Introduction to the Management

of Critical Ill Patient

KURSUS CRITICAL CARE
HOSPITAL SERDANG

Definition Of Critically Patient

Critically ill patients:
Decompensation of the status of the patient leading
without therapeutic intervention to the multiorgans failure
and to the death
Critically ill patients:
Those patients who are at high risk for actual or potential
life-threatening health problems.
The more critically ill the patient is, the more likely he or
she is to be highly vulnerable, unstable and complex,
thereby requiring intense and vigilant nursing care.

Every Critically Ill Patients are constantly in

EMERGENCY OR RED ALERT condition.
Potentially to advance to life threatening event
such as cardiac or pulmonary event.
THUS
Active Treatment and Prevention including closed
monitoring, fast and correct actions are
mandatory.

Number of Admission into

ICU/HDW, Hospital Serdang

ICU
HDW

2006

2007

2008

307

407

461

624
(Mei Dis)

AMI &
HEART FAILURE

MAJOR OPERATION

TRAUMA & BURN

PESAKIT KRITIKAL
UNCONTROL MEDICAL
PROBLEM
i. DKA
ii. CVA
iii. Renal Failure
iv. Acute Br. Asthma

SEVERE INFECTION
& SEPTICAEMIA
i. Pneumonia
ii. Diabetic Foot
iii. Peritonitis
iv. Meningitis

Causes
Trauma

Infection
Shock & Hypotension

Tumour
Pulmonary embolism
Postoperative

Metabolism disorder

Head injury
Uncontrol Chronic Disease

Which organ systems are most

commonly involved in critically ill
patients?
Respiratory System
Cardiovascular system
Internal or Metabolic environment
Central Nervous System
Gastrointestinal Tract

AIM OF ASSESSMENT
1. Identify the physiologically abnormalities
2. Identify the most appropriate way to correct the
abnormalities
3. Diagnose the underlying problem
History taking, examination and initial resuscitation often
occurring simultaneously.

Overview Of The Systems Function

Respiratory
CO2

Cardiovascular

O2

Tissue &
Capillary

Blood With Low Oxygen Content, High CO2 Content

Blood with High Oxygen Content, Low CO2 Content
Gas Exchange: i. In the lung: between alveolar and blood in pulmonary circulation
ii. In the tissue: between cells in tissue & blood in systemic circulation

In Normal Condition:
The Circulation System will
Carry the blood all over the body
At the Lungs
O2
O2
CO2
At the Tissue

Glucose + O2 CO2 + H2O + E

CO2

In Normal Condition: The Cellular Respiration happened in

the cytoplasma and proceed into the mitochondria. This
process need O2 (Aerobic metabolism)

In Abnormal condition when the CVS and Respiratory System

function reduced, the systems failed to supply O2 to the cells for
aerobic metabolism. The cells will go into anarobic metabolism.
This lead to organs failure and production of lactate
(lactic acid).

Effects of Hypoxia
Aerobic metabolism at the Cytochrome oxidase
system is replaced by anaerobic metabolism
( increased lactate production)
Membrane
pumps
cease
functioning;
irriversible cell damage may follow.
Brain & heart function reduced (most
susceptible). Followed by other organs if
prolonged.
Critical value of O2 at mitochondrial level is 1
mmHg.

What
system
evaluated first?

should

be

First few minutes of evaluation

should
address
life-threatening
physiologic abnormalities.
Usually involving the airway, the
respiratory
system,
or
the
cardiovascular system.
Then the evaluation should expand
to include all organ system
ABC of resuscitation

How is vital organ perfusion assessed?

