Treatment of cardiac arrest. Recent aspects of cardiopulmonary resuscitation

Opinions are still not unanimous about the mechanism behind circulation during external cardiac compression and this leads to uncertainty regarding the correct frequency, force of compression and its duration. Adrenaline and other alpha-stimulators increase blood flow during external cardiac compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis on account of hyperventilation and venous acidosis. No communications exist about the favourable effect of administration of bicarbonate during cardiac arrest. On the other hand, several conditions suggest that bicarbonate increases the intracellular acidosis with poorer possibilities for resuscitation with this form of treatment. Ischaemia results inter alia in intracellular accumulation of calcium which initiates potential cell destructive processes. No investigations are available which favour employment of calcium during cardiac arrest. Conversely animal experiments suggest the possibility of favourable effects from calcium-entry blockers. Ischaemia and, in particular, reperfusion release cell and vessel damaging free oxygen redicals. Intensive investigations are being conducted at present about the value of anti-oxidants for cerebral and myocardial protection.