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Respiratory Failure.4
Respiratory Failure.4
RESPIRATORY FAILURE
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Respiratory failure in patients admitted to critical gaseous exchange functions that is oxygenation failure
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care unit (CCU) is a major cause of morbidity and (arterial hypoxaemia) or CO2 removal failure (hypercapnia,
mortality. Patients can get into CCU because of respiratory ventilatory failure) or failure of both the functions. Non –
failure secondary to pulmonary pathology like pneumonia; respiratory functions of the lung include metabolic,
in many other patients respiratory failure is secondary to secretory and immunologic functions. These functions are
sepsis, cardiac failure or neurological disorders. Obviously, not discussed further in this review.
respiratory failure involves diverse pathology.
This review is mainly confined to physiology of
The respiratory system performs the vital function respiration and pathophysiological mechanisms that lead to
of gaseous exchange.1 O2 is transported through the upper respiratory failure. Various disorders that cause different
airways to the alveoli that diffuses across the types of respiratory failure are also briefly mentioned.
alveolocapillary membrane and enters the capillary blood. Though, a general guideline of management is presented,
There, it combines with haemoglobin and is transported a detailed discussion on management is out of the scope
by the arterial blood to the tissues. In the tissues the O2 of this review
is utilized for adenosine triphosphate production which is
essential for all metabolic processes. The major by product Physiology of respiration
of cellular metabolism, CO2, diffuses from the tissues into Gaseous exchange between the environment and the
the capillary blood, where a major portion of it is hydrated pulmonary capillary blood constitutes external respiration.
as carbonic acid and transported to the lungs by the venous The functioning unit of the lung is alveolus with its capillary
blood. In the lungs, it diffuses from the pulmonary blood network. Various factors govern transport of air from the
into the alveoli and is exhaled into the atmosphere environment to the alveoli (ventilation) and supply of blood
(Expiration). Gaseous exchange appropriate to the metabolic to the pulmonary capillaries (perfusion).
demand is essential to maintain homeostasis (the milieu Henry’s law dictates that when a solution is exposed
interior of the body). Respiration is accomplished and to an atmosphere of gas an equilibration of partial pressures
regulated by an intricate set of structures.2 These structures follow between the gas molecules dissolved in the liquid
include: (1) the lungs that provide the gas exchange surface; and the gas molecules in the atmosphere. Consequently,
(2) the conducting airways that convey the air into and out partial pressure of O2 and CO2 in the blood leaving the
of the lungs; (3) the thoracic wall that acts as a bellows pulmonary capillaries (pulmonary venous blood) is equal
and supports and protects the lungs; (4) the respiratory to the partial pressure of O2 and CO2 achieved in the
muscles that creates the energy necessary for the movement alveolus after equilibration.3 At equilibrium, the partial
of air into and out of the lungs; and (5) the respiratory pressure of O2 and CO2 results from a dynamic equilibrium
centres with their sensitive receptors and communicating between O2 delivery to the alveolus and O2 extraction
nerves that control and regulate ventilation. Pathologic from the alveolus; and CO2 delivery to the alveolus and
processes can affect any of these functional components. CO2 removal from the alveolus.
