The physiology of cerebral blood flow during cardiopulmonary resuscitation.

Abstract

For decades after Kouwenhoven'z original description of cardiopulmonary resuscitation (CPR), I antegrade blood flow during was generally assumed to result from the direct compression of the heart between the sternum and the vertebral column, thereby forcing blood out of the ventricle cardiac mechanism of blood flow. If this hypothesis is correct, the fotlowing haemodynamie findings and flow events would be expected. During chest compression or systole, a ventricular-atrial pressure gradient should develop that would close the atrioventricular valves. Synchronous left and right ventricular ejection would be associated with a reduction in ventricular volume. During chest relaxation or diastole ventricular pressure would fall below atrial pressure with subsequent atrioventricnlar valve opening and ventricular filling. Such a mechanism of blood flow generation is obviously operative during open-chest, internal cardiac massage. Several observations of early investigators, however, did not support the cardiac pump hypothesis of antegrade blood flow. Weale and Rothwel]-Jackson 2 measured equivalent elevations in arterial and right atrial pressures with external chest compression and Gall et al. using a cardioscope demonstrated that the mitral valve is open during chest compression. Other clinical observations also raised questions about direct cardiac compression as a sole mechanism of blood flow. has certainly been successful in resuscitating either extremely large individuals or patients with severe emphysema. Nevertheless, in these patients it is physically impossible to depress the sternum enough to squeeze the heart against the sternum. External is frequently ineffective in patients with flail chests, a situation that should more readily permit direct cardiac compression. 3 Furthermore, a knowledge of anatomy would reveal that it is the right ventricle that is placed below the sternum and that the left ventricle is laterally placed and less likely to be squeezed by chest compression. Despite these observations, it was not until the dramatic observations of Criley in 1976, 4,s that Kouwenhoven's cardiac compression hypothesis was seriously ques tinned. Criley reported that several patients who developed ventricular fibrillation during cardiac eatheterization maintain a cardiac output adequate to maintain consciousness by repetitive coughing and phasically elevating intrathoracic pressure. This observation of cough CPR focused research on whether either direct cardiac compression or large fluctuations in intrathoracic pressure was the mechanism for forward blood flow during CPR. In 1980, the demonstration that manoeuvres that increased intrathoracic pressure with chest compression, increased aortic pressure and carotid blood flow during CPR, led to a new theory accotmting for forward blood flow during CPR. 6'7 This hypothesis proposed that blood flow produced by external chest compression could be generated by phasle changes in intrathoraeic pressure without the direct compression of the heart. According to this model, external chest compression produced a generalized elevation of intrathoracic pressure, that was transmitted equally to all cardiac chambers and intrathoracic vascular structures. This increase in intravascular pressure was transmitted from the intrathoracic to extrathoracic arteries but not to extrathoracic veins because of the presence of venous valves, a compliant exttalhoracic venous system and easily collapsible veins but not arteries at the thoracic inlet. The difference in pressure between the intrathoracic arteries and extratboracic veins caused blood to move from the chest into the extrathoracic vascular system. 67 The mechanism implies that with chest compression-systole blood flows from the lungs through the left atrium, and an open mitral valve, left ventricle and aorta into the systemic circulation. During the release of chest compression-diastole intrathuracic pressure falls below that of the extrathoracic venous pressure and blood returns to the lungs. With this