The vital organs & their method of initial
evaluation are as follows:
Skin : assess warmth, capillary refill in all
extremities.
CNS : assess level of consciousness &
orientation.
Heart : measure BP & HR, ask for symptoms
of myocardial ischemia (eg., chest pain)
Kidneys : measure urine output
Lungs : (as slides before)

Warning Signs of a Severely Ill Patient

Blood pressure
Heart rate
Respiratory rate
Conscious level
Oliguria
Sodium
Potassium
pH
PaO2
PaCO2
Bicarbonate

: SBP <90 or mean < 70 mmHg

: > 150 or < 50 bpm
: > 30 or < 8 breaths/min
: GCS < 12
: < 0.5 ml/kg/hr
: < 120 or > 150 mmol/l
: < 2.5 0r > 6 mmol/l
: < 7.2
: < 94%
: < 35 mmol/L and > 45 mmol/L
: <18 mmol/l

Arterial Blood Gas

pH
: 7.35 7.45
PaO2 : > 60 mmHq
PaCO2 : 35 45 mmHq
SaO2 : 90% - 100%
Standard Bicarbonat : 21 27 mmol/L
Actual Bicarbonate
: 23 -25 mmol/L
Base Excess (BE)
: -5 5
Lactate : 0.4 1.4 mmol/l

ABG : Interpretation Guidelines

Step 1: Look at pH - this is the starting point.
If within normal range, a normal or compensated state exists. If outside normal
limits, assess whether acidosis or alkalosis is present. The body never
overcompensates. Whichever state exists on the pH scale is the primary
abnormality.
Step 2: Assess hypoxemic state.
If PaO2 is <60 mmHg, hypoxic state exists. If PaO2 is between 80 -100 mmHg,
a normal condition exists. If PaO2 is >100 mmHg, a hyperoxic state exists.
Step 3: Assess ventilatory status.
If PaCO2 is <35 mmHg, it is termed "alkalosis" (alveolar hyperventilation or
hypocarbia). If PaCO2 is between 35-45 mmHg, it is within normal limits.
If PaCO2 is >45 mmHg, it is termed "acidosis" (ventilatory failure or hypercarbia).
If possible, determine whether this is an acute or chronic state (see the
compensation explanation).
Step 4: Assess metabolic component.
1. If bicarbonate (HCO3-) is <22 mEq/l, it is termed "acidosis".
2. If bicarbonate is between 22-28 mEq/l, it is within normal limits.
3. If bicarbonate is >28 mEq/l, it is termed "alkalosis".
4. If possible, determine whether this is an acute or chronic state

Arterial Blood Gas

Disturbances in acid-base balance
Respiratory Phatology

Metabolic Phatology

Respiratory acidosis (that is,

ventilatory failure) the drop in
pH is explained by the change
in PaCO2

Respiratory alkalosis (that

is, alveolar hyperventilation)
the decreased PaCO2
explains the increased pH

Metabolic acidosis reduced

pH not explained by increased
PaCO2. It is usually associated
with an increased anion gap
due to the accumulation of
renal acids, lactic acids, and
ketoacids (from diabetes or
starvation)

Metabolic alkalosis raised pH

out of proportion to changes in
PaCO2. It is associated with
hypokalaemia, volume
contraction, or exogenous alkali
administration

Groups of patients who are difficult to

assess
Young adults

Compensatory mechanisms tend to mask signs of

severe illness until the illness is very advanced
Significant physiological abnormalities in these patient
therefore indicate very severe illness

Elderly or
immunocompromised
pt

The inflammatory response may be damped, again

hiding signs of severe illness. In addition the
physiological reserve of these patients is often severely
compromised.

Trauma
patients

Difficult to assess due the multitude of possible

injuries & the effect of the distracting pain making
injuries difficult to localize. Detailed mechanism of
injury very useful

Subsequent Assessment

REVIEW
- on going review of response to treatment
- plan for subsequent management

ACUTE RESPIRATORY
FAILURE

CAUSE OF RESPIRATORY FAILURE

What is the Diagnosis ?

CAUSE OF RESPIRATORY FAILURE

Definition
Hypoxemic respiratory failure (type I) is present when
the arterial partial pressure of oxygen (PaO2) is <8
kPa (60 mmHg) when the patient is breathing room
air.
Hypercapnic respiratory failure (type II) is present
when the arterial partial pressure of CO2 (PaCO2) is
> 6.7 kPa (50 mmg).
Disorders that initially causes hypoxemia may be
complicated by respiratory pump failure and
hypercapnia.