The interactions of cardiopulmonary, nervous and
musculoskeletal systems can be disrupted by disease, by Delivery of O2 to the alveolus is directly related
surgery and by anaesthetic agents. Respiratory failure can to the sweep rate of air (ventilation), and composition of
be defined as a significant impairment in the gaseous the sweeping gas (partial pressure of O2 in the inspiratory
exchange capacity of the respiratory system. Traditionally air; FIO2). In general, alveolar O2 tension (PAO2) increases
respiratory failure has been a clinical diagnosis; however, with increase in inspiratory O2 tension and increase in
with the easy availability of blood gas analysis, respiratory ventilation. Extraction of O2 from the alveolus is determined
failure is considered in terms of impairment of its actual by the saturation, quality and quantity of the haemoglobin
of the blood perfusing the alveoli. The O2 saturation of the
1. M.D., PDCC
Associate Professor, Department of Anaesthesiology, haemoglobin in the pulmonary capillary blood is affected
Sree Chitra Tirunal Institute for Medical Sciences and by the supply of O2 to the tissues (cardiac output) and the
Technology, Trivandrum, Kerala. extraction of the O2 by the tissues (metabolism). In general,
Correspond to : lower the haemoglobin saturation in the blood perfusing
E-mail : praveenneema@yahoo.co.in
the pulmonary capillaries, a result of low cardiac output
NEEMA : RESPIRATORY FAILURE IN ICU 361
Effect of low-haemoglobin saturation in the 3. Dead space effect, the volume of inspired air that do
pulmonary capillary (venous) blood: Low cardiac output not participate in gaseous exchange
and increased tissue metabolism are the reasons of low Vd/VT = PaCO2 – PECO2/PaCO2
haemoglobin saturation. Normal haemoglobin saturation in
the mixed venous blood that perfuses through pulmonary Where Vd is wasted ventilation; dead space, VT is
capillaries is 75%. Low-haemoglobin saturation per se tidal volume, PaCO2 and PECO2 are partial pressure of
does not affect oxygenation in the alveoli provided CO2 in arterial blood and mixed exhaled gas. Unfortunately,
ventilation is adequate. However, ventilation-perfusion the clinical usefulness of all the three measurements is
mismatch will exist in the presence of low cardiac output. limited because of the fact that they are influenced by both
Low-haemoglobin saturation produces arterial hypoxaemia – the changes in minute ventilation and the cardiac output
by three mechanisms – first, the blood leaving the areas apart from ventilation-perfusion imbalance.
of low ventilation-perfusion will contribute blood with a Classification of respiratory failure
lower partial pressure of O2 because of the lower
equilibration partial pressure (haemoglobin with low On the basis of arterial blood gas analysis,
saturation will extract more O2 before becoming saturated respiratory failure may be divided into three types. Type
thereby reducing partial pressure of O2 in the alveolus), I or oxygenation failure, Type II or ventilatory failure,
second, the effect of the shunt units will be exaggerated Type III or combined oxygenation and ventilatory failure.
due to low saturation of venous blood, third, decreased Type I Respiratory Failure (Oxygenation Failure;
arterial O2 content will lead to further decrease in O2 Arterial Hypoxaemia): Partial pressure of O2 in the arterial
supply to the tissues, if tissue O2 consumption remains blood reflects: (1) Partial pressure of O2 in inspiratory
unchanged, venous O2 saturation will further decrease. It gas; (2) minute ventilation; (3) quantity of blood flowing
is clear that the presence of low-cardiac output state through pulmonary capillaries; (4) O2 saturation of the
compounds the effects of low ventilation-perfusion areas haemoglobin in the blood flowing through pulmonary
and shunt areas. capillaries (an effect of tissue metabolism and cardiac
NEEMA : RESPIRATORY FAILURE IN ICU 363
output); (5) diffusion across alveolar membrane; and (6) 8. Pulmonary embolism
ventilation-perfusion matching (Fig. 3). Type I failure is 9. Pulmonary hypertension
characterized by an abnormally low partial pressure of O2
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in the arterial blood. It may be caused by any disorder that Type II Respiratory Failure (Ventilatory Failure:
produces areas of low ventilation-perfusion or a right to Arterial Hypercapnia): Partial pressure of CO2 in the
left intrapulmonary shunt and is characterized by low partial arterial blood reflects the efficiency of ventilatory
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pressure of O2 in the arterial blood (PaO2 < 60 mm Hg mechanism that clears (washes out) CO2 produced during
while breathing room air), an increase in PAO2 – PaO2 tissue metabolism. Type II failure can be caused by any
difference, venous admixture and Vd/VT. 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.
Compensatory Mechanisms in presence of respiratory high AOP 0.1 value during acute respiratory failure
failure: indicates increased respiratory drive and neuromuscular
The response to hypoxaemia depends on the ability activity and, if sustained, may result in inspiratory muscle
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of the patient to recognize the hypoxemic state and then fatigue. Modern ventilators provide facility for measurement
to increase cardiac output and minute ventilation to improve of airway resistance and lung compliance and AOP in the
the situation. Peripheral chemoreceptors located in the arch ventilated patient.
