Indian J. Anaesth.
2003; 47 (5) : 360-366
360
RESPIRATORY FAILURE
Dr. Praveen Kumar Neema
Respiratory failure in patients admitted to critical
care unit (CCU) is a major cause of morbidity and
mortality. Patients can get into CCU because of respiratory
failure secondary to pulmonary pathology like pneumonia;
in many other patients respiratory failure is secondary to
sepsis, cardiac failure or neurological disorders. Obviously,
respiratory failure involves diverse pathology.
The respiratory system performs the vital function
of gaseous exchange.1 O2 is transported through the upper
airways to the alveoli that diffuses across the
alveolocapillary membrane and enters the capillary blood.
There, it combines with haemoglobin and is transported
by the arterial blood to the tissues. In the tissues the O2
is utilized for adenosine triphosphate production which is
essential for all metabolic processes. The major by product
of cellular metabolism, CO2, diffuses from the tissues into
the capillary blood, where a major portion of it is hydrated
as carbonic acid and transported to the lungs by the venous
blood. In the lungs, it diffuses from the pulmonary blood
into the alveoli and is exhaled into the atmosphere
(Expiration). Gaseous exchange appropriate to the metabolic
demand is essential to maintain homeostasis (the milieu
interior of the body). Respiration is accomplished and
regulated by an intricate set of structures.2 These structures
include: (1) the lungs that provide the gas exchange surface;
(2) the conducting airways that convey the air into and out
of the lungs; (3) the thoracic wall that acts as a bellows
and supports and protects the lungs; (4) the respiratory
muscles that creates the energy necessary for the movement
of air into and out of the lungs; and (5) the respiratory
centres with their sensitive receptors and communicating
nerves that control and regulate ventilation. Pathologic
processes can affect any of these functional components.
The interactions of cardiopulmonary, nervous and
musculoskeletal systems can be disrupted by disease, by
surgery and by anaesthetic agents. Respiratory failure can
be defined as a significant impairment in the gaseous
exchange capacity of the respiratory system. Traditionally
respiratory failure has been a clinical diagnosis; however,
with the easy availability of blood gas analysis, respiratory
failure is considered in terms of impairment of its actual
1. M.D., PDCC
Associate Professor, Department of Anaesthesiology,
Sree Chitra Tirunal Institute for Medical Sciences and
Technology, Trivandrum, Kerala.
Correspond to :
E-mail : praveenneema@yahoo.co.in
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
360
gaseous exchange functions that is oxygenation failure
(arterial hypoxaemia) or CO2 removal failure (hypercapnia,
ventilatory failure) or failure of both the functions. Non –
respiratory functions of the lung include metabolic,
secretory and immunologic functions. These functions are
not discussed further in this review.
This review is mainly confined to physiology of
respiration and pathophysiological mechanisms that lead to
respiratory failure. Various disorders that cause different
types of respiratory failure are also briefly mentioned.
Though, a general guideline of management is presented,
a detailed discussion on management is out of the scope
of this review
Physiology of respiration
Gaseous exchange between the environment and the
pulmonary capillary blood constitutes external respiration.
The functioning unit of the lung is alveolus with its capillary
network. Various factors govern transport of air from the
environment to the alveoli (ventilation) and supply of blood
to the pulmonary capillaries (perfusion).
Henry’s law dictates that when a solution is exposed
to an atmosphere of gas an equilibration of partial pressures
follow between the gas molecules dissolved in the liquid
and the gas molecules in the atmosphere. Consequently,
partial pressure of O2 and CO2 in the blood leaving the
pulmonary capillaries (pulmonary venous blood) is equal
to the partial pressure of O2 and CO2 achieved in the
alveolus after equilibration.3 At equilibrium, the partial
pressure of O2 and CO2 results from a dynamic equilibrium
between O2 delivery to the alveolus and O2 extraction
from the alveolus; and CO2 delivery to the alveolus and
CO2 removal from the alveolus.
