My clinical experience in an active emergency department makes me dubious about the ACLS course’s PEA algorithm. My experience is that this is commonly fatal. Comments?

When sudden loss of cardiac output is associated with a “physiologic” ECG rhythm, several obvious issues need to be considered. This includes looking at various possible causes such as:

Hypovolemia: When this is the cause of sudden loss of cardiac output, the issue is usually acute rupture of a major vessel such as the abdominal aorta. Any chance of survival requires immediate surgical intervention. If the patient is in the OR when this happens, there is chance of survival. However, if the abdominal aorta is ruptured, such as secondary to a motor vehicle crash, there is not much hope of resuscitation. However, it is important to recognize hemorrhage and engage in early intervention prior to losing cardiac output. This group of patients is likely to survive.

Hypoxia: In the case of hypoxia, CPR and supplemental oxygen are indicated; but when global hypoxia exists, it is usually indicative of total perfusion failure. Again, finding a treatable cause is the key to treatment, and early intervention prior to the arrest is paramount.

Hydrogen Ion (Acidosis): This is most typically hypoxic lactic acidosis. The treatment is restoration of perfusion systemically. Using buffering agents has a long negative track-record when it comes to dealing with increased hydrogen ions that are associated with inadequate perfusion.

Hyper/Hypokalemia: There are certain patients, such as those on dialysis, for whom rapid shifts in serum potassium should be considered. Administering CaCl or supplemental potassium are logical interventions. However, when such massive electrolyte shifts occur, the clinical likelihood of reversing them in the arrested patient is usually poor.

Hypothermia: This should always be quickly identified and emergency re-warming should take place immediately. The literature is replete with reports of long-duration arrest and survival.

Tension Pneumothorax: Patients who are developing this issue are typically receiving positive airway pressure (unlike patients with spontaneous pneumothorax). Thus, identification of these patients should be relatively simple. Because of the clear mechanism of this sudden state of pulselessness, the treatment is equally simple: decompression of the chest to relieve compression of the thoracic vessels. This is a very treatable form of arrest. It should always be ruled out in any patient who is receiving positive airway pressure therapy and who suddenly develops PEA.

Cardiac Tamponade: Sudden ventricular rupture could clearly result in PEA. However, the difficulty in emergency intervention suggests that unless an immediate thoracotomy can be performed and the muscle wall is closed, insertion of a needle would not be useful. So, is this theoretically treatable? Perhaps. But mortality is the most likely outcome for most of these patients.

Thrombosis: The ability to dissolve or remove a clot in the pulmonary artery, or an acute blockage of the LAD to reverse arrest is not common. However, when clinically feasible, all efforts should be made to accomplish vessel patency.

Remember, every practitioner caring for patients who are receiving positive airway pressure should first rule out a tension pneumothorax because it is routinely treatable. Virtually all critically ill or arrested patients receive emergency ventilation or airway support. Treatment requires nothing more than decompression of the pleural space under tension. Failure to identify this syndrome results in guaranteed death as would treating a tension pneumothorax with CPR and IV pressor agent therapy.