Holiday Heart Syndrome Medication

Updated: May 30, 2018
  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jose M Dizon, MD  more...
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Medication Summary

Symptoms of acute alcohol toxicity generally resolve spontaneously, and management is largely supportive (ie, intravenous [IV] hydration and correction of electrolyte derangements). Arrhythmia monitoring and observation are sufficient in many patients. In patients with atrial tachyarrhythmias and a rapid ventricular response (eg, atrial fibrillation or flutter), ventricular rate control is important for those who are symptomatic. The use of beta-blockers or nondihydropyridine calcium channel blockers (CCBs) is appropriate. Digoxin is a third-line option; chronic therapy with this drug is rarely indicated. Patients who are hemodynamically unstable should be treated with direct-current cardioversion.

As discussed earlier under Prognosis, although the majority (>90%) of cases of alcohol-related atrial fibrillation self-terminate, approximately 20%-30% will recur within 12 months. [11] When considering the type of atrial fibrillation, moderate to heavy alcohol consumption has been demonstrated to be the strongest risk factor for progression from paroxysmal atrial fibrillation to persistent atrial fibrillation. [25]

As discussed under Diagnostic Considerations, although long-term anticoagulation is indicated for patients with paroxysmal, persistent, or permanent atrial fibrillation plus risk factors for stroke or systemic thromboembolism, it may be prudent to be cautious about anticoagulating patients with expected acute alcohol toxicity, especially if there is a history of possible trauma. Unless high-risk features are present (ie, prior stroke, mechanical heart valve, or other indication for anticoagulation) a reasonable approach may be to allow the patient to recover from the acute episode, and then initiate anticoagulation once they are clinically stable.

Note that when considering initiating anticoagulation, the most recent American College of Cardiology/American Heart Association (ACC/AHA) guidelines do not specifically consider "reversible" causes as a reason to forgo anticoagulation for stroke risk reduction. That is, a single episode of atrial fibrillation may result in a significant change in a patient's medical regimen for the forseeable future. [30]  In this scenario, anticoagulation would be initiated after a patient-physician discussion regarding the risks and benefits of anticoagulation. Integral to this discussion is calculation of both the CHA2DS2VASc (Cardiac failure, Hypertension, Age >75 years [doubled], Diabetes, prior Stroke or TIA [transient ischemic attack] or thromboembolism [doubled], Vascular disease, Age 65-75 years, Sex category) score and the HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding history or predisposition, Labile INR [international normalized ratio], Elderly, Drugs/alcohol concomitantly ( score. [30, 31]

Because atrial fibrillation with rapid ventricular response (RVR) is the primary acute concern with holiday heart syndrome (HHS), commonly used medications for heart rate control are outlined in the next sections. (Also see the Guidelines section, under Rate Control.) Although there is no clear consensus about what heart rate should be targeted, a goal based on symptoms is reasonable (eg, A heart rate < 85 beats per minute is reasonable in a symptomatic patient, whereas a more lenient heart rate goal is reasonable in an asymptomatic patient.) Other antiarrhythmic medications and anticoagulants are outside the scope of this article. Information regarding these ageents can be found here.


Beta-Blockers, Beta-1 Selective

Class Summary

Beta-blockers (also known as beta-antagonists) function via sympatholytic effects. The beta-1 adrenoreceptor is the adrenoreceptor responsible for myocardial effects. Thus, beta-1 selective agents are generally preferred if possible to avoid off-target effects. In general, they are the treatment of choice in the setting of acute myocardial ischemia or left ventricular systolic dysfunction.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a beta-1 selective (ie, cardioselective) beta-blocker that may be given IV or PO for acute rate control.

Metoprolol is not avaliable as an infusion. Thus, once rate controlled, the patient must be switched to scheduled IV or PO doses.

Esmolol (Brevibloc)

Esmolol is another cardioselective beta-blocker. It is administered as an IV bolus with maintenance infusion. Its main clinical utility is its short half-life (9 minutes, with a clinical hemodynamic effect commonly quoted at 10-30 minutes).


Calcium Channel Blockers, Non-dihydropyridine

Class Summary

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit the movement of calcium ions across the cell membrane, thus depressing both impulse formation (automaticity) and conduction velocity.

Diltiazem (Cardizem CD, Dilacor, Tiazac)

Diltiazem has a relatively balanced effect on both the myocardium as well as the peripheral vasculature. Similar to verapamil, this agent should be used with caution whenever left ventricular systolic dysfunction is present.

Diltiazem may be given as an IV bolus or as an infusion.

Verapamil (Calan, Covera-HS, Verelan)

Verapamil is the most cardioselective of the calcium channel blockers, with minimal effect on the peripheral vasculature. It should be used with caution whenever left ventricular systolic dysfunction is present.

Verapamil may be given as an IV bolus or as an infusion. In general, verapamil infusions are used less commonly when compared with use of diltiazem.


Cardiac Glycosides

Class Summary

Cardiac glycosides have direct and indirect cardiac effects. Their direct effect is in inhibiting the membrane sodium-potassium (Na+-K+) pump, raising intracellular levels of sodium and leading to an accumulation of intracellular calcium. This in turn increases cardiac contractility. Their indirect effect is in enhancing vagal tone.

Digoxin (Lanoxin, Lanoxicaps)

Digoxin's effects on atrioventricular nodal conduction are mediated via increased vagal tone. It is also characterized by positive inotropic effects on the myocardium via inhibition of the sodium-potassium ATPase, and the resultant increase in intracellular calcium. Digoxin has fallen out of favor in relatively recent years over concerns of proarrhythmias, drug-drug-interactions, and variable effects on overall long-term mortality depending on the population studied. In general, it should only be used for rate control in the presence of heart failure with reduced ejection fraction.


Antidysrhythmics, III

Class Summary

Class III antiarrhythmic agents inhibit adrenergic stimulation; affect sodium, potassium, and calcium channels; markedly prolong action potential and repolarization; and decrease atrioventricular conduction and sinus node function.

Amiodarone (Cordarone, Nexterone, Pacerone)

Amiodarone is perhaps the most effective of all the antiarrhythmic drugs. It has effects in all four of the Vaughn Williams antiarrhythmic classes. In general, however, amiodarone should not be a first-line agent. When used for acute rate control in the acute setting, only IV amiodarone is practical. It is useful for rate control when heart failure or hypotension are present, as amiodarone tends to cause less hypotension than beta-blockers and calcium channel blockers.  

NOTE: There is a theoretical concern for cardioversion with amiodarone which must be considered if selecting this drug.  

In this particular context of alcohol-induced atrial fibrillation, keep in mind that amiodarone is also associated with many adverse effects, one of which is hepatotoxicity.