The Effects of Insulin in Treating Bupivacaine-Induced Cardiac Depression / 대한마취과학회지

Backgroud: Bupivacaine blocks the sodium channels enhanced by hypokalemia. Bupivacaine also inhibits the transient outward K+ current (Ito). Insulin, in contrast, enhances Ito and induces hypokalemia. The current study was performed to confirm the efficacy of insulin for the treatment of bupivacaine- induced cardiac depression in dogs. METHODS: After dogs were anesthetized with pentobarbital, 0.5% bupivacaine was administered at a rate of 0.5 mg/kg/min until S O2 decreased to 60% or less, which was defined as the point of cardiac depression in this study. The insulin group (n = 9, 16.9 +/- 3.1 kg) received 2 ml/kg of a mixed solution of regular insulin 30 units and 5% D/W 50 ml, followed by a glucose infusion (50 ml 5% dextrose in water) over 15 min. The control group (n = 9, 15.8 +/- 3.4 kg) received 2 ml/kg of 5% D/W 50 ml, followed by a normal saline infusion over 15 min. Mean arterial pressure (MAP), heart rate (HR), pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), SO2, blood gas analysis, serum electrolytes, ECG and the local anesthetic concentraton of the blood were taken. RESULTS: Changes in hemodynamic variables and ECG of the insulin group normalized more rapidly than in the control group. There were no statistical differences in serum Na and Ca2 concentratons between the two groups. The serum K concentration of the insulin group was lower than that of the control group after 5 min of resuscitation. The changes in plasma bupivacaine concentration over time were not significantly different between groups. CONCLUSIONS: Insulin is effective in reversing bupivacaine-induced cardiac depression. This study suggests insulin can be considered an immediate treatment for cardiac depression by bupivacaine.

The Influence of Serum Potassium Change on Bupivacaine-Induced Cardiac Toxicity in Dogs with Normal Serum Potassium Concentration / 대한마취과학회지

BACKGROUND: Bupivacaine blocks the sodium channels and inhibits the depolarization of myocardium. The inward sodium current (INa) could be activated by decreasing potassium in the extracellualr spaces. We hypothesized that the bupivacaine dose which creates the cardiac toxicity may have the correlation with serum potassium concentration which is in the normal range. METHODS: After the dogs were anesthetized with pentobarbital, 0.5% bupivacaine was administrated at a rate of 0.5 mg/kg/min until SvO2 decreased to 60% or less, which was defined as the point of cardiac depression in this study. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), SvO2, ETCO2, arterial blood gas analysis, serum electrolytes (Na+ , K+ , Ca2+ ), and ECG were taken at baseline and cardiac depression point. Infused bupivacaine dose and blood concentration to make cardiac depression were taken. RESULTS: PaO2, PaCO2, pH, serum electrolytes (Na+ , K+ , Ca2+ ) were within nornal range at baseline and cardiac depression point. MAP, HR, CO, SvO2, and ETCO2 were within normal range at baseline point but decreased significantly at cardiac depression point. Bupivacaine made QRS duration on EKG to prolong significantly. Infused bupivacaine dose to make cardiac depression had an strong negative correlation with concentration of serum potassium (P < 0.05, rs: -. 501). CONCLUSIONS: We conclude that the increase of serum potassium concentration enhances the cardiotoxic effects of bupivacaine, even though it is in the normal range.

The Effect of Hyperventilation on Serum Potassium Concentration During Infusion of Mannitol / 대한마취과학회지

BACKGROUND: Mannitol is widely used in neurosurgical patients and may induce an increase in serum potassium concentration according to doses and administration rates with unknown mechanism. The treatment of hyperkalemia is aimed at eliminating the causes and includes calcium, sodium bicarbonate, glucose with insulin, loop diuretics and hyperventilation. This study was undertaken to observe the effects of hyperventilation on the serum potassium concentration following infusion of mannitol (2.0 gm/kg). METHODS: We studied 30 patients who were operated brain aneurysm clipping surgery and were divided into 3 groups (n=10). In control group, mild hypocapnia was maintained (PaCO2, 32 2 mmHg) before and after mannitol infusion. In group I, moderate hypocapnia was maintained (PaCO2, 27 2 mmHg) before and after mannitol infusion. In group II, mild hypocapnia (PaCO2, 32 2 mmHg) was maintained before 30 minutes of mannitol infusion and moderate hypocapnia (PaCO2, 27 2 mHg) after mannitol infusion. We started infusion of 20% mannitol with a dosage of 2.0 gm/kg, 15~20 min after cranium was opened. RESULTS: The changes of serum potassium were as follows (Mean SD mEq/l) (just before and 15min, 30min, 60min after mannitol infusion): 3.79 0.48, 4.66 0.60, 4.44 0.48, 4.13 0.40 (Control group), 3.62 0.18, 3.63 0.42, 4.14 0.51, 3.95 0.33 (Group I), 3.76 0.20, 3.91 0.15, 4.11 0.30, 4.04 0.23 (Group II). After 15 minutes of mannitol infusion, the serum potassium levels of group I and II were lower than that of control group (p<0.05) and there was no significant difference between group I and II. CONCLUSIONS: These results suggest that hyperventilation may blunt the increase in serum potassium concentration following rapid infusion of high dose mannitol.

Effect of Esmolol on Serum Potassium Changes Induced by Succinylcholine / 대한마취과학회지

BACKGROUND: The purpose of this study was to determine whether esmolol augmented the increase in serum K+ following administration of succinylcholine. METHODS: Forty patients were randomly divided esmolol group (n=20) and control group (n=20). The esmolol group received a 1 minute rapid infusion of 500 mcg/kg/min followed by a continuous infusion of 200 mcg/kg/min for 4 minutes before administration of succinylcholine. Serum potassium level, mean arterial blood pressure and pulse rate were measured prior to induction(baseline) and 1, 3, 5, 10, 15, 30, 45, 60, 75, 90 minutes after administration of succinylcholine. RESULTS: Serum potassium level was significantly higher in esmolol group after 3 and 15 minutes after succinylcholine than control group. Mean arterial blood pressure was not significantly different between two groups except 10 minute but the pulse rate significantly lower 1, 3, 5, 10 and 15 minutes in esmolol group than control group. CONCLUSIONS: Esmolol does not significantly elevate serum potassium level in clinical use(1 minute infusion of 500 mcg/kg/min followed by infusion of 200 mcg/kg/min for 4 minutes) after administration of succinylcholine. So succinylcholine can be used safely in the presence of beta-1-selective adrenergic blockade. And esmolol can attenuate more effectively increase of pulse rate than mean arterial pressure.