Author/Editor		Noč, Marko; Pernat, Andrej
Title		Patofiziologija kardiopulmonalnega oživljanja
Translated title		Pathophysiology of cardiopulmonary resuscitation
Type		članek
Source		In: Bručan A, Gričar M, Fink A, et al, editors. Urgentna medicina: izbrana poglavja 7. Zbornik 8. mednarodni simpozij o urgentni medicini; 2001 jun 13-16; Portorož. Ljubljana: Slovensko združenje za urgentno medicino,
Publication year		2001
Volume		str. 55-64
Language		slo
Abstract		Cardiac arrest results in abrupt cessation of mechanical activity of the heart and thereby spontaneous circulation. The consecutive ischemia triggers process of dying; which immediately affects aerobic organs such as central nervous system and heart. Primary cardiac arrest, which is most frequent, is due to sudden malignant ventricular arrhythmia-mainly ventricular fibrillation. Secondary cardiac arrest, which evolves as a consequence of preceding respiratory failure or circulatory shock, accounts for only 15-20% of episodes. The only definite treatment of ventricular fibrillation is early electrical defibrillation. To reduce time delays to defibrillation, automated external defibrillators evolved during the last years. Since these devices automatically analyze cardiac rhythm and defibrillate if required, they can be easily operated by lay-personnel. If defibrillation fails, the likelihood that further electrical shocks may restore spontaneous circulation is related to the ability of chest compression and vasopressors to restore critical myocardial perfusion. Myocardial perfusion is linearly related to the coronary perfusion pressure, which is defined as arhythmetic difference between aortic and right atrial pressure in the relaxation phase of chest compression. The resuscitation attempts in humans are universally unsuccessful if coronary perfusion pressure does not exceed 15 mm Hg.
Descriptors		CARDIOPULMONARY RESUSCITATION HEART ARREST RESPIRATION, ARTIFICIAL