Bosen, Diane M. MSN, RN, APRN-BC, CCRN
ATRIAL FIBRILLATION (AF) is the most common sustained dysrhythmia encountered in clinical practice settings, affecting healthcare costs and patient quality of life, and posing the risk of death from heart failure or stroke.1 This article reviews the mechanisms of AF, its clinical manifestations, and pacing therapies.
AF can occur in patients with or without diagnosed heart disease (see Clinical conditions associated with AF). In AF, numerous areas in the atria are stimulated at different rates, so depolarization can't occur normally. This disorganized atrial depolarization interrupts normal atrial mechanical contraction and places the patient at increased risk for thrombus formation and stroke.
A patient with AF usually has decreased cardiac output because of the loss of synchronous atrial mechanical activity (atrial kick). The patient may experience signs and symptoms such as chest discomfort, dyspnea, palpitations, near-syncope or syncope, dizziness or lightheadedness, fatigue, or orthostatic hypotension. Pulmonary edema secondary to reduced diastolic filling time, increased myocardial oxygen demands, or functional impairment of the ventricle may be an initial sign of AF with an uncontrolled ventricular rate (higher than 100 beats/minute).
The treatment priority for AF is rate control rather than rhythm control.2 A poorly controlled ventricular rate may lead to dilated ventricular cardiomyopathy, also known as tachycardia-induced cardiomyopathy, with subsequent heart failure.
Pharmacologic therapy is the first-line treatment; multiple drugs may be needed to maximize rate control. Unfortunately, patients may not achieve rate control if the maximum recommended dosage of the medication doesn't control the responsiveness of the atrioventricular (AV) node, and if the patient can't tolerate the medication, doesn't adhere to the medication regimen, can't afford the medication, or has comorbid conditions that limit therapy. Patients with chronic obstructive pulmonary disease (COPD), for example, may not be able to tolerate the beta-blockers typically used to optimize rate control.
Setting the pace
For patients who don't achieve ventricular rate control despite optimal medical therapy, and for patients with an intractable dysrhythmia, atrial pacing can be combined with drug therapy. This treatment isn't a primary treatment.
The choice of atrial pacemaker depends on the desired outcome, and various pacing protocols are available to treat AF. Atrial pacing may have an antiarrhythmic effect; on the other hand, ventricular pacing may be more proarrhythmic.3
Some studies suggest that AF may be initiated by a premature beat or may be the end result of a bradydysrhythmia. By controlling the atrial rate with pacing, AF may be prevented. The pacemaker may prevent a bradydysrhythmia or suppress a premature beat through overdrive pacing—that is, initiating a paced rate that's higher than the patient's intrinsic rate. Patients with an intrinsic heart rate less than 60 beats/minute are more likely to benefit from pacing therapy to prevent bradycardia-induced AF.
Different types of atrial pacemakers may be used.
* A single-lead atrial pacemaker is rarely used because other, more effective options are now available. However, a single-lead pacemaker can be used to directly stimulate the right atrium if indicated, with the lead positioned in the high right atrium.
* A biatrial pacemaker positions a lead in each atrium and stimulates both simultaneously. This shortens intra-atrial conduction delays, corrects atrial dyssynchrony, and may reduce the frequency or degree of conduction blocks. The pacemaker leads may be placed in the high right atrium and the distal coronary sinus, which indirectly paces the left atrium. Biatrial pacing is preferred over single-lead atrial pacing, but may not have any benefit over AV sequential pacing (more on this shortly).3
* A dual-site atrial pacemaker positions two leads in the right atrium. This type of pacemaker is preferred to single-lead atrial pacing because it's more effective in achieving rate control. The dual-site pacemaker also reduces left-sided AV delay, resulting in improved atrial filling and improved atrial kick. When dual-site pacing is used, the leads are positioned near the septum, near the ostium (opening) of the coronary sinus, or in the area of Bachmann bundle.3
* Dual-chamber pacing or AV sequential pacing paces the right atrium and right ventricle sequentially, mimicking normal cardiac physiology and preserving atrial kick. AV sequential pacing also can reduce the frequency and degree of conduction blocks.4
* Right ventricular pacing. Some studies suggest that ventricular pacing alone may be detrimental because the loss of atrial kick may produce negative hemodynamic effects.5 Also, ventricular pacing alone may predispose the patient to AF. Right ventricular pacing has been shown to increase the risk of death or exacerbate heart failure in patients who have left ventricular systolic dysfunction (that is, an ejection fraction less than 35%). Right ventricular pacing also can worsen mitral regurgitation in patients with valvular disease.5
Atrial pacing also may be used to terminate an atrial tachycardia that could deteriorate to AF. Therapies include atrial overdrive pacing and an implantable atrial cardioverter defibrillator.
Atrial overdrive pacing paces the atrium at a rate higher than the patient's intrinsic rate, then gradually decreases the pacing rate. Because the atrial rate can reach well over 200 beats/minute without pharmacologic therapy, atrial overdrive pacing is used in combination with drug therapy. However, this type of therapy may not be well tolerated by patients because the increased heart rates pose the risk of hypotension and syncope.2
An implantable atrial cardioverter defibrillator may be used alone or in conjunction with ventricular defibrillation. When an atrial defibrillator is used, two atrial defibrillation leads are used: one coil is placed in the right atrium and the other in the distal coronary sinus. Tiered shock therapy can be delivered with moderate discomfort to the patient, so the use of this therapy is limited. Generally one to two shocks are needed to convert AF into normal sinus rhythm. Complications associated with device implantation include surgical-site infection and bleeding. This treatment is indicated for patients who can't tolerate pharmacologic therapy, and who aren't candidates for ablation or in whom ablation wasn't effective.3
Ablate and pace
Radiofrequency ablation of the AV node and implantation of a permanent pacemaker, a technique known as "ablate and pace," may be used in patients who aren't candidates for curative procedures such as surgical ablation. This therapy also may be used in the 10% of patients with AF who are severely symptomatic and either are intolerant or fail to respond to pharmacologic therapy, or have a refractory dysrhythmia.
The ablate and pace procedure leaves the patient fully dependent on the pacemaker. However, if a rate-responsive pacemaker is used, the patient's heart rate will adjust to accommodate exercise or increased respiratory effort as well as periods of rest.
Another advantage of the ablate and pace procedure is that the patient's cardiac output and cardiac performance are optimized (and therefore quality of life is improved) without the adverse effects of drug therapy. The patient may have improved exercise tolerance, and because no long-term drug therapy is needed, the procedure is cost-effective. Compared with other atrial pacing therapies, ablate and pace is easy to perform and less likely to cause complications. Although not a cure for AF, it is palliative therapy.2
Biventricular pacing has been shown to be more effective than right ventricular pacing alone with the ablate and pace strategy, and is the preferred pacing modality for patients who've undergone AV node ablation.6
Caring for your patient
If pacing is used for AF, monitor your patient's response to therapy and assess his cardiac rhythm for appropriate pacemaker sensing and capture depending on the type of pacing used.
Notify the patient's healthcare provider if the patient develops recurrent AF or the pacemaker doesn't function properly.
If your patient had AV node ablation and the pacemaker fails to capture, be prepared to perform CPR and initiate transcutaneous pacing.
Patients with AF requiring pacing therapies may need anticoagulation therapy. Teach patients about anticoagulation, including the need for frequent monitoring (prothrombin time and international normalized ratio), signs and symptoms of bleeding and stroke, and when to contact a healthcare provider.2
By understanding the types of atrial pacing, you can help your patient deal with this common dysrhythmia.
Clinical conditions associated with AF2
* systemic hypertension
* coronary artery disease (especially of the right coronary artery)
* heart failure
* valvular heart disease (especially mitral)
* cardiac surgery
* left atrial enlargement
* rheumatic heart disease
* congenital heart disease
* sick sinus syndrome
* Wolff-Parkinson-White syndrome
* degeneration of the conduction system
* electrolyte imbalances
* acute alcohol intoxication
* parasympathetic (vagal) or sympathetic nervous system imbalances
* pulmonary disease such as COPD
* septic or febrile illness
* toxins including cocaine and caffeine
* genetic predisposition
* advanced age
* pulmonary embolism
1. Josephson ME. Clinical Cardiac Electrophysiology. 4th ed. Philadelphia, PA: Wolters Kluwer Health; 2008.
2. Natale A, ed. Handbook of Cardiac Electrophysiology. London, UK: Informa Healthcare; 2008.
3. Ellenbogen KA, Wilkoff BL, Kay GN, Lau CP. Clinical Cardiac Pacing, Defibrillation, and Resynchronization Therapy. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2007.
4. Fogoros RN. Electrophysiology Testing. 4th ed. Malden, MA: Blackwell Publishing; 2006.
5. Zipes DP, Jalife J. Cardiac Electrophysiology, From Cell to Bedside. 5th ed. Philadelphia, PA: Elsevier Saunders; 2009.
6. Doshi RN, Daoud EG, Fellows C, et al. Left ventricular-based cardiac stimulation post AV nodal ablation evaluation (the PAVE study). J Cardiovasc Electrophysiol. 2005;16(11):1160–1165.
© 2011 Lippincott Williams & Wilkins, Inc.