Cardiopulmonary Interactions in the Management of Acute Obstructive Disease

The heart and lung are mechanically coupled both by virtue of their common exposure to the pleural pressure and the direct effects of lung inflation on the pulmonary vasculature. Derangements in pulmonary mechanics that occur with obstructive lung disease may thus result in hemodynamic abnormalities. In the setting of airflow obstruction, changes in pulmonary compliance, airway resistance, or airflow limitation may result in prolonged expiratory times and the possibility of incomplete exhalation. When this occurs, alveolar pressure is greater than airway opening pressure at end expiration, a phenomenon known as auto-PEEP; this also increases mean intrathoracic pressure and dynamically increases end-expiratory lung volume. Dynamic hyperinflation and increased mean intrathoracic pressure result in increased work of breathing, increased dead space, and, potentially, in substantial hemodynamic compromise. Hemodynamic compromise may also occur through the effects of intrathoracic pressure on cardiac filling pressures, cardiac afterload, and venous return. The primary determinants of auto-PEEP are tidal volume, expiratory time, severity of airway obstruction, and lung compliance. To minimize auto-PEEP, ventilator parameters should be chosen to maximize expiratory time. The dominant determinant of expiratory time is respiratory rate. In a spontaneously breathing patient, auto-PEEP also presents an inspiratory threshold load which increases the work of breathing. In the presence of auto-PEEP, extrinsic PEEP can reduce the threshold load. However, extrinsic PEEP greater than auto-PEEP can also worsen hyperinflation. Reduction of auto-PEEP can improve venous return and cardiac output and is thus a primary therapeutic goal in the ventilatory management of patients with obstructive disease.