Cardiovascular changes after naloxone administration in propofol-sedated piglets during opioid overdose.

BACKGROUND: Naloxone is an opioid receptor antagonist. Even when used in modest doses, it has been associated with serious cardiopulmonary side-effects. In this experimental porcine study, we examined the cardiac effects of naloxone during an opioid overdose. METHODS: Cardiac parameters, changes in the left ventricular compliance and the magnitude of catecholamine release were evaluated in eight spontaneously breathing piglets under propofol sedation. Cardiac parameters were recorded every 30 s and transthoracic echocardiography was used for the continuous assessment of cardiac performance. Respiratory arrest was induced by morphine (8 mg/kg). Ten minutes after morphine administration, naloxone (80 microg/kg) was injected intravenously. Every 5 min, arterial blood gases were measured and, every 10 min, a sample for the analysis of plasma catecholamines was drawn. RESULTS: There were no statistically significant changes in left ventricular ejection fraction and no signs of pulmonary hypertension. There was a statistically significant increase in the mean arterial pressure immediately after naloxone administration and in norepinephrine concentration before naloxone administration. After naloxone administration, the plasma catecholamine levels decreased in all but one animal. Two animals developed cardiac arrest (pulseless electrical activity and ventricular fibrillation) shortly after receiving naloxone. Although they were both administered naloxone prematurely due to hypoxic bradycardia, naloxone could have contributed to the development of ventricular fibrillation. CONCLUSION: Naloxone did not cause changes in ejection fraction or mean pulmonary artery pressure in hypoxic and hypercarbic conditions. After naloxone administration, the plasma catecholamine levels returned to baseline in all but one animal, and two animals developed cardiac arrest.

Association between R-wave amplitude of the electrocardiogram and myocardial function during coronary artery bypass grafting.

OBJECTIVE: The recovery of R-wave amplitude in the V5 lead of the electrocardiogram (ECG) was recently found to be worse in nonsurvivors than in survivors after coronary artery bypass grafting (CABG). On the contrary, an increase in R-wave amplitude has been found to reflect myocardial dysfunction in exercise testing. The purpose of this study was to examine whether the changes in R-wave amplitude are associated with changes of myocardial function during CABG. DESIGN: A prospective clinical study. SETTING: Cardiothoracic division of surgery in a university hospital. PARTICIPANTS: Ten consecutive patients undergoing CABG. MEASUREMENTS: R-wave amplitude was measured at eight different time points. Left ventricular end-systolic wall tension, wall stress at isovolumic contraction (afterload), end-diastolic wall stress (preload), end-systolic wall stress per end-systolic area (contractility), and stroke work were calculated using transesophageal echocardiography and arterial pressure. MAIN RESULTS: Linear regression was calculated between changes in R-wave amplitude and echo parameters. A weak positive association within subjects was noted among R amplitude and all measured cardiac function parameters except preload. R2 value varied from 0.101 to 0.266, and R2 for preload was 0.017. CONCLUSIONS: These results suggest that only 10% to 27% of variation in R-wave amplitude can be explained by left ventricular function indices measured by echocardiography in patients with CABG. Thus, R-wave amplitude changes in an individual patient undergoing CABg have very limited utility as a noninvasive measure of left ventricular function.