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    Atrial fibrillation: Nurses' guide to this common arrhythmia

    Rapid-fire impulses hijack the heart in atrial fibrillation


    ATRIAL FIBRILLATION is one of the most common arrhythmias in the United States.1,2 This arrhythmia, a supraventricular rhythm, affects up to 2.8 million people and costs over $1 billion in estimated healthcare costs annually.2 To discuss how an atrial fibrillation arrhythmia alters cardiac blood flow, we first must understand how normal electrophysiology works within the heart.

    For the body to operate effectively, a functioning heart must pump blood through the vascular system to perfuse body tissues. If the heart doesn't contract, oxygen and nutrients don't travel to body cells, and carbon dioxide and other waste products aren't released from body cells.

    Each heartbeat is a combination of electrical and mechanical impulses. The electrical impulses stimulate the mechanical contractions of the heart. Let's start with the mechanical portion, which stimulates the cardiac tissue to contract.3 At first, cells in cardiac tissue are at rest in a polarized state, with more potassium in the cell and the majority of the sodium outside the cell. When a cell is electrically stimulated, this electrolyte balance is altered by sodium rushing into the cell and potassium moving outside the cell. This change in intracellular electrolyte concentration causes cardiac contraction known as depolarization. Once the cell has depolarized, the cell uses active transport—sodium-potassium pump—to remove the sodium from the cell and allow potassium to return into the cell. This process is known as repolarization and brings the cell full-circle back to a resting polarized state, so it can start all over again. The process of depolarization and repolarization produces the waveforms that are captured on a cardiac monitor or electrocardiogram (EKG).3 Normally, the heart follows a specific pattern, which provides a smooth and coordinated contraction of cardiac tissue, resulting from electrical conduction that starts in the sinoatrial (SA) node.

    Known as the pacemaker for the heart, the SA node initiates the electrical impulse, which normally occurs between 60 and 100 times per minute in an adult. The impulse moves across the atria and depolarizes these cells, which is the atrial depolarization as seen as a P wave on an EKG. The impulse then travels down to the atrioventricular (AV) node, which conducts the impulse through to depolarize the ventricles. The ventricular depolarization is seen as the QRS complex on an EKG. It's a systematic and functional method to promote an organized contraction of the cardiac tissue.3 Although the SA node is the natural pacemaker for the heart, other cardiac cells can initiate an electrical impulse, though once an impulse starts, other cardiac cells will conduct that rogue or ectopic impulse across cell membranes of the cardiac tissue. Adhering to the same electromechanical properties as an appropriate impulse from the SA node, the ectopic impulse depolarizes cardiac tissue, but proceeds along an altered path from the normal SA node's conduction route. As the altered conduction route cycles, an irregular pattern of cardiac contraction transmits to the EKG. These rhythms will show various different electrical tracings on an EKG and are known as arrhythmias.2,3 The important thing to remember is that the cells that initiate the fastest electrical impulse are the cells that will control the heart rate. If some rogue atrial cells stimulate other atrial cells faster than the SA node is able to stimulate them, then these ectopic cells will be in charge of the heart's contractions.3

    ATRIAL FIBRILLATION By employing the foundation of cardiac conduction, it's time to tackle atrial fibrillation. In many cases of this specific arrhythmia, multiple areas of the atria fire simultaneously and quickly—some 300 to 600 sporadic atrial impulses per minute. Atrial cells are stimulated individually and do not allow for an organized depolarization through the atria muscle. Because of this, the atria does not contract as a unit, rather it quivers in a chaotic fashion. On an EKG, there will not be identifiable P waves. Instead, an undulating baseline with bizarre, rapid deflections off the baseline occur; these are known as F waves. The AV node works as a filter to protect the ventricles from being stimulated at this rate, so not all the atrial impulses are conducted through for ventricular depolarization. Since the problem is above the AV node, the conduction pattern for the ventricles is not affected and is conducted normally. So, an EKG will show a normal and narrow QRS for ventricular depolarization. With the continuous bombardment of impulse stimