Information ⬇
- Hemodynamics
- Volatile anesthetics produced dose-dependent and similar decreases in systemic blood pressure (Fig. 17-6: Heart rate and systemic blood pressure changes (from awake baseline) in volunteers receiving general anesthesia with a volatile anesthetic). The primary mechanism to decrease blood pressure with increasing dose is related to their potent effects to lower regional and systemic vascular resistance (Fig. 17-7: Cardiac index (CI), systemic vascular resistance (SVR), and central venous pressure (CVP) changes from awake baseline in volunteers receiving general anesthesia with a volatile anesthetic).
- In volunteers, sevoflurane to about 1 MAC results in minimal changes in heart rate; isoflurane and desflurane are associated with an increase of 5% to 10% from baseline 10 to 15 (see Fig. 17-6: Heart rate and systemic blood pressure changes (from awake baseline) in volunteers receiving general anesthesia with a volatile anesthetic).
- Rapid increases in the delivered concentration of desflurane (and to a lesser extent, isoflurane) may transiently increase heart rate and systemic blood pressure.
- Administration of an opioid or clonidine blunts the heart rate responses evoked by volatile anesthetics, including responses associated with abrupt increases in the delivered concentration of volatile drug.
- Myocardial Contractility. Human studies with isoflurane, sevoflurane, and desflurane have not demonstrated significant changes in echocardiographic-determined indices of myocardial function.
- Other Circulatory Effects
- Nitrous oxide is associated with increased sympathetic nervous system activity when administered alone or in combination with other volatile anesthetics.
- Isoflurane, sevoflurane, and desflurane do not predispose patients to ventricular arrhythmias or sensitize the heart to the arrhythmogenic effects of epinephrine.
- Coronary Steal, Myocardial Ischemia, and Cardiac Outcomes
- Most potent volatile anesthetics increase coronary blood flow beyond that of myocardial oxygen demand. (No evidence that coronary steal occurs with resulting increased incidence of myocardial infarction or perioperative death.)
- Myocardial ischemia and cardiac outcome seem more related to events that alter myocardial oxygen delivery rather than the specific anesthetic drug selected.
- Cardioprotection from Volatile Anesthetics
- Volatile anesthetics mimic ischemia preconditioning and initiate a cascade of intracellular events resulting in myocardial protection against ischemia and reperfusion injury that last beyond elimination of the anesthetic.
- It is likely that anesthetic cardioprotection lessens myocardial damage (based on troponin levels) during cardiac surgery with or without cardiopulmonary bypass.
- Sulfonylurea oral hyperglycemic drugs close KATP channels and abolish anesthetic preconditioning. Hyperglycemia also prevents preconditioning, so insulin therapy should be started when oral agents are discontinued before surgery.
- Recent evidence suggests that volatile anesthetics, including xenon, may protect other organs from ischemic injury, including the kidneys, liver, and brain.
- Autonomic Nervous System
- Isoflurane, desflurane, and sevoflurane produce similar dose-dependent depression of reflex control of sympathetic nervous system outflow.
- Desflurane is unique in evoking increased sympathetic nervous system outflow (paralleled by increased plasma concentrations of catecholamine) when the delivered concentration of this drug is abruptly increased (Fig. 17-8: Stress hormone responses to a rapid increase in anesthetic concentration from 4% to 12% inspired).
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