Two mechanisms have been proposed to explain blood flow with closed chest compressions.
The thoracic pump theory suggests that the heart acts as the passive conduit, with systolic and mean arterial pressures and blood flow to the carotid artery augmented by increased thoracic pressure. Intrathoracic pressure is transmitted into the extrathoracic arteries to a greater extent than into the extrathoracic veins. This is reflected in an extrathoracic arterial-venous pressure gradient. The unequal transmission of intrathoracic pressure into the extrathoracic arteries and veins results from the presence of venous valves and unequal arterial and venous capacitance and collapsibility.
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Arteries resist collapse and therefore transmit the intrathoracic pressure into the extrathoracic arterial bed.
The cardiac theory suggests that the heart itself is compressed, creating a pressure gradient between intracardiac and extracardiac structures. However, there are not enough data at present to determine which mechanism predominates.
Describe the common reversible causes of cardiac arrest and their specific treatment.
Cardiac arrest may be successfully resuscitated in a number of cases if the underlying etiology is recognized and promptly treated.
Ventricular fibrillation and ventricular tachycardia. Immediate defibrillation should be performed before other procedures, as the success rate decreases by 4% with every minute of delay.
Tension pneumothorax. This condition should be suspected following positive pressure ventilation in a cardiac arrest patient who has a decrease in breath sounds on the affected side, subcutaneous air, or resistance to airflow with bagging. The treatment is needle decompression at the fifth intercostal space, followed by thoracotomy.
Hyperkalemia. Heralded by wide QRS complexes and the absence of P waves, hyperkalemia should be suspected as the cause of arrest in patients with renal failure. Calcium chloride should be administered immediately, followed by sodium bicarbonate and an insulin-glucose drip.
Anaphylaxis. This should be suspected whenever cardiac arrest occurs following administration of parenteral medication. As asphyxia or shock is the underlying mechanism, aggressive intervention with endotracheal intubation, fluids, and intravenous epinephrine should be performed immediately.
When should intravenous calcium be used in the patient in cardiac arrest?
Overall, patients in cardiac arrest do not appear to benefit from the use of intravenous calcium. Indications are thus limited to three specific causes of cardiac arrest: hyperkalemia, hypocalcemia, and possibly calcium antagonist overdose. Calcium chloride should be administered at a dose of 2-4 mg/kg of a 10% solution intravenously every 10 minutes.
Can neurologic outcome be predicted following successful resuscitation of cardiac arrest?
Several reports have attempted to develop prognostic signs for cerebral recovery following CPR. The duration of coma is the most reliable prognostic sign. However, recovery of consciousness has occurred after 10 days of coma. Reactive pupils, oculocephalic reflexes, spontaneous respirations, and purposeful response to painful stimuli are associated with a higher percentage of neurologic recovery. However, a favorable outcome may rarely occur in patients with poor prognostic signs.