Bradycardia fentanyl

WARNING Exacerbation of ischemic heart Dz w/ abrupt D/C Uses HTN MI Action p-Adrenergic receptor blocker, pj, P2 Dose HTN 10-20 mg bid, up to 60 mg/d MI 10 mg bid Caution [C (1st tri D if 2nd or 3rd tri), +] Contra CHF, cardiogenic shock, bradycardia, heart block, COPD, asthma Disp Tabs SE Sexual dysfxn, arrhythmia, dizziness, fatigue, CHF Interactions t Effects W/ antihyper-tensives, ciprofloxacin, fentanyl, nitrates, quinidine, res pine t bradycardia and... 

Answer This feature of bradycardia is typical of patients who take (3-blockers, which should be continued so they result ultimately in better anesthetic management. The drugs given could have been modified (i.e., etomidate instead of propofol, which does not raise or may cause a slower heart rate). The potent opioids in the fentanyl family all cause vagal transmitted bradycardia. The muscle relaxant vecuronium (norcuron) has no effect on heart rate and could have been replaced by pancuronium, which has a vagolytic effect and will counter bradycardia in the usual induction bolus doses. 

Most of the haemodynamic effects of opioids are related to decreased central sympathetic outflow, specific vagal effects or, in the case of morphine and pethidine, histamine release. Fentanyl and its analogues do not cause histamine release. All opioids, with the exception of pethidine, produce bradycardia by actions on the afferent fibres of the vagus and the nucleus tractus solitarius and nucleus commissuralis, which have very high densities of opioid receptors. Pethidine often produces tachycardia, possibly due to its structural similarity to atropine. In isolated heart or heart-muscle preparations, opioids produce a dose-related negative inotropic effect, but only at concentrations 100 to several thousand times those found clinically. 

Nearly all opioids induce bradycardia (Bowdle, 1998), most likely mediated via central stimulation of the vagus nerve. Cardiovascular depression associated with most opioids is moderate and only the stronger opioids of the fentanyl group induce a more severe effect. Morphine and some of its analogs induce a non-opioid receptor-mediated release of histamine, which can result in a decrease in blood pressure and compensatory... 

A 44-year-old woman developed atropine-resistant but isoprenaline-sensitive bradycardia (36 beats/minute), thought to be due to sinus node dysfunction related to lithium, fentanyl, and propofol (120). 

Sinus bradycardia (36/minute) developed in a 44-year-old woman taking lithium who received fentanyl and propofol (120). 

PROCARBAZINE ANALGESICS-OPIOIDS Unpredictable reactions may occur associated with hypotension and respiratory depression when procarbazine is co-administered with alfentanil, fentanyl, sufentanil or morphine Opioids cause hypotension due to arterial and venous vasodilatation, negative inotropic effects and a vagally induced bradycardia. Procarbazine can cause postural hypotension. Also attributed to an accumulation of serotonin due to inhibition of MAO Recommended that a small test dose (one-quarter of the usual dose) be administered in initially to assess the response... 

Kuczkowski KM. Severe persistent fetal bradycardia following subarachnoid administration of fentanyl and bupiva-caine for induction of a combined spinal-epidural analgesia for labor pain. J Clin Anesth 2004 16(l) 78-9. 

Cardiovascular adverse effects are minimal with pancuronium. Ganglion blockade does not occur. Shght dose-dependent rises in heart rate, blood pressure, and cardiac output are common (5), but are often masked by the actions of other co-administered agents, such as fentanyl or halothane, which cause bradycardia or hypotension. These adverse effects of pancuronium are thus often beneficial and can be deliberately harnessed. Several mechanisms contribute vagal blockade via selective blockade of cardiac muscarinic receptors (6), release of noradrenaline from adrenergic nerve endings (7), increased blood catecholamine concentrations (8), inhibition of neuronal catecholamine reuptake (9-11), and direct effects on myocardial contractility (12). These have been reviewed (13-15). 

In a prospective randomized comparison of combined sevoflurane plus remifentanil with combined fentanyl plus etomidate for induction of anesthesia in 10 patients with ischemic heart disease, 3 of the 20 patients given sevoflurane plus remifentanil developed severe bradycardia (heart rate less than 40) and one developed asystole, but the difference between the two groups did not reach statistical significance (20). Therefore, in patients with ischemic heart disease remifentanil should be used with caution, and concurrent administration of glycopyr-rolate 0.2 mg is advisable to reduce the incidence of bradycardia, hypotension, or both, without increasing the heart rate. 

Bradycardia and other dysrhythmias are common (80% in some series) and occur after the first and subsequent injections of suxamethonium in infants and children. In adults, these effects are seen more commonly after second or later injections, particularly when the interval between the doses is 2-5 minutes. However, it has been suggested that bradycardia and asystole may now be more frequently seen than previously in adults after a single injection of suxamethonium, as a result of the increased use of fentanyl or the omission of atropine beforehand (6). Nodal rhythm and wandering pacemaker are frequent. The bradycardia is sometimes extreme (asystoUc periods of 15-30 seconds duration have been reported). Usually these minor dysrhythmias revert to normal after a few minutes. Halothane can prolong their presence. The incidence of bradycardic asystole is not known, as atropine (the effective therapy) is usually quickly given. 

The expected cardiovascular stability of vecuronium has been confirmed in man (2,21-23). Even doses as large as 0.28 mg/kg in patients undergoing coronary artery bypass grafting produced negligible effects (24). Bradycardia is the only cardiovascular adverse effect reported, and this is seen in association with opioids such as fentanyl (25) and sufentanil (SEDA-11, 125) (26) or other drugs that are themselves capable of producing bradycardia. The lack of vagolytic and sympathomimetic activity of vecuronium... 

Fentanyl overdose leads to the classic triad of symptoms consistent with the opioid intoxication syndrome miosis, respiratory depression, and CNS depression. Additional toxic effects of fentanyl include bradycardia, hypotension, decreased gastrointestinal motility, euphoria, and acute lung injury. 

The toxic effects of illicit fentanyl derivatives include rapid onset respiratory and central nervous system depression. Patients often present comatose and apneic. Other signs and symptoms consistent with opioid intoxication such as bradycardia, hypotension, miosis, and decreased gastrointestinal motility also occur. 

Severe hypotension has been reported in patients taking calcinm-channel-blocking agents who undergo fentanyl anesthesia. Overdosage with nicardipine may prodnce hypotension, bradycardia, drowsiness, confusion, and slnrred speech. 

Fentanyl [437-38-7] (Subhmaze, Leptanal), C22H2gN20, (9) has been extensively used since its introduction into clinical practice in the 1960s (119). Because of its potency, which is 50—100 times that of morphine, a rapid onset of action and a short duration, its use as an iv anesthetic is widespread The short duration results from redistribution from the brain to other tissues, rather than elimination. It does, however, have the usual opiate disadvantages respiratory depression, chest wall rigidity, nausea, and bradycardia. Fentanyl has an extremely wide therapeutic ratio. The size of the dose influences its duration of action which, after iv administration, may last from approximately 30 min to 2 to 3 h (120,121). In cardiac surgery fentanji is administered in very laige doses to produce profound analgesia and suppress cardiovascular reflex responses. This technique is particulady useful for patients with compromised circulation where any increase in cardiac demand could precipitate myocardial ischemia (122). 

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