[Functional circulatory arrest (heart arrest) in traffic accidents].
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STUDY OBJECTIVE: The aim of the study was to examine the relation between zero flow pressure and intramyocardial pressure in the inner and outer layers of the myocardium. DESIGN: Zero flow pressure was obtained in maximally vasodilated excised hearts by decreasing perfusion pressure (at 2 mm Hg.s-1) during transient heart arrest. Intramyocardial pressures in inner and outer myocardium were measured simultaneously with needle tip pressure transducers at depths of 8.0(SD 2.6) and 3.3(1.2) mm from the epicardium respectively. Ventricular and atrial pressure could be controlled at will. EXPERIMENTAL MATERIAL: The excised hearts of eight mongrel dogs, body weight 14.0(0.8) kg, were used. MEASUREMENTS AND MAIN RESULTS: During left ventricular pressure elevation (0, 15, 30 mm Hg), zero flow pressures were 9.1(2.4), 13.8(2.2), and 19.1(5.1) mm Hg, respectively. Corresponding values of intramyocardial pressure at the outer myocardium were in good agreement with the zero flow pressures, at 9.1(3.4), 13.4(2.8), and 20.8(5.4) mm Hg. Values at the inner myocardium increased from 7.4(2.4) to 18.9(8.6) and 32.9(13.0) mm Hg. The latter two values were significantly higher than the corresponding values of zero flow pressure and intramyocardial pressure at the outer myocardium (p less than 0.05, p less than 0.01). In isotransmural pressure elevation, the three pressures increased almost equally. CONCLUSIONS: The results show that zero flow pressure is strongly affected by intramyocardial tissue pressure, and if uneven intramyocardial pressure distribution is present the value of zero flow pressure depends on the lower values of intramyocardial pressure.
Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.
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Intraoperative pulmonary embolism with acute cardiac arrest can successfully be managed by immediate open cardiac massage followed by rt-PA injection, an inter-disciplinary approach is mandatory. The scheduled tumor nephrectomy was performed 6 weeks after the initial event. The tumor was embolised with intravascular coils placed in a supraselective manner by the radiologist. During the secondary procedure it was found to be necrotic. In the second case the event occurred at the end of a radical cystectomy. Instead of an ileal conduit cutaneous ureterostomies were used for urinary drainage after cardiac output had been restored and rt-PA had been administered.
INTRODUCTION: The Mobile Emergency Care Unit (MECU) in Arhus includes an experienced anaesthesiologist and a specially trained rescuer. It covers a radius of 25 km from the centre of Arhus with 330,000 inhabitants. Rescue workers in Denmark are permitted to give basic life support and defibrillation. The MECU carriers out advanced cardiac life support in accordance with "The 1998 Guidelines of the European Resuscitation Council". MATERIAL AND METHODS: Data collected by the MECU doctor on a standardised chart and survival data received from the Central Hospital Database were analysed retrospectively. RESULTS: In 1998, 4725 emergency calls were received. Twenty-five per cent of the calls were for trauma, 515 patients had cardiac disease, 158 of whom had cardiac arrest. In 86 patients, death was determined on the spot and no treatment was given. Seventy-two patients received advanced cardiac life support. Twenty-five patients were admitted to hospital. Thirteen patients were alive one year later, which gives a survival rate of 52% of the patients admitted to hospital. Of the 25 patients who were resuscitated and admitted to hospital, 21 received defibrillation, 16 were intubated, 19 had adrenaline, 11 lidocaine, and 9 amidarone. Other drugs used were atropine, NaHCO3, sotalol, and CaCl. DISCUSSION: These results illustrate that for patients with out-of-hospital cardiac arrest early treatment with advanced cardiac life support performed by experienced doctors probably had a positive impact on survival, as compared to basic cardiac life support.
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