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Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Management of AF is a highly nuanced clinical scenario that involves considerations of AF type, duration, patient history, patient goals, and potential sequelae and manifestations in the cardiovascular system as well as other systems. There are many potential management options for AF within conventional medicine, and these options are further expanded by the addition of natural or complementary and alternative (CAM) therapies.
AF is a disturbance of the normal conduction of electricity in the heart. The sinoatrial (SA) node is the normal pacemaker of the heart. It is situated in the right atrium of the heart near the junction with the superior vena cava. The SA node releases an impulse of depolarization (electricity) that is conducted through both the right and left atrium, causing them to contract. The impulse makes its way down to the atrioventricular (AV) node at the junction between the atria and the ventricles. The AV node collects this depolarization, holds it for about a fifth of a second, and then releases the electricity down into the ventricles.
The atria and ventricles are electrically isolated from one another. The only way for electricity from the upper rooms of the heart (the atria) to get down to the lower rooms of the heart (the ventricles) is through the AV node and the normal conduction system. The conduction system is the "wiring" of the heart. Its job is to conduct electricity in a rapid and organized fashion from the SA node to the AV node and then down through the lower conduction pathways to the ventricles.
The problem in AF is that the SA node has lost control of the pace of the heart. The atria are beating disorganizedly and rapidly, which is to say fibrillating. Because of this rapid, disorganized beating, electrical impulses are only making it through the AV node and down to the ventricles every so often and with irregular timing. As a result, the systolic ejection of the heart (the pulse) becomes erratic.
There are several methods for classifying AF. While pathological and molecular classifications will play an important role in our clinical strategies, the first decisions to be made in the clinical setting of a case of acute AF typically hinge upon the heart rate (the pulse).
At the most basic, we can classify AF as having a controlled ventricular response or a rapid ventricular response. If the heart rate remains under 110 beats per minute (bpm), we consider the ventricular response to be controlled. If the heart rate is over 110 bpm, we consider the ventricular response to be rapid.1
Rapid ventricular response to AF can be immediately life-threatening. The higher the heart rate, the more immediately concerned we are about heart failure.2 It does not take long, in some cases less than 24 hours, for a heart in a sustained rapid rate to begin failing. The heart simply does not have enough time to fill and eject completely when the rate is so fast for so long. The signs and symptoms of this type of heart failure are typically identical to other types of systolic failure (shortness of breath, orthopnea, pulmonary edema, peripheral edema, fatigue). The difference is simply that the failure is not a result of a weak pump, but rather the result of a pump that is working too fast.
This brings up our first important clinical point: the radial pulse is not a reliable indicator of the heart rate when a patient is in AF. Due to the irregularly irregular timing of the ventricular ejection, not every contraction of the heart causes an equal volume of blood or strength of pulse to reach the periphery. Moreover, because the rate is irregularly irregular, if the pulse per minute is estimated from a 15- or 30-second pulse count, the estimate of the heart rate can be very different from the actual because the number of beats over any period of time is not regular. Therefore, it is of the utmost importance to document the heart rate in AF by listening to the heart and counting the number of beats over a full minute as they occur at the cardiac apex. If this can be done several times over a visit and the pulse from multiple measures averaged, an even better estimate of ventricular response can be ascertained.
For example, a recent patient presented to us in AF. His radial pulse was 60 bpm, by palpation and a finger tip pulse oximeter also read his heart rate as 60 bpm; his oxygen saturation as 99%. When counting his apical pulse by auscultation, the patient's actual heart rate was 90 bpm. The radial pulse was only receiving 66% of the heart's impulses. Moreover, we have a completely different assessment of the patient's rate control and potential for complications when the resting rate is 90 bpm as opposed to 60 bpm.
A rapid ventricular response to AF must be controlled to prevent heart failure. For the majority of CAM providers and midlevel practitioners, AF with rapid ventricular response is a condition that warrants referral to the emergency department, the patient transported there by another person or by EMS. The decision about how to control the rapid heart rate depends upon the heart rate, duration and type of AF with which we are dealing, and the present complications.3
The most useful clinical classification of AF (other than the ventricular response) is based on the instances and durations of the arrhythmia. We classify instances and durations as lone, paroxysmal, persistent, or permanent.4-6
A lone episode of AF is just that, it is a first-time episode. It is typically treated by returning the heart to a normal sinus rhythm. There may never be another episode of the arrhythmia thereafter or not for many years.