Delivery of O2 to the alveolus is directly related
to the sweep rate of air (ventilation), and composition of
the sweeping gas (partial pressure of O2 in the inspiratory
air; FIO2). In general, alveolar O2 tension (PAO2) increases
with increase in inspiratory O2 tension and increase in
ventilation. Extraction of O2 from the alveolus is determined
by the saturation, quality and quantity of the haemoglobin
of the blood perfusing the alveoli. The O2 saturation of the
haemoglobin in the pulmonary capillary blood is affected
by the supply of O2 to the tissues (cardiac output) and the
extraction of the O2 by the tissues (metabolism). In general,
lower the haemoglobin saturation in the blood perfusing
the pulmonary capillaries, a result of low cardiac output
NEEMA : RESPIRATORY FAILURE IN ICU
(increased tissue extraction) and/or increased tissue
metabolism, higher the extraction of O2 in the alveoli and
lower the equilibration partial pressure of O2. Similarly
the absolute quantity of haemoglobin in the circulating
pulmonary blood also increases or decreases extraction of
O2, though this particular factor is less important. The
partial pressure of O2 in the alveolus is further affected by
the partial pressure of CO2 in the pulmonary capillary
blood. As mentioned earlier partial pressure of CO2 in the
alveolus is because of dynamic equilibrium between CO2
transported to the alveolus and CO2 removed from the
alveolus. Amount and the partial pressure of CO2 in the
alveolus increases with the increase in tissue metabolism
and in presence of low cardiac output (CO2 produced in
the tissues is transported in less amount of the venous blood).
Ventilation and perfusion is further influenced by
variation in distribution of ventilation and perfusion. The
major determinants of distribution of pulmonary blood flow
include cardiac output, pulmonary artery pressure, gravity,
posture, and interaction of pulmonary artery pressure with
airway pressure and pulmonary venous pressure. In general,
perfusion is more at the lung bases as compared to the
apex and this difference increases with decrease in cardiac
output, hypotension and with the application of positive
pressure ventilation. Distribution of ventilation is influenced
by regional transpulmonary pressure (TPP) gradient and
changes in the TPP during inspiration. In general alveolar
volume is bigger in the apical regions as compared to the
alveolar volume at the base and ventilation is more at the
base as compared to the apex.
Theoretically, the most efficient gaseous exchange
would occur if a perfect match exists between ventilation
and perfusion in each of the functioning unit of the lung.
The partial pressure of O2 and CO2 contained in each
alveolus, and therefore of the capillary blood leaving it,
are primarily determined by the ventilation perfusion ratio
of that alveolus.4 The functioning unit can exist in one of
the four absolute relationships (Fig. 1): (1) the normal
unit in which both ventilation and perfusion are matched;
(2) the dead space unit in which the alveolus is normally
ventilated but there is no blood flow through the capillary;
(3) the shunt unit in which the alveolus is not ventilated
but there is normal blood flow through the capillary; and
(4) the silent unit in which the alveolus is unventilated and
the capillary has no perfusion. The complexities of the
ventilation-perfusion (VA/Q) relationship are caused
primarily by the spectrum between the two extremes of
dead space and shunt units (Fig 2). The lung consists of
millions of alveoli with its network of capillaries. In health
and disease states ventilation and perfusion relationship
can exist in various combinations. Needless to say, the
361
partial pressure of O2 and CO2 in the arterial blood
obviously reflects sum total of effect of all the factors
discussed in the preceding section.
Effect of ventilation-perfusion imbalance: The
partial pressure of O2 and CO2 in each alveolus and
therefore of the capillary blood leaving it are primarily
determined by the ventilation-perfusion (VA/Q) ratio of
that alveolus. As the ratio between ventilation and perfusion
decreases, the partial pressure of the O2 falls and that of
CO2 rises in the blood leaving that alveolus. The opposite
occurs as ventilation perfusion ratio increases (Fig. 2).
Any pathological process that affects the airways, lung
parenchyma and vasculature of the lungs will cause an
imbalance between ventilation and perfusion and will
produce areas of abnormal ventilation-perfusion ratio. The
extent to which gas exchange is impaired depends on both
the values of the ventilation-perfusion and the shape of
their distribution. It is important to realize that arterial
hypoxaemia and hypercapnia results from regions of lungs
with low ventilation-perfusion ratio. Areas with high
ventilation-perfusion ratio do not adversely affect the arterial
blood gas tensions; however they increase the amount of
wasted ventilation (Dead space effect). Areas of the lung
with low ventilation-perfusion contribute blood with a low
partial pressure of O2 to the pulmonary venous blood.
