Halothane

Cardiovascular

Halothane, isoflurane, and sevoflurane are potent coronary vasodilators, able to produce some degree of coronary steal in ischemic regions. Despite this, halothane may preferentially dilate large coronary arteries and/or interfere with platelet aggregation [ ].

Halothane has a mild depressive effect on cardiac performance [ ]. In human ventricular myocardium, halothane interacted with L-type calcium channels by interfering with the dihydropyridine binding site; this may, at least in part, explain its negative inotropic effect [ ].

Halothane depressed cardiovascular function significantly more than isoflurane in younger adults, but the falls in systolic and diastolic blood pressures in elderly patients were significantly greater with isoflurane [ ].

Respiratory

Halothane is not irritant to the respiratory tract. Respiratory depression is a consequence only of high concentrations of halothane. A certain degree of bronchodilatation is observed, and may explain the fact that a beneficial effect of halothane was described in a 17-year-old woman with acute severe asthma who did not respond to conventional treatment [ ].

Preterm infants can become apneic during the immediate postoperative period, even if the ventilatory response to CO ₂ is not depressed after halothane anesthesia [ ]. In a prospective study in 167 preterm infants after inguinal herniorrhaphy with halothane/nitrous oxide anesthesia, only one had an episode of apnea up to 2 days postoperatively; however, the authors recommended careful monitoring until complete recovery from anesthesia has occurred [ ].

Nervous system

In contrast to enflurane, cerebral irritability is very rare with halothane [ ].

Halothane can cause an increase in intracranial pressure [ ], as can other inhalational anesthetics, which can constitute a particular risk if the pressure is already raised before anesthesia. In neonates, the intracranial pressure may fall [ ].

A child who underwent induction of anesthesia with halothane developed hiccups associated with pulmonary edema [ ].

• An 8-year-old girl with a history of seizures and cerebral ischemic strokes secondary to moyamoya disease underwent anesthetic induction with halothane and 70% nitrous oxide. She had had three previous uneventful anesthetics. Hiccups started within seconds of induction of anesthesia and did not cease until 20 minutes later, when she was paralysed, intubated, and ventilated. During the next 20 minutes a period of hemodynamic instability ensued, with increasing oxygen requirements. The procedure was stopped and pulmonary edema was confirmed on chest X-ray. The child was transferred to the intensive care unit and ventilated overnight. Further recovery was uneventful.

Hiccups during anesthesia are often thought to be benign. Negative pressure pulmonary edema is usually associated with an obstructed airway, as occurs with laryngospasm, or other causes of upper airway obstruction, but was presumably the cause in this child.

The effect of increasing and decreasing concentrations of halothane on the cerebral circulation has been studied in 11 young children (aged 4 months to 3.5 years) undergoing minor urological surgery under general relaxant and caudal anesthesia [ ]. Cerebral blood flow velocity was measured in the middle cerebral artery using transcranial Doppler ultrasound. There was significantly increased cerebral blood flow velocity when the dose was increased from 0.5 to 1.0 MAC (minimum alveolar concentration) and from 0.5 to 1.5 MAC, but not when it was increased from 1.0 to 1.5 MAC. When the halothane concentration was reduced from 1.5 to 1.0 MAC, cerebral blood flow velocity fell significantly, whereas there was no effect when the concentration was reduced from 1.0 to 0.5 MAC. These results suggest that there is cerebrovascular hysteresis in response to increasing and decreasing concentrations of halothane.

Psychiatric

Slight depression of mood, lasting up to 30 days, along with a non-specific slowing of the electroencephalogram for 1–2 weeks, was observed in 16 healthy young men, in whom halothane anesthesia had negative effects on postoperative mood and intellectual function, the changes being greatest 2 days after anesthesia, with restoration of function after 8 days [ ]. In seven subjects, serial electroencephalography, serum bromide determinations, and psychological tests before and after halothane anesthesia showed that there was significant psychological impairment 2 days after anesthesia [ ].

The effect of a single preoperative dose of the opioid oxycodone on emergence behavior has been studied in a randomized trial in 130 children [ ]. Oxycodone prophylaxis, compared with no premedication, significantly reduced the incidence of post-halothane agitation.

Mineral balance

Halothane can cause an increase in circulating concentrations of bromide and fluoride [ ], which can be associated with impaired urine-concentrating ability in response to antidiuretic hormone [ ].

Hematologic

Halothane produced inhibition of in vitro platelet aggregation and an increase in bleeding time [ ].

Gastrointestinal

Postoperative nausea and vomiting can occur after halothane anesthesia [ ]. In one series, postoperative vomiting occurred in 13 of 29 patients who had received halothane for induction, but when dyxirazine was added during anesthesia the incidence of postoperative vomiting was significantly reduced (three of 29 patients) [ ].