Asystole causes

Causes of obstructive shock should be entertained in patients with PEA/asystole with absent or low levels of ETC02 after placement of invasive airway. 

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

Use quinidine with extreme caution in incomplete AV block, because complete block and asystole may result. The drug may cause unpredictable dysrhythmias in digitalized patients. Use cautiously in patients with partial bundle branch block, severe CHF, and hypotensive states due to the depressant effects of quinidine on myocardial contractility and arterial pressure. 

Adverse effects With chronic use, procainamide causes a high incidence of side effects, including a reversible lupus erythe-matosus-like syndrome that develops in 25 to 30% of patients. Toxic concentrations of procainamide may cause asystole or induction of ventricular arrhythmias. Central nervious system (CNS) side effects include depression, hallucination and psychosis. With this drug, gastrointestinal intolerance is less frequent than with quinidine. 

A 24-year-old man took a presumed cumulative dose of 420 mg of olanzapine and 10 mg of alprazolam (252). He had a cardiac arrest with asystole, from which he was initially resuscitated. Recurrent cardiac arrest, probably caused by hyperkalemia, occurred in the intensive care unit and he died within 1 hour. 

DISOPYRAMIDE CALCIUM CHANNEL BLOCKERS Risk of myocardial depression and asystole when disopyramide is co administered with verapamil, particularly in the presence of heart failure Disopyramide is a myocardial depressant like verapamil and can cause ventricular tachycardia, ventricular fibrillation or torsades de pointes Avoid co administering verapamil with disopyramide if possible. If single-agent therapy is ineffective, monitor PR, BP and ECG closely watch for heart failure... 

Disequilibrium in the eleetrolyte balanee ean provide diagnostic clues. For example, hyperkalemia causes tail T-waves in leads II, III, V2 to V4, when the potassium balance exceeds 5.5 mmol/1. In conjunction, the amphtude of the P wave is reduced and QRS is widened. Hyperkalemia is usually present when the amphtude of the T-wave is higher than that of the R-wave. With increasing potassium concentration, P-waves widen and eventually disappear. Accentuated hyperkalemia results in asystole. 

A 49-year-old woman was given intravenous edrophonium chloride 2 mg as part of the investigation of an acute myopathy following gastrointestinal surgery. She had also received 60 mg of intravenous labetalol in the 14 hours before the edrophonium was given presumably this was for a raised blood pressure, but that was not specified. Labetalol caused transient but severe bradycardia (heart rate about 20/mmute). Immediately after the injection of edrophonium, she developed asystole, which was treated immediately with atropine and recovered in 10 seconds. 

Patients with impaired function of the sinus node or impaired atrioventricular conduction can develop sinus bradycardia, sinus arrest, heart block, hypotension and shock, and even asystole, with verapamil (139) or diltiazem. These drugs should not be given to patients with aberrant conduction pathways associated with broad-complex tachydysrhythmias, and they can cause severe conduction disturbances in hypertrophic cardiomyopathy. 

Three cases of carbamazepine-induced Stokes-Adams attacks caused by intermittent total atrioventricular block, sinoatrial block with functional escape rhythm, and intermittent asystole have been described it was suggested that cardiac conduction should be assessed if syncope or changes in seizure tjrpe occur in patients taking carbamazepine (5). 

The combination of disopjramide and practoioi can cause profound sinus bradycardia and asystole (40,41). 

Lidocaine can cause dysrhythmias and hypotension. The dysrhythmias that have been reported include sinus bradycardia, supraventricular tachycardia (11), and rarely torsade de pointes (12). There have also been rare reports of cardiac arrest (2) and worsening heart failure (13). Lidocaine can also cause an increased risk of asystole after repeated attempts at defibrillation (14). Lidocaine may increase mortality after acute myocardial infarction, and it should be used only in patients with specific so-called warning dysrhythmias (that is frequent or multifocal ventricular extra beats, or salvos) (15). 

