Nursing Center - Journal Article

Abstract

Atrial fibrillation is the most common arrhythmia found in older adults that places them at a high risk for stroke. The presence of AF in an individual, especially older than 60 years, increases the risk of mortality, affects quality of life, and increases prevalence of heart failure. The goal of AF treatment is to maintain heart rate or rhythm control and stroke prevention through anticoagulation. With appropriate management of AF an improvement of symptoms and a reduced morbidity from stroke or heart failure can be achieved. The best treatment for AF is prevention and early diagnosis.

ATRIAL fibrillation (AF) affects approximately 2.2 million people in the United States. The presence of AF in an individual, especially older than 60 years, increases the risk of mortality, affects quality of life, and increases prevalence of heart failure.1 Often patients do not know they have AF until they become symptomatic with palpitations, dizziness, and shortness of breath. There are 3 types of AF-first detected, recurrent, and lone.2 The goal of AF is to maintain heart rate or rhythm control and stroke prevention through anticoagulation. This in turn will improve symptoms, reduce morbidity from stroke or heart failure, and reduce mortality.3 For the purpose of this article, the recommendations for rate control and anticoagulation therapy for home maintenance will be discussed.

PATHOPHYSIOLOGY OF ATRIAL FIBRILLATION

Atrial fibrillation is a supraventricular tachycardia characterized by multiple rapid reentry impulses that lead to inadequate contractions and decreased emptying of the atria.4 Patients who have "valvular disease, dilated cardiomyopathy, aortic stenosis, hypertension, and coronary artery disease, undergo cardiac surgery, pulmonary disease, or use alcohol in excess or have alcohol withdrawal" are at increased risk of developing AF.4^(p26) Patients without symptoms of cardiac disease may have obesity, hyperthyroidism, diabetes, metabolic disorders, or obstructive sleep apnea as the precipitating cause of AF.5

A patient with cardiovascular disease has an increased risk of swelling and inflammation in the atrial tissue that leads to development of fibrosis. When fibrotic tissue is present, an erratic electrical conduction pattern can develop from foci within the atria.5 When a patient is experiencing multiple foci triggering randomly within the atria, a rapid ventricular rate can occur. This happens due to only half to one third of the impulses fired conducting through the atrioventricular (AV) node. With that small amount of impulses conducting, an irregular heart rate occurs along with a decrease in cardiac output due to decreased filling in the ventricles. If the patient remains in a rapid ventricular rate, they will develop clinical symptoms, hemodynamic compromise, and tissue and electrical damage within the atria.5

According to the American College of Cardiology and American Heart Association clinical guidelines, AF can be classified into 3 categories-first detected, recurrent/persistent, and lone.6 When the patient first presents with AF, a cause needs to be identified for proper treatment. A patient with recurrent AF has had 2 or more episodes where they are in sinus rhythm and then found in AF. Recurrent AF is further broken down into paroxysmal and permanent. Paroxysmal AF occurs but the patient converts back into sinus rhythm within 7 days of onset. Chronic or permanent AF lasts more than 7 days and does not respond to pharmacologic or nonpharmacologic treatment. Last, a patient who presents with lone AF is usually younger than 60 years and does not have any history of cardiovascular disease or hypertension, and the cause of the atrial fibrillation is unknown.4,6

Many patients do not know they have AF and are asymptomatic. Patients who present with symptoms can have minimal symptoms to very severe symptoms mimicking heart failure. When patients do experience AF symptoms, they commonly complain of shortness of breath, decreased exercise tolerance, palpitations, chest pain, or syncopal episodes. This is caused by the rapid ventricular rate that prevents the ventricles from filling appropriately and in turn causes hypotension and decreased oxygen transport to cells and the brain.5

Atrial fibrillation is diagnosed by an electrocardiogram (ECG) and the patient description of any symptoms. When interpreting an ECG, the absence of a discernible P wave is present along with a rapid rate of 350 to 600 bpm. The QRS complex and conduction through the ventricles are normal but the rate appears irregular because the AV node cannot keep up with the rapid rate firing from the atria.2,3 A patient may also have a cardiac ultrasonography performed to determine atrial enlargement or ventricular thickening and a Holter monitor to establish which type of AF they experience and effectiveness of heart rate control.

