Respiratory failure is defined as inadequate gas exchange due to malfunction of one or more components of the respiratory system. There are two main types of acute respiratory failure: hypoxemic and hypercarbic. Hypoxemic respiratory failure is defined by arterial O2 saturation <90% while receiving an increased inspired O2 fraction. Acute hypoxemic respiratory failure can result from pneumonia, pulmonary edema (due to elevated pulmonary microvascular pressures in heart failure and intravascular volume overload, or with normal pulmonary microvascular pressures in acute respiratory distress syndrome [ARDS]), and alveolar hemorrhage. Hypoxemia results from ventilation-perfusion mismatch and intrapulmonary shunting. Lung injury in ARDS can be worsened by mechanical ventilation, and lower tidal volumes can reduce lung injury.
Hypercarbic respiratory failure is characterized by alveolar hypoventilation and respiratory acidosis. Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Conditions associated with hypercarbic respiratory failure include neuromuscular diseases (e.g., myasthenia gravis), disease processes causing diminished respiratory drive (e.g., drug overdose, brainstem injury), and respiratory diseases associated with respiratory muscle fatigue (e.g., exacerbations of asthma and chronic obstructive pulmonary disease [COPD]). The primary therapeutic goal in hypercarbic respiratory failure is to reverse the underlying cause of respiratory failure. Noninvasive positive-pressure ventilation may be effective, especially in COPD exacerbations.
Two other types of respiratory failure are commonly considered: (1) perioperative respiratory failure related to lung atelectasis, which can be treated with physiotherapy, positional changes, and/or noninvasive positive-pressure ventilation; and (2) hypoperfusion of respiratory muscles related to shock, which typically improves with intubation and mechanical ventilation.
For intubated pts receiving volume-controlled modes of mechanical ventilation, respiratory mechanics can be followed easily. The peak airway pressure is regularly measured by mechanical ventilators, and the plateau pressure can be assessed by including an end-inspiratory pause. The inspiratory airway resistance is calculated as the difference between the peak and plateau airway pressures (with adjustment for flow rate). Increased airway resistance can result from bronchospasm, respiratory secretions, or a kinked endotracheal tube. Static compliance of the respiratory system is calculated as the tidal volume divided by the gradient in airway pressure (plateau pressure minus PEEP). Reduced respiratory system compliance can result from pleural effusions, pneumothorax, pneumonia, pulmonary edema, or auto-PEEP (elevated end-expiratory pressure related to insufficient time for alveolar emptying before the next inspiration).
Many pts receiving mechanical ventilation require treatment for pain (typically with opiates) and for anxiety (non-benzodiazepine sedatives are preferred since benzodiazepines are associated with worse pt outcomes). Protocol-driven approaches to sedation or daily interruption of sedative infusions can prevent excessive sedative drug accumulation. Less commonly, neuromuscular blocking agents (e.g., cisatracurium) are required to facilitate ventilation when there is extreme dyssynchrony between the pt’s respiratory efforts and the ventilator that cannot be corrected with manipulation of the ventilator settings; aggressive sedation is required during treatment with neuromuscular blockers. Neuromuscular blocking agents should be used with caution because a myopathy associated with prolonged weakness can result.
Weaning from mechanical ventilation should be considered when the disease process prompting intubation has improved. Daily screening of intubated pts for weaning potential should be performed. Stable oxygenation (with oxygen supplementation levels that are achievable off of mechanical ventilation and at low positive end-expiratory pressure [PEEP] levels), intact cough and airway reflexes, and lack of requirement for vasopressor agents are required before considering a trial of weaning from mechanical ventilation. The most effective approach for weaning is usually a spontaneous breathing trial, which involves 30–120 min of breathing without significant ventilatory support. Either an open T-piece breathing system or minimal amounts of ventilatory support (pressure support to overcome resistance of the endotracheal tube and/or low levels of continuous positive airway pressure [CPAP]) can be used. Failure of a spontaneous breathing trial has occurred if tachypnea (respiratory rate <35 breaths/min for >5 min), hypoxemia (O2 saturation <90%), tachycardia (>140 beats/min or 20% increase from baseline), bradycardia (20% reduction from baseline), hypotension (systolic blood pressure <90 mmHg), hypertension (systolic blood pressure >180 mmHg), increased anxiety, or diaphoresis develops. At the end of the spontaneous breathing trial, the rapid shallow breathing index (RSBI or f/VT), which is calculated as respiratory rate in breaths/min divided by tidal volume in liters, can be used to predict weanability. An f/VT value <105 at the end of the spontaneous breathing test warrants a trial of extubation. Daily interruption of sedative infusions in conjunction with spontaneous breathing trials can limit excessive sedation and shorten the duration of mechanical ventilation. Despite careful weaning protocols, up to 10% of pts develop respiratory distress after extubation and may require reintubation.
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