Areas of the lung with high ventilation-perfusion contribute
blood with a high partial pressure of O2 to the pulmonary
venous blood; however, these areas of high and low
ventilation-perfusion do not counterbalance each other for
two reasons – first, the areas of low ventilation-perfusion
generally receive more blood flow than the areas of high
ventilation-perfusion; second, because of non-linear shape
of the O2- haemoglobin dissociation curve,5 the higher
partial pressure of O2 of the blood leaving high ventilation-
perfusion areas does not translate into a proportionate
362
increase in haemoglobin saturation and O2 content and
therefore provides little extra O2 to the blood leaving these
areas of high ventilation-perfusion. As mentioned earlier
in the perfused alveoli with no ventilation, the shunt units,
(Fig. 1 C) venous blood passes unchanged through these
units. This is an intrapulmonary right to left shunt and
causes hypoxaemia by addition of the venous blood to the
arterial blood. Ventilation-perfusion mismatch usually does
not lead to increase in the partial pressure of CO2 because
stimulation of the chemoreceptor increases minute
ventilation to maintain partial pressure of CO2 within the
normal range. However, increase in partial pressure of
CO2 will occur if an increase in the ventilation is limited
by respiratory depression, neuromuscular disability or
excessive work of breathing.
Effect of low-haemoglobin saturation in the
pulmonary capillary (venous) blood: Low cardiac output
and increased tissue metabolism are the reasons of low
haemoglobin saturation. Normal haemoglobin saturation in
the mixed venous blood that perfuses through pulmonary
capillaries is 75%. Low-haemoglobin saturation per se
does not affect oxygenation in the alveoli provided
ventilation is adequate. However, ventilation-perfusion
mismatch will exist in the presence of low cardiac output.
Low-haemoglobin saturation produces arterial hypoxaemia
by three mechanisms – first, the blood leaving the areas
of low ventilation-perfusion will contribute blood with a
lower partial pressure of O2 because of the lower
equilibration partial pressure (haemoglobin with low
saturation will extract more O2 before becoming saturated
thereby reducing partial pressure of O2 in the alveolus),
second, the effect of the shunt units will be exaggerated
due to low saturation of venous blood, third, decreased
arterial O2 content will lead to further decrease in O2
supply to the tissues, if tissue O2 consumption remains
unchanged, venous O2 saturation will further decrease. It
is clear that the presence of low-cardiac output state
compounds the effects of low ventilation-perfusion areas
and shunt areas.
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
Evaluation of ventilation-perfusion imbalance
The severity of ventilation-perfusion imbalance may
be assessed by several measurements based on ideal alveolar
gas equation which represents mixed alveolar gas in the
absence of ventilation–perfusion imbalance. The PAO2 is
calculated from a modified alveolar gas equation.
PAO2 = (PB – PH2O) FIO2 – PaCO2/R,
Where PB is the barometric pressure, PH2O is the
water vapour pressure in the alveoli, R is the respiratory
quotient, and PaCO2 is the partial pressure of CO2 in the
arterial blood. The different measurements used in the
clinical practice to evaluate ventilation-perfusion imbalance
are –
1. Alveolar-arterial O2 partial pressure difference (PAO2
– PaO2),
2. Venous admixture effect or shunt effect – Qva/Qt =
(Cc’O2 – CaO2)/(Cc’O2 – CvO2)
Where Qva is venous admixture, Qt is cardiac
output; Cc’O2, CaO2, and C½”O2 are O2 content in ideal
capillary blood (blood leaving the alveoli with a perfect
match between ventilation and perfusion), arterial blood
and mixed venous blood, respectively. Calculation of venous
admixture at 100% inspiratory O2 tension (FIO2=1)
removes the contribution of low ventilation-perfusion units
and measures the true shunt fraction (Qs/Qt).
