Liver transplantation for massive hepatic haemangiomatosis causing restrictive lung disease.

A 34-yr-old man with hepatic haemangiomatosis presented for orthotopic liver transplantation. His massively distended abdomen caused thoracic compression and severe restrictive lung disease. Respiratory failure was the principal indication for transplantation. Increased airway pressures, pulmonary hypertension, systemic hypotension caused by aorto-caval compression, and blood loss, complicated the intra-operative anaesthetic management. Weaning from mechanical ventilation was impaired by acute and chronic metabolic alkalosis, and diaphragmatic laxity.

Monitoring equipment induced tachycardia in patients with minute ventilation rate-responsive pacemakers.

Minute ventilation-sensing pacemakers enable the paced heart to respond to an increased workload. Two patients with such a pacemaker developed pacemaker-driven tachycardia when connected to an electrocardiogram (ECG) monitor also capable of documenting ventilatory frequency and ECG lead disconnection. This tachycardia stopped when the ECG leads were removed. These pacemakers and monitors emit a low-amplitude electrical current and measure the resultant impedence signal across the chest. When patients are connected to the monitor the pacemaker sensor summates both impedence signals and the paced heart rate is increased as a result.

Altered release and metabolism of norepinephrine in superfused canine saphenous veins in the presence of halothane and hypoxia.

BACKGROUND: Hypoxia and halothane are both known to have different effects on the release and disposition of norepinephrine at sympathetic nerve terminals during neurotransmission. In adverse clinical situations, both conditions may be present, but the effects of halothane and hypoxia together are not known. Therefore, studies were made of the effects of low partial pressures of oxygen and of halothane on the release, action, and metabolism of norepinephrine at sympathetic nerve endings in isolated segments of a blood vessel in which halothane is known to affect norepinephrine release and action profoundly. METHODS: Saphenous veins were removed from dogs, suspended for superfusion with Krebs-Ringer solution, and stimulated electrically. The veins were exposed to either 0%, 0.75%, or 1.5% halothane in the presence of 95% O2, 5% CO2, or 5% O2, 5% CO2, and 90% N2. Superfusates were collected under basal conditions, during and after electrical field stimulation, and poststimulation. Norepinephrine and its intraneuronal metabolite, 3,4-dihydroxyphenylglycol, were measured in superfusates and in the tissues after superfusion using high-performance liquid chromatography with electrochemical detection. RESULTS: Halothane decreased 1) evoked release of norepinephrine, 2) contractile response of the smooth muscle to nerve stimulation, 3) formation of 3,4-dihydroxyphenylglycol, and 4) tissue content of norepinephrine. However, hypoxia 1) increased evoked release of norepinephrine but decreased 2) contractile response during nerve stimulation, 3) formation of 3,4-dihydroxyphenylglycol, and 4) tissue content of norepinephrine. When halothane and hypoxia were present together, their effects on 3,4-dihydroxyphenylglycol formation, tissue content of norepinephrine, and the contractile responses appeared to be additive, but norepinephrine release was decreased compared with control concentrations. CONCLUSIONS: Although halothane and hypoxia had similar and additive effects on the intraneuronal metabolism of norepinephrine and on the postjunctional responses of smooth muscle to nerve stimulation, they had opposite effects on norepinephrine release from sympathetic nerve endings. The halothane-induced decrease in norepinephrine release overrode the increased release of norepinephrine caused by hypoxia.