Halothane cardiovascular effects

Halogenated hydrocarbon inhalation anesthetics may increase intracranial and CSF pressure. Cardiovascular effects include decreased myocardial contractility and stroke volume leading to lower arterial blood pressure. Malignant hyperthermia may occur with all inhalation anesthetics except nitrous oxide but has most commonly been seen with halothane. Especially halothane but probably also the other halogenated hydrocarbons have the potential for acute or chronic hepatic toxicity. Halothane has been almost completely replaced in modern anesthesia practice by newer agents. 

In 190 patients taking tricyclic antidepressants that could not be discontinued before surgery, who underwent general and 61 local or regional anesthesia, there were no changes in the cardiovascular effect of halothane, induction time with pentobarbital, propanidid, or ketamine, or the duration of depolarization or recovery time (160). The general conclusion was that it is safer to continue treatment with tricyclic antidepressants than to risk potential disruption from withdrawal before surgery. 

Mckinney MS, Fee JP. Cardiovascular effects of 50% nitrous oxide in older adult patients anaesthetized with isoflurane or halothane. Br J Anaesth 1998 80(2) 169-73. 

McKinney MS, Fee JP, Clarke RS. Cardiovascular effects of isoflurane and halothane in young and elderly adult patients. Br J Anaesth 1993 71(5) 696-701. 

From RP, Pearson KS, Choi WW, Abou-Donia M, Sokoll MD. Neuromuscular and cardiovascular effects of mivacurium chloride (BW B1090U) during nitrous oxide-fentanyl-thiopentone and nitrous oxide-halothane anaesthesia. Br J Anaesth 1990 64(2) 193-8. 

Steffey E P, Howland D Jr 1978a Cardiovascular effects of halothane in the horse. American Journal of Veterinary Research 39 611-615... 

Blackmore WP, Erwin KW, Wiegand OF, Lipsey R. Renal and cardiovascular effects of halothane. Anesthesiology 1960 21 489-495. 

Cardiovascular effects Most inhaled anesthetics decrease arterial blood pressure moderately. Enflurane and halothane are myocardial depressants that decrease cardiac output, while isoflurane causes peripheral vasodilation. Nitrous oxide is less likely to lower blood pressure than are other inhaled anesthetics. Blood flow to the liver and kidney is decreased by most inhaled agents. Halothane may sensitize the myocardium to the arrhythmogenic effects of catecholamines. 

In a study during open heart surgery, the cardiovascular effects of halothane, enflu-rane, methoxyflurane and fluroxene were compared (22C). The strongest cardiovascular depression was found after the use of halothane and enflurane. In a comparison of the 2 latter agents in equipotent dosages (23C) it was found that although the blood pressure decreased more markedly with enflurane, halothane caused significantly more myocardial depression. 

Karliczek, G., Hempelmann, G. and Piepen-brock, S. (1975) A comparison of tlic cardiovascular effects of enflurane, halothane, methoxy-flurane and fluroxene during open cardiac surgery./I efa ana est/r. belg., 26, 81. 

The local risks of vasoconstrictors in local anaesthetic solutions, particularly when the latter are used in the fingers or other extremities, have long been recognized. In addition, it is well known that the use of adrenaline or noradrenaline for this purpose can lead to marked rises in blood pressure, especially in patients who are taking MAO inhibitors the cardiovascular effects can be dangerous in patients with existing cardiovascular disease or where there is simultaneous treatment with either a tricyclic antidepressant (SED VIII) or with those general anaesthetics which sensitize the myocardium to the effects of catecholamines (e.g. chloroform, cyclopropane, halothane). 

Methoxyflurane (Penthmne) is the most potent inhala-tional agent available, but its high solubility in tissues limits its use as an induction anesthetic. Its pharmacological properties are similar to those of halothane with some notable exceptions. For example, since methoxyflurane does not depress cardiovascular reflexes, its direct myocardial depressant effect is partially offset by reflex tachycardia, so arterial blood pressure is better maintained. Also, the oxidative metabolism of methoxyflurane results in the production of oxalic acid and fluoride concentrations that approach the threshold of causing renal tubular dysfunction. Concern for nephrotoxicity has greatly restricted the use of methoxyflurane. 

The most common use of NjO is in combination with the more potent volatile anesthetics. It decreases the dosage requirement for the other anesthetics, thus lowering their cardiovascular and respiratory toxicities. For example, an appropriate anesthetic maintenance tension for N2O and halothane would be N2O 40% and halothane 0.5%. With this combination in a healthy patient, anesthesia is adequate for major surgery, and the dose-dependent cardiac effects of halothane are reduced. 

Isoflurane has a dose-dependent depressant effect on the myocardium. In vitro studies indicate that it reduces myocardial contractility to a similar extent as halothane. In vivo, isoflurane appears to be less of a cardiovascular depressant than other volatile agents. 

