Because all inhaled anesthetics produce a dose-dependent decrease in arterial blood pressure, activation of autonomic nervous system reflexes may trigger increased heart rate. However, halothane, enflurane, and sevoflurane have little effect on heart rate, probably because they attenuate baroreceptor input into the autonomic nervous system. Desflurane and isoflurane significantly increase heart rate because they cause less depression of the baroreceptor reflex. In addition, desflurane can trigger transient sympathetic activation—with elevated catecholamine levels—to cause marked increases in heart rate and blood pressure during administration of high desflurane concentrations or when desflurane concentrations are changed rapidly.
Inhaled anesthetics tend to reduce myocardial oxygen consumption, which reflects depression of normal cardiac contractility and decreased arterial blood pressure. In addition, inhaled anesthetics produce coronary vasodilation. The net effect of decreased oxygen demand and increased coronary flow (oxygen supply) is improved myocardial oxygenation. However, other factors, such as surgical stimulation, intravascular volume status, blood oxygen levels, and withdrawal of perioperative β blockers, may tilt the oxygen supply-demand balance toward myocardial ischemia.
Halothane and, to a lesser extent, other volatile anesthetics sensitize the myocardium to epinephrine and circulating catecholamines. Ventricular arrhythmias may occur when patients under anesthesia with halothane are given sympathomimetic drugs or have high circulating levels of endogenous catecholamines (eg, anxious patients, administration of epinephrine-containing local anesthetics, inadequate intraoperative anesthesia or analgesia, patients with pheochromocytomas). This effect is less marked for isoflurane, sevoflurane, and desflurane.
C. Respiratory Effects
All volatile anesthetics possess varying degrees of bronchodilating properties, an effect of value in patients with active wheezing and in status asthmaticus. However, airway irritation, which may provoke coughing or breath-holding, is induced by the pungency of some volatile anesthetics. The pungency of isoflurane and desflurane makes these agents less suitable for induction of anesthesia in patients with active bronchospasm. These reactions rarely occur with halothane and sevoflurane, which are considered nonpungent. Therefore, the bronchodilating action of halothane and sevoflurane makes them the agents of choice in patients with underlying airway problems. Nitrous oxide is also nonpungent and can facilitate inhalational induction of anesthesia in a patient with bronchospasm.
The control of breathing is significantly affected by inhaled anesthetics. With the exception of nitrous oxide, all inhaled anesthetics in current use cause a dose-dependent decrease in tidal volume and an increase in respiratory rate, resulting in a rapid, shallow breathing pattern. However, the increase in respiratory rate varies among agents and does not fully compensate for the decrease in tidal volume, resulting in a decrease in alveolar ventilation. In addition, all volatile anesthetics are respiratory depressants, as defined by a reduced ventilatory response to increased levels of carbon dioxide in the blood. The degree of ventilatory depression varies among the volatile agents, with isoflurane and enflurane being the most depressant. By this hypoventilation mechanism, all volatile anesthetics increase the resting level of Paco2 in spontaneously breathing patients.