Term Paper: Atrial Fibrillation as a Post Operative Complication

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Atrial Fibrillation as a Post Operative Complication

Atrial Fibrillation and Heart Surgery

Atrial fibrillation represents a serious post-operative complication in many types of heart surgery. Nearly 40% of all patients undergoing coronary and valve surgery experience this side effect (Saltman, 2004). Post operative atrial fibrillation is an enigma that remains refractory to both pharmacologic and nonpharmacologic attempts at prevention (Saltman, 2004). Reducing the incidence of atrial fibrillation (AF) is a serious concern for heart surgeons in all types of heart surgery. The following will explore the mechanisms that trigger AF, risk factors, monitoring procedures, and new treatments aimed at reducing the occurrence of post operative AF.


One of the key reasons for the ineffectiveness of procedures to minimize AF is a lack of understanding surrounding the mechanism that triggers it (Saltman, 2004). AF is a serious arrhythmia that has recently been classified as a reentrant arrhythmia. In order for a reentrant arrhythmia to occur, two conditions must be met. The first is that there must be some even that initiates the reentrant circuit. There must also be a substrate available that is capable of maintaining the arrhythmia. Understanding these two conditions will help us to develop methods to prevent and control this arrhythmia by short-circuiting either the initiating event or the maintenance event.

First, let us look at the initiation event in the arrhythmia cycle. The initiation event occurs when excitable tissue demonstrates unidirectional conduction block and slow conduction (Saltman, 2004). Unidirectional block occurs when an excitation wave can no longer penetrate tissue in a normal manner. Prolonged refractoriness as is the result of an excitation wave that encounters cell that have not recovered their full excitability potential (Saltman, 2004). Slow conduction occurs when an excitation wave is restricted long enough to permit abnormal tissue to recover excitability. This typically sets the stage for retrograde reentry of the excitation wave (Saltman, 2004).

This is the sequence that triggers normal atrial fibrillation. The only difficulty is determining if this reentry sequence is the culprit behind post operative atrial fibrillation or if some other mechanism is responsible. It is not difficult to imagine how a properly timed impulse may encounter refractory tissue in some areas and normal tissues in others after the trauma of surgery (Saltman, 2004). Atrial fibrillation can be heralded by frequent premature atrial contractions and bursts of atrial tachychardia (Frost et al., 1995). Saltman surmises that these contractions are the likely agents that set up the unidirectional block.

Slow conduction presents a slightly different mechanism. It results from a decrease in cell to cell coupling and a decline in the rapid inward Sodium current. This condition is unusual in normal atrial tissue. Recently, it was discovered that the inflammatory mediator, arachidonic acid can reversibly depress the conduction up to 60% less than the baseline in normal canine and human atrial tissues (Saltman, et al., 2002). This suggests that post-surgical inflammation may alter the normal atrial electrophysiology in such a way as to initiate slow conduction.

However, this effect is only seen in a direction that is transverse to the fiber's long axis, with no effect apparent parallel to the long axis (Saltman, et al., 2000). This suggests that there is no change in the properties of depolarizing sodium ion currents or repolarizing potassium currents (Saltman, 2004). This led to the application of steroidal and non-steroidal anti-inflammatory drugs for the prevention of fibrillation in sterile talc pericarditis in animals (Saltman, et al., 2000). Research demonstrates that inflammatory markers are particularly increased in patients that exhibit post operative atrial fibrillation (Chung, et al., 2001). These findings would lead us to suspect that an agent in the inflammatory cascade is to blame, but at the current time, which one or the exact mechanism is not known.

Janse, (1997) found that atrial fibrillation is associated when the atrial muscle is enlarged or stretched. This stretching may cause electrophysiological changes that could be attributed to the effects seen in reentry sequence. According to Janse, an acute stretch might cause action potential shortening. The effects of an acute stretch may be different from those experienced in a chronic stretch. Refractory periods were found to be shorter in human atrial tissue that had been stretched. These findings offer a plausible explanation for atrial fibrillation after heart surgery. It was also found that atrial fibrillation begets atrial fibrillation. Once the heart starts fibrillating it tends to develop a vicious cycle that is difficult to stop (Allesse et al., 1998).

