POSITIVE-PRESSURE VENTILATION

The iron lung is a form of noninvasive negative-pressure ventilation that was widely used to treat respiratory failure during the polio epidemics of the 1950s and was the first widely used method of mechanical ventilation. With the advent of endotracheal intubation in the 1960s, PPV became and remains the predominant method for treating respiratory failure. PPV refers to the application of higher than ambient airway pressures during inspiration and/or exhalation in order to improve respiratory function. This form of therapy is potentially useful for ventilatory or hypoxic respiratory failure. Invasive PPV via an endotracheal tube is presently the most commonly used method for the inhospital treatment of respiratory failure; however, it is associated with a multitude of potential complications including vocal cord injury, dental injury, tracheal stenosis, and ventilator-associated pneumonia. For this reason there has been a renewed interest in noninvasive forms of mechanical ventilation. The following section discusses the physiology and the commonly available modes of PPV and the practice of NIPPV.

Physiology of Positive-Pressure Ventilation

Normal breathing is a process of negative pressure ventilation. Gas is moved into the tracheobronchial tree by displacement of the diaphragm caudally, and the chest wall is expanded; in doing so, negative intrapleural pressure is created and the lungs are expanded, creating a pressure gradient from the oropharynx to the alveoli and thus initiating air movement into the lungs. Air is then moved out of the tracheobronchial tree when the diaphragm and chest wall are relaxed and the lungs are passively deflated as the pressure gradient from the environment to the lungs is reversed. When positive pressure is applied to the respiratory system, either continuously or at end expiration, a host of physiologic changes occur. The bulk of these changes occur in the cardiopulmonary system.

Pulmonary Effects

Positive end-expiratory pressure/continuous positive airway pressure (PEEP/CPAP) therapy produces two well-described salutary effects on the pulmonary system and thus on oxygenation: (1) redistribution of extravascular water, and (2) increase in the functional residual capacity (FRC). There are other potential beneficial pulmonary effects, but these are usually specific to individual disease processes. The redistribution of extravascular water leads to improved oxygenation, lung compliance, and ventilation-perfusion matching.^{[56] [57] [58] [59]} The increase in FRC results from an increase in the volume of patent alveoli at lower levels of PEEP and from inflation of previously collapsed alveoli, a process known as alveolar recruitment, at higher levels of PEEP.^[60] Studies have demonstrated that there is a critical airway pressure necessary to reopen or recruit collapsed alveolar units. This critical pressure is referred to as the inflection point and is determined in large part by PEEP.^{[61] [62] [63]} This concept is the basis on which low tidal volume-high PEEP protocols for the treatment of acute respiratory distress syndrome (ARDS) are based (see Chapter 74 ). By expanding atelectatic alveoli and increasing the FRC, the proportion of alveoli that is perfused but not ventilated is decreased—that is, shunt is decreased and thus oxygenation improved.

Cardiovascular Effects

PPV causes a decrease in cardiac output that can be attributed to at least three mechanisms: (1) decreased venous return (2) right ventricular dysfunction, and (3) alteration of left ventricular distensibility. Decreased venous return is generally the most significant factor causing decreased cardiac output with PPV. Increased intrathoracic pressure results in decreased end-diastolic volume and stroke volume of both ventricles.^{[64] [65]} Augmenting preload with additional intravascular fluid will minimize this effect. In the second mechanism, PPV increases pulmonary vascular resistance and thereby increases right ventricular afterload.^{[67] [68]} This effect is most pronounced in patients with pre-existing right ventricular dysfunction. ^[69] The third mechanism by which PPV can cause reduction in cardiac output is alteration of left ventricular distensibility. Elevated pulmonary pressures can cause an elevation in right ventricular end-diastolic volume, resulting in a leftward shift of the intraventricular septum.^[70] This shift limits left ventricular distensibility and causes a decrease in cardiac output.^{[71] [72]}

In some patients with left ventricular dysfunction, positive pressure may actually improve cardiac output. This occurs by several mechanisms: (1) patients with elevated filling pressures may have a decrease in end-diastolic volume and improved cardiac performance as the

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PPV can also affect hemodynamic measurements. The degree to which intrapulmonary pressures affect central venous, pulmonary artery, and pulmonary capillary pressures is variable and depends in large part on pulmonary compliance. There is evidence that even in the presence of normal compliance, PEEP of greater than 10 cm H₂ O makes measurement of pulmonary capillary wedge pressure unreliable. ^[74]