Respiratory Failure

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO 2 value of less than ! mm "g while breathing air or a Pa#O 2 of more than $! mm "g. %urthermore, respiratory failure may be acute or chronic. &hile acute respiratory failure is characteri'ed by life(threatening derangements in arterial blood gases and acid(base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. Classification of respiratory failure Respiratory failure may be classified as hypoxemic or hypercapnic and may be either acute or chronic. "ypoxemic respiratory failure )type I* is characteri'ed by a PaO2 of less than ! mm "g with a normal or low Pa#O2. +his is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. ,ome examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage. "ypercapnic respiratory failure )type II* is characteri'ed by a Pa#O2 of more than $! mm "g. "ypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. +he p" depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. #ommon etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders )eg, asthma, chronic obstructive pulmonary disease -#OP./*. Distinctions between acute and chronic respiratory failure 0cute hypercapnic respiratory failure develops over minutes to hours1 therefore, p" is less than 2.3. #hronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. +herefore, the p" usually is only slightly decreased. +he distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. +he clinical mar4ers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long(standing disorder. Pathophysiology: Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, #5,, peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shoc4 often present with respiratory failure. 1

Hypoxemic respiratory failure: +he pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are ventilation(perfusion )678* mismatch and shunt. +hese 2 mechanisms lead to widening of the alveolar(arterial oxygen difference, which normally is less than 9$ mm "g. &ith 678 mismatch, the areas of low ventilation relative to perfusion )low 678 units* contribute to hypoxemia. 0n intrapulmonary or intracardiac shunt causes mixed venous )deoxygenated* blood to bypass ventilated alveoli and results in venous admixture. +he distinction between 678 mismatch and shunt can be made by assessing the response to oxygen supplementation or calculating the shunt fraction following inhalation of 9!!: oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. Hypercapnic respiratory failure: 0t a constant rate of carbon dioxide production, Pa#O2 is determined by the level of alveolar ventilation )6a*, where 6#O2 is ventilation of carbon dioxide and ; is a constant value )!.< 3*. )6a = ; x 6#O2*7Pa#O2 0 decrease in alveolar ventilation can result from a reduction in overall )minute* ventilation or an increase in the proportion of dead space ventilation. 0 reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and #5, depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy. The diagnosis of acute or chronic respiratory failure begins with clinical suspicion of its presence. #onfirmation of the diagnosis is based on arterial blood gas analysis. >valuation of an underlying cause must be initiated early, fre?uently in the presence of concurrent treatment for acute respiratory failure.

+he cause of respiratory failure often is evident after a careful history and physical examination.
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#ardiogenic pulmonary edema usually develops in the context of a history of left ventricular dysfunction or valvular heart disease. 0 history of previous cardiac disease, recent symptoms of chest pain, paroxysmal nocturnal dyspnea, and orthopnea suggest cardiogenic pulmonary edema. 5oncardiogenic edema )eg, acute respiratory distress syndrome -0R.,/* occurs in typical clinical contexts such as sepsis, trauma, aspiration, pneumonia, pancreatitis, drug toxicity, and multiple transfusions.

Physical: +he signs and symptoms of acute respiratory failure reflect the underlying disease process and the associated hypoxemia or hypercapnia. @ocali'ed pulmonary findings reflecting the acute cause of hypoxemia, such as pneumonia, pulmonary edema, asthma, or #OP., may be readily 2

apparent. In patients with 0R.,, the manifestations may be remote from the thorax, such as abdominal pain or long(bone fracture. 5eurological manifestations include restlessness, anxiety, confusion, sei'ures, or coma.

0sterixis may be observed with severe hypercapnia. +achycardia and a variety of arrhythmias may result from hypoxemia and acidosis. Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. +his helps assess the severity of respiratory failure and also helps guide management. #yanosis, a bluish color of s4in and mucous membranes, indicates hypoxemia. 6isible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least $ g7d@. .yspnea, an uncomfortable sensation of breathing, often accompanies respiratory failure. >xcessive respiratory effort, vagal receptors, and chemical stimuli )hypoxemia and7or hypercapnia* all may contribute to the sensation of dyspnea. Aoth confusion and somnolence may occur in respiratory failure. Byoclonus and sei'ures may occur with severe hypoxemia. Polycythemia is a complication of long(standing hypoxemia. Pulmonary hypertension fre?uently is present in chronic respiratory failure. 0lveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of the affected smooth muscles and narrowing of the pulmonary arterial bed. +he increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure. +his, in turn, causes enlargement of the liver and peripheral edema. +he entire se?uence is 4nown as cor pulmonale. #riteria for the diagnosis of acute respiratory distress syndrome
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#linical presentation ( +achypnea and dyspnea1 crac4les upon auscultation #linical setting ( .irect insult )aspiration* or systemic process causing lung inCury )sepsis* Radiologic appearance ( +hree(?uadrant or D(?uadrant alveolar flooding @ung mechanics ( .iminished compliance )ED! m@7cm water*

Fas exchange ( ,evere hypoxia refractory to oxygen therapy )PaO27%IO2 E2!!* 5ormal pulmonary vascular properties ( Pulmonary capillary wedge pressure E9< mm "g

Causes: +hese diseases can be grouped according to the primary abnormality and the individual components of the respiratory system, as follows:

#entral nervous system disorders

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0 variety of pharmacological, structural, and metabolic disorders of the #5, are characteri'ed by depression of the neural drive to breathe. +his may lead to acute or chronic hypoventilation and hypercapnia. >xamples include tumors or vascular abnormalities involving the brain stem, an overdose of a narcotic or sedative, and metabolic disorders such as myxedema or chronic metabolic al4alosis.