Definition

Disorders that
initially causes
hypoxemia may be
complicated by
respiratory pump
failure and
hypercapnia.

Diseases that produce

respiratory pump failure
are frequently
complicated by
hypoxemia resulting
from secondary
pulmonary parenchymal
processes (eg.
pneumonia) or vascular
disorders (eg.
pulmonary embolism)

Signs And Symptoms of Resp.

Failure
Dyspnea, Tachypnea, Gasping
Used of Respiratory Accessory muscle
Kaussmals Breathing
Cyanosis
Hypertension (early) Hypotension (later)
Tachycardia (early) Bradycardia (later)
Reduce Sensorium and Concious level.
Poor Arterial Blood Gaseous (ABG) reading

Type Of Respiratory Failure

Respiratory Failure Type I:
PaO2 < 60 mmHq (hypoxia)
PaCO2 < 40 mmHq
* Hyperventilating when PaCO< 35 mmHq.
Respiratory Failure type II:
PaO2 < 60 mmHq.
PaCO2 > 45 mmHq (Hypercarbia)
* Hypoventilating

Causes
Pulmonary Causes

Extrapulmonary causes

Airway obstruction
Diaghpragm Pathology And
Phrenic nerve
palsy/paralyse
Neuromuscular disease:
Myasthenia Gravis &
Guillains Barre
Ribs Fracture
Cervical bone fracture (esp.
above C3)
Septicaemia
Severely Blood loss

Pneumonia
Bronchitis
Emphysema
Pneumothorax
Lung Contusion
Pulmonary Oedema
Lung Collaps

This will lead to hypoventilation

and hypoxia

Causes of Respiratory Failure

1. Low inspired partial pressure of oxygen
2. Hypoventilation
3. Ventilation perfusion mismatch
4. Diffusion abnormality

Common causes of breathlessness based on

speed of onset
minutes

hours

Days-weeks

Pneumothorax

Asthma

Pleural effusion

Pulmonary
embolism

Pneumonia

Exacerbation of
COPD

Pulmonary
oedema

Pulmonary
oedema
Metabolic
acidosis

pneumonia

Cross Section Of Airway

During Infection: Bronchitis

Bronchial tissue
: Edema, Inflammed
& hyperamia
: Br. Smooth muscle
contraction

Bronchial lumen
narrowed

Effect Of Infection
Cough reflex
Resp. Muscle activity
Cilia Function
iv. Bronchial smooth muscle
contraction

Increased sputum
& mucus production

Bronchial Asthma
Abnormal Bronchi

Normal Bronchi

Chest Physio
&
Sputum mobilisation
Oxygen
Therapy

Bronchodilator
Management Of
Respiratory Failure

Nursing Care

Antibiotic

Chest Physio & Sputum Mobilisation

Encourage sputum clearance:
: chest physio
: encourage cough and regular tracheal suction
: Humidifier & sputum diluents drugs
Spontaneous breathing and cough movement
help to reduce respiratory muscle atrophy.
Humidifier and sputum diluents drug help:
: to dilute the sputum/mucus
: reduce and prevent cilia dysfunction
: Remember: O2 gas is a dry and cold gas. It need
to be humidified

Bronchodilator
Action:
Reduced bronchoedema.
Reduced mucus secretion.
Bronchial smooth muscle relaxation
Can be given through:
Nebuliser, Inhaler, Intravenous, Oral and
Subcutaneous.
Group:
-2 stimulant (Terbutaline)
Anticholinergic (Atrovent)
Aminophyline (theophyline)

Bronchodilator

Dilated Bronchi,
Sputum still present

C.Physio
Clearance Of sputum

Effect Of Broncho dilator

& Chest physio

Bronchial dilatation

Bronchodilator

C.Physio
Sputum clear up,
Bronchi still narrow

Nursing care
Very important.
Patient in prop up position.
: Reduce the effect of splinting abdomen
: Increased respiratory effort and reduced work
of breathing
: Reduced atelectasis (lung unit collapes)
especially at the lower zone.
: Easy to cough.
It help to reduce the complications such as Bed
sore, DVT and Nosocomial infection.

