Heart rate is unchanged by halothane. In addition, halothane also inhibits the baroreceptor-increased heart rate usually seen with lowered blood pressure. Stroke volume is reduced and is consistent with decreased myocardial contractility. Patients with impaired contractility secondary to congestive heart failure are particularly vulnerable to inhaled anesthetics. Systemic vascular resistance is unchanged, but halothane does have venodilating effects and increases skin blood flow.
All volatile anesthetics increase cerebral blood flow, with halothane having the greatest effect.
Autoregulation seems to remain intact in coronary arterioles. Right atrial pressure is increased in a dose-dependent fashion. Halothane does reduce the amount of circulating epinephrine required to elicit ventricular premature contractions. The ability of halothane to impair cardiac conduction appears to be a necessary part of the etiology of these arrhythmias. Junctional rhythm is common with halothane from suppression of sinus node activity.