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Health Protocols


Conventional Treatment Strategies

Several strategies are available for treating arrhythmias, and the approach varies depending on the type of arrhythmia. For bradycardia, or slow heart rate, a pacemaker can be implanted to help ensure the heart beats quickly enough. Tacchycardias (fast heart rate) and fibrillations (irregular heart rate) can be treated with medications to slow the heart rate. A procedure called cardioversion uses electrical current, either synchronized or unsynchronized (defibrillation) with the cardiac cycle, to treat abnormally fast heart rate (tachyarrhythmia) or uncoordinated & irregular electrical activity in the heart (fibrillation). Another treatment option involves ablation of portions of heart tissue from which improper electrical signals are originating. In addition, since atrial fibrillation increases ischemic stroke risk, anticoagulant medications such as warfarin (Coumadin®) or dabigatran (Pradaxa®) are used to prevent blood clot formation in people with this arrhythmia (Gallego 2012; Ho 2012; MayoClinic 2011a).

This section will outline several arrhythmia treatment considerations:

Vagal Maneuvers

It may be possible to stop an arrhythmia that begins above the ventricles by using vagal maneuvers that affect the vagus nerve, which is a part of the nervous system responsible for controlling the heartbeats. Some examples of these maneuvers, which often cause the heart rate to slow, include holding your breath and straining (Valsalva maneuver), dunking your face in icy water, and coughing; a physician may be able to recommend other maneuvers to slow down a fast heartbeat (NHLBI 2011b).


Arrhythmias can be treated with a variety of medications. The type of arrhythmia present and the unique characteristics of each patient determine which type of drug should be used and how. Because the clinical assessment of arrhythmias and the algorithm that physicians employ to determine the best pharmacologic treatment strategy is complex, this protocol will not discuss all of the specific roles of drugs in the various types of arrhythmias. Rather, we will outline the basic classification of drugs that may be utilized as part of pharmacologic arrhythmia management. Individuals with any type of arrhythmia should consult with a physician experienced in arrhythmia management to be properly evaluated and treated.

A classification method called the Vaughan-Williams system is widely used to categorize antiarrhythmic agents based on their effects on the electrophysiological system of the heart. This classification system characterizes antiarrhythmic drugs as follows (Weirich 2000; Ganjehei 2011; Homoud 2008):

Class I agents: Sodium-Channel Blockers. Class I antiarrhythmic agents are further subclassified as class IA, IB, or IC agents depending on how strongly they block sodium channels. Examples of class I agents include procainamide (Procanbid®), disopyramide (Norpace®), and flecainide (Tambocor®).

Class II agents: Beta-Adrenergic Blockers or “Beta-Blockers”. Some common beta-blockers are carvedilol (Coreg®), metoprolol (Lopressor®), and propranolol (Inderal®).

Class III agents: Potassium-Channel Blockers. Drugs in this class include sotalol (Betapace®), dofetilide (Tikosyn®), and ibutilide (Corvert®).

Class IV agents: Calcium Channel Blockers. A few common drugs that fall into this category include amlodipine (Norvasc®), diltiazem (Cardizem®), verapamil (Calan®).

Other agents: There are several antiarrhythmic drugs whose mechanisms are complex and/or not fully understood; they are usually grouped into this category. One frequently used drug that falls into this category is digoxin (Campbell 2001).

It should be noted that the Vaughan-Williams System has some considerable limitations because some drugs – such as amiodarone (which is typically considered a class III agent) for example – exhibit actions characteristic of more than one Vaughan-Williams class (Schmidt 2011). Therefore, physicians cannot rely solely on classification of antiarrhythmic agents in this manner when determining the best drug strategy for each patient.

Newer alternatives to amiodarone – budiodarone and dronedarone

Amiodarone (Cordarone®) is one of the most frequently used antiarrhythmic agents because it effectively treats potentially deadly ventricular arrhythmias; it is also used in the management of atrial fibrillation (Siddoway 2003; Singh 2005). However, it can cause some serious side effects, including the development of fibrous tissue in the lungs and thyroid dysfunction (Maseeh uz 2012; Van Herendael 2010). Therefore, a drug capable of delivering similar efficacy with less side effects would be a promising antiarrhythmic agent (Morey 2001).

