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.