RATE CONTROL

Management of patients with chronic AF includes controlling the heart rate by decreasing the ventricular rate. This is accomplished with beta-blockers, calcium channel blockers, and digoxin.1 According to the American College of Cardiology and American Heart Association guidelines for AF management, the goal of heart rate control is less than 110 bpm in patients with persistent AF.6 Clinicians may choose rate or rhythm control to treat an AF patient depending on severity of symptoms, degree of cardiac disease, and age. Uncontrolled tachycardia can cause deterioration of ventricular function leading to tachycardia-induced cardiomyopathy. Rate control may also be preferred because antiarrhythmic medications have many adverse effects and can be proarrhythmic.7

BETA-BLOCKERS

Beta-blockers are antidysrhythmic agents that affect the heart in 3 areas. First, they reduce automaticity in the sinoatrial (SA) node; second, they slow conduction in the AV node; and third, they reduce contractility in the atria and ventricles. Beta-blockers block cardiac beta1 adrenergic receptors by decreasing sinus node discharge and suppressing transmission of atrial impulses in the AV node.8 Beta1 receptors are also coupled with calcium channels so that when a beta-blocker is administered it closes the calcium channels and decreases calcium channel influx. This lowers the ventricular rate and allows for more filling time of the ventricles and increased amounts of oxygen carrying blood to the tissues.8

Propranolol is a first-generation nonselective beta-blocker. It blocks beta 1 and beta 2 receptors creating a reduction in heart rate, decreased ventricular contraction, and suppressed conduction through the AV node. Because it is nonselective, it also affects the lungs by causing bronchoconstriction, the liver causing decreased glycogenolysis and blood vessels causing vasoconstriction. Propranolol can be given intravenously (IV) or orally and is highly lipid soluble so that it can cross cell membranes easily. It has a high first pass effect when taken orally, and only 30% of the medication is systemically circulated. Propranolol is widely distributed to all tissues and the central nervous system (CNS). It is metabolized by the liver and excreted by the kidneys. There are many adverse effects of propranolol. The main adverse effect is bradycardia due to the slowing of the AV conduction and heart rate. Other adverse effects are AV heart block caused by slowing conduction of AV impulses, heart failure from decreasing myocardial contractility, and rebound tachycardia caused by abrupt withdrawal. Because propranolol is nonselective, the beta 2 blocking ability can cause bronchoconstriction in the lungs; this medication is contraindicated in asthma patients because of bronchoconstriction. Propranolol also inhibits glycogenolysis in the liver, which can affect diabetic patients by not allowing the production of glucose and causing hypoglycemia when insulin is administered and also masking symptoms of hypoglycemia such as tachycardia.7,8

Metoprolol is a second-generation beta-blocker that mainly affects beta1 receptors of the heart. The action of metoprolol is similar to propranolol in that it decreases heart rate, contractility, and AV node conduction. Metoprolol can also be given IV or orally. It is highly lipid soluble and metabolized by the liver and excreted through the kidneys. Metoprolol also has a high first pass effect when taken orally so that only 40% of the medication circulates systemically. Metoprolol adverse effects are bradycardia, heart block, and rebound tachycardia, but because it only works on the beta 1 receptors it does not affect glycogenolysis or cause bronchoconstriction. Metoprolol can mask the symptoms of hypoglycemia in diabetic patients because it suppresses tachycardia.5,8

Patients who are prescribed beta-blockers for heart rate control need education regarding the adverse effects and potential complications. When a patient begins taking a beta-blocker, they need to be taught how to monitor their heart rate and blood pressure with administration and also monitor the effect of the medication. Diabetic patients need education on monitoring their glucose levels and not relying on their body to tell them when they may be hypoglycemic because beta-blockers mask signs of hypoglycemia. Patients should also be cautioned against abrupt discontinuation of a beta-blocker because of the potential for it to cause rebound tachycardia. If the patient is going to stop the medication, it needs to be slowly tapered. Patients should be advised to take the first dose at night and not to drive or perform other hazardous activities because of a large first pass effect that can lead to orthostatic hypotension. Patients should be taught to get up slowly from a lying or sitting position and of they feel dizzy or lightheaded to sit or lie back down.8

CALCIUM CHANNEL BLOCKERS

Diltiazem and verapamil are calcium channel blockers that work in vascular smooth muscle and the heart. Calcium channels in the heart regulate the myocardium, SA node, and AV node. They couple with beta 1 adrenergic receptors and allow calcium to flow in the cells. Calcium channel blockers inhibit calcium influx in the cells, cause decreased SA node automaticity, suppress AV node conduction, and decrease contractility. For patients experiencing AF, calcium channel blockers slow the ventricular rate and AV node reentry circuit.

Verapamil affects the heart and blood vessels in several different ways. It acts on the blood vessels by causing peripheral arteriole dilation that lowers blood pressure and increases coronary perfusion. It also blocks the actions of the SA node to decrease heart rate, blocks AV node impulses thereby decreasing AV conduction, and blocks calcium in cardiac muscle to decrease contractility. An indirect effect occurs when a patient takes verapamil, as verapamil lowers blood pressure and stimulates baroreceptors in the aortic arch to activate the sympathetic nervous system and release norepinephrine. This action neutralizes the effects of verapamil on the heart and leaves its primary action as vasodilation that increases coronary perfusion and lowers arterial pressures. Verapamil is administered IV or orally with a large first pass effect and only 20% of the medication circulating in the blood. It is eliminated through hepatic metabolism and dosages should be adjusted for patients with hepatic impairment.

