Physiology of cardiopulmonary resuscitation.

Abstract

.,7410Myron L. Weisfeldt, M. D. and Nisha Chandra, M. D.,Peter Belfer Laboratory for Myocardial Research and the Cardiology Division,The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205INTRODUCTIONFor 20 years sternal compression has been used to create artificialcirculation in patients following cardiac arrest (15), and the mechanism forthe resulting movement of blood to the brain was thought to be understood.The arrested heart was viewed as a rubber ball filled with fluid with one-wayvalves at its entrance and exit. The heart is situated between the sternumand the vertebral column, thus chest compression moves the ster-num and was thought to compress the heart against the vertebral col-umn. Such compression, like internal cardiac massage, moved blood fromthe left ventricle into the aorta as the aortic valve opened. Retrograde flowwas prevented by mitral valve closure. Following the period of compressionthe left ventricle filled with blood when the mitral valve opened.This widely held concept appeared inconsistent with a number of obser-vations in animal models (21) and man (17), but no alternative mechanismsfor the movement of blood were suggested. In the dog arterial and venouspressures during chest compression were similar if not identical (21). fact, the high intrathoracic venous pressure was considered by some (17, 21 to point to an important injurious effect of external massage. It wasassumed that the very high intrathoracic venous pressures were transmittedperipherally to the brain and caused brain injury.Only recently did it become clear that other mechanisms beside cardiaccompression operate during chest compression. These new suggestions (20)