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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003360Indian J. Anaesth. 2003; 47 (5) : 360-366

RESPIRATORY FAILURE

Dr. Praveen Kumar Neema

1. M.D., PDCC

Associate Professor, Department of Anaesthesiology,

Sree Chitra Tirunal Institute for Medical Sciences andTechnology, Trivandrum, Kerala.

Correspond to :

E-mail : praveenneema@yahoo.co.in

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 O2is 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 andregulated 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 canbe 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 CO2removal 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).

Henrys law dictates that when a solution is exposed

to an atmosphere of gas an equilibration of partial pressuresfollow 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 O2and CO

2results 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 ofthe sweeping gas (partial pressure of O

2in the inspiratory

air; FIO2). In general, alveolar O

2tension (PAO

2) increases

with increase in inspiratory O2

tension and increase in

ventilation. Extraction of O2from 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 O2by the tissues (metabolism). In general,

lower the haemoglobin saturation in the blood perfusing

the pulmonary capillaries, a result of low cardiac output

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NEEMA : RESPIRATORY FAILURE IN ICU 361

(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 circulatingpulmonary 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 byvariation 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 thealveolar 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 normallyventilated 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: Thepartial pressure of O

2and CO

2in each alveolus and

therefore of the capillary blood leaving it are primarily

determined by the ventilation-perfusion (VA/Q) ratio ofthat 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 animbalance between ventilation and perfusion and willproduce areas of abnormal ventilation-perfusion ratio. The

extent to which gas exchange is impaired depends on boththe 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 lungswith low ventilation-perfusion ratio. Areas with highventilation-perfusion ratio do not adversely affect the arterial

blood gas tensions; however they increase the amount ofwasted ventilation (Dead space effect). Areas of the lung

with low ventilation-perfusion contribute blood with a lowpartial pressure of O

2to 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 lowventilation-perfusion do not counterbalance each other fortwo reasons first, the areas of low ventilation-perfusion

generally receive more blood flow than the areas of highventilation-perfusion; second, because of non-linear shapeof the O

2- haemoglobin dissociation curve,5 the higher

partial pressure of O2

of the blood leaving high ventilation-

perfusion areas does not translate into a proportionate

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NEEMA : RESPIRATORY FAILURE IN ICU 363

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 thatproduces 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.

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) CO2produced 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

PaO2difference, 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 O2in the inspired air

3. Underventilated alveoli (areas of low ventilation-

perfusion)

B Intrapulmonary shunt (areas of zero ventilation-perfusion)

C Decreased mixed venous O2content (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

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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003364

Compensatory Mechanisms in presence of respiratory

failure:

The response to hypoxaemiadepends on the ability

of the patient to recognize the hypoxemic state and thento 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 parenchymaprovides 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 oftenfocused on auscultatory findings; however, considerableinformation can be obtained from careful inspection andexamination of the pattern of breathing. Presence ofwheeze, crepitations, increased respiratory rate,suprasternal and intercostal recession, accessory muscleactivity (sternomastoid) and rib cageabdominal paradoxindicates increased work of breathing. Various tests aredescribed to assess different components. Measurement ofairway resistance and lung compliance allow evaluation of

load put on the neuromuscular component while assessment

of the function of respiratory centre and the strength ofrespiratory muscle allow evaluation of the efficiency ofneuromuscular component. Measurement of airwayocclusion pressure (AOP) at 0.1 second bears a closerelationship to the intensity of respiratory neural drive.6

The occlusion pressure is measured by transiently andsurreptitiously occluding the airway during early inspirationand measuring the change in airway pressure after 0.1second before the patient react to the occlusion. AlthoughAOP 0.1 values represent negative pressure, it is customaryto 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 measurementof 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 P

emax,) 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). P

imax and P

emax in healthy

adult men are approximately 11134 and 15168 cm ofH

2O 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 tensiontime index are

used to detect the presence or development of muscle

fatigue.11

Recently, diaphragmatic ultrasonography has beenfound 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

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NEEMA : RESPIRATORY FAILURE IN ICU 365

delirium. Cyanosis of the nail beds may be evident.

