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Surgery for Atrial Fibrillation

AORN Journal, July, 2007 by Patricia C. Seifert, Jill Collins, Niv Ad

Approximately 2.3 million people in North American and 4.5 million people in the European Union suffer from atrial fibrillation (AF), (1) a supraventricular cardiac rhythm disturbance characterized by uncoordinated, rapid atrial contractions of up to 350 or more impulses per minute. These rapid atrial contractions produce an irregular ventricular response rate that can vary from 130 to 150 or more beats per minute. This chaotic cardiac rhythm affects normal movement of blood through the heart, diminishes cardiac output, and increases the person's risk for thromboembolic stroke as a result of stasis of blood in the atria. (2)

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Atrial fibrillation was documented as early as 1906, when Cushney and Edmunds (3) studied venous and arterial pulse tracings that demonstrated irregularities of the heartbeat. Using an electrocardiograph machine invented by Einthoven four years earlier, Cushney and Edmunds recorded the first electrocardiogram (ECG) of AF. (3) The ECG remains the primary diagnostic test for AF.

ANATOMY AND PHYSIOLOGY

The heart's electrical conduction system (Figure 1) coordinates cardiac contractile force, heart rate, and stroke volume and allows these to be adjusted individually or collectively in order to maintain an adequate cardiac output. Individual cardiac myocytes, however, have the intrinsic ability to contract (ie, contractility) and to initiate an action potential (ie, automaticity). In normal sinus rhythm (Figure 2), the process of excitation and contraction originates in the sinoatrial (SA) node--the heart's natural pacemaker--which is located at the junction of the superior vena cava and the right atrial wall. The electrical impulse initiated by the SA node travels through internodal tracts that carry the electrical signal to the atrioventricular (AV) junction that houses the AV node, located medial to the entrance of the coronary sinus in the right atrium, close to the tricuspid valve.

[FIGURES 1-2 OMITTED]

The impulse generated by the SA node is delayed briefly in the AV junction, allowing the atria time to contract and generate the P wave on the ECG. Atrial contraction contributes 30% more blood to the right and left ventricles in addition to the blood passively draining into the ventricles from the venae cavae and the pulmonary veins, respectively. (4) Atrial contraction also promotes self-washing of the left atrial endocardium, in particular, and reduces the potential for pooling of stagnant blood that can lead to intra-atrial thrombus formation. The formation of an intra-atrial clot as a result of the loss of effective contraction and atrial stasis increases the likelihood of a thromboembolic event. (5)

From the AV junction, the impulse spreads to the bundle of His, which extends down the right side of the interventricular septum. The bundle divides into the right and left bundle branches, which terminate in a network of fibers called the Purkinje system. The Purkinje fibers are spread throughout the inner surface of both ventricles and the papillary muscles, which when stimulated, produce contraction of the heart muscle. (6,7) If the SA node fails to initiate a signal, the AV node assumes the function of pacemaker, albeit at a slower rate, and generates an impulse.

ELECTROPHYSIOLOGY OF ATRIAL FIBRILLATION

In patients with AF, an impulse may be generated by the SA node, but that impulse is interrupted by cells in the atrium discharging electrical impulses, which interrupts normal conduction. As a result of this re-entry mechanism, multiple, uncoordinated atrial impulses are generated from ectopic foci faster than the SA node impulse and supersede the normal SA impulse; these ectopic impulses produce random and chaotic pathways to form an irregularly irregular ventricular response. (6) There is no effective atrial contraction and no obvious P wave. Occasionally, atrial electrical activity may be seen on the ECG as small undulations called f waves (Figure 3); but more often, the ECG does not illustrate organized or consistent atrial electrical wave forms. The atria may discharge 300 to 600 beats per minute. Most of these impulses do not pass the AV junction to stimulate the ventricles, but the ventricular response can be 100 to 160 beats per minute in untreated patients with normal AV conduction. In patients with abnormal AV conduction, a greater number of impulses may pass into the ventricles, producing ventricular tachyarrhythmias and increasing the risk of ventricular fibrillation. (8)

[FIGURE 3 OMITTED]

Historically, the irregularity of AF was attributed to random, multiple wavelets generated throughout the atria that propagated new (ie, daughter) wavelets to create the re-entry mechanism. In studying the characteristics of conduction in general, and in AF in particular, that could lead to a surgical treatment for AF, Cox and other early researchers found that electrical impulses cannot cross areas of the heart that have been incised and sutured (Figure 4). (5) This finding encouraged Cox et al (5) to develop the first Maze procedure in which multiple incisions were made and sutured in such a way as to interrupt the aberrant impulses within the atrium (Figure 5). These incisions allow the SA node to initiate and propagate its impulses throughout the atria to the AV node via the pathway created by the Maze incisional lesions. (9)

Health Care Industry

Surgery for Atrial Fibrillation

AORN Journal, July, 2007 by Patricia C. Seifert, Jill Collins, Niv Ad

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