Inhaled anesthetics change heart rate either directly by altering the rate of sinus node depolarization or indirectly by shifting the balance of autonomic nervous system activity. Bradycardia is often seen with halothane, probably through vagal stimulation. In contrast, enflurane, and sevoflurane have little effect, and both desflurane and isoflurane increase heart rate. In the case of desflurane, cardiovascular responses include a transient sympathetic activation that can lead to marked increases in heart rate and blood pressure when high inspired gas concentrations are administered. 

Usui T, Sugiyama A, Ishida Y, Satoh Y, Sasaki Y, Hashimoto K (1998) Simultaneous assessment of the hemodynamic, car-diomechanical and electrophysiological effects of terfenadine on the in vivo canine model. Heart Vessels 13 49-57 Weissenburger J, Nesterenko VV, Antzelevitch C (2000) Transmural heterogeneity of ventricular repolarization under baseline and long QT conditions in the canine heart in vivo torsades de pointes develops with halothane but not pentobarbital anesthesia. Journal of Cardiovascular Electrophysiology ll(3) 290-304... 

INHALATIONAL -HALOTHANE OXYTOCICS Report of arrhythmias and cardiovascular collapse when halothane was given to patients taking oxytocin Uncertain possibly additive effect. High-dose oxytocin may cause hypotension and arrhythmias Monitor PR, BP and ECG closely give oxytocin in the lowest possible dose. Otherwise consider using an alternative inhalational anaesthetic... 

The effect of the sympathomimetic drugs on the pregnant uterus is Vciriable and difficult to predict, but serious fetal distress can occur, due to reduced placental blood flow as a result both of contraction of the uterine muscle (a) and arterial constriction (a). Pj-agonists are used to relax the uterus in premature labour, but unwanted cardiovascular actions can be troublesome. Sympathomimetics were particularly likely to cause cardiac arrhythmias (p, effect) in patients who received halothane anaesthesia (now much less used). 

Halothane can be used as an anesthetic by maternal inhalation for fetal surgery and improves surgical exposure by relaxing the uterus. However, the effects of halothane on fetal cardiovascular homeostasis have been evaluated, and the authors concluded that halothane had a significant negative effect on the fetal heart and peripheral vasculature it was therefore considered a poor anesthetic for this purpose (57). 

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). 

Muir W W 1995 The haemodynamic effects of milrinone HCI In halothane anaesthetized horses. Equine Veterinary Journal Supplement 19 108-113 Muir W W, Mcguirk S M 1985 Pheirmacology and pharmacokinetics of drugs used to treat cardiac disease in horses. Veterinary Clinics of North America Equine Practice 1 335-352 Muir W W D, Mcguirk S 1987 Cardiovascular drugs. Their pharmacology and use In horses. Veterinary Clinics of North America Equine Practice 3 37-57 Muir W W D, Reed S M, Mcguirk S M 1990 Treatment of atrial fibrillation in horses by intravenous administration of quinidine. Journal of the American Veterinary Medical Association 197 1607-1610... 

Lidocaine is used in cardiovascular medicine for its antiarrhythmic properties (see Ch. 12). More recently, studies have looked at the i.v. administration of lidocaine to horses with colic (see Ch. 6). It appears that i.v. lidocaine (without epinephrine (adrenaline)) may have some desirable effects on jejunal distension and peritoneal fluid accumulation and is well-tolerated periop-eratively in horses with colic (Brianceau et al 2002). In addition, i.v. lidocaine reduced the halothane MAC significantly (Doherty Frazier 1998) in ponies. 

In addition, to its hypotensive effect, rilmenidine has additional beneficial effects. In the cardiovascular field, it was shown to powerfully prevent the occurrence of experimental ventricular arrhythmias. Mammoto et al. (1996) reported that rilmenidine prevented the halothane-adren-aline induced arrhythmias in dogs. Our group has shown that rilmenidine was able to prevent the occurrence of ventricular arrhythmias caused by bicuculline injected i.c. in anaesthetized rabbits. This effect of potential clinical relevance was observed when rilmenidine was injected either i.c. or intravenously (Roegel et al., 1996). It is notable that this anti-arrhythmic action was observed at doses of rilmenidine too low to reduce blood pressure and that it was antagonized by idazoxan. Similar results were also obtained with moxonidine (Lepran and Papp, 1994 Mest et al., 1995). 

Cardiovascular System The most predictable side effect of halothane is a dose-dependent reduction in arterial blood pressure. Mean arterial pressure typically decreases -20-25% at MAC concentrations of halothane, primarily as a result of direct myocardial depression, and perhaps an inability of the heart to respond to the effector arm of the baroreceptor reflex. Halothane-induced reductions in blood pressure and heart rate generally disappear after several hours of constant halothane administration, presumably because of progressive sympathetic stimulation. 

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