Rationale

The most important advantage of noninvasive ventilation is the avoidance of complications associated with invasive mechanical ventilation. These include complications related to direct upper-airway trauma, bypass of the upper-airway defense mechanisms, increased risk of nosocomial pneumonia, and interference with upper-airway functions, including the ability to eat and communicate normally.⁶ By averting airway intubation, noninvasive ventilation leaves the upper airway intact, preserves airway defenses, and allows patients to eat orally, vocalize normally, and expectorate secretions. Compared with invasive mechanical ventilation, noninvasive ventilation reduces infectious complications including pneumonia, sinusitis, and sepsis.^7–9 Strengthening the rationale for its use is evidence accumulated over the past decade that noninvasive ventilation lowers morbidity and mortality rates of selected patients with acute respiratory failure and may shorten hospital length of stay or avoid hospitalization altogether,¹⁰ thus reducing costs.

The main indication for mechanical ventilatory assistance is to treat respiratory failure, either type 1 (hypoxemic), type 2 (hypercapnic), or both. Figure 51-1 shows that airspace collapse, surfactant abnormalities, and airway narrowing and closure contribute to ventilation-perfusion abnormalities and shunt, which cause hypoxemia. By opening collapsed airspaces and narrowed airways, positive airway pressure reduces shunt and improves ventilation-perfusion relationships, ameliorating hypoxemia. In addition, positive airway pressure can reduce the work of breathing by improving lung compliance as a consequence of opening collapsed airspaces. Another potential benefit of positive airway pressure is enhanced cardiovascular function via the afterload-reducing effect of increased intrathoracic pressure. Conversely, deleterious cardiovascular effects may occur if the preload-reducing effect outweighs the afterload-reducing effect, as may be seen in patients with reduced intravascular fluid volume.

Figure 51-1 Pathophysiology of acute hypoxemic respiratory failure and points where positive-pressure and oxygen supplementation interrupt the process. Low ventilation-perfusion ratios, shunt, and alveolar hypoventilation cause hypoxemia. Hypoxemia is treated by increasing inspired oxygen fraction (FIO₂) (limited benefit with shunt) and applying positive pressure (continuous positive airway pressure [CPAP] or positive end-expiratory pressure [PEEP]) to increase functional residual capacity, open collapsed alveoli and narrowed airways, and enhance compliance. An additional beneficial effect of CPAP may occur in patients with cardiogenic pulmonary edema, because it reduces both venous return and left ventricular afterload, which may enhance cardiovascular performance in patients with dilated, hypocontractile left ventricles.

Mechanisms of Action

Figure 51-2 shows the pathophysiologic mechanisms that contribute to ventilatory failure. Increased airway resistance, reduced respiratory system compliance, and intrinsic positive end-expiratory pressure (PEEP) contribute to increased work of breathing, predisposing to respiratory muscle fatigue. In patients with chronic obstructive pulmonary disease (COPD), the increased radius of the diaphragmatic curvature, which increases muscle tension and thereby increases impedance to blood flow, exacerbates the situation. By counterbalancing intrinsic PEEP with extrinsic PEEP and by augmenting tidal volume with intermittent positive-pressure ventilation, NIPPV reduces the work of breathing and averts the vicious circle leading to respiratory failure. Work of breathing measurements, including transdiaphragmatic pressure, diaphragmatic pressure-time product, and diaphragmatic electromyographic amplitude, are all decreased when NIPPV is delivered to patients with exacerbations of COPD. In such patients, continuous positive airway pressure (CPAP) and pressure-support ventilation (PSV) both reduce the work of breathing, but the combination of the two (PSV + PEEP) is more effective than either alone.¹¹

Figure 51-2 Pathophysiology of acute hypercapnia and points where continuous positive airway pressure (CPAP), positive end-expiratory pressure (PEEP), and pressure support (PS) interrupt the process (large arrows). Hypercapnia (increased partial pressure of carbon dioxide in arterial blood [PaCO₂]) occurs when respiratory muscles fail to adequately ventilate alveoli to maintain homeostasis with carbon dioxide production. Respiratory muscle failure occurs when work of breathing is normal (e.g., acute or chronic neuromuscular disease) or increased (e.g., patients with chronic obstructive pulmonary disease, asthma, or obesity hypoventilation syndrome), and presumably because of inadequate oxygen delivery to respiratory muscles (e.g., ~ a third of patients presenting with cardiogenic pulmonary edema). Strategies to counter these pathophysiologic mechanisms include applying CPAP or PEEP to counterbalance intrinsic PEEP (PEEPi), increasing alveolar ventilation by augmenting tidal volume (VT), using intermittent positive-pressure ventilation (IPPV), and reducing CO₂ production by decreasing the work of breathing.

Indications

A number of causes of acute respiratory failure are now considered appropriate for noninvasive ventilation therapy and are listed in Box 51-1. Evidence supporting these indications is rated and briefly discussed here; guidelines for patient selection are discussed later.