Ventricular arrhythmias

Cardiovascular and cerebrovascular Coca me has cardiotoxic effects, sometimes resulting in arrhythmia, ventricular fibrillation, or cardiac arrest (Nanji and Filipenko 1984 Sherief and Carpentier 1991). Vaso-... 

Propranolol is used in treating arterial hypertonicity, angina, extrasystole, superventric-ular arrhythmia, ventricular tachycardia, migraines, hypertrophic subaortic stenosis, and pheochromocytoma. It also is used in the postanginal phase of myocardial infarctions. Universally accepted synonyms of this drug are anaprilin, inderal, and many others. 

Lidocaine Post-myocardial infarct arrhythmias Ventricular tachycardia... 

It is indicated in ventricular arrhythmia, ventricular premature depolarization and paroxysmal ventricular tachycardia, supra-ventricular tachycardia and atrial arrhythmia. 

Autonomic symptoms are most common and include gastrointestinal disturbance (nausea, diarrhea), general somatic distress (myalgias, malaise, headache, rhinorrhea), sleep disturbances (insomnia, nightmares), and cardiovascular symptoms (arrhythmias, ventricular ectopy). Psychotic decompensation, withdrawal mania, and general anxietylike symptoms have been attributed to abrupt withdrawal of cyclic antidepressants. 

OPs cause QT prolongation on the ECG that subsequently can degenerate into TdP. In one reported OP case, 79.7% had QT prolongations with ST segment and T wave abnormalities (Karki et al, 2004 Rubinshtein et al, 2002 Saadeh, 2001 Saadeh et al, 1997). Changes are ultimately expressed in arrhythmia, ventricular fibrillation and TdP, and severe disturbance of the energy homeostasis of the heart. 

Atrial fibrillation Atrioventricular block Bundle Branch Block Cardiac failure Flushing Hypertension Ventricular arrhythmia Ventricular tachycardia... 

Intentional inhalation, or huffing, of volatile organic chemicals for the purpose of inducing euphoria can bring on cardiac arrhythmia, ventricular fibrillation, myocardial infarction, cardiac arrest, and dilated cardiomyopathy, a condition in which the heart becomes enlarged and weakened, thereby limiting its ability to pump bloodJ4 15l Table 29.2 contains a list of cardiotoxic chemicals frequently, intentionally inhaled and the common sources of these chemicals. 

Cardiovascular Cardiac arrhythmias (ventricular fibrillation, torsades de pointes, ordigoxin-induced arrhythmias), sudden cardiac death, and hypertension may be present. ECG abnormalities include widened QRS complex and peaked T waves with mild hypomagnesemia and prolonged PR interval, progressive widening of QRS complex, and flattened T waves with moderate to severe hypomagnesemia. 

The localization of adducts to the epicardial border zone suggested the possibility that IsoK/LG adducts contribute to cardiac arrhythmias. Ventricular tachycardia/fibrillation following myocardial infarction is a major cause of sudden cardiac death. Arrhythmias in ischemic myocardium arise from sodium channel blockade. Sodium channels are hypothesized to cycle between three conformational states a deactivated closed state, an activated open state, and an inactivated closed state. Upon depolarization, the deactivated state converts to the activated state and sodium current flows for a brief time before the channel enters the inactive state. The channel only converts from the inactive state to the deactivated state when the membrane repolarizes during the falling phase of the action potential. Changes in the ability to convert from the inactive to the deactivated state are critical to the initiation and perpetuation of arrhythmias. 

Local and spinal anesthetic also used for treatment of status epilepticus migraine and cluster headaches ventricular arrhythmias, ventricular fibrillation cardiac arrest neuropathic pain, postherpetic neuralgia... 

Flecainide is absorbed well, has a long half-hfe of 3 to 5 days, is metabolized to -O-deaUcylated flecainide (active antiarrhythmic agent with less potency than flecainide) and to -0-deaUcylated lactam of flecainide, which is an inactive metabolite. A portion of flecainide is excreted unchanged. Flecainide, like other antiarrhythmic agents, can cause new or worsen supraventricular or ventricular arrhythmias. Ventricular proarrhythmic effects range from an increase in frequency of premature ventricular complexes (PVCs) to the development of more severe ventricular tachycardia, e.g., tachycardia that is more sustained or more resistant to conversion to sinus rhythm, with potentially fatal consequences. 

