C.1. What are the cardiovascular effects of commonly used intravenous anesthetic and coinduction agents?
Answer:
Propofol
Propofol is a potent sympatholytic and vascular smooth muscle dilator. This results in hypotension from vasodilation, preload reduction from venodilation, and myocardial depression. It blunts the baroreceptor reflex while preserving vagal tone, and bradycardia can ensue. The overall effect is a decrease in venous return, CO, and systemic arterial pressure, which would hasten cardiovascular collapse in this patient if given in standard induction doses.
Etomidate
Etomidate is characterized by its stable hemodynamic profile when used for induction of anesthesia. Its imidazole-based structure bears structural similarities to α2-agonists and is thought to be responsible for peripheral vasoconstriction and the occasional hypertensive response when injected rapidly as the sole agent. Minor decreases in SVR, much less than with propofol or thiopental, can occur in conjunction with a volatile agent. Baroreceptor and sympathetic reflexes are preserved, and there is minimal effect on myocardial contractility. Because hemodynamic responses to laryngoscopy are not affected by etomidate, a significant increase in HR and BP should be expected when given as a sole induction agent. The primary disadvantage of etomidate is the adrenocortical suppression with its use, which can occur after a single dose. However, this has not translated into increased postoperative hypotension, morbidity, or mortality in cardiac surgery patients. Taken together, etomidate is the most cardiostable intravenous anesthetic and is the drug of choice in patients with impending hemodynamic collapse.
Ketamine
Ketamine is associated with an increase in norepinephrine release that increases sympathetic outflow and is largely responsible for its stable hemodynamic profile. The mechanism by which it causes this norepinephrine release is unclear, but a direct central effect and reuptake inhibition has been postulated. An induction dose of ketamine increases blood pressure, HR, CO, and myocardial oxygen consumption. Ketamine should be used with caution in patients with depleted endogenous catecholamine levels, such as those who are critically ill, because this can unmask its direct negative inotropic effects. This patient's sympathetic outflow appears intact, as evidenced by her tachycardia and increased SVR. In the absence of myocardial ischemia, ketamine is a reasonable choice for induction.
Thiopental
Thiopental is included here for historical interest. It is a direct myocardial depressant and also has indirect negative inotropic effects through the suppression of sympathetic outflow. It also causes vascular dilation, but because the baroreceptor reflex is preserved, there is less hypotension when compared with an equivalent dose of propofol, and the subsequent tachycardia minimizes the decrease in CO from venodilation. In a patient with cardiac tamponade, however, the hypotensive effects are exaggerated, and its use is not recommended.
Fentanyl
The hallmark of fentanyl is that it causes minimal to no myocardial depression. However, its strong vagotonic effect leads to a decrease in HR, which can lead to a decrease in CO. It preserves coronary autoregulation and has no histaminergic effects. When given in combination with midazolam or other sedatives, however, fentanyl can produce more clinically significant hypotension.
Midazolam
Midazolam exerts a dose-related venous and arterial vasodilatory effect. When given in typical anxiolytic doses, it can decrease SV and SVR by 10%, but because the baroreceptor reflex is preserved, CO is maintained. Hypotension can become marked if it is used in higher doses or in combination with fentanyl. It suppresses sympathetic outflow and decreases myocardial oxygen consumption. Because of its rapid onset and MAC-sparing effect, midazolam can be a useful coinduction agent in this patient. Some hypotension should be expected because of her dependence on sympathetic tone to compensate for her shock state.
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