These mechanisms explain how AF may be initiated, but it must be sustained to develop into an episode. In order for the AF to achieve continue to perpetuate, the reentrant circuit must be small enough to fit within the confines of the affected tissue (Saltman, 2004). In chronically fibrillating atrial tissue the conduction velocity was found to be normal, yet the refractory period is greatly shortened (Allessie et al., 1998). This same study also found that once the heart returned to normal rhythm the risk of atrial fibrillation increased.

The mechanisms of initiation of atrial fibrillation are only suspected at this point and even less is known about the maintenance mechanism. However, it appears that many agree that postsurgical changes in the atrium are responsible for making it susceptible to both the initiation and maintenance of this arrhythmia (Saltman, 2004).

Risk Factors

Several risk factors have been identified that place a person in the general population at risk for atrial fibrillation. The first factor is that the risk of AF increases with age. More men than women tend to develop AF. Factors such as diabetes, hypertension, congestive heart failure, and valve disease were also found to be major contributors to the risk of atrial fibrillation (Benjamin, et al., 1994). Body mass index and alcohol use were not found to be factors in the development of AF in this study in the original analysis. However, a reexamination of the cohorts used in the study did reveal a correlation between atrial fibrillation and obesity (Iacobellis, 2005).

As we found, stretching and inflammation place a person at greater risk of developing AF. However, cardiovascular diseases including hypertension, coronary disease, and heart failure also place a person at greater risk for AF (Benjamin, et al., 1994). This same study also indicates that interventions meant to treat these conditions also decrease the risk of AF in a patient. The results of this study raise some important questions. The first is whether the patient that develops AF as the result of a surgical procedure may have been at greater risk than the normal population because they already had an underlying condition before the surgery. The second is that the risk of post operative AF may be reduced by eliminating some of the risk factors associated with it.

Koray et al., (2005) found that several preoperative histopathologic factors could be identified that increased the risk of post operative atrial fibrillation. Chronic obstructive pulmonary disease was found to be the only reliable predictor for post operative atrial fibrillation. Those that developed post operative atrial fibrillation were found to have larger sized myolytic valves than those that maintained a normal rhythm. In a study of patients undergoing coronary bypass surgery there was no difference between those that had on-pump and off-pump procedures (Mariscalco, 2006). This study did concur with Koray and associates that pre-existing histopathologic changes in the right atrium increase the chances of post operative AF.

Leung et al. (2004) found that impairment of the left atrium was a significant predictor of post operative atrial fibrillation (also in Osranek and Associates, 2006). Left Atrial Volume Predicts the Risk of Atrial Fibrillation After Cardiac Surgery: A Prospective Study J. Am. Coll. Cardiol., August 15, 2006; 48(4): 779-786.. This study found that similar changes occurred in the elderly population that were seen post operatively in the surgical patients.

The process of the development of AF is not completely understood. However, these structural anomalies associates with increased risk of AF may provide clues to this elusive mechanism. Studies are concentrating on discovering the mechanism that drives AF. Guler et. al., (2007) found that an increase in AngII and the decrease in SubP after may be a factor in postoperative AF.


Better monitoring of patients after heart surgery of any type has led to decreased lengths of stay. Electrocardiogram is the most frequently used form of monitoring. This type of monitoring increases the likelihood that the atrial fibrillation will be detected and managed quickly and effectively. In 1991 the presence of atrial fibrillation increased the stay in intensive care from 1.9 to 3.6 days in intensive care (Loew et al., 1991). Research studies provide the best indication of how monitoring and length of stay have decreased since 15 years ago.

2002 study revealed that the presence of AF after surgery increased the average hospital stay by a total of 5.5 days (Thompson et al., 2002). A meta analysis of studies regarding the effectiveness of post operative treatments for AF revealed that the most common monitoring regime currently being… [END OF PREVIEW]

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