Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 22/04/2025
This article have been viewed 2849 times
Kent H. Rehfeldt, MD, FASE
Anesthesiologists frequently administer opioids preoperatively, intraoperatively, and postoperatively, most often to provide analgesia or as part of a balanced anesthetic. A predominantly opioid-based anesthetic may be selected for hemodynamically unstable patients because, compared with other classes of anesthetic drugs, opioids usually cause fewer unwanted changes in the hemodynamic profile. Nonetheless, opioids, especially in large doses, can alter hemodynamics. Changes in heart rate, cardiac conduction, blood pressure, and myocardial contractility are possible. Whether these effects are beneficial or detrimental depends on the clinical setting.
The administration of opioids (with the exception of meperidine) usually results in decreased heart rate. The tendency of meperidine to increase heart rate has been attributed to its atropine-like structure or to the effect of its principal metabolite, normeperidine. The reduction in heart rate that typically accompanies the use of opioids other than meperidine is seen in conjunction with reduced sympathetic tone and may be desirable in some patients, such as those at risk for developing coronary ischemia. When compared with the use of fentanyl and sufentanil, the use of alfentanil less reliably prevents increases in heart rate and blood pressure in response to surgical stimulation during cardiac operations. Additionally, opioids directly stimulate μ receptors in medullary vagal nuclei, an effect that can be attenuated by bilateral vagotomy. Some investigators have also noted decreases in heart rate with the use of remifentanil, even in the absence of enhanced parasympathetic tone, suggesting a direct effect on cardiac conduction tissue. Severe bradycardia and even asystole have been reported following the administration of opioids, such as remifentanil; fortunately these serious reactions are rare and may be more likely to occur when remifentanil is given as a bolus or when administered to patients who are also receiving β-adrenergic receptor or calcium channel blocking agents. Similarly, profound bradycardia may be more likely to occur when opioids are given during vagotonic procedures. For example, fentanyl, sufentanil, and alfentanil significantly augment the oculocardiac reflex, contributing to intraoperative bradycardia during some eye operations. Pretreatment with drugs such as pancuronium or atropine diminishes the likelihood of occurrence of opioid-induced decreases in heart rate.
Besides causing bradycardia, opioid administration can also lower blood pressure. Decreased sympathetic tone probably accounts for most of the blood pressure reduction. The tone of both venous capacitance vessels and arteriolar resistance vessels may decrease. Hypotensive effects are most prominent in patients with increased sympathetic tone, such as those with congestive heart failure or hypovolemia. Blood pressure changes are less common in isovolemic supine patients. However, orthostatic hypotension may be seen in patients with autonomic nervous system impairment (e.g., autonomic neuropathy in patients with diabetes). Besides reducing sympathetic tone, a direct opioid effect on vascular smooth muscle has also been observed when sufentanil and remifentanil have been administered in experimental settings. These direct effects on vascular smooth muscle appear to be independent of a neurogenic or systemic mechanism and may contribute to the hypotension sometimes encountered when sufentanil and remifentanil are used clinically. Interestingly, pretreatment with glycopyrrolate may attenuate the decrease in blood pressure that can accompany remifentanil administration.
In addition to reducing sympathetic tone and direct vascular effects, morphine and meperidine also activate mast cells and trigger histamine and tryptase release, which can contribute to vasodilatation and hypotension. The use of fentanyl, sufentanil, alfentanil, and remifentanil does not promote histamine release.
Hypertension is occasionally observed in patients receiving opioid medications intraoperatively. Most frequently seen in patients with preserved left ventricular function, hypertensive responses probably result from either too low of an opioid dose or inadequate administration of other types of anesthetic agents.
The inotropic effects of opioids are probably not clinically important in most settings when typical doses are used. However, some investigators have noted dose-dependent increases in myocardial contractility with the use of agents such as fentanyl and sufentanil, possibly related to direct myocardial adrenergic stimulation. The use of alfentanil may increase myocardial contractility by augmenting the sensitivity to calcium. On the other hand, meperidine may have detectable negative inotropic effects. Variable effects on myocardial contractility have been reported in response to morphine use.
Opioids are often selected for patients who currently have or have a history of ischemic heart disease. In fact, morphine is included in advanced cardiac care algorithms for the treatment of patients presenting with acute myocardial ischemia. The benefits of morphine in these patients include a reduction in sympathetic tone, lowering of the heart rate, and vasodilatation, resulting in reduced preload without altering the responsiveness of large coronary arterioles to vasoactive agents. Overall, a more favorable myocardial oxygen supply/demand ratio is maintained. Similarly, opioid-based anesthetic agents promote a more favorable myocardial oxygen supply/demand ratio when compared with inhalation-based anesthesia. Opioid use is not associated with coronary steal. Although it is not well established clinically, the use of opioids may confer an ischemic preconditioning benefit similar to that seen with the use of inhalation anesthetic agents.
Anesthesiologists are frequently asked to provide care for patients undergoing catheter-based electrophysiology investigations and procedures. Thus, an understanding of the impact of commonly used sedative and anesthetic drugs on electrophysiology parameters is essential. As noted, opioids typically reduce sympathetic outflow and enhance parasympathetic tone by direct stimulation of vagal nuclei. The enhanced vagal tone that follows fentanyl administration may manifest during electrophysiology procedures as prolonged sinus node recovery time, which is a measure of sinus node automaticity. Remifentanil also prolongs sinus node recovery time, increases sinoatrial conduction time, and prolongs the ventricular effective refractory period. Ideally, the use and possible effects of opioids on measured electrophysiology parameters should be discussed with the interventional cardiologist prior to beginning the procedure.
The impact of perioperatively administered drugs on the QT interval and the possible promotion of torsades de pointes in patients with congenital long QT syndrome have recently been reviewed. A few reports link the use of sufentanil and high-dose methadone to QT prolongation or torsades de pointes. On the other hand, remifentanil seems to have no effect on the QT interval, at least, as has been shown in a large animal model. Although conflicting evidence exists, fentanyl and morphine may be the preferred opioids for use in patients with congenital long QT syndrome.
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