Comparative cardiotoxicity of bupivacaine and lidocaine in the isolated perfused mammalian heart.

This study was designed to compare the direct actions of bupivacaine and lidocaine on the isolated perfused guinea pig Langendorff heart preparation. Sixty min after mounting, either bupivacaine HCl (0.3 or 3 micrograms/ml) or lidocaine HCl (10 or 30 micrograms/ml) was added to the perfusate, and the effect (if any) was compared to untreated control values 30, 60, and 90 min later. Although the highest concentrations of both drugs invariably produced statistically significant reductions in heart rate, df/dt, coronary blood flow, and myocardial oxygen consumption (MVO2), these reductions were consistently greater after bupivacaine. Moreover, arrhythmias occurred in 6 of 12 preparations in those hearts exposed to 3 micrograms/ml of bupivacaine. Most often these arrhythmias consisted of heart block and bi- or trigeminy. Additional studies indicated that the reduction in coronary blood flow and MVO2 produced by 3 micrograms/ml of bupivacaine was a consequence of its direct negative inotropic and chronotropic action. Although the myocardial depression produced by bupivacaine and lidocaine could be reversed readily by substituting fresh perfusate, increasing the extracellular calcium concentration in stepwise increments did not augment the negative inotropic or chronotropic effect produced by 3 micrograms/ml of bupivacaine or 10 micrograms/ml of lidocaine. We conclude that 3 micrograms/ml of unbound bupivacaine is more cardiotoxic than 30 micrograms/ml of unbound lidocaine in this model.

The value of lorazepam in gas encephalography: a preliminary report.

Lorazepam is of value in the performance of gas encephalography. Given with judicious and individualized doses of IV narcotic, it has significantly lessened the morbidity of this examination. We have been particularly impressed with the lack of unpleasant memories for the procedure. The quality of the examination was good through the patients had to be reminded, because of the amnestic effects of the drug, to hold still throughout the 6-s exposure needed for polytomography.

Lidocaine and increased respiratory resistance produced by ultrasonic aerosols.

Respiratory resistance significantly increased from 5.0 to 8.0 cm H2O/1/sec in anesthetized patients who were given ultrasonically nebulized water for 20 minutes via an endotracheal tube. Intravenous administration of lidocaine failed to reverse the provoked increase in resistance. In another group, respiratory resistance significantly increased from 5.8 to 7.5 cm H2O/1/sec in response to nebulized water despite prior and con-current intravenous administration of lidocaine. In a third group, initial respiratory resistance was 5.6 cm H2O/1/sec and did not increase during a 20-minute challenge with intratracheally administrered ultrasonically nebulized 2 per cent lidocaine. In a final group, resistance was increased from 5.0 to 6.9 cm H2O/1/sec with nebulized water. When challenge was continued with nebulized 2 per cent lidocaine, resistance remained elevated for about 10-12 minutes. It then decreased and returned to its initial control value at about 17 minutes, despite continuing lidocaine aerosol administration. Lidocaine, when administered intratracheally as an aerosol, both prevented and reversed provoked increases in respiratory resistance. Intravenously administered lidocaine was ineffective. Intratracheal administration of ultrasonically nebulized lidocaine might be another useful technique for management of bronchoconstriction in anesthetized patients.