Arrhythmia, evaluation

Ebert SN, Liu XK, Woosley RL. Female gender as a risk factor for drug-induced cardiac arrhythmias Evaluation of clinical and experimental evidence. J WomeiVs Health 1998 7 547-57. 

Asymptomatic therapy, or ineffective therapy (antitachycardia pacing) Unknown Consider reprogramming the detection criteria to more rapidly provide therapy for ventricular arrhythmias. Evaluate effectiveness of antitachycardia pacing electrograms or via NIPS... 

The use of voltage clamp studies for unbiased and standardized decision-making in arrhythmia evaluation will necessitate the development of consensus on best practices and/or standardization of protocols, positive/negative controls, and experimental conditions. This effort will reduce variability, allow comparisons across assays and laboratories, and generate movement towards more uniform data quality for purposes of decision-making, both by sponsors internally and by regulatory... 

Monitor the patient s 12-lead ECG or single rhythm strips to determine if an arrhythmia is present and to identify the specific arrhythmia, and evaluate and monitor the patient s symptoms. 

Low-dose dopamine is not without adverse reactions and most studies have failed to evaluate its potential toxicities. Adverse reactions that may be associated with low-dose dopamine include tachycardia, arrhythmias, myocardial ischemia, depressed respiratory drive, and gut ischemia. Low-dose dopamine has also been postulated to impair resistance to infection through a reduction in prolactin concentrations.21 Furthermore, significant overlap in receptor activation occurs. Therefore, doses considered to activate only dopamine receptors may increase cardiac output and blood pressure through dopamine s effect on 3- or a-adrenergic receptors. 

During the initial evaluation, providing for the safety of the patient is of paramount importance. The severity of intoxication and potential for withdrawal must be quickly and accurately determined. Extreme alcohol intoxication can be fatal either by the production of cardiac arrhythmias, aspiration (the inhalation of stomach contents that are vomited), or other causes. We have all seen reports of college students dying from alcohol poisoning. Likewise, up to 10% of patients in severe alcohol withdrawal can die without treatment. Fortunately, most patients do not experience the most severe forms of alcohol withdrawal such as the DTs. Mild withdrawal can be managed in the outpatient setting with appropriate support and patient adherence, but severe withdrawal requires an inpatient hospitalization. See Section 6.5 for further discussion of the initial evaluation. 

The ICH guideline lists the assessment of effects on blood pressure, heart rate and ECG. In vivo, in vitro and/or ex vivo evaluations, including methods for electrical repolarisation and conductance abnormalities, should also be considered. These abnormalities can be associated with risks for fatal ventricular arrhythmias called Torsade de pointes. 

Proarrhythmic effects Antiarrhythmic agents may cause new or worsened arrhythmias. It is essential that each patient be evaluated electrocardiographically and clinically prior to and during therapy to determine whether the response to the drug supports continued treatment. ... 

Proarrhythmic effects Propafenone may cause new or worsened arrhythmias. Such proarrhythmic effects range from an increase in frequency of PVCs to the development of more severe ventricular tachycardia, ventricular fibrillation or torsade de pointes, which may lead to fatal consequences. It is essential that each patient be evaluated electrocardiographically and clinically prior to, and during therapy to determine whether response to propafenone supports continued use. Non-life-threatening arrhythmias Use of propafenone is not recommended in patients with less severe ventricular arrhythmias, even if the patients are symptomatic. 

Perform clinical and ECG evaluation as needed to determine whether the desired antiarrhythmic effect has been obtained and to guide titration and dose adjustment. Initial dose 200 mg every 8 hours when rapid control of arrhythmia is not essential, with a minimum of 2 to 3 days between adjustments. Adjust dose in 50 or 100 mg increments. 

QT prolongation, recent acute Ml, uncompensated heart failure, cardiac arrhythmia). Discontinue treatment if the QT interval is over 500 msec. Patients who experience symptoms that may be associated with the occurrence of torsade de pointes (eg, dizziness, palpitations, syncope) may warrant further cardiac evaluation in particular, consider Holter monitoring. 

Cardiovascular Specifically, screen and evaluate patients with coronary heart disease, serious cardiac arrhythmias or vasospastic diseases before nicotine is prescribed. There have been occasional reports of tachyarrhythmias associated with nicotine use therefore, if an increase in cardiovascular symptoms occurs, discontinue the drug. 

Exercise-related VT frequently arises from the right ventricular outflow tract and may be easily evaluated by catheter mapping in an electrophysiology laboratory. The treatment of first choice for chronic therapy of this arrhythmia has been -blockers, but radiofrequency catheter ablation should also be considered. 

Moricizine is indicated for the treatment of documented ventricular arrhythmias, particularly sustained ventricular tachycardia. Moricizine was evaluated in the CAST II clinical trial for the prevention of postinfarction ventricular premature complexes. It was ineffective and found to be proarrhythmic. Patients in the moricizine arm of the trial exhibited a greater incidence of sudden cardiac death than did controls. 

Amiodarone blocks the peripheral conversion of thyroxine (T4 ) to triiodothyronine (T3). It is also a potential source of large amounts of inorganic iodine. Amiodarone may result in hypothyroidism or hyperthyroidism. Thyroid function should be evaluated before initiating treatment and should be monitored periodically. Because effects have been described in virtually every organ system, amiodarone treatment should be reevaluated whenever new symptoms develop in a patient, including arrhythmia aggravation. 

Calcium ion facilitates the toxic actions of cardiac glycosides by accelerating the overloading of intracellular calcium stores that appears to be responsible for digitalis-induced abnormal automaticity. Hypercalcemia therefore increases the risk of a digitalis-induced arrhythmia. The effects of magnesium ion appear to be opposite to those of calcium. These interactions mandate careful evaluation of serum electrolytes in patients with digitalis-induced arrhythmias. 

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. 

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