3. Dead space effect, the volume of inspired air that do
not participate in gaseous exchange
Vd/VT = PaCO2 – PECO2/PaCO2
Where Vd is wasted ventilation; dead space, VT is
tidal volume, PaCO2 and PECO2 are partial pressure of
CO2 in arterial blood and mixed exhaled gas. Unfortunately,
the clinical usefulness of all the three measurements is
limited because of the fact that they are influenced by both
– the changes in minute ventilation and the cardiac output
apart from ventilation-perfusion imbalance.
Classification of respiratory failure
On the basis of arterial blood gas analysis,
respiratory failure may be divided into three types. Type
I or oxygenation failure, Type II or ventilatory failure,
Type III or combined oxygenation and ventilatory failure.
Type I Respiratory Failure (Oxygenation Failure;
Arterial Hypoxaemia): Partial pressure of O2 in the arterial
blood reflects: (1) Partial pressure of O2 in inspiratory
gas; (2) minute ventilation; (3) quantity of blood flowing
through pulmonary capillaries; (4) O2 saturation of the
haemoglobin in the blood flowing through pulmonary
capillaries (an effect of tissue metabolism and cardiac
NEEMA : RESPIRATORY FAILURE IN ICU
output); (5) diffusion across alveolar membrane; and (6)
ventilation-perfusion matching (Fig. 3). Type I failure is
characterized by an abnormally low partial pressure of O2
in the arterial blood. It may be caused by any disorder that
produces areas of low ventilation-perfusion or a right to
left intrapulmonary shunt and is characterized by low partial
pressure of O2 in the arterial blood (PaO2 < 60 mm Hg
while breathing room air), an increase in PAO2 – PaO2
difference, venous admixture and Vd/VT.
Pathophysiologic mechanisms of arterial hypoxaemia:
A. Decreased partial pressure of O2 in alveoli
1. Hypoventilation
2. Decreased partial pressure of O2 in the inspired air
3. Underventilated alveoli (areas of low ventilation-
perfusion)
B Intrapulmonary shunt (areas of zero ventilation-perfusion)
C Decreased mixed venous O2 content (low-haemoglobin
saturation)
1. Increased metabolic rate
2. Decreased cardiac output
3. Decreased arterial O2 content
Causes of Type I (Oxygenation) respiratory failure:
1. Adult respiratory distress syndrome (ARDS)
2. Asthma
3. Pulmonary oedema
4. Chronic obstructive pulmonary disease (COPD)
5. Interstitial fibrosis
6. Pneumonia
7. Pneumothorax
363
8. Pulmonary embolism
9. Pulmonary hypertension
Type II Respiratory Failure (Ventilatory Failure:
Arterial Hypercapnia): Partial pressure of CO2 in the
arterial blood reflects the efficiency of ventilatory
mechanism that clears (washes out) CO2 produced during
tissue metabolism. Type II failure can be caused by any
disorder that decreases central respiratory drive, interferes
with the transmission of signals from the central nervous
system, or impedes the ability of respiratory muscles to
expand the lungs and chest wall. Type II failure is
characterized by an abnormal increase in the partial pressure
of CO2 in the arterial blood (PaCO2 > 46 mm Hg), and
is accompanied by simultaneous fall in PAO2 and PaO2,
therefore PAO2 - PaO2 difference remains unchanged.
Common causes of Type II Respiratory Failure:
A. Disorders affecting central ventilatory drive
1. Brain stem infarction or haemorrhage
2. Brain stem compression from supratentorial mass
3. Drug overdose, Narcotics, Benzodiazepines,
Anaesthetic agents etc.
B. Disorders affecting signal transmission to the respiratory
muscles
1. Myasthenia Gravis
2. Amyotrophic lateral sclerosis
3. Gullain-Barrè syndrome
4. Spinal –Cord injury
5. Multiple sclerosis
6. Residual paralysis (Muscle relaxants)
C. Disorders of respiratory muscles or chest-wall
1. Muscular dystrophy
2. Polymyositis
3. Flail Chest
Type III Respiratory Failure (Combined Oxygenation
and Ventilatory Failure): Combined respiratory failure
shows features of both arterial hypoxaemia and hypercarbia
(decrease in PaO2 and increase in PaCO2). Assessment
based on alveolar gas equation shows an increase in PAO2
– PaO2 difference, venous admixture and Vd/VT. In theory,
any disorder causing Type I or Type II respiratory failure
can cause Type III respiratory failure.
Common causes of Type III respiratory Failure:
1. Adult respiratory distress syndrome (ARDS)
2. Asthma
3. Chronic obstructive pulmonary disease
364
Compensatory Mechanisms in presence of respiratory
failure:
The response to hypoxaemia depends on the ability
of the patient to recognize the hypoxemic state and then
to increase cardiac output and minute ventilation to improve
the situation. Peripheral chemoreceptors located in the arch
of aorta and at the bifurcation of carotid artery send afferent
signals to the brain.
Assessment of Pulmonary Function in Critically Ill
Patients:
The primary aim of respiratory system is gaseous
exchange (cardiopulmonary interaction) in the lung
parenchyma. Airways provide conduit for the passage of
air from the environment to the lungs, the neuromuscular
system ensures ventilation and the lung parenchyma
provides the ground for interaction between ventilation
and perfusion. Health of the lung parenchyma and the
airways determines the load (work of breathing) placed on
the neuromuscular system; increased load due to lung
disease or airway disease can stress and precipitate failure
of the neuromuscular system. Deterioration in pulmonary
function in critically ill patients can be because of the
inadequacy of airways, lung parenchyma, cardiopulmonary
interaction and neuromuscular system. The assessment of
pulmonary function is of particular importance in (1)
deciding whether ventilation is indicated, (2) assessing
response to therapy, (3) optimising ventilator management,
and (4) to decide on weaning from ventilator.
Clinical assessment of the respiratory system is often
focused on auscultatory findings; however, considerable
information can be obtained from careful inspection and
examination of the pattern of breathing. Presence of
wheeze, crepitations, increased respiratory rate,
suprasternal and intercostal recession, accessory muscle
activity (sternomastoid) and rib cage–abdominal paradox
indicates increased work of breathing. Various tests are
described to assess different components. Measurement of
airway resistance and lung compliance allow evaluation of
load put on the neuromuscular component while assessment
of the function of respiratory centre and the strength of
respiratory muscle allow evaluation of the efficiency of
neuromuscular component. Measurement of airway
occlusion pressure (AOP) at 0.1 second bears a close
relationship to the intensity of respiratory neural drive.6
The occlusion pressure is measured by transiently and
surreptitiously occluding the airway during early inspiration
and measuring the change in airway pressure after 0.1
second before the patient react to the occlusion. Although
AOP 0.1 values represent negative pressure, it is customary
to report them in positive units, which in the normal subject
during relaxed breathing is 0.93 ± 0.48(SD) cm H2O.7 A
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
high AOP 0.1 value during acute respiratory failure
indicates increased respiratory drive and neuromuscular
activity and, if sustained, may result in inspiratory muscle
fatigue. Modern ventilators provide facility for measurement
of airway resistance and lung compliance and AOP in the
ventilated patient.
Respiratory muscle strength is assessed by measuring
the maximum inspiratory and maximum expiratory pressure
(Pimax and Pemax,) generated against an occluded airway.
These measurements can be obtained readily with an
inexpensive aneroid manometer.8 The maximum force that
can be generated by the inspiratory or expiratory muscle
is related to their initial length. Consequently these
measurements are made at residual volume (Pimax) or at
total lung capacity (Pemax). Pimax and Pemax in healthy
adult men are approximately 111±34 and 151±68 cm of
H2O respectively.9 The values tend to decrease with age
and are lower in women.10 In ambulatory patients with
neuromuscular disease but who are free of lung disease,
hypercapnia is likely to develop when Pimax is reduced to
one-third of the normal predicted value. Respiratory system
performs continuously, and for sustained ventilation, the
muscles of respiration must perform (endurance) without
getting fatigued. A number of techniques, such as
transdiaphragmatic pressure measurement, phrenic nerve
stimulation, and determination of tension–time index are
used to detect the presence or development of muscle
fatigue.11 Recently, diaphragmatic ultrasonography has been
found to be very helpful in assessment of diaphragmatic
function. The method assesses change in the thickness of
diaphragm during inspiration and easily recognizes
diaphragm palsy.12
Vital capacity (VC) is the only lung volume
commonly measured in the CCU. In a study of patients
with Guillain Barre syndrome, the VC measurement was
found to be a reliable predictor of respiratory failure
hours before actual intubation13 and a fall in VC to
<15 mlkg-1 indicates the need of intubation.
