5
19.50
3.07
37.94
12.11
11.91
0.30
20.83
79
377638
35
Closed Head
Injury DAI
60.1
50.9
120.5
70.12
49.5
220.15
3.00
38.05
10
10
0.5
20.50
3.72
38.05
11.2
13.64
0.30
22.05
80
302149
21
OP POISONING
62.15
52.1
124.3
83.12
50.5
214.15
3.15
37.31
10
12.6
0.5
25.80
3.21
37.31
10.87
12.17
0.30
25.35
81
375966
55
Post Laprotomy ARDS
65.15
60.1
130.3
84.12
45.9
220.15
3.30
36.68
10
11
0.5
28.10
3.09
36.68
10.54
11.84
0.30
27.73
82
377539
42
ARDS
66.15
56.2
132.2
86.4
45.9
274.27
4.05
35.83
11.42
0.5
24.50
3.37
35.83
6.11
11.34
0.30
24.24
83
376916
24
thrombocytopeni
a
72.1
55.4
144.2
82.14
40.9
287.14
4.15
36.6
10
13.83
0.5
18.50
4.25
36.6
8.6
15.17
0.30
18.50
84
376189
87
COPD
62.15
54.8
124.3
85.14
40.5
287.27
4.20
36.35
10
13.77
0.5
19.50
4.15
36.35
13.23
0.30
19.78
85
317097
64
IHD c PTCA
49.9
54.1
124.75
84.4
38.5
287.4
4.15
33.35
10
13.83
0.4
20.50
3.05
33.35
6.71
11.45
0.30
21.05
86
326410
42
Head injury
59.9
50.9
149.75
79.9
49.9
120.47
3.02
39.63
10
10.78
0.4
28.90
3.51
39.63
8.45
11.26
0.3
28.00
87
333534
56
IHD
60.1
48.5
150.25
86.6
38.6
284.36
2.65
39.21
10
8.68
0.4
17.80
3.32
39.21
10.14
11.43
0.3
17.80
COPD c RENAL
FAILURE
Met.
Encephalopathy
COPD c RENAL
FAILURE
Met.
Encephalopathy
SEPSIS with
ARDS
Closed Head
Injury c SDH
Traumatic Head
Injury
77.85
32
0.411
78
130
50
84
137.5
47
8.25
4.33
10
78.98
33
0.418
88
135
50
94.83
147.8
54.13
8.33
4.5
11
80.09
34
0.412
110
110
60
123.41
116.9
71.11
7.29
4.16
17
18
20
68.75
33
0.480
68
100
50
75.75
92.75
57.5
2.4
10
15
72.72
32
0.440
110
110
50
109.66
106.2
57.66
8.16
3.14
16
68.58
31
0.450
98
117
50
103.85
111
59.71
9.14
3.5
17
71.57
34
0.475
108
110
60
122.72
102.5
63.9
9.27
3.2
11
16
1.5
71.12
34
0.478
88
117
62
96
111
62
8.33
4.5
10
71.11
32
0.450
110
100
50
112
124
59.88
6.77
4.16
12
17
66.23
31
0.468
110
117
62
107.8
109.2
56.8
4.16
13
71.12
34
0.478
121
100
51
112.75
105.3
54.75
8.25
15
67.76
33
0.487
110
110
50
124
106.7
56.66
10
10
16
79.43
34
0.428
120
110
50
122.66
106.7
46
10
10
3.57
17
1.5
72.36
33
0.456
113
100
50
123
87.5
47.5
3.25
20
69.47
33
0.475
128
100
54
123.2
80
58.6
8.6
2.66
21
2.5
130
110
58
120
97.5
59.75
9.25
6.7
10
10
69.92
33
0.474
127
110
55
115.16
100
58.33
8.16
3.1
10
16
65.81
33
0.471
103
107
54
112.16
105.3
57.33
9.83
3.57
17
2.5
113
110
54
123.2
98
58
8.8
79.81
34
0.426
108
100
54
106.2
94.4
58.2
8.8
10
1.5
70.51
33
0.468
108
120
54
109
125.5
54.75
4.25
10
2.0
77.43
35
0.452
110
100
55
105.62
98.12
58
9.62
3.5
10
16
1.0
111
100
54
121.75
100.1
60.25
9.5
6.14
10
10
111
124
54
110.11
132.9
57.44
6.44
6.1
10
15
10
78.57
33
0.420
90
151
55
99.4
136.2
58.4
6.6
10
10
16
3.5
81.92
34
0.415
100
100
54
113.27
98.9
61.63
7.36
11
16
2.5
79.8
32
0.401
121
126
48
125.57
132.4
52
8.42
4.12
10
3.00
0.00
108
128
54
117.16
130.7
56.16
8.33
3.33
13
115
130
40
123
116.6
45.2
9.4
3.5
12
14
81.48
33
0.405
108
120
40
116.75
112.8
47
9.5
3.91
12
17
1.00
73.89
30
0.406
110
110
40
122.5
114.5
47
10
10
3.9
10
18
81.92
34
0.415
110
105
52
115
108.2
46.2
9.6
4.16
12
15
100
110
48
116.6
100
50.2
4.4
3.3
10
18
79.13
33
0.417
120
106
66
121.5
92.66
69
5.06
15
15
76.55
32
0.418
130
110
78
125.16
95
75.83
7.33
4.37
16
16
80
34
0.425
110
100
70
92.85
105.3
64
5.11
17
17
81.48
33
0.405
120
100
72
122.25
98.5
76.12
9.5
4.83
12
15
79.8
32
0.401
110
100
78
120.55
86.44
67.33
8.11
5.06
15
21
110
100
72
111.3
98.8
71.6
5.3
6.4
10
10
20
110
80
72
120.87
87.5
57
5.12
7.41
12
15
78.57
33
0.420
110
90
72
118
100
72.27
8.9
4.8
11
15
17
2.5
80.56
34
0.422
110
110
60
122.11
100
62.44
7.77
4.37
16
15
1.5
71.77
30
0.418
121
90
50
118.6
99.6
48
7.8
3.3
10
13
66.66
30
0.450
110
110
60
118.57
92.85
64.28
4.12
13
2.5
81.33
34
0.418
130
110
62
126.42
99.57
53.71
3.64
14
15
3.5
131
100
72
128.36
108.7
58.27
5.25
4.5
11
10
10
79.51
33
0.415
113
117
78
113.14
96.71
66
8.57
3.8
10
2.4
GLOBAL OUTCOME
2
2
2
2
1
3
2
2
1
3
1
1
2
2
2
1
1
1
1
1
1
1
2
2
3
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Chest Physiotherapy in Mechanical Ventilated Patients

