The standard technique of external precordial compression has changed little since it was described in the landmark paper of Kouwenhoyen.,et.a/: (I960). External chest compressions are applied by the rescuer who places the heel of one hand over the lower half of the victim's sternum and the other hand on top of the first hand. Downward force displaces the sternum for a distance of 3.5 to 5 cm for adult patients. The compressions are repeated at a rate of 80 to 100/min with equal compression-relaxation intervals.
The efficacy of precordial compression progressively decreases with increasing duration of the resuscitation effort. This is coincident with a loss of myocardial compliance, deformation of the chest wall, fractured ribs, and fatigue on the part of the operator. The technique is maximally effective when cardiopulmonary resuscitation is initiated after only a brief interval of untreated cardiac arrest and during the initial 10 min of precordial compression.
The mechanism by which blood flow is generated during external precordial compression has been the subject of vigorous debate. Echocardiographic recordings now quite securely support the so-called cardiac pump theory. This theory holds that the heart is compressed and blood is actively ejected into both the pulmonary and systemic circulation during chest compression. Cardiac valve function is preserved so as to assure forward blood flow. When compression is released, corresponding declines in intrathoracic and intracardiac pressures allow for venous return and cardiac filling. Precordial compression is associated with closure of the mitral valve and opening of the aortic valve. Pressure gradients between the atria, ventricles, and aorta have also been documented under experimental conditions. These observations contrast with the thoracic pump theory which claims that chest compression increases intrathoracic pressure, and that this pressure is transmitted to the intrathoracic vasculature with extrusion of blood from the intrathoracic vessels and forward blood flow. Therefore this theory holds that the heart is a passive conduit, and that arterial-venous pressure gradients between intrathoracic and extrathoracic arteries and veins account for forward blood flow. The observation that patients who developed ventricular fibrillation during cardiac catheterization were effectively sustained by vigorous coughing, the so-called 'cough cardiopulmonary resuscitation', has been cited in support of the thoracic pump theory. The current consensus is that high-impulse compression does represent a cardiac pump mechanism, but that there is a thoracic component to the extent that the increase in intrathoracic pressure itself accounts for cardiac compression together with or independently of direct ventricular compression.
Injury to both thoracic and abdominal structures follows chest compression in as many as 60 per cent of victims. Most frequently the ribs and sternum are fractured, with occasional injuries occurring to the heart, great vessels, lungs, and liver. Other pathological findings include pulmonary edema, hemothorax, pneumothorax, and hemoperitoneum.
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