Cardiovascular effects are primarily due to increased production of norepinephrine, and include atrial and ventricular arrhythmias, ventricular tachycardia, and atrial fibrillation. These effects are markedly reduced with concurrent administration of an inhibitor of peripheral LAAD. 

There are anecdotal reports of fatal cardiac arrhythmia (ventricular fibrillation) with a combined phenylpropanolamine and thioridazine regimen. 

In the auricular arrhythmias (premature auricular systole, auricular paroxysmal tachycardia, auricular flutter, and auricular fibrillation), the auricles contract in chaotic, incomplete fashion and there is inefficient transfer of blood to the ventricles. While the auricular arrhythmias are not fatal, unless a normal rhythm is restored there will be a serious strain on the heart that will contribute to its failure or there is an increased likelihood of lethal emboli formation. The ventricular arrhythmias (ventricular premature systole, ventricular tachycardia, and ventricular fibrillation)... 

B. With chronic intoxication, visual disturbances, weakness, sinus bradycardia, atrial fibrillation with slowed ventricular response rate or junctional escape rhythm, and ventricular arrhythmias (ventricular bigeminy or trigeminy, ventricular tachycardia, bidirectional tachycardia, and ventricular fibrillation) are common. Accelerated junctional tachycardia and paroxysmal atrial tachycardia with block are frequently seen. Hypokalemia and hypomagnesemia from chronic diuretic use may be evident and appear to worsen the tachyarrhythmias. 

D. For treatment of life-threatening arrhythmias (ventricular tachycardia or fibrillation associated with hypomagnesemia) in adults, give 1-2 g (8-16 mEq) IV, which can be given over 1-2 minutes. It should be diluted to 20% or less and infused no faster than 1 g/min (see IV, above). It can also be administered as a loading dose of 1-2 g (8-16 mEq) IV diluted in 50-100 mL of D5W or NS and infused over 5 to 60 minutes. A common regimen for adults is 2 g IV over 20 minutes. 

In the heart, fatty acid oxidation defects can cause cardiomyopathy. The cardiomyopathy is usually associated with a degree of hypertrophy. Cardiomyopathy is typical for severe fatty acid oxidation defects of long-chain fatty acids. Cardiomyopathy in those with carnitine transporter defect is typically dilated in nature without hypertrophy. Severe ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation, torsades de pointes) occur in fatty acid oxidation defects. They are frequent in severe fatty acid oxidation defects of long-chain fatty acids and particularly prominent in camitine-acylcamitine translocase deficiency but can also occur in MCAD deficiency during decompensation. Atrioventricular block can occur but is rare. 

The AVID trial, a large multicenter prospective NIH-sponsored trial, compared antiarrhythmic drug (amiodarone or sotalol) therapy to ICD implant in patients who survived life-threatening hemodynamically destabilizing ventricular arrhythmias (ventricular tachycardia and ventricnlar fibrillation). One thousand sixteen patients were randomized (45% with ventricnlar fibrillation and 55% with poorly tolerated ventricular tachycardia). The mean ejection fraction was 0.32. Patients with sustained ventricular tachycardia who were enrolled had associated syncope or a left ventricular ejection fraction < 0.40 (118). The AVID trial is the most persuasive and influential secondary prevention trial to date. At the time this trial was initiated, several centers refnsed to participate because of the belief that the ICD had already been shown to be the best therapy. Fifty-six U.S. and Canadian centers participated. 

Treatment of intoxication is supportive. No specific antidote is presently known. M-cholinoblockers (atropine) are indicated to treat bradycardia. Amiodarone and flecainide can be recommended for the treatment of aconitine-induced arrhythmia. Ventricular arrhythmias provoked by aconitine are often refractory to direct current cardioversion and antiarrhythmic drugs. In refractory cases of ventricular arrhythmias and cardiogenic shock, the cardiopulmonary bypass is recommended. 

Both conditions predispose the patient to dangerous ventricular arrhythmias (Ventricular Tachycardia/Fibrillation and/or Torsades). 

Calcium channel blockers are clinically used for the treatment of hyjtertension, angina pectoris, and arrhythmia (ventricular and supraventricular). Although all CCBs will slow down influx of extracellular Ca through calcium channels it is quite dear that not all CCBs affect the same caldum channd. Different CCBs show different sdectivity and activity toward different caldum channds in different tissues and organs, leading to spedfic bioactivity at that tissue or organ. 

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