How do chest compressions produce a cardiac output?
It used to be assumed that chest compressions produced a cardiac output by directly compressing the ventricles against the vertebral column. This was thought to produce systole, with forward flow out of the aorta and pulmonary artery, and backward flow prevented by closure of the atrioventricular (AV) valves.
This explanation is probably not completely valid. Echocardiographic images during arrest show that the AV valves are not closed during chest compressions. There are reports of patients who, during episodes of monitored VF, have developed systolic pressures capable of maintaining consciousness by coughing. This demonstrates that chest compressions per se are not necessary to maintain a cardiac output. Furthermore, CPR is frequently ineffective in patients with a flail chest until chest stabilization is achieved. If direct compression were the etiology of blood circulation in CPR, then a flail chest would be an advantage by increasing the efficiency of the “direct” compression. These observations have led to the proposal of the “thoracic pump” theory of CPR.
The “thoracic pump” theory proposes that forward blood flow is achieved because of phasic changes in intrathoracic pressure produced by chest compressions. During the downward phase of the compression, positive intrathoracic pressure propels blood out of the chest into the extrathoracic vessels that have a lower pressure. Competent valves in the venous system prevent blood from flowing backwards. During the upward phase of the com-pression, blood flows from the periphery into the thorax because of the negative intrathoracic pressure created by release of the compression. With properly performed CPR, systolic arterial blood pressures of 60–80 mmHg can be achieved, but with much lower diastolic pressures. Mean pressures are usually less than 40 mmHg. This only provides cerebral blood flows of approximately 30% and myocardial blood flows of about 10% compared with pre-arrest values.