Diagnosis
As discussed earlier, the diagnosis of respiratory
failure is based on analysis of arterial blood gas. However,
it is important to suspect its presence on clinical
grounds. The patients with respiratory failure will have
clinical features of underlying disease; in addition they
may have signs of hypoxaemia and hypercapnia.
Hypoxaemia may be accompanied by the presence of
tachypnoea, tachycardia, dyspnea, hypertension, intercostal
retraction, and use of accessory muscles of ventilation.
Cerebral hypoxia produces changes in mentation that
can range from mental confusion and restlessness to
NEEMA : RESPIRATORY FAILURE IN ICU
delirium. Cyanosis of the nail beds may be evident.
Hypercapnia exerts its major effects on central nervous
system. As the PaCO2 increases, patients typically progress
through the stages of lethargy, stupor and finally coma
(CO2 narcosis). Other symptoms are secondary to
catecholamine release and simultaneous hypoxaemia. The
patient is often described as appearing “fatigued” or “tired
out.” However, the clinical manifestations described are
non-specific and may occur in the absence of respiratory
failure. Therefore, the diagnosis of respiratory failure must
be confirmed by arterial blood gas analysis.
Management of respiratory failure:
A clear understanding of physiology of respiration
and pathophysiological mechanisms of respiratory failure
is mandatory for managing these patients. The extent of
abnormality in arterial blood gas values is a result of the
balance between the severity of disease and the degree of
compensation by cardiopulmonary system. Normal blood
gases do not mean there is an absence of disease because
the homeostatic system can compensate. However, an
abnormal arterial blood gas value reflect uncompensated
disease that may be life threatening. Obviously, ABG should
be interpreted along with the features of compensatory
mechanisms. Apart from definitive treatment of primary
disease, the management should be focused to enhance O2
delivery to the tissues by emphasizing airway management,
ventilation and oxygenation.
Patient’s ability to maintain, clear and protect the
airway (against aspiration) is the most important
considerations. Respiratory failure is frequently associated
with depressed level of consciousness; this is commonly
seen in patients with neurological disease (Stroke, Mass
lesion) or ventilatory failure (Myasthenia Gravis, Guillain
– Barrè Syndrome). Depressed consciousness can result in
partial airway obstruction due to loss of muscle tone.
Airway obstruction unduly increases work of breathing,
aggravates respiratory failure and potentially can interfere
with cardiac output. The obstruction can easily be relieved
by lifting the mandible or by inserting an oropharyngeal
airway. However, if protective reflexes are poor or patient
is unable to clear airway, consideration should be given
for endotracheal intubation and ventilation. Recovery from
neuromedical diseases is usually prolonged and it may be
prudent to separate the airway electively even if the blood
gases are within acceptable limits.
Ventilation: Hypercapnia signifies the presence of
alveolar hypoventilation. This may result from a fall in
minute ventilation or an inadequate ventilatory response to
areas of low ventilation-perfusion imbalance. An abrupt
rise in PaCO2 is always associated with respiratory acidosis.
However, chronic ventilatory failure (PaCO2>46 mmHg)
365
is usually not associated with acidosis because of metabolic
compensation. And it is the correction of respiratory
acidosis (pH < 7.25) that matters not the correction of
PaCO2. In patient’s, where early recovery is expected,
non-invasive mechanical ventilation by nasal or face mask
is an effective alternative, however, as discussed in the
preceding section, in the likelihood of delayed recovery,
endotracheal intubation with assist-control mode or
synchronized intermittent ventilation with a set rate close
to the patients spontaneous rate ensures maximum comfort
to the patient.
