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Hypoxemic respiratory failure is characterized by a failure to oxygenate. Hypercapnic respiratory failure is a failure of the ventilatory pump (ventilatory muscles). Frequently, respiratory failure is a result of both hypoxemic and hypercapnic failure, and can be classified as compensated or uncompensated.
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Hypercapnic Respiratory Failure
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The ventilatory pump comprises the diaphragm and chest wall muscles, as well as the neural control of them. This is responsible for ensuring adequate alveolar ventilation. Four aspects of the ventilatory pump, either alone or in combination, can result in pump failure: weak muscles, excessive load, impaired neuromuscular transmission, motor neuron disease, or decreased respiratory drive (Table 14-1). Hypercapnic respiratory failure results in an elevated Paco2.
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Weak respiratory muscles may occur as a result of inherited myopathies and muscular dystrophies malnutrition, electrolyte imbalance, inadequate peripheral nerve function, or compromised substrate delivery. Long term use of corticosteroids and aminoglycoside antibiotics or calcium channel blockers can impair neuromuscular transmission. Chronic pulmonary disease and neuromuscular disease may precipitate pump failure because of a decrease in the force-velocity relationship of the muscle, decreasing maximal muscular contraction. Ventilatory muscle force may also be decreased by the mechanical disadvantage caused by a flattening of the diaphragm as in severe chronic obstructive pulmonary disease or a deformed thoracic cage as in kyphoscoliosis. Patients in the ICU who are mechanically ventilated, especially those paralyzed and receiving steroids, may develop critical illness myopathies. In addition, chronic pulmonary disease or neuromuscular disease may lead to detraining, atrophy, or fatigue of ventilatory muscles, all leading to a reduced efficiency of ventilation and carbon dioxide retention.
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Excessive load may cause hypercapnic failure, but it is usually associated with other factors that compromise pump function. For patients with chronic pulmonary or neuromuscular disease, the increased load resulting from secretion accumulation, mucosal edema, or bronchospasm may precipitate failure. For patients with thoracic deformities, increased ventilatory load is a chronic problem. Any factor that elevates minute ventilation requirements increasing ventilatory load may precipitate failure when associated with reduced neuromuscular capability.
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Depressed respiratory drive may be caused by drugs, hypothyroidism, or diseases affecting the respiratory center. Increased respiratory drive may also precipitate acute respiratory failure, especially when coupled with compromised pump function and increased ventilatory load. For example, metabolic acidosis, increased carbon dioxide production, and dyspnea-related anxiety may result in an intolerable increase in ventilatory drive.
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Hypoxemic Respiratory Failure
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Failure of the lungs to maintain arterial oxygenation is hypoxemic respiratory failure (Table 14-2). Hypoxemic respiratory failure usually does not result in carbon dioxide retention unless acute or chronic pump failure is also present. Hypoxemic respiratory failure can usually be treated with oxygen, but mechanical ventilation may be necessary in severe cases of acute respiratory distress syndrome (ARDS), heart failure, or pneumonia.
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