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of aorta and at the bifurcation of carotid artery send afferent Respiratory muscle strength is assessed by measuring
signals to the brain. the maximum inspiratory and maximum expiratory pressure
(Pimax and Pemax,) generated against an occluded airway.
Assessment of Pulmonary Function in Critically Ill
These measurements can be obtained readily with an
Patients:
inexpensive aneroid manometer.8 The maximum force that
The primary aim of respiratory system is gaseous can be generated by the inspiratory or expiratory muscle
exchange (cardiopulmonary interaction) in the lung is related to their initial length. Consequently these
parenchyma. Airways provide conduit for the passage of measurements are made at residual volume (Pimax) or at
air from the environment to the lungs, the neuromuscular total lung capacity (Pemax). Pimax and Pemax in healthy
system ensures ventilation and the lung parenchyma adult men are approximately 111±34 and 151±68 cm of
provides the ground for interaction between ventilation H2O respectively.9 The values tend to decrease with age
and perfusion. Health of the lung parenchyma and the and are lower in women.10 In ambulatory patients with
airways determines the load (work of breathing) placed on neuromuscular disease but who are free of lung disease,
the neuromuscular system; increased load due to lung hypercapnia is likely to develop when Pimax is reduced to
disease or airway disease can stress and precipitate failure one-third of the normal predicted value. Respiratory system
of the neuromuscular system. Deterioration in pulmonary performs continuously, and for sustained ventilation, the
function in critically ill patients can be because of the muscles of respiration must perform (endurance) without
inadequacy of airways, lung parenchyma, cardiopulmonary getting fatigued. A number of techniques, such as
interaction and neuromuscular system. The assessment of transdiaphragmatic pressure measurement, phrenic nerve
pulmonary function is of particular importance in (1) stimulation, and determination of tension–time index are
deciding whether ventilation is indicated, (2) assessing used to detect the presence or development of muscle
response to therapy, (3) optimising ventilator management, fatigue.11 Recently, diaphragmatic ultrasonography has been
and (4) to decide on weaning from ventilator. found to be very helpful in assessment of diaphragmatic
Clinical assessment of the respiratory system is often function. The method assesses change in the thickness of
focused on auscultatory findings; however, considerable diaphragm during inspiration and easily recognizes
information can be obtained from careful inspection and diaphragm palsy.12
examination of the pattern of breathing. Presence of Vital capacity (VC) is the only lung volume
wheeze, crepitations, increased respiratory rate, commonly measured in the CCU. In a study of patients
suprasternal and intercostal recession, accessory muscle
with Guillain Barre syndrome, the VC measurement was
activity (sternomastoid) and rib cage–abdominal paradox
found to be a reliable predictor of respiratory failure
indicates increased work of breathing. Various tests are
hours before actual intubation13 and a fall in VC to
described to assess different components. Measurement of
<15 mlkg-1 indicates the need of intubation.
airway resistance and lung compliance allow evaluation of
load put on the neuromuscular component while assessment Diagnosis
of the function of respiratory centre and the strength of
As discussed earlier, the diagnosis of respiratory
respiratory muscle allow evaluation of the efficiency of
failure is based on analysis of arterial blood gas. However,
neuromuscular component. Measurement of airway
occlusion pressure (AOP) at 0.1 second bears a close it is important to suspect its presence on clinical
relationship to the intensity of respiratory neural drive.6 grounds. The patients with respiratory failure will have
The occlusion pressure is measured by transiently and clinical features of underlying disease; in addition they
surreptitiously occluding the airway during early inspiration may have signs of hypoxaemia and hypercapnia.
and measuring the change in airway pressure after 0.1 Hypoxaemia may be accompanied by the presence of
second before the patient react to the occlusion. Although tachypnoea, tachycardia, dyspnea, hypertension, intercostal
AOP 0.1 values represent negative pressure, it is customary retraction, and use of accessory muscles of ventilation.
