Magnesium flux and cardiac surgery. A study of the relationship between magnesium exchange, serum magnesium levels and postoperative arrhythmias.

A prospective study of 128 adult cardiac surgical patients was undertaken in order to quantify net magnesium loss and its relationship to serum magnesium levels and postoperative problems, particularly arrhythmias. Peri-operative magnesium flux on the first day was calculated from the administered magnesium (in cardioplegia solution and intravenous infusion) and urinary magnesium loss. Magnesium input ranged from 24 mmol to 40 mmol, resulting in a net magnesium gain in 94% of patients. Hypomagnesaemia, identified in 34% of patients pre-operatively and 30% of patients postoperatively, had no significant correlation with the measured peri-operative magnesium flux or the electrocardiograph corrected-QT interval. Fifty-three patients developed postoperative arrhythmias, but there was no significant correlation with the serum total magnesium concentration, or with the peri-operative change in serum magnesium level, magnesium flux, or QT interval. The data suggest that serum total magnesium is not a useful measurement upon which to base preventive or therapeutic measures in cardiac surgical patients.

Alveolar oxygenation and mouth-to-mask ventilation: effects of oxygen insufflation.

The effect on alveolar oxygen fraction (FAO2) of insufflating oxygen under a mask (or through an inflow nipple provided in the mask) during simulated mouth-to-mask ventilation was investigated using a lung model. A variety of commercially produced masks were evaluated. Two patterns of artificial ventilation were applied: 1. 500 ml tidal volume at 20 breaths per minute, and 2. 900 ml tidal volume at 12 breaths per minute. The ventilating gas mixture was oxygen 16% in nitrous oxide, and oxygen was insufflated at flow rates of 2, 4, 6, 8, 10, 12 or 14 litres per minute. The rate of rise of FAO2 and the equilibrium FAO2 attained were greatest at high oxygen inflow rates. The relationship between oxygen flow and FAO2 was not linear however, and an oxygen flow rate of 10 l/min was adequate to generate FAO2's around 50% with either ventilatory pattern. The equilibrium FAO2 achieved was greater with smaller tidal volumes and with larger mask deadspace. We also found that several breaths were required for equilibration of FAO2 during each trial, supporting recommendations that several breaths should be given on commencement of artificial ventilation during cardiopulmonary resuscitation.

Isoflurane and large coronary artery haemodynamics. A study in dogs.

In the dog, stepped increases in isoflurane concentration (up to 1.5 MAC) caused peripheral and coronary vasodilatation. In the presence of significant decreases in arterial pressure (-35%), contractility (-46%), cardiac output (-17%) and coronary perfusion pressure (-40%), coronary blood flow remained unchanged, while the effective coronary vascular resistance was halved. The coronary reserve, estimated by the hyperaemic response to short periods (10 s) of coronary occlusion was reduced by the stepped increases in isoflurane concentration. Linear relationships were observed between peak hyperaemic flow, volume repayment, repayment: deficit ratio and coronary perfusion pressure. The vasodilation induced by isoflurane was of such magnitude that, at 1.5 MAC, the repayment: deficit ratio was close to unity, indicating that the vasodilatory reserve was almost exhausted.

Endocardial viability ratio and ischaemic dysfunction of the left ventricle during halothane anaesthesia.

In normal hearts, the critical value of the endocardial viability ratio (EVR) is thought to be less than 0.5. As myocardial regional dysfunction is a sensitive index of subendocardial ischaemia, the relationship between EVR and regional function has been studied in an experimental model of coronary artery constriction. In 13 dogs anaesthetized with halothane (0.5-2.0% inspired concentration), diastolic and systolic pressure time indices were obtained by planimetry, and their ratio (EVR) correlated with regional function. Halothane alone caused a significant reduction in EVR from 1.38 +/- 0.08 to 1.15 +/- 0.04 (mean +/- SEM). In the presence of coronary artery constriction a similar decrease in EVR was observed and was accompanied by post-systolic shortening (PSS), an indicator of regional dysfunction. At high concentrations of halothane, there was an inverse correlation between reduction in EVR and increase in PSS. Mean EVR of approximately 0.9 (mean = 0.92 +/- 0.02) was associated with significant worsening of regional function.

Beta-blockade reverses regional dysfunction in ischemic myocardium.

To determine the protective effect of oxprenolol-induced beta-blockade on the compromised myocardium (critical constriction of the left anterior descending coronary artery) against the adverse effect of high concentrations of halothane, halothane dose-response curves were obtained in six dogs in each of three phases: preconstriction (control), critical constriction, and critical constriction with the addition of 0.3 mg/kg intravenous oxprenolol. The extent of depression of ventricular function was essentially the same in the three phases. However, at high halothane concentrations (2.0% inspired), the depression of systolic shortening in the compromised segment was significantly minimized after oxprenolol so that shortening was 10.2% +/- 1.8 instead of 6.5% +/- 1.4 (P less than 0.05); moreover the large increase in postsystolic shortening observed during critical constriction was abolished after oxprenolol. This suggests a protective effect of oxprenolol on regional myocardial function in the presence of critical constriction, possibly by an effect on myocardial metabolism or endocardial blood flow.

Halothane-verapamil causes regional myocardial dysfunction in the dog.

Regional myocardial function was studied using sonomicrometry in six mongrel dogs, anaesthetized with halothane (1% inspired), as increasing doses of verapamil were given i.v. In addition to a gradual increase in end-diastolic length and a reduction in systolic shortening, an abnormal (paradoxical) contraction pattern appeared in the apical region. This occurred in the absence of coronary artery damage and at coronary perfusion pressures unlikely to result in ischaemia. Administration of verapamil in the presence of halothane results in regional dysfunction similar to that caused by the intracoronary administration of nifedipine.

The interactions between beta-blockers and anaesthetics. Experimental observations.

The possibility of interactions between beta-adrenoceptor antagonists and anaesthetic drugs is particularly relevant to the anaesthetic management of patients suffering from arterial hypertension and ischaemic heart disease. Maintenance of adrenergic beta-receptor blockade in patients with ischaemic heart disease and arterial hypertension is now widely accepted in order to avoid the cardiac risks of its sudden withdrawal and also to minimize the effects of sympathetic overactivity on the cardiovascular system. However, maintenance of adrenergic beta-receptor blockade may impose some constraints on the choice of the anaesthetic agent. While no adverse interaction has been found between beta blockade and anaesthesia with halothane, halothane supplementing nitrous oxide, or isoflurane, substantial reductions of cardiac performance have been observed in the case of the association of beta blockade and anaesthesia using methoxyflurane or trichloroethylene. An adverse interaction has also been observed between propranolol and enflurane anaesthesia but not between oxprenolol and enflurane anaesthesia. Recent studies of the effects of anaesthesia in the presence of critically narrowed coronary arteries have shown that both halothane and enflurane may cause regional myocardial dysfunction. This dysfunction is minimized by oxprenolol and it appears that adrenergic beta-receptor blockade, besides improving cardiovascular stability, protects the myocardium supplied by narrowed coronary arteries.