In a study of 32 patients, 84% of those who received paclitaxel developed hypersensitivity reactions characterized by hypotension, respiratory distress, and urticaria (35). These symptoms further confirm that histamine is likely to be the cause of the reaction. The majority of reactions (53%) occurred within 2-3.minutes after the administration of paclitaxel and 78% within 10 minutes. There was one fatal reaction, characterized by hypotension and asystole. Most reactions to paclitaxel occurred after the first or second dose, and hypersensitivity reactions were more common with shorter infusion schedules. Since the duration of the infusion affected the incidence of hypersensitivity reactions, an extension of the infusion duration was investigated. Longer infusion schedules were associated with a reduced incidence of hypersensitivity reactions, the frequency of severe reactions being reduced from 12% or more to 5% with longer infusion times (5,15,49). 

The primary toxicities observed with procainamide are cardiovascular in nature. Initially, a tachycardia may occur due to procainamide s anticholinergic properties or as a reflex response to vasodilation. Cardiac conduction disturbances may occur. On the ECG, these may be displayed as prolongation of the QRS and/or QTc duration. Heart block, bradycardia, and asystole have been reported. Procainamide can also cause ventricular tachycardia, ventricular fibrillation, and Torsades de Pointes. Severe hypotension due to decreases in cardiac output and/or vasodilation may be seen. Altered mental status and seizure activity can occur in procainamide toxicity. 

Early signs of tricyclic antidepressant toxicity are due to anticholinergic effects and include tachycardia, mydriasis, dry mouth, low-grade fever, diminished bowel sounds, CNS excitation, and delirium. More serious toxicity is manifested by coma, respiratory depression, seizures, and cardiovascular toxicity including conduction disturbances, hypotension, ventricular arrhythmias, and asystole. Seizures cause hyperthermia, rhabdomyolysis, and metabolic acidosis. Clinical deterioration can be rapid and catastrophic in patients with tricyclic antidepressant overdose. Death most often occurs due to dysrhythmia and circulatory collapse. The typical therapeutic dose of a tricyclic antidepressant is 2-4 mg kg day Doses of 15-20 mg kg are potentially lethal. Therapeutic drug levels for most tricyclic antidepressants range from 100 to... 

Therapy for phenothiazines is generally supportive and similar to that for tricyclic antidepressant overdose. Physostigmine can reverse the central and peripheral anticholinergic manifestations of phenothiazines however, because these manifestations are rarely life-threatening and because physostigmine may cause severe bradycardia or asystole it is not recommended for treatment of pheno-thiazine overdose. Because of the large volume of distribution and extensive protein binding, hemodialysis or hemoperfusion is not beneficial for phenothiazine overdose. 

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

Heart disease is the leading cause of death in the United States and is responsible for approximately 870,000 deaths per year (1). Sudden cardiac death (SCD) is responsible for almost half of these deaths, claiming 350,000 to 400,000 lives per year (2). SCD is defined by the World Health Organization as death due to any cardiac disease that occurs out of hospital, in an emergency room, or a patient who is dead on arrival to a care facility. Of note, the death must occur within one hour after the onset of symptoms. The majority of SCD is likely arrhythmic in etiology. In women, up to 88% of sudden cardiac arrests may be due to arrhythmic causes (3). Of SCD due to cardiac arrhythmias, greater than 80% of events are due to ventricular tachycardia (VT) and ventricular fibrillation (VF), with the remainder due to bradyarrhythmias and asystole (4). Coronary artery disease (CAD), manifesting acutely as ischemic ventricular arrhythmias or chronically as scar-mediated... 

Overdosage with mexiletine causes dizziness, drowsiness, nausea, hypotension, sinus bradycardia, paresthesia, seizures, intermittent left-bundle branch block, and temporary asystole. With massive overdoses, coma and respiratory arrest may occur (see also Eigure 84). 

B. Complications. Bradycardia and AV block frequently cause hypotension, which may progress to asystolic cardiac arrest. 

Overdose may cause sedation, confusion, coma, seizures, respiratory arrest, and cardiac toxicity (sinus arrest, atrioventricular [AV] block, asystole. 

Overdose causes hypotension, bradycardia, AV block, and asystole. The QRS and QT intervals are prolonged, and ventricular arrhythmias may occur. 

A small dose of physostigmine (see p 489), 0.5-1 mg IV in an adult, can be given to patients with severe toxicity (eg, hyperthermia, severe delirium, or tachycardia). Caution physostigmine can cause atrioventricular block, asystole, and seizures, especially in patients with tricyclic antidepressant overdose. 

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