To investigate changes of electrocardiogram (ECG) wave amplitudes in dogs with early bupivacaine-induced cardiac depression.

Bupivacaine was infused into pentobarbital-anesthetized mongrel dogs (n = 9) at a rate of 0.5 mg/kg/min for 30 min. R-wave, S-wave, T-wave amplitude in lead II and III, and cardiac output (CO) were measured every 5 min after the initiation of bupivacaine infusion. PR interval, QRS complex duration, corrected QT interval were also measured. MAP (mean arterial blood pressure), HR (heart rate), and cSvO₂ (continuous mixed venous oxygen saturation) were recorded at 5 min intervals. Arterial blood gas, serum electrolytes and bupivacaine concentration were measured at 10 min intervals. The relationships between CO and ECG amplitudes, and of CO versus hemodynamic variables were compared by regression analysis.

With bupivacaine infusion, R-wave amplitude decreased to zero and S-wave amplitude increased negatively in both leads. The best correlation with CO was seen in S-wave (r = 0.751) in lead III among the ECG parameters.

Close monitoring of S-wave amplitude in lead III can be helpful for detecting the early Bupivacaine-induced cardiotoxicity.