medication for pulseless electrical activity

MEDICATION FOR PULSELESS ELECTRICAL ACTIVITY HOW TO

Metabolic acidosis without hyperkalemia is usually the consequence rather than the cause of PEA. When the presentation is wide-complex PEA or nonshockable pulseless wide-complex tachycardia, the most likely causes include severe hyperkalemia or sodium channel blocker toxicity. The clinical scenario and, if available, bedside ultrasonography should quickly distinguish among these. Among the mechanical causes we have listed cardiac tamponade, tension pneumothorax, mechanical hyperinflation and pulmonary embolism. Second, within each category we have markedly reduced the number of listings to those diagnoses that have the highest likelihood and clinical relevance. Narrow-complex PEA is usually due to a mechanical cause, whereas wide-complex PEA is usually due to a metabolic cause. First, rather than randomly listing 10-13 causes of PEA with terms starting with the letters H or T, our algorithm categorizes the possible causes based on the easy finding of QRS complexes being narrow or wide in a simple telemetry or rhythm strip (fig. Our simplified and structured approach offers three new elements compared to official European and American guidelines. There is considerable debate surrounding the most appropriate approach to cardiac arrest due to PEA. The New PEA Algorithm: Therapeutic Considerations Of the other possible ‘Ts', we have excluded trauma, as have the newest guidelines, because traumatic arrests have unique management strategies separate from current ACLS guidelines, and signs are usually apparent on exam. Standard treatments are available for these conditions. Some of these do progress to PEA but by that time the diagnosis is usually well established. Of ‘toxins', the initial presentation of β-blocker, calcium channel blocker and digitalis toxicity is almost always hypotension, sinus bradycardia, sinus arrest or atrioventricular block.

Hypothermia is not listed in our new algorithm, but there the clinical picture is usually quite obvious. A recent thorough review of the PEA literature by Desbiens and our independent review did not find any evidence that hypoxemia, hypokalemia or hypoglycemia presents primarily with PEA.

In these cases too, bedside ultrasound can quickly point to a mechanical cause.Īn important question is whether this simplified algorithm covers all important causes of PEA? We believe that it does. Other possible causes of wide-complex PEA include a mechanical etiology with preexisting aberrancy or pulmonary embolism - a mechanical cause that can be associated with complete right bundle branch block. In wide-complex PEA, a metabolic or ischemic cause is supported by the echocardiographic observation of left ventricular hypokinesis or standstill (fig. In patients who were ‘found down' or who present following ingestion or suicide attempt, the cause of wide-complex PEA is almost always sodium channel blocker toxicity. Identification of an arteriovenous fistula or dialysis catheter also suggests hyperkalemia.

Again, the clinical scenario is usually helpful: in patients with critical illness, sepsis, shock or renal failure, the diagnosis of wide-complex PEA is usually hyperkalemia. Wide-complex PEA usually suggests a metabolic problem such as severe hyperkalemia with or without metabolic acidosis, or sodium channel blocker toxicity (fig.

MEDICATION FOR PULSELESS ELECTRICAL ACTIVITY HOW TO

Moreover, even if such a list can be generated, the ACLS does not provide guidance on the relative likelihood of the specific causes, nor does it offer suggestions on how to individualize treatments based on simple initial findings. Studies, however, have shown that during cardiopulmonary resuscitation it is difficult to recall up to 13 causes of PEA. Memory aids list numerous conditions whose English names start with the letters H or T as potentially treatable causes of PEA (fig.

Both the European and American ACLS guidelines, therefore, stress the significance of quickly finding and addressing the cause of PEA. Higher-dose epinephrine has actually been shown to be associated with worse outcomes. Studies suggest that cause-specific treatment of PEA is more effective than general treatments offered by advanced cardiac life support (ACLS) guidelines such as cardiac massage, epinephrine and vasopressin. The survival rate of patients with PEA is much worse than that of cardiac arrest patients with shockable rhythms. Patients with pulseless electrical activity (PEA) account for up to 30% of cardiac arrest victims.

Medication for pulseless electrical activity