to report them in positive units, which in the normal subject Cerebral hypoxia produces changes in mentation that
during relaxed breathing is 0.93 ± 0.48(SD) cm H2O.7 A can range from mental confusion and restlessness to
NEEMA : RESPIRATORY FAILURE IN ICU 365
delirium. Cyanosis of the nail beds may be evident. is usually not associated with acidosis because of metabolic
Hypercapnia exerts its major effects on central nervous compensation. And it is the correction of respiratory
system. As the PaCO2 increases, patients typically progress acidosis (pH < 7.25) that matters not the correction of
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through the stages of lethargy, stupor and finally coma PaCO2. In patient’s, where early recovery is expected,
(CO2 narcosis). Other symptoms are secondary to non-invasive mechanical ventilation by nasal or face mask
catecholamine release and simultaneous hypoxaemia. The is an effective alternative, however, as discussed in the
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patient is often described as appearing “fatigued” or “tired preceding section, in the likelihood of delayed recovery,
out.” However, the clinical manifestations described are endotracheal intubation with assist-control mode or
non-specific and may occur in the absence of respiratory synchronized intermittent ventilation with a set rate close
failure. Therefore, the diagnosis of respiratory failure must to the patients spontaneous rate ensures maximum comfort
be confirmed by arterial blood gas analysis. to the patient.
this reason serial measurement of O2 delivery, not just 7. Tobin MJ, Gardener WN: Monitoring of the control of
PaO2 are essential when PEEP is used in patients with breathing. In principles and practice of intensive care
acute respiratory failure. Other adjuncts for improving monitoring. Tobin MJ (Ed). New York, McGraw-Hill,
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membrane oxygenation (ECMO) is increasingly used in 9. Koulouris N, Mulvey DA, Laroche CM et al: Comparison of
paediatric patients. two different mouth-pieces for the measurement of Pimax
and Pemax in normal and weak subjects. Eur Respir J 1:
Arterial hypoxaemia in postoperative setting is 1988; 863.
common and is because of atelectasis following retention 10. Chen H-I, Kuo C-S: Relationship between respiratory muscle
of secretions, decrease in functional residual capacity or function and age, sex and other factors. J Appl Physiol 1989;
diaphragmatic splinting due to pain. In cardiac surgical 66: 943.
patients, multiple causes like ventilation-perfusion imbalance 11. Tobin MJ, Laghi F: Monitoring of respiratory muscle function.
due to low cardiac output or pulmonary congestion due to In Principles and practice of Intensive care monitoring. Tobin
cardiac failure are associated with hypoxaemia. Hypoxaemia MJ (Ed). New York, McGraw- Hill, 1998; 945-988.
is usually responsive to supplemental O2 and incentive 12. Gottesman E, McCool FD: Ultrasound evaluation of the
spirometry. Chest physiotherapy and coughing initiated paralysed diaphragm. Am J Respir Crit Care Med 1997;
soon after the onset of collapse can quickly reverse most 155: 1570.
cases of atelectasis due to airway plugging. Fiberoptic 13. Chevrolet JC, Deleamont P: repeated vital capacity
bronchoscopy should be attempted in patients who are measurement as predictive parameter for mechanical
unable to tolerate vigorous respiratory physiotherapy. ventilation need and weaning success in the Guillain –Barre
syndrome. Am Rev Respir Dis 1991; 144: 814.
Conclusion 14. Chatte G, Sab JM, Dubois JM et al: Prone positioning in
Respiratory failure in critical care unit is a medical mechanically ventilated patients with severe acute respiratory
emergency and a real threat to the life of the patient. failure. Am J Respir Crit Care Med 1997; 155: 473-478.
Though many diseases of diverse aetiology are associated 15. Hirschi RB, Pranikoff T, Wise C et al: Initial experiment with
with respiratory failure the initial management of respiratory partial liquid ventilation in adult patients with acute respiratory
failure is same. A sound knowledge of underlying distress syndrome. JAMA 1996; 275: 383-389.
pathophysiological mechanisms producing disturbances in 16. Anzueto A, Baughman RP, Guntupalli KK et al: Aerosolised
gaseous exchange will allow selection of optimal surfactant in adults with sepsis induced acute respiratory
management strategy. distress syndrome. Exosurf acute respiratory distress syndrome
study group. N Eng J Med. 1996; 334: 1417-1421.
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