Arrhythmias premature ventricular contraction

Unlabeled Uses Atrial arrhythmias, complete and nonsustained ventricular arrhythmias, premature ventricular contractions (PVCs)... 

Scarring was the second most common com-plicahon reported, with the most frequent sites being the lip, chin, and perioral areas [315]. Thirteen percent of these plastic surgeons had experienced systemic cardiac complicahons (tachycardia, arrhythmias, premature ventricular contractions (PVCs), paroxysmal atrial tachycardia (PAT), and hypertension) during phenol peeling [315]. Of these, tachycardia was the most frequent [315]. An 11-year-old boy treated with phenol for xeroderma pigmentosum developed multifocal ventricular arrhythmias with heart rates up to 220 beats/min [329]. 

Cardiac-changes in pulse rate or rhythm electrocardiographic changes, such as bradycardia, tachycardia, premature ventricular contractions, bigeminal (two beats followed by a pause), or trigeminal (three beats followed by a pause) pulse. Other arrhythmias (abnormal heart rhythms)also may be seen. 

The uses of the antiarrhythmic drug are given in the Summaiy Drug Table Antiarrhythmic Drug3. In general these drugp are used to prevent and treat cardiac arrhythmias, such as premature ventricular contractions (PVCs), ventricular tachycardia (VT), premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), atrial fibrillation, and atrial flutter. Some of the antiarrhythmic dru are used for other... 

In an undated study, HCFC-141b was administered to male SpragueDawley rats at concentrations of 5,000, 10,000, or 20,000 ppm for 30 min (Eger, unpublished data). As exposure continued, bolus intravenous epinephrine, characterized as three times the dose that produced arrhythmias in the same rats anesthetized with halothane, was administered. The dose of epinephrine was defined as a maximum of 12 fig/kg. For this study, three or more premature ventricular contractions was considered an arrhythmic response (Table 4—5). Marked arrhythmias occurred at all concentrations. The author further compared the concentrations of halothane and HCFC-141b that produced arrhythmias with administration of various doses of exogenous epinephrine. The nominal chamber concentration for HCFC-141b did not differ from that of halothane. Furthermore, the arrhythmias were characterized as relatively mild and within acceptable limits for surgical anesthesia in humans. 

Genera/-Arrhythmias changes in AV conduction ECG changes (most frequently with toxic doses) flushing heart block hot flushes hypertension hypotension orthostatic hypotension palpitations precipitation of CHF premature ventricular contractions stroke sudden death syncope tachycardia. 

Disopyramide Premature ventricular contractions Atrial arrhythmias, episodic ventricular tachycardia... 

Inappropriate use of oxytocin can lead to uterine rupture, anaphylactoid and other allergic reactions, and possibly maternal death. Prolonged stimulation of uterine contractions can result in the following fetal adverse reactions persistent uteroplacental insufficiency, sinus bradycardia, premature ventricular contractions, other arrhythmias, and fetal death. Prolonged use of oxytocin can lead to water intoxication secondary to the antidiuretic hormone-like effects of oxytocin. Maternal and fetal cardiovascular parameters should be monitored during oxytocin administration. 

I Unlabeled Uses Angina pectoris, premature ventricular contractions, supraventricular arrhythmias... 

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial... 

During arrhythmias Atrial tachycardia, atrial fibrillation AV nodal tachycardia, AV blockade Premature ventricular contractions, bigeminy, ventricular tachycardia, ventricular fibrillation... 

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial infarction and ventricular ectopy (see The Cardiac Arrhythmia Suppression Trial). The drug is well absorbed and has a half-life of approximately 20 hours. Elimination is both by hepatic metabolism and by the kidney. The usual dosage of flecainide is 100-200 mg twice a day. 