Oxygen Therapy
O2 is widely used across all medical
specialities
It is life saving & part of first line treatment in
many acute critical situations
It should always be considered along with mx
of the airway, breathing, circulation, constant
monitoring and reassesment of treatment.
Method of O2 delivery is part of this mx.

When O2 therapy indicated?

Cardiac and respiratory arrest (give 100%
O2)
Hypoxaemia ( PaO2<60mmHg, SaO2<90% )
Systemic hypotension ( SBP<100mmHg )
Low COP & metab.acidosis ( HCO3
<18mmol/L)
Resp.distress ( RR>24/min )
In anaesthesia ( during & after )
Septicaemia

Prescribing oxygen:
controlled or uncontrolled?
As with any drug, O2 should be prescribed.
Most pts benefit from uncontrolled O2
However a small group COAD patients requires
controlled O2 therapy (used Ventimask).
They depend on hypoxia drive to stimulate respiration
These pts should received carefully controlled O2 therapy,
starting at 24 - 28%, which is progressively increased.
Aiming to achieve a PaO2 > 50mmHg or SpO2 of 85 92%.

Oxgen Delivery System

Oxygen Flowmeter

Water bath Humidifier

Without Humidifier

Pin Index Flow meter

& Oxygen
Pressure regulator

Bull Nose Flow meter

& Oxygen Pressure
Regulator

Oxygen Delivery Devices

2 main types of devices :
Fixed performance devices
pt receives a constant inspired O2 concentration
(fix FiO2) despite any changes in minute
ventilation
Variable performance devices
the O2 conc. delivered is variable depending on
pts minute ventilation (pts effort), O2 flow rate &
peak inspire flow rate.

Fixed performance devices

VentiMask

Adjustable oxygen
Concentration
Delivery system

Variable Performance
Devices

Nasal cannula
Simple face mask
Trachaemask
High flow mask
Head box

Oxygen flow must be adequate to prevent

rebreathing of carbon dioxide

Variable Performance Devices

Method Of Oxygen therapy

Nasal Pronged

OFlow < 4 L/m (FiO2 24%-36%)

Face mask

OFlow > 5 L/m (FiO2 35%-70%)

Ventimask

FiO: 24%- 60%

High Flow Mask

OFlow > 10 L/m

Mechanical Vent.

Inadequate flow can cause

rebreathing and hypercarbia

Progress Of Oxygen therapy

Nasal Pronged
Face mask
Ventimask
High Flow Mask
Mechanical Vent.

SpO2 & PaO2

worsening
Inspite O2 therapy

Worsening of
other Vital signs
in spite of Mx.
: BP
: Tachycardia/
bradycardia
: PaCO2
: GCS
: persistence
tachypnoe/dyspnea

Wean Of Oxygen therapy

Nasal Pronged
Face mask
Ventimask
High Flow Mask
Mechanical Vent.

SpO2 & PaO2

beter
With O2 therapy

Improving of
other Vital signs &
optimisation of Mx.
: BP
: HR normalised
: PaCO2 normalised
: GCS improved
: tachypnoe/dyspnea
stop.

Danger of Respiratory Failure

Hypoxia:

Hypercarbia :

Brain damage
Cardiac event: AMI,
arrthymias
Acute Renal Failure
Acute Liver Failure

Stimulation Adrenal
Activity
Acid-base
disturbance:
Respiratory Acidosis
Electrolites
imbalance: danger
of hyperkalaemia

Death

Effects of Hypoxia
Aerobic metabolism at the Cytochrome
oxidase system is replaced by anaerobic
metabolism ( increased lactate production)
Membrane
pumps
cease
functioning;
irriversible cell damage may follow.
Brain & heart most susceptible.Followed by
other organs if prolonged.
Critical value of O2 at mitochondrial level is 1
mmHg.

