Pulseless electrical

Pulseless Electrical Activity Causes (HATCH HMO pH) and Management... 

The absence of a pulse does not guarantee VF, as the pulse may also be absent in patients with asystole, VT, or pulseless electrical activity. 

Pulseless electrical activity (PEA) is the absence of a detectable pulse and the presence of some type of electrical activity other than VF or PVT. 

CPR, cardiopulmonary resuscitation D5W, 5% dextrose in water PEA, pulseless electrical activity PVT, pulseless ventricular tachycardia ROSC, return of spontaneous circulation VF, ventricular fibrillation. 

PDGF platelet-drived growth factor PE pulmonary embolus, physical examination, pleural effusion PEA pulseless electrical activity PFT pulmonary function test pg picogram... 

When the cardiac electrical activity is maintained, but there is no mechanical output (pulseless electrical activity, electromechanical dissociation), then hypovolaemia, tension pneumothorax, pulmonary embolism, cardiac tamponade, and various forms of metabolic or pharmacological disturbance may be responsible. In asystole or pulseless electrical activity (with an underlying rate of less than 60 beats per minute) a single intravenous bolus of 3 mg atropine is recommended. 

Epinephrine (adrenaline) should be given every 3-5 min whilst the patient remains in cardiac arrest, immediately if the patient has an initially non-shockable rhythm (asystole or pulseless electrical activity) but delayed until before the third shock for shockable rhythms. Continued administration of epinephrine (adrenaline), cardiac massage, and DC shock may be required for several cycles. 

Asystole, slow pulseless electrical activity IV 1 mg may repeat q3-5min up to total... 

For pulseless electrical activity (PEA) and asystole, the primary focus should be diagnosis and identification of a reversible cause. 

PAD public-access deflbrillation PEA pulseless electrical activity PVT pulseless ventricular tachycardia ROSC return of spontaneous circulation VF ventricular fibrillation... 

Vasopressin levels in patients with vasodilatory shock are inappropriately low, and such patients are extraordinarily sensitive to the pressor actions of vasopressin. The combination of vasopressin and norepinephrine is superior to NE alone in the management of catecholamine-resistant vasodilatory shock. Although the efficacy of vasopressin in the resuscitation of patients with ventricular fibrillation or pulseless electrical activity is similar to that of epinephrine, vasopressin followed by Epi appears to be more effective than Epi alone in the treatment of patients with asystole. 

Sudden death caused by cardiac arrest due to ventricular tachycardia or ventricular fibrillation remains a serious health problem worldwide. In the United States alone, cardiovascular disease accounts for over 900,000 deaths annually (1). Of these deaths, 350,000 are due to out-of-hospital cardiac arrest (2), two-thirds of which occur without prior recognition of cardiac disease (1). In the United States, 15-20% of all fatalities and 50% of all cardiac fatalities are sudden. Although sudden death caused by asystole or pulseless electrical activity is not preventable, sudden death caused by a ventricular arrhythmia can be. Prompt treatment to stop the ventricular arrhythmia before it causes death is possible. 

A case study of pulseless electrical activity (PEA) arrest with postresuscitation prolonged QT in a 47-year-old American man on chronic methadone after 3 days of azithromycin highlights potential interactions with other arrhythmogenic drugs [100 ]-... 

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