Premature ventricular contractions (PVCs) are commonly recorded in patients convalescing from myocardial infarction. Since such arrhythmias have been associated with an increased risk of sudden cardiac death, it had been the empiric practice of many physicians to treat PVCs, even if asymp-tomatic, in such patients. In CAST (Cardiac Arrhythmia Suppression Trial [CAST], Echt et al, 1991), an attempt was made to document the efficacy of such therapy in a controlled clinical trial. The effects of several antiarrhythmic drugs on arrhythmia frequency were first evaluated in an open-label fashion. Then, patients in whom antiarrhythmic therapy suppressed PVCs were randomly assigned, in a double-blind fashion, to continue that therapy or its corresponding placebo. 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably due to -adrenergic activation. The cause of this activation is not fully understood, but the effects can be ameliorated by the use of B-blockers (see below). Cardiac arrhythmias include atrial tachycardias, premature ventricular contractions, and ventricular tachycardia. In severe poisoning (eg, acute overdose with serum level > 100 mg/L), seizures often occur and are usually resistant to common anticonvulsants. Toxicity may be delayed in onset for many hours after ingestion of sustained-release tablet formulations. 

Therapeutic uses Flecainide is useful in treating refractory ventricular arrhythmias. It is particularly useful in suppressing premature ventricular contraction. Flecainide has a negative inotropic effect and can aggravate congestive heart failure. 

By increasing the rates of ventricular contraction and relaxation, Epi preferentially shortens systole and usually does not reduce the duration of diastole. Epi speeds the heart by accelerating the slow depolarization of sinoatrial (SA) nodal cells that takes place during phase 4 of the action potential (see Chapter 34). The amplitude of the AP and the maximal rate of depolarization (phased) also are increased. A shift in the location of the pacemaker within the SA node often occurs, owing to activation of latent pacemaker cells. In Purkinje fibers, Epi accelerates diastolic depolarization and may activate latent pacemakers. If large doses of Epi are given, premature ventricular contractions occur and may herald more serious ventricular arrhythmias. Conduction through the Purkinje system depends on the level of membrane potential at the time of excitation. Epi often increases the membrane potential and improves conduction in Purkinje fibers that have been excessively depolarized. 

TheophyUine decreases peripheral resistance, increases cardiac output, and causes a central vagal effect. Palpitations, sinus bradycardia, extrasystoles, hypotension, ventricular tachycardia, premature ventricular contractions (PVCs), and cardiac arrest have been reported. Although cardiovascular effects are generaUy mUd and transient, serious reactions, such as ventricular arrhythmias, can develop without warning. Patients should be carefuUy monitored. 

In theophyUine acute overdose patients are more likely to exhibit hypotension, hypokalemia, and/or metaboUc acidosis than are patients receiving chronic overmedication. Patients suffering chronic overmedication can develop seizures and serious arrhythmias with serum concentrations of 28-70 /xg/mL. Cardiac arrhythmias include atrial fibriUation or atrial flutter, multifocal atrial tachycardia, sinus tachycardia, supraventricular tachycardia and premature ventricular contractions with hemodynamic instabUity. 

Additionally excessive cortisol may lead to a type of arrhythmia called premature ventricular contractions (PVCs). These abnormal heartbeats originate in the lower chambers of the heart and may be associated with more severe arhythmias that can lead to a heart attack. Cortisol also encourages the body to store fat around the abdomen instead of the hips, a well-known but little understood risk factor for heart disease. 

A. Amantadine intoxication causes agitation, visual hallucinations, nightmares, disorientation, delirium, slurred speech, ataxia, myoclonus, tremor, and sometimes seizures. Anticholinergic manifestations include dry mouth, urinary retention, and mydriasis. Rarely, ventricular arrhythmias including torsade de pointes (see p 14) and multifocal premature ventricular contractions may occur. Amantadine has also been reported to cause heart failure. 

Two patients developed ventricular arrhythmias while anaesthetised with halothane and nitrous oxide/oxygen when given terbutaline 250 to 350 micrograms subcutaneously for wheezing. Both developed unifocal premature ventricular contractions followed by bigeminy, which responded to lidocaine. Halothane was replaced by enllurane in one case, which allowed the surgery to be completed without further incident. ... 

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