Hypercapnia exerts its major effects on central nervous

system. As the PaCO2increases, patients typically progress

through the stages of lethargy, stupor and finally coma(CO

2narcosis). 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 respirationand pathophysiological mechanisms of respiratory failureis mandatory for managing these patients. The extent of

abnormality in arterial blood gas values is a result of thebalance between the severity of disease and the degree ofcompensation by cardiopulmonary system. Normal blood

gases do not mean there is an absence of disease because

the homeostatic system can compensate. However, anabnormal arterial blood gas value reflect uncompensated

disease that may be life threatening. Obviously, ABG shouldbe interpreted along with the features of compensatorymechanisms. 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 theairway (against aspiration) is the most importantconsiderations. Respiratory failure is frequently associated

with depressed level of consciousness; this is commonly

seen in patients with neurological disease (Stroke, Masslesion) or ventilatory failure (Myasthenia Gravis, Guillain

Barr Syndrome). Depressed consciousness can result inpartial airway obstruction due to loss of muscle tone.Airway obstruction unduly increases work of breathing,

aggravates respiratory failure and potentially can interferewith cardiac output. The obstruction can easily be relievedby lifting the mandible or by inserting an oropharyngeal

airway. However, if protective reflexes are poor or patientis unable to clear airway, consideration should be givenfor endotracheal intubation and ventilation. Recovery from

neuromedical diseases is usually prolonged and it may beprudent 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)

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 haemoglobinconcentration therefore increases in the cardiac output and

haemoglobin concentration should be considered. Sufficient

supplemental O2should be provided to ensure the PaO

2to

approximately 60-70 mmHg. Because of the shape of the

O2-haemoglobin dissociation curve; at a PaO

2below 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

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 COPDexperience 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 ofO

2is 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 PaO2and

arterial haemoglobin saturation and yet cause a fall in O2

delivery to the tissues by decreasing cardiac output. For

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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003366

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 liquidventilation15 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 incentivespirometry. 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 ingaseous exchange will allow selection of optimal

management strategy.

References1. Kreit JW and Rogers RM: Approach to the patient with

respiratory failure. In Shoemaker, Ayres, Grenvik, Holbrook

(Ed) Textbook of Critical Care. WB Saunders, Philadelphia,

1995; 680-687.

2. Papadakos PJ: Perioperative evaluation of pulmonary disease

and function. In Murray MJ, Coursin DB, Pearl RG, Prough

DS (Ed) Critical Care Medicine. Lippincot-Williams and

Wilkins, Philadelphia, 2002; 374-384.

3. Shapiro BA and Peruzzi WT: Physiology of respiration. InShapiro BA and Peruzzi WT (Ed) Clinical Application of

Blood Gases. Mosby, Baltimore, 1994; 13-24.

4. West JB: Ventilation-perfusion relationships. Am Rev Respir

Dis 1977; 116: 919-925.

5. Stoelting RK: Pulmonary gas exchange and blood transport

of gases. In Stoelting RK (Ed) Pharmacology and physiology

in anesthetic practice. JB Lippincott, Philadelphia, 1987;

721-733.

6. Whitelaw WA, Derenne JP: Airway occlusion pressure. J Appl

Physiol 1993; 74: 1475.

7. Tobin MJ, Gardener WN: Monitoring of the control of

breathing. In principles and practice of intensive care

monitoring. Tobin MJ (Ed). New York, McGraw-Hill,

1998; 415-464.8. Tobin MJ: State of the art: Respiratory monitoring. Am Rev

Respir Dis 1988; 138: 1625.

9. Koulouris N, Mulvey DA, Laroche CM et al: Comparison of

two different mouth-pieces for the measurement of Pimax

and Pemax in normal and weak subjects. Eur Respir J 1:

1988; 863.

10. Chen H-I, Kuo C-S: Relationship between respiratory muscle

function and age, sex and other factors. J Appl Physiol 1989;

66: 943.

11. Tobin MJ, Laghi F: Monitoring of respiratory muscle function.

In Principles and practice of Intensive care monitoring. Tobin

MJ (Ed). New York, McGraw- Hill, 1998; 945-988.

12. Gottesman E, McCool FD: Ultrasound evaluation of theparalysed diaphragm. Am J Respir Crit Care Med 1997;

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13. Chevrolet JC, Deleamont P: repeated vital capacity

measurement as predictive parameter for mechanical

ventilation need and weaning success in the Guillain Barre

syndrome. Am Rev Respir Dis 1991; 144: 814.

14. Chatte G, Sab JM, Dubois JM et al: Prone positioning in

mechanically ventilated patients with severe acute respiratory

failure. Am J Respir Crit Care Med 1997; 155: 473-478.

15. Hirschi RB, Pranikoff T, Wise C et al: Initial experiment with

partial liquid ventilation in adult patients with acute respiratory

distress syndrome. JAMA 1996; 275: 383-389.

16. Anzueto A, Baughman RP, Guntupalli KK et al: Aerosolised

surfactant in adults with sepsis induced acute respiratory

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17. Rossaint R, Falke K, Lopez F et al: Inhaled nitric oxide for

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18. Walmrath D, Schneider W, Pitch J et al: Aerosolized

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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 Taylors Physiological basis of medical

practice. 12th ed. BI Waverly pvt ltd. New-Delhi. 1996.