Paroxysmal AF describes an arrhythmia that comes and goes. The episodes (paroxysms) are short, often less than 24 hours and certainly less than 7 days. The heart may be converted back to normal sinus rhythm (NSR) by interventional means, but often returns to NSR spontaneously.
Persistent AF is a circumstance in which the duration of arrhythmic episodes become quite long, usually lasting more than 7 days and sometimes months or years. Persistent AF may still spontaneously convert back to NSR, but as the duration of the episodes becomes longer and their instances more frequent, intervention is more often required to return the heart to normal rhythm.
The saying goes, "AF begets AF," and this is certainly the natural history of the condition. The longer and more often the heart is in AF, the more its anatomy becomes deranged, typically beginning with enlargement of the atria. As the atria enlarge, the conduction system becomes distorted and AF episodes typically begin to occur more frequently and last for longer periods. It becomes progressively more difficult to return the heart to a normal rhythm and the heart does a progressively poorer job of staying out of AF.7
Permanent AF is defined by the point at which we accept AF as the new "normal" rhythm of the heart and give up on attempts to return the heart to NSR. Patients can live a long, happy, and otherwise healthy life in permanent AF as long as their two largest risk factors are controlled; namely, those risks are rapid heart rate and thromboembolic risk.
While in AF, the contractions of the atria are disorganized. As a result, the blood within the atria is not moved through them efficiently. Rather, the blood pools, eddies, and becomes stagnant, especially near the walls of the atria. The stagnation of blood greatly increases the probability for a clot to form within the atrium. Along the wall of the atrium (especially within the small alcove of the left atrium called the left atrial appendage) it is possible for very large clots (thrombi) to form. This is the primary underlying etiology for an increased risk of thromboembolic events in AF, especially strokes.
If a clot forms on the left side of the heart, then breaks loose and enters the systemic circulation (an embolism), it will become lodged in the first artery that it reaches that is smaller in caliber than it is itself. If that artery is in the brain it will cause and ischemic stroke, but the clot could become lodged anywhere in the circulatory system.
The risk of thromboembolic events begins to rise within the first 5 hours of an episode of AF and reaches maximum risk within 72 hours.8,9 This fact forms the basis of much of the decision making around when, how, and if an attempt to convert the heart back to normal rhythm will occur.
If the heart is returned to normal rhythm, the risk of heart failure and thromboembolic events is dramatically reduced. If the heart cannot be returned to normal rhythm, then it is mandatory that we control the accompanying risk factors. Therefore, we say that the basic management strategy in AF is to (1) convert the rhythm (if possible and safe), (2) control the rate, and (3) prevent thromboembolic events.10
Cardioconversion, or cardioversion, is the term for our attempt to return a heart from a state of arrhythmia back to normal sinus rhythm. Cardioversion can be achieved by any of several methods. In AF, the most reliable method of conversion is to use a moderate level (50–200 joules) direct current electrical shock (delivered to the heart while the patient is under sedation) to reset the electrical conduction of the heart. This kind of shock causes all of cells of the heart to depolarize at the same time. Since the SA node (the natural pacemaker of the heart) is the part of the heart that resets the fastest it typically resumes beating first and is thereby able to resume control of the heart rate and rhythm.
This process of electrocardioversion has a high success rate at first, but its success rate decreases as episodes of AF get longer and the left atrium gets larger. It does not prevent the heart from returning to AF or prevent the need for subsequent conversions.11-14
Other conventional management techniques are available to attempt to return the heart to a normal rhythm and keep it there. These techniques include procedural, surgical, medical, and device therapies based on individual circumstances; and all of these are the purview of conventional cardiologists, especially electrophysiologists who subspecialize in cardiac dysrhythmias.
Sometimes the very process of bringing the AF rate under control with medication causes rhythm conversion. Most frequently this occurs in the emergency department with delivery of intravenous (IV) rate control drugs such as beta blockers or certain calcium channel blockers, though on occasion we have seen it happen in the outpatient setting with delivery of the same drugs by oral administration.
There are several methods available to attempt to convert the cardiac rhythm using natural interventions and CAM therapies. As a word of caution: conversion is not a process to be undertaken without due consideration. The process of conversion can cause an existing blood clot in the heart to become dislodged and enter circulation, resulting in an embolic event that can be far more serious than the arrhythmia itself. This is why, when the duration of the present episode of AF is unknown, the conventional standard of care requires weeks to months of anticoagulation therapy prior to any attempt at cardioversion.3
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