Introduction

RESPIRATORY FAILURE
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. In many other patients, respiratory failure is secondary to diseases
like pneumonia; sepsis, cardiac failure or neurological disorders. Obviously, respiratory
failure involves diverse pathology. The respiratory process involves of gaseous exchange. O2
is transported through the upper system performs the vital function 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 is utilized for adenosine triphosphate production which is O2 essential for all
metabolic processes.1 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 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.1 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). Henrys law dictates that when a
solution is exposed to an atmosphere of gas, there will be 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 (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).2
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.2 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.3

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 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.2
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 ventilationperfusion do not counter balance each other for two reasons first, the areas of low
ventilation-perfusion generally receive more blood flow than the areas of high ventilationperfusion; second, because of non-linear shape of the O2- haemoglobin dissociation curve,
the higher partial pressure of O2 of the blood leaving high ventilation perfusion areas does
not translate into a proportionate increase in haemoglobin saturation and O2 content and
therefore provides little extra O2 to the blood leaving these areas of high ventilationperfusion. 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 sedoes 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 ventilationperfusion 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. 4

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 = (CcO2 CaO2)/(CcO2 CvO2)
Where Qva is venous admixture, Qt is cardiac output; CcO2, CaO2, and CO2 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 ventilationperfusion imbalance.
Classification of respiratory failure
On the basis of arterial blood gas analysis, respiratory failure may be divided into three types.
TypeI 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 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.
7. Pulmonary embolism
8. Pulmonary hypertension
Type II Respiratory Failure (Ventilatory Failure: Arterial Hypercapnia):

Partial pressure of CO2 in the arterial blood reflects the efficiency of ventilator 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-Barr 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
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 ventilationperfusion)
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
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 auscultator findings; however, considerable
information can be obtained from careful inspection and examination of the pattern of
breathing. Presence of wheeze, crepitation, increased respiratory rate, suprasternal and
intercostal recession, accessory muscle activity (sternomastoid) and rib cageabdominal
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. The occlusion pressure is measured by
transiently and surreptitiously occluding the airway during early inspiration and measuring
the change in airway pressure after 0.1second 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 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. The maximum force that can be generated by the inspiratory

or expiratory muscleis 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 11134 and 15168 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. 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. 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.4

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 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.5

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. Patients 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 ventilator failure (Myasthenia Gravis, Guillain Barr 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. 6The 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 ventilator response to areas of low ventilation-perfusion
imbalance. An abrupt rise in PaCO2 is always associated with respiratory acidosis.
However, chronic ventilator failure (PaCO2>46 mmHg) 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 patients, 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 patients where underlying mechanism is ventilationperfusion 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 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, partial liquid ventilation and use of
surfactant, nitric oxide (NO), and prostacycline inhalation. 7 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. Fibre optic
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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