First set of experiments was designed to investigate atrial mechanical and electrical functions during ventricular fibrillation (VF) of 8 min or longer duration. In addition, we wanted to quantitate the amount and direction of blood flow generated by atrial contractions in this setting. To demonstrate preserved electrical function of the atria, epicardial right atrial electrograms in the isolated rat hearts were recorded during VF. To demonstrate preserved atrial contractions we continuously recorded right atrial pressure pulses prior to and during VF in 10 rats. Finally, we measuredmagnitude and direction of blood flow across the mitral valve during VF in 15 pigs utilizing transesophageal echo-Doppler methodologies. In isolated perfused rat hearts, we demonstrated regular atrial depolarizations that accompanied atrial contractions during VF. In each of the rats regular right atrial pressure pulsations were demonstrated during VF. These persisted over an average interval of 7.5 min. In pigs, atrial contractions generated stroke volumes of approximately 12 ml or 25 % of pre-arrest values during the first minute after the onset of VF. Stroke volumes gradually declined to approximately 6 ml after 10 min of untreated arrest. However, blood flow from the left atrium failed to advance significantly into systemic circuit. During atrial diastole we observed reversal of blood flow into the left atrium. In conclusion, atrial contractions are preserved during the initial 8 min or moreafter the onset of VF. Substantial forward flow generated by atrial contractions failed to advance into the systemic circuit. In the second set ofexperiments our goal was to measure stroke volumes produced by precordial compression during cardiopulmonary resuscitation and to quantitate relationships of stroke volume to measurements of end-tidal carbon dioxide (ETCO2). Eighteen anestethized pigs weighing between 40 and 45 kg were investigated. (Abstract truncated at 2000 characters).

In patients with acute myocardial infarction a transient fall in blood pressure frequently occurs during streptokinase (SK) infusion. This fall can depress efficacy of coronary thrombolysis induced by thrombolytic agents. The aim of our study was to evaluate whether treatment with hydrocortisone reducesfall in blood pressure (BP) during SK infusion in patients with acute myocardial infarction. We also wanted to identify subgroups of patients which would especially benefit from the effect of hydrocortisone, and to find out factors which affect BP during SK infusion. 182 patients with acute myocardialinfarction were included in a double blind, placebo controlled prospective study. A11 were treated with systemic infusion of SK. Half of themreceived 100 mg of hydrocortisone intravenously before the start of SK infusion, the other half received 2 ml of saline intravenously. Blood pressurewas measured twice before SK infusion, at the beginning of infusion and 5, 10, 15, 20, 25, 30, 35, 40, 50, 60, 80, 100 and 120 minutes after the beginning of infusion. In patients who received hydrocortisone, the maximal fall in systolic BP during SK infusion was 18% lower than in patients who received placebo (28 +- 23 (SD) vs 34 +- 24 mm Hg, p=0.046). There were no significant differences in the maximal fall in mean and diastolic BP between the two groups. In the subgroup with systolic BP lower than 100 mm Hg the effect of hydrocortisone was even more pronounced. In patients who received hydrocortisone the maximal fall in systolic BP was 65% lower, the maximal fallin mean BP 40% lower, and the maximal fall in diastolic BP 29% lower than in the placebo group. However, the difference between the two groups is not significant. The only factor with a significant correlation with the lowest systolic BP during infusion was systolic BP before SK infusion. (Abstract truncated at 2000 characters).