Diltiazem is another frequently used calcium channel blocker. Its actions within the heart are the same as verapamil. It blocks calcium channels in the heart producing arterial dilation, which in turn is countered by the sympathetic reflex, and little affect is actually seen in the heart. Diltiazem is also administered IV or orally. Oral diltiazem is absorbed and metabolized through the liver; its first pass effect is around 50%. It begins working within 30 minutes and is excreted through urine and feces.8

Verapamil can cause constipation especially in elderly patients. Patients should be encouraged to increase fiber and fluid intake. Because of the vasodilatory effects of verapamil, edema in the extremities, dizziness, and headaches may occur. Patients should be cautioned to sit up or adjust positions carefully. Both verapamil and diltiazem can have cardiovascular effects in each area of the heart they affect. Bradycardia can occur from SA node suppression, AV node suppression causes heart block, and decreased contractility leads to heart failure. When patients are taking beta-blockers or digoxin with a calcium channel blockers, they need to be monitored closely for exacerbation of cardiac symptoms. Verapamil also increases the plasma levels of digoxin putting patients at increased risk of digoxin toxicity. Patients with sick sinus syndrome, heart failure, or heart block should not take a calcium channel blocker. Diltiazem can also cause a rash in elderly patients.8 Patients should notify their clinician if they experience bradycardia, weight gain, or peripheral edema.

CARDIAC GLYCOSIDE

Digoxin acts as a positive inotrope in the heart by increasing ventricular contraction when it inhibits the enzyme N+, K⁺-ATPase. When digoxin inhibits this enzyme, it helps to increase intercellular calcium that in turn acts on actin and myosin to increase contractility. Digoxin can also be affected by potassium in the cells. Digoxin and potassium compete with each other to bind to the N+, K⁺-ATPase. If potassium levels are low, the digoxin has increased binding, which increases the serum levels. If potassium levels are high, the digoxin does not bind as much with the N+, K⁺-ATPase and will not be as effective.8 Digoxin is prescribed to patients in AF because it decreases conduction in the AV node by direct suppression of it and it also acts on the CNS to increase parasympathetic impulses. Digoxin affects automaticity in the SA node by increasing parasympathetic flow and decreasing sympathetic flow in the node. This direct action slows the number of impulses that pass through the AV node and in turn slows the ventricular rate.8

Digoxin can initially be given in an IV loading dose and then be taken orally at home. It has a half-life of one and a half days, and it takes 4 half-lives to be excreted from the body. Digoxin has a variable rate of absorption between the different manufacturers. It is not recommended to switch brands because of this difference. Digoxin is mainly excreted through the kidneys, so patients with kidney impairment are at an increased risk of digoxin toxicity.

Digoxin has many adverse effects, and it can be affected by electrolyte balance with potassium. It has a narrow therapeutic range, and patients need to have their blood levels monitored closely. Patients also need to be taught symptoms of dioxin toxicity such as fatigue, gastrointestinal discomfort, anorexia, nausea, vomiting, blurred vision, or halos of light around objects. The most common adverse effect on patients taking digoxin is toxicity that induces dysrhythmias. Patients need to be taught how to take their apical pulse before administration; if the heart rate is less than 60, the dose should be held. Patients should also be taught not to double a dose if they have missed one, but to maintain compliance with the medication to prevent dysrhythmias from occurring. Patients should also take digoxin cautiously when they are also taking diuretics or angiotensin-converting enzyme inhibitors or angiotensin receptor binders because of the effects of potassium in the cells. Patients taking diuretics should also have their potassium levels monitored and be prescribed potassium-sparing diuretics and cautioned when taking potassium supplements.

RHYTHM CONTROL

When the goal of treatment is rhythm control, restoring sinus rhythm with medications or procedures occurs.1 Rhythm control is the first choice of therapy for patients younger than 60 years or when the patient in very symptomatic despite rate control. Once a regular rate in obtained, patients may need to take medications to keep their rate regular.

Amiodarone is often used for long-term rhythm control in AF patients. It works on the heart by delaying repolarization and delaying the action potential, with effects similar to potassium channel blockers. Amiodarone blocks sodium, calcium, and beta-receptors to decrease SA node automaticity and reduces contractility and AV node conduction. Amiodarone is lipid soluble and metabolized in the liver by CYP3A4 with an extremely long half-life of 25 to 110 days. There are many adverse effects of amiodarone with the main effect on the pulmonary system. Patients on amiodarone need to have a baseline chest x-ray obtained and pulmonary function tests. Because amiodarone is highly soluble, it crosses into all tissues and can cause interstitial lung disease, pulmonary fibrosis, and hypersensitivity pneumonitis. Patients may also develop corneal microdeposits that can cause blurred vision. Because amiodarone affects the AV node, SA node, and contractility, it also has adverse complications of bradycardia and heart failure.