Oxygenation : Correction of arterial hypoxaemia is
one of the cornerstones in the management of respiratory
failure. It is important to realize that PaO2 is only one of
the determinants of O2 delivery to the tissues. The other
determinants are cardiac output and haemoglobin
concentration therefore increases in the cardiac output and
haemoglobin concentration should be considered. Sufficient
supplemental O2 should be provided to ensure the PaO2 to
approximately 60-70 mmHg. Because of the shape of the
O2-haemoglobin dissociation curve; at a PaO2 below 60
mmHg, a small increase results in a significant improvement
in saturation. The initial concentration of O2 should be
selected based on the underlying mechanism of arterial
hypoxaemia. In patient’s where underlying mechanism is
ventilation-perfusion imbalance (asthma, COPD), a small
increase (FIO2 - 0.24-0.40) in inspiratory O2 is usually
sufficient. It is well known that some patients with COPD
experience hypercapnia and respiratory acidosis on
administration of supplemental O2. This was believed to
be due to fall in minute ventilation; however, it is shown
to be due to worsening ventilation-perfusion imbalance.
However, it is recommended that the hypoxaemia must be
corrected, if necessary, hypercapnia and respiratory acidosis
can be managed with mechanical ventilation.
As discussed earlier, hypoxaemia due to intrapulmonary
shunt producing lesions (pneumonia, ARDS, pulmonary
oedema, etc) is difficult to treat and should be managed
with administration of high concentration of O2. The usual
practice of beginning treatment with low concentration of
O2 is not recommended. Often it is not possible to correct
hypoxaemia by high concentration of O2 delivered by face
mask, in such cases; continuous positive airway pressure
via a face mask or endotracheal intubation and controlled
ventilation with high concentration of O2 is necessary and
should be tried. Patients with ARDS may need positive
end expiratory pressure (PEEP); however, its use is often
associated with a decrease in cardiac output by its effect
on venous return. It may, therefore, increase the PaO2 and
arterial haemoglobin saturation and yet cause a fall in O2
delivery to the tissues by decreasing cardiac output. For
366
this reason serial measurement of O2 delivery, not just
PaO2 are essential when PEEP is used in patients with
acute respiratory failure. Other adjuncts for improving
oxygenation include: prone positioning,14 partial liquid
ventilation15 and use of surfactant,16 nitric oxide (NO),17
and prostacycline inhalation.18 Recently, extra corporeal
membrane oxygenation (ECMO) is increasingly used in
paediatric patients.
Arterial hypoxaemia in postoperative setting is
common and is because of atelectasis following retention
of secretions, decrease in functional residual capacity or
diaphragmatic splinting due to pain. In cardiac surgical
patients, multiple causes like ventilation-perfusion imbalance
due to low cardiac output or pulmonary congestion due to
cardiac failure are associated with hypoxaemia. Hypoxaemia
is usually responsive to supplemental O2 and incentive
spirometry. Chest physiotherapy and coughing initiated
soon after the onset of collapse can quickly reverse most
cases of atelectasis due to airway plugging. Fiberoptic
bronchoscopy should be attempted in patients who are
unable to tolerate vigorous respiratory physiotherapy.
Conclusion
Respiratory failure in critical care unit is a medical
emergency and a real threat to the life of the patient.
Though many diseases of diverse aetiology are associated
with respiratory failure the initial management of respiratory
failure is same. A sound knowledge of underlying
pathophysiological mechanisms producing disturbances in
gaseous exchange will allow selection of optimal
management strategy.
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Suggested Reading
1. Stoelting RK (Ed): Pharmacology and physiology in anesthetic
practice. 2nd ed. JB lippincott, Philadelphia, 1991.
2. Ayres SM, Grenvik A, Holbrook PR, Shoemaker WC, (Ed):
Textbook of Critical Care. 3 rd ed. WB Saunders,
Philadelphia,1995.
3. Murray MJ, Coursin DB, Pearl RG, Prough DS (Ed): Critical
Care Medicine. 2nd ed. Lippincot-Williams & Wilkins,
Philadelphia, 2002.
4. Shapiro BA and Peruzzi WT (Ed): Clinical Application of
Blood Gases. 5th ed. Mosby, Baltimore, 1994.
5. West JB (Ed): Best and Taylor’s Physiological basis of medical
practice. 12th ed. BI Waverly pvt ltd. New-Delhi. 1996.