Heart contractility halothane

Enflurane (Ethrane) depresses myocardial contractility and lowers systemic vascular resistance. In contrast to halothane, it does not block sympathetic reflexes, and therefore, its administration results in tachycardia. However, the increased heart rate is not sufficient to oppose enflurane s other cardiovascular actions, so cardiac output and blood pressure fall. In addition, enflurane sensitizes the myocardium to catecholamine-induced arrhythmias, although to a lesser extent than with halothane. Enflurane depresses respiration through mechanisms similar to halothane s and requires that the patient s ventilation be assisted. 

Sevoflurane, in common with all volatile agents, reduces cardiac output and systemic blood pressure. It does so mainly through a reduction in peripheral vascular resistance. Although it is a systemic vasodilator it does not appear to produce significant dilatation of small coronary vessels and there is no possibility of coronary steal as hypothesised for isoflurane. A small increase in heart rate may be observed. This is less pronounced than with isoflurane and desflurane and is almost certainly the result of reflex activity secondary to the reduction in peripheral vascular resistance. Sevoflurane is associated with a stable heart rhythm and does not predispose the heart to sensitisation by catecholamines. In children, halothane causes a greater decrease in heart rate, myocardial contractility and cardiac output than sevoflurane at all concentrations. For these reasons sevoflurane is advocated for use in outpatient dental anaesthesia, especially in children. 

Enflurane produces a dose-related decrease in systemic arterial blood pressure secondary to reductions in cardiac output and systemic vascular resistance. There is evidence that cardiac output is partially maintained by a compensatory increase in heart rate. This effect seems dependent on a degree of hypercardia and does not occur during controlled ventilation. Enflurane and halothane depress myocardial contractility to a similar extent and less than isoflurane. Enflurane does not sensitise the heart to the effects of catecholamines to any significant extent and adrenaline (epinephrine) may be given subcutaneously for control of bleeding. 

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). 

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