Amiodarone has significant drug interactions especially with other antiarrhythmic agents such as digoxin, verapamil, diltiazem, quinidine, and statins. Adjunctive use of these medications with amiodarone often requires a reduction in their dosage. Amiodarone levels can be reduced by medications that block absorption or CYP3A4 inducers. Patient education should be focused on how to recognize symptoms of pulmonary, cardiac, or optic affects so that intervention can occur before too much damage is caused.1,8

Dronedarone is a new antiarrhythmic medication related to amiodarone but does not cause the adverse effects as amiodarone. It is a noniodinated benzofuran derivative with methane-sulfonyl that keeps it from being too lipid soluble. Because dronedarone does not contain iodine and is less lipid soluble than amiodarone, it is believed to not cause the pulmonary and thyroid complications of amiodarone.1

In the ATHENA study, dronedarone was shown to decrease paroxysmal or persistent AF and decrease hospitalizations related to cardiovascular complications. It has a half-life of 24 hours and is eliminated in the fecal system.3 Dronedarone is metabolized by the CYP3A4 system that inhibits CYP2D6. Administration of dronedarone is contraindicated with medications that are CYP3A4 inhibitors and can cause QT prolongation. If dronedarone is given with digoxin or statins, the dose of digoxin or statins should be decreased because of the CYP3A4 inhibition to prevent toxicity. Patients should be educated on the potential adverse effects of dronedarone such as nausea, diarrhea, and skin rash. Frequent ECG monitoring of the QTC interval is needed to determine prolongation. Dronedarone is contraindicated for use with patients having heart failure due to the QTC prolongation and decreased AV and SA node conduction pathways.6

EVIDENCE FOR STROKE PREVENTION WITH ANTICOAGULATION

Warfarin is the most commonly prescribed anticoagulant for AF. It is a vitamin K antagonist that has been shown to reduce the risk of stroke but has increased risk of hemorrhage. Warfarin has interactions with many foods and requires frequent monitoring, causing decreasing patient compliance and increasing discontinuation.9 Warfarin decreases production of vitamin K-dependent clotting factors VII, IX, X, and prothrombin. This inhibits VKORC1 enzyme that converts vitamin K to an active form. Warfarin is taken orally and binds to albumin in the blood. Warfarin is inactivated in the liver by CYP2C9 and excreted in urine and feces.8 Warfarin has a half-life of 11/2 to 2 days so a therapeutic range may not develop for 3 to 5 days requiring bridging with heparin or enoxaparin (Lovenox, Sanofi-Aventis, Bridgewater, NJ). Patients are monitored using the international normalized ratio range of 2 to 3. Warfarin also has a narrow therapeutic range, and strict adherence to diet and monitoring must be followed to avoid adverse effects.

The biggest adverse effect of warfarin is hemorrhage. Patients should be taught to be aware of bleeding from any area of the body and to seek medical assistance immediately. They should also be given instructions on dosage, time of administration, food and medications to avoid, and a schedule to have international normalized ratio checked. If they are going to be scheduled for surgery, they need to stop taking warfarin and bridge with a low-molecular-weight heparin therapy until told to resume warfarin.

Dabigatran is a new oral direct thrombin inhibitor. Once taken, it has a rapid onset of action where 80% is absorbed in the gastrointestinal tract and anticoagulation occurs within 2 hours with a half-life of 12 to 17 hours and is eliminated renally. Because of its renal excretion, dabigatran is not used in hemodialysis patients or patients with a creatinine clearance less than 15 mL/min.1 This eliminates bridge therapy for 3 to 5 days with heparin when warfarin is used. Dabigatran compared with warfarin in the RE-LY trial has demonstrated anticoagulation control that does not have the dietary restrictions or monitoring requirements of warfarin thereby increasing patient compliance.3 It does not interfere with CYP inhibition or induction like warfarin and is not inhibited by dietary intake. In the RE-LY study, dabigatran was shown to decrease risk of hemorrhagic stroke and major bleeding complications when compared with warfarin. Patients do need education for the adverse effects of dyspepsia due to tartaric acid in the dabigatran that decreases gastric pH levels to increase medication absorption.9,10

CONCLUSIONS

Atrial fibrillation is the most common arrhythmia found in older adults that places them at a high risk for stroke. Heart disease such as valvular disease, hypertension, heart failure, and coronary atherosclerosis leads to arterial dilation, which in turn can lead to AF. The main goal of treatment, whether controlling heart rate or rhythm, is to reduce hemodynamic symptoms and prevent development of thrombi. The best treatment for AF is prevention and early diagnosis. Patients who are at high risk for developing AF should be monitored closely and be given education regarding when to contact a medical provider for signs and symptoms of deterioration.