Support of circulation while an antidote or reversing agent is obtained is of primary importance. Physical signs include bradycardia, pupil symptoms, and other neurological changes. ECG signs of toxicity include prolongation of the QT interval. Cocaine is the most common street drug that increases incidence of pulseless arrest. Street drugs and other chemicals can precipitate pulseless arrest. Some of the most common include : tricyclics, digoxin, betablockers, and calcium channel blockers). Core temperature should be raised above 86 F (30 C) as soon as possible.Īccidental overdose of a number of different kinds of medications can cause pulseless arrest. The hypothermic patient may be unresponsive to drug therapy and electrical therapy (defibrillation or pacing). If a patient has been exposed to the cold, warming measures should be taken. Hypoglycemia was removed from the H’s but is still to be considered important during the assessment of any person in cardiac arrest. Treat hypoglycemia with IV dextrose to reverse a low blood glucose. Hypoglycemia or low serum blood glucose can have many negative effects on the body, and it can be associated with cardiac arrest. Treatment of hypokalemia involves infusion of potassium. The major signs of hypokalemia (low potassium) are flattened T-waves, prominent U-waves, and possibly a widened QRS complex on the EKG. This can be treated in a number of ways which include sodium bicarbonate (IV), glucose + insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. The major sign of hyperkalemia (high potassium) are taller peaked T-waves and widening of the QRS-wave on the EKG. Prevent metabolic acidosis by giving the patient sodium bicarbonate.īoth high and low potassium levels can contribute to cardiac arrest. Respiratory acidosis is treated with adequate ventilation. To determine if the patient is “acidotic”, an arterial blood gas evaluation must be performed. Also ensure that your oxygen source is connected properly. You must ensure that the patient’s airway is open, and that the patient has chest rise and fall and bilateral breath sounds with ventilation.

Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest. A fluid challenge or fluid bolus may also help determine if the arrest is related to hypovolemia. After CPR, the most import intervention is obtaining intravenous access/IO access.

Looking for obvious blood loss in the patient with pusleless arrest is the first step in determining if the arrest is related to hypovolemia. Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac arrest. Toxins, Tamponade (cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), and Trauma. Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper/hypokalemia, Hypoglycemia, Hypothermia. The H’s and T’s of ACLS is a mnemonic used to help recall the major contributing factors to a pulseless cardiac arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. Out of hospital survival rates (even with emergency intervention) are less than 2%. Survival rates in a cardiac arrest patient with asystole are much lower than with a rhythm amenable to an electrical shock (defibrillation).

Even in the rare case that a rhythm reappears, after 10-15 minutes or more the brain will have been deprived of oxygen long enough to cause brain death. When all emergency treatments are unsuccessful, death is confirmed. With both asystole and PEA there is no blood flow to the brain unless immediate CPR is performed.

Pulseless electrical activity has previously been referred to as electromechanical dissociation (EMD). Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and no palpable pulse but with some organized cardiac electrical activity.