Low inspired partial pressure of Oxygen

High altitude
Inadvertent oxygen disconnection on a
patient receiving oxygen

Hypoventilation
1.

2.

Respiratory center
depression
- drug ingestion,
anaesthesia, head injury,
encephalopathy, fatigue etc
Disruption of respiratory
signal during transmission
along the nerves to the
respiratory muscles
- spinal injury, motor neurone
disease, Guillain-Barre
syndrome

3. Dysfunction of the neuromuscular junction

- paralytic agents, myasthenia
gravis
4. Dysfunction of the muscles
of respiration
- myopathy, fatigue,
malnutrition, dystrophy
5. Chest wall abnormalities
- kyphoscoliosis, ankylosing
spondylitis, pleural fibrosis

Ventilation perfusion mismatch

1.

2.

3.

Physiological shunting
- pneumonia, pulmonary oedema, pulmonary
haemorrhage and contusion, atelectasis
Anatomical shunting
-intracardiac shunting (eg. Fallots tetralogy,
Eisenmenger syndrome)
Increased physiologic dead space
- hypovolemia, pulmonary embolus, poor cardiac
function, or high intrathoracic pressures ( from
positive pressure ventilation)

Diffusion abnormality
The alveolar and
capillary distand
increased d/t interstitel
infiltrate or fluid in the
alveolar sac.
Thus the gasseos (O2
and CO2) difficult to
travel.
Common in Pneumonia
pulmonary oedema &
ARDS
Severe destructive
disease of the lung
late fibrosing diseases,

Respiratory Monitoring
1. Clinical
a. Increased work of breathing :
tachypnea, use of accessory
respiratory muscles, nasal
flaring,
intercostal/suprasternal/supracla
vicular retraction, or a
paradoxical breathing.
b. Sweating
c. Tachycardia
d. Hypertension (hypotension and
bradycardia are late signs)
e. Altered mental status- ranging
from agitation to coma and
seizures
f. Cyanosis central and peripheral
2. Arterial blood gases

3. Pulse oximetry
- Extremely useful monitor
- Estimates arterial saturation
- The relationship between saturation
and PaO2 is described by
Oxyhemoglobin Dissociation Curve
- Desaturation ~94% is critical
threshold because below this level a
small fall in PaO2 produces sharp
fall in SpO2.
- Conversely, a rise in an arterial
PaO2 has little effect on saturation.
- The main determinant of O2 content
of blood and O2 delivery to tissues is
the SATURATION, not the PaO2.
4. Capnography

Oxygen Dissociation Curve

SaO2
(%)

SaO2 above than: 90%

100
94

SaO2

Lower alarm limit

Small increased in SaO2

Large increased in PaO2

THUS
Falls in PaO2 may be
Tolerated well

90
PaO2

SaO2

SaO2 below than : 90%

Large dropped in SaO2
Small dropped in PaO2

PaO2

THUS

40

Reduced the Oxygen

Content

40

60 70

100

PaO2 (mmHq)

Oxygen Content /100 ml blood = 1.34 x Hb (g/%) x SaO2 + 0.03 x PaO2 (mmHq)

 Pulse oximetry
- common source of error is poor peripheral
perfusion which will lead to a discrepancy between
the heart rate displayed by the pulse oximetry and
HR measure by the ECG
- other sources of error : bilirubine pigments, false
nails or nail varnish, bright ambient light, poorly
adherent probe, excessive motion, methaemoglobin
& carboxyhemoglobin.

Management Principles

Must correct the hypoxemia

If uncorrected, FATAL
Rapid reversal of hypoxemia is obviously critical
Hypoxemia should be treated by oxygen
supplementation (increase FiO2) or increase
mean airway pressure ( mechanical ventilation)
Risk of oxygen induced hypoventilation in
hypercarbic patients with an acute exacerbation
of COPD is low.

Thank you