LITERATURE REVIEW Carol L. Lake, MD, Editor

Hohnloser SH, Verrier RL, Lown B, et ah Effect of hypokalemia on susceptibility to ven- tricular fibrillation in the normal and ischemic canine heart. Am Heart J 112:32-35, 1986

The importance of hypokalemia in the anesthetized patient remains a subject of controversy with recent work suggesting that it is of little consequence. However, in this experimental animal study, an acute decrease of serum potassium by hemodialysis reduced the ventricular fibrilla- tion threshold by 25% and the repetitive extrasystole thresh- old by 30%. The thresholds for repetitive extrasystoles and ventricular fibrillation were determined by scanning elec- trical diastole in 5-msec intervals beginning at the boundary of the effective refractory period and continuing through the end of the T wave and applying constant current cathodal pulses of 5 msec duration, increasing the intensity of the test stimulus in 2-mA increments.

The authors also noted that acute ligation of the anterior descending coronary artery further enhanced ven- tricular vulnerability to fibrillation, during both normokal- emia (44% decrease in fibrillation threshold) and hypokal- emia (58% decrease in fibrillation threshold). Restoration of serum potassium concentrations normalized ventricular excitability in the nonischemic animals. Hypokalemia ex- acerbates dysrhythmias by (1) transformation of nonpace, maker cells into pacemakers and (2) creation of an inhomo- geneity in excitable properties of adjacent myocardial tissue increasing reentry. The authors conclude that hypokalemia enhances cardiac electrical instability, with ischemia causing an additional proarrhythmic effect.

Wolff G, Brunner JX, Gradel E: Gas exchange during mechanical ventilation and spon- taneous breathing. Intermittent mandatory venti- lation after open heart surgery. Chest 90:11-17, 1986

The authors studied ventilatory parameters during the progression from controlled positive pressure ventilation (CPPV) through intermittent mandatory ventilation (IMV) to continuous positive airway pressure (CPAP) spontaneous breathing in eight patients after unspecified cardiac proce- dures. Unfortunately, the level of anesthesia probably varied during the measurements and there was no randomization of the ventilatory techniques applied as each patient progressed sequentially from controlled to spontaneous ventilation. All measurements were made during ventilation via a modified Monaghan M-250 ventilator (Monaghan, Inc, Littleton, CO) with those on CPPV at 6, on IMV at 10, and the final set on CPAP at 12 hours postoperatively. Intermittent mandatory ventilation decreased mean airway pressure and slightly

increased dead space to tidal volume ratio (Vd/Vt), because small spontaneous tidal volumes during IMV demonstrated higher series dead space ventilation-to-tidal volume ratios. The efficiency of alveolar carbon dioxide elimination was also greater during spontaneous than mandatory breaths because there was better matching of perfusion and ventilation.

Compared to CPAP, IMV failed to reduce the work of breathing. During CPAP, functional residual capacity (FRC) decreased without a change in shunt or arterial oxygenation. The advantages of early weaning to IMV dem- onstrated in this study were a reduction in mean airway pressure and dead space ventilation without changes in FRC or oxygenation.

Quon CY, Gorczynnski R J: Pharmacody- namics and onset of action of esmolol in anesthe- tized dogs. J Pharmacol Exp Ther 237:912-918, 1986

The pharmacodynamics of esmolol, an ultrashort- acting cardioselective beta agonist with weak cardiodepres- sant activity and minimal intrinsic sympathomimetie action, were studied in anesthetized dogs. Specifically, the authors evaluated the relationship between plasma drug concentra- tions and beta blockade. The percent inhibition of isoprotere- nol-induced tachycardia was used to evaluate the level of beta blockade. A loading infusion of 500 #g/kg/min followed by maintenance infusions of 12.5, 25, or 50 ~g/kg/min rapidly achieved beta blockade in a dose-dependent manner.

The onset of beta blockade began within 15 seconds of the loading infusion with peak blockade at 30 to 45 seconds on the maintenance infusion. Steady-state levels of blockade occurred within 10 minutes of infusion. Peak blood levels occurred immediately after discontinuation of the infusion, with steady-state levels within 30 minutes of continuous administration. Beta blockade correlated well with the loga- rithm of the steady-state blood concentration.

The termination of blockade was rapid with an 80% recovery within 17 minutes, similar to the 15-minute elimina- tion half-life. Unlike propranolol, the onset and termination of beta blockade correlated closely with blood concentrations of esmolol. The pharmacologic properties of esmolol permit easily titratable beta-adrenergic blockade.

Jureidini SB, Alpert BS, Durant RH, et al: Two-dimensional echocardiographic assessment

From the Department of Anesthesiology, University of Virginia, Charlottesville.

© 1987 by Grune & Stratton, Inc.

Journal of Cardiothoracic Anesthesia, Vol I , No 1 (February), 1987: pp 8 7 - 8 9 87