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Chest Physiotherapy in Mechanical Ventilated Patients

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EFFECT OF MULTIMODALITY CHEST PHYSIOTHERAPY

(Accredited A Grade by NAAC)

For the award of the degree of

Renu B. Pattanshetty M.P.T

Under the Guidance of

Prof. Dr. Gajanan. S. Gaude M.D.,DNB, F.C.C.P.

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

(Accredited A Grade by NAAC)

PROSPECTIVE STUDY IN MEDICAL AND SURGICAL INTENSIVE CARE UNITS

a bonafide and original research carried out by me under the guidance of

Professor, Department of Pulmonary Medicine,

K.L.E Universitys JN Medical College, Belgaum. The thesis or any part

Renu B. Pattanshetty M. P.T.

KLEU Institute of Physiotherapy,

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

(Accredited A Grade by NAAC)

entitled EFFECT OF MULTIMODALITY

CHEST PHYSIOTHERAPY ON THE RATE OF RECOVERY AND PREVENTION OF

PROSPECTIVE STUDY IN MEDICAL AND SURGICAL INTENSIVE CARE UNITS

a bonafide and genuine research carried out by Renu B. Pattanshetty under

Prof. & Head,

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

(Accredited A Grade by NAAC)

entitled EFFECT OF MULTIMODALITY

CHEST PHYSIOTHERAPY ON THE RATE OF RECOVERY AND PREVENTION OF

PROSPECTIVE STUDY IN MEDICAL AND SURGICAL INTENSIVE CARE UNITS

a bonafide and genuine research carried out by Renu B. Pattanshetty under

Prof. Dr. Sanjiv Kumar

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

(Accredited A Grade by NAAC)

entitled EFFECT OF MULTIMODALITY

CHEST PHYSIOTHERAPY ON THE RATE OF RECOVERY AND PREVENTION OF

PROSPECTIVE STUDY IN MEDICAL AND SURGICAL INTENSIVE CARE UNITS

a bonafide and genuine research carried out by Renu B. Pattanshetty under

Prof. Dr. V.D. Patil

Dean, Faculty of Medicine,

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

(Accredited A Grade by NAAC)

DR. GAJANAN S. GAUDE M.D.,DNB, FCCP

KLE ACADEMY OF HIGHER EDUCATION AND RESEARCH,

MATERIAL AND METHODS

ANNEXURE I- Ethical clearance certificate

ANNEXURE II Informed consent form

ANNEXURE III Photographs

ANNEXURE V- Master chart

I am grateful to Mr. M.D. Mallapur, Assistant Professor, Dept. of

Renu B. Pattanshetty M.P.T

Discharge against medical advice-

Was defined as an outcome that was

physicians and/or surgeons advice due to what so ever reasons.

Discontinuation of the treatment was defined as abrupt stopping of the chest

Acute respiratory distress syndrome

Acute physiology and chronic health evaluation system II

Acute lung injury

Assist pressure release ventilation

Arterial blood gas analysis

Clinical pulmonary infection score

Coronary artery by - pass graft

Dynamic lung compliance

Diastolic blood pressure

Discharge against medical advice

End expiratory lung volume