Chapter 14 Positive pressure ventilation effects on cardiac function
The effects of mechanical ventilation on the cardiovascular system depend on the baseline myocardial reserve, circulating intravascular volume, intrathoracic pressure (ITP), and autonomic tone of the patient. Unlike spontaneous inspiration, ITP increases during positive-pressure ventilation during lung expansion. Increased ITP causes a reduction of right ventricular filling and pulmonary perfusion. The right atrial pressure and systemic venous pressure increase. Venous return to the heart becomes greatest during expiration which is opposite with spontaneous respiration. The consequence of increased ITP and decreased venous return could be deleterious in patients who are hypovolemic at baseline. These patients may require large volume resuscitation to increase their cardiac output. However, in patients whose intravascular volume is normal or increased, positive pressure ventilation does not impair cardiac output as long as hyperinflation is avoided. Hyperinflation compresses the alveolar vessels, increases pulmonary vascular resistance, and can cause pulmonary artery hypertension. The consequence of hyperinflation in any patient on mechanical ventilation could be acute right ventricular ischemia and failure. Increased right ventricular afterload elevates right ventricular end-diastolic pressure which can result in ventricular septal shift toward the left ventricular cavity.
On the other hand, increased ITP reduces left ventricular afterload, which in turn, augments left ventricular systolic function and cardiac output. This beneficial effect is even more pronounced in patients with myocardial ischemia at baseline. Positive pressure ventilation decreases the work of breathing, increases oxygen delivery to other organs, and decreases myocardial oxygen demand. These effects improve myocardial contractility and cardiac output and reduce ischemia. The opposite situation develops during transition from positive pressure ventilation to spontaneous breathing. The weaning from positive pressure ventilation to spontaneous breathing usually represents an acute cardiovascular stress. Therefore, withdrawal of ventilator support in patients with reduced cardiovascular reserve can precipitate myocardial ischemia, heart failure, and pulmonary edema.
The autonomic balance is altered in patients with acute respiratory failure. These patients have elevated catecholamine levels secondary to anxiety, dyspnea, and hypoxia. Mechanical ventilation is useful in protecting the myocardium from the excessive catecholamine release by eliminating dyspnea, anxiety, and maintaining ventilator support. This effect is also beneficial in reducing the dysrhythmias induced by elevated adrenergic tone.
In summary, the effects of positive pressure ventilation on cardiac function are very complex and variable since most of these changes depend on the baseline cardiovascular status of the patient and the etiology of the respiratory compromise. These effects are minimized by using the lowest possible mean airway pressure. The maintenance cardiac output and systemic blood pressure can be achieved by volume repletion with or without vasopressor drugs when a high mean airway pressure is necessary. The most common effects on the cardiovascular system in a usual patient without accompanying significant comorbidities are summarized in the following table.
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