.isorders of the peripheral nervous system, respiratory muscles, and chest wall
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+hese disorders lead to an inability to maintain a level of minute ventilation appropriate for the rate of carbon dioxide production. #oncomitant hypoxemia and hypercapnia occur. >xamples include Fuillain(AarrG syndrome, muscular dystrophy, myasthenia gravis, severe 4yphoscoliosis, and morbid obesity.

0bnormalities of the airways

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,evere airway obstruction is a common cause of acute and chronic hypercapnia. >xamples of upper airway disorders are acute epiglottitis and tumors involving the trachea1 lower airway disorders include #OP., asthma, and cystic fibrosis.

0bnormalities of the alveoli

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+he diseases are characteri'ed by diffuse alveolar filling, fre?uently resulting in hypoxemic respiratory failure, although hypercapnia may complicate the clinical picture. #ommon examples are cardiogenic and noncardiogenic pulmonary edema, aspiration pneumonia, or extensive pulmonary hemorrhage. +hese disorders are associated with intrapulmonary shunt and an increased wor4 of breathing.

#ommon causes of type I )hypoxemic* respiratory failure

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#hronic bronchitis and emphysema )#OP.* Pneumonia Pulmonary edema Pulmonary fibrosis 0sthma Pneumothorax Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Franulomatous lung diseases #yanotic congenital heart disease Aronchiectasis 0dult respiratory distress syndrome %at embolism syndrome ;yphoscoliosis Obesity

#ommon causes of type II )hypercapnic* respiratory failure

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#hronic bronchitis and emphysema )#OP.* ,evere asthma .rug overdose Poisonings Byasthenia gravis Polyneuropathy Poliomyelitis Primary muscle disorders Porphyria #ervical cordotomy "ead and cervical cord inCury Primary alveolar hypoventilation Obesity hypoventilation syndrome Pulmonary edema 0dult respiratory distress syndrome Byxedema +etanus

Imaging tudies:

#hest radiograph
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#hest radiography is essential because it fre?uently reveals the cause of respiratory failure. "owever, distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult. Increased heart si'e, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat(wing distribution of infiltrates suggest hydrostatic edema1 the lac4 of these findings suggests 0R.,.

>chocardiography
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>chocardiography need not be performed routinely in all patients with respiratory failure. "owever, it is a useful test when a cardiac cause of acute respiratory failure is suspected. +he findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. 0 normal heart si'e and normal systolic and diastolic function in a patient with pulmonary edema would suggest 0R.,. >chocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure.

!ther Tests:

Patients with acute respiratory failure generally are unable to perform pulmonary function tests )P%+s*. "owever, P%+s are useful in the evaluation of chronic respiratory failure.
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5ormal values of forced expiratory volume in one second )%>6 9* and forced vital capacity )%6#* suggest a disturbance in respiratory control. 0 decrease in %>69(to(%6# ratio indicates airflow obstruction, whereas a reduction in both the %>6 9 and %6# and maintenance of the %>69(to(%6# ratio suggest restrictive lung disease.

Respiratory failure is uncommon in obstructive diseases when the %>69 is greater than 9 @ and in restrictive diseases when the %6# is more than 9 @.

0n >#F should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure1 it also may detect dysrhythmias resulting from severe hypoxemia and7or acidosis.

Procedures:

Right heart catheteri'ation

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+his remains a controversial issue in the management of critically ill patients. Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, ade?uacy of volume resuscitation, and systemic oxygen delivery remain, right heart catheteri'ation should be considered. Beasurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema. +he pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function

Treatment "ypoxemia is the maCor immediate threat to organ function. +herefore, the first obCective in the management of respiratory failure is to reverse and7or prevent tissue hypoxia. "ypercapnia unaccompanied by hypoxemia generally is well tolerated and probably is not a threat to organ function unless accompanied by severe acidosis. Bany experts believe that hypercapnia should be tolerated until the arterial blood p" falls below 2.2. 0ppropriate management of the underlying disease obviously is an important component in the management of respiratory failure. 0 patient with acute respiratory failure generally should be admitted to a respiratory care or intensive care unit. Bost patients with chronic respiratory failure can be treated at home with oxygen supplementation and7or ventilatory assist devices along with therapy for their underlying disease.

0irway management o 0ssurance of an ade?uate airway is vital in a patient with acute respiratory distress. o +he most common indication for endotracheal intubation )>++* is respiratory failure.

>++ serves as an interface between the patient and the ventilator. o 0nother indication for >++ is airway protection in patients with altered mental status. #orrection of hypoxemia o 0fter securing an airway, attention must turn to correcting the underlying hypoxemia, the most life(threatening facet of acute respiratory failure. o +he goal is to assure ade?uate oxygen delivery to tissues, generally achieved with a PaO2 of ! mm "g or an arterial oxygen saturation ),aO2* of greater than H!:. o ,upplemental oxygen is administered via nasal prongs or face mas41 however, in patients with severe hypoxemia, intubation and mechanical ventilation often are re?uired. #oexistent hypercapnia and respiratory acidosis may need to be addressed. +his is done by correcting the underlying cause or providing ventilatory assistance.
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Bechanical ventilation is used for 2 essential reasons: )9* to increase PaO2 and )2* to lower Pa#O2. Bechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue.

+reatment of underlying cause

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0fter the patientIs hypoxemia is corrected and the ventilatory and hemodynamic status have stabili'ed, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place. +he specific treatment depends on the etiology of respiratory failure