One reason that amiodarone can cause significant side effects is that it remains in the body for a long time (ie, it has a very long half-life) and can build up in tissues (Morey 2001; Mason 2009).

Budiodarone and dronedarone (Multaq®) are similar to amiodarone in both chemical structure and mechanism of action. However, they are metabolized more quickly than amiodarone, potentially resulting in less tissue accumulation and side effects (Mason 2009). Dronedarone was approved by the Food and Drug Administration (FDA) in 2009 for atrial fibrillation and atrial flutter; budiodarone is still undergoing trials as of the time of this writing (FDA 2009; Ezekowitz 2012).

Clinical trials and data analyses have shown that both of these new drugs have efficacy and side effect profiles comparable or superior (at least in some aspects) to amiodarone.


In a comprehensive analysis of data from 4 trials involving nearly 6000 subjects with atrial fibrillation, treatment with dronedarone significantly reduced stroke risk compared to placebo treatment (Dagres 2011). In another analysis, this time grouping data from 39 atrial fibrillation treatment trials, dronedarone was again shown to reduce stroke risk and produce fewer arrhythmic events than amiodarone, and amiodarone was shown to be associated with a higher mortality rate than dronedarone. However, dronedarone was not as efficacious at preventing recurrence of atrial fibrillation as amiodarone (Freemantle 2011).

Dronedarone is associated with increased risk of cardiovascular death, stroke, and heart failure in patients with permanent atrial fibrillation (ie, those who cannot be converted to normal heart rhythm). Therefore, the FDA does not advise that doctors prescribe dronedarone to this population (FDA 2011).


In a 12 week study, patients with atrial fibrillation and a previously implanted pacemaker who stopped taking antiarrhythmic agents for a period sufficient to “wash out” the drug from their systems were treated with budiodarone for 12 weeks. In the group receiving the highest dose of the drug (600 mg twice daily), atrial tachycardia / atrial fibrillation was reduced by 74% (Ezekowitz 2012).

Although more studies are needed before dronedarone and/or budiodarone can be asserted as unequivocally superior or inferior to amiodarone, data so far suggest that these agents may become an important treatment consideration for select arrhythmia patients.

Electrical Cardioversion

In some cases of arrhythmia, cardioversion (ie, the process of delivering an external electrical jolt through the chest to the heart) may be utilized to reset the heart to its normal rhythm. The machine used to deliver the electrical current is called a defibrillator (Hebbar 2002a; Shea 2008; Sucu 2009).

Ablation Therapy

Another technique often employed to treat arrhythmias is catheter ablation. This procedure involves the insertion of a thin wire catheter into a blood vessel in the groin, arm, or neck, which is then guided to the heart. Radiofrequency energy is then delivered through the wire to generate heat and destroy (ablate) small sections of tissue in the heart responsible for triggering the arrhythmia (Davoudi 2012). Other ablation techniques include application of extreme cold (ie, “cryoablation”) or high frequency ultrasound through the catheter to destroy the arrhythmogenic tissue (Narayan 2012; Joseph 2012).

Implantable Devices

Treatment for heart arrhythmias may also involve the use of an implantable device. Several types of such devices are currently available.


A pacemaker is an implantable, battery-operated device that is used in cases of slow or irregular heart rate. Implanting a pacemaker involves surgically placing the device under the skin, near the collarbone. An insulated wire connects the device to the right side of the heart, where it is permanently anchored. In cases of slow or abnormal heart rhythms, the device emits an electrical signal that stimulates the heart to beat at a normal rate. The device typically remains in a “switched off” mode when the heartbeat is normal (NHLBI 2011a; ExitCare 2012).

Implantable Cardioverter-Defibrillator

In ventricular fibrillation, which is a potentially life-threatening disorder, an implantable cardioverter-defibrillator (ICD) may be placed near the left collarbone, similarly to a pacemaker. The ICD does not turn off and monitors heart beats continuously. It acts as a pacemaker in cases of bradycardia and sends high-energy electrical impulses to reset the heart in cases of ventricular fibrillation or tachycardia (Estes 2011; Vlay 2009; NHLBI 2011a).

Surgical Treatments

In some cases, surgery may be the recommended treatment for heart arrhythmias.

Maze Procedure

This procedure involves making surgical incisions in the atria, which heal into carefully placed scars that force cardiac electrical impulses to travel along a preset pathway and cause the heart to beat efficiently. The resulting scars form boundaries and create a ‘maze’ for electrical impulse to travel along. Rather than using a scalpel, scars can be created by using a ‘cryoprobe’ to apply extreme cold or a radiofrequency device that applies heat. Since this procedure requires open-heart surgery, it is typically reserved for patients who do not respond to other types of treatment (Nakamura 2012; MayoClinic 2011a).

Coronary Bypass Surgery

Coronary bypass surgery or coronary artery bypass graft (CABG) is performed in cases of severe coronary artery disease with frequent ventricular tachycardia. This procedure may help improve the blood supply to the heart and reduce the frequency of ventricular tachycardia (MayoClinic 2011a).

Stroke Prevention in Atrial Fibrillation

A major potential complication of atrial fibrillation is ischemic stroke that occurs as a result of blood stagnating and clotting in the fibrillating atria. The blood clot can then travel to the brain and lodge in a blood vessel, causing an ischemic stroke. Therefore, anticoagulant medications, which reduce the likelihood of blood clots forming, are an important stroke-prevention strategy in patients with atrial fibrillation (Davoudi 2012).

Without anticoagulants, the rate of ischemic stroke in patients with atrial fibrillation is approximately 5% per year. With anticoagulant therapy, the rate of stroke is reduced to less than 1.5% (You 2012; Davoudi 2012). The most commonly used blood thinners include warfarin (Coumadin®), clopidogrel (Plavix®), and aspirin. Standard recommendations, including those by the American College of Chest Physicians, state that patients with atrial fibrillation at a lower risk of stroke should be prescribed a dose of aspirin ranging from 75 to 325 mg daily while patients at high risk should be prescribed warfarin (You 2012). Warfarin has a narrow therapeutic index, which refers to a very small dose range in which it is effective as an anticoagulant. Below this range, the compound is ineffective, and above these levels it is extremely toxic; therefore, patients on warfarin must be closely monitored (Martin 2012). However, not all patients are suitable candidates for warfarin therapy, in which case aspirin and clopidogrel may be used together to reduce stroke risk; although this combination increases bleeding (hemorrhage) risk and is not FDA-approved for prevention of stroke in individuals with atrial fibrillation (Connolly 2009).

Other anticoagulant drugs include dabigatran (Pradaxa®), apixaban (EliquisTM) (Martin 2012), and rivaroxaban (XareltoTM), all of which inhibit components of the blood coagulation cascade. Dabigatran inhibits a coagulation factor called thrombin, while the other three are direct inhibitors of factor Xa, a component of the coagulation cascade (Van Mieghem 2012). Dabigatran has been approved for the prevention of stroke, and research has found 150 mg of dabigatran twice daily may be superior to warfarin for stroke prophylaxis (Schwartz 2010). Based on clinical trials, all three drugs – dabigatran, apixaban, and rivaroxaban – significantly reduced the occurrence of hemorrhagic stroke as compared with warfarin (Van Mieghem 2012). Only dabigatran reduced the occurrence of ischemic stroke as compared with warfarin, but the other two compounds performed as well as warfarin (Van Mieghem 2012; Martin 2012).

Advantages of Pradaxa® vs. warfarin include:

  • Rapid onset of action
  • Predictable, consistent anticoagulant effects
  • Low potential for drug-drug interaction
  • No requirement for anticoagulant blood test monitoring
  • Preliminary efficacy and safety advantages vs. warfarin based on initial head-to-head, hard-endpoint data
  • No need to maintain low vitamin K levels. Insufficient vitamin K promotes arterial calcification.

Disadvantages of Pradaxa® vs. Warfarin include:

  • No antidote for reversal of over-anti-coagulation effect. When too much warfarin is given and the patient's INR indicates they are at risk for a major bleed (or are pathologically bleeding), vitamin K can be injected to immediately reverse warfarin's anti-coagulant effect. If too much Pradaxa® is taken, there is no immediate antidote.
  • No long-term safety data on Pradaxa® (the case with virtually all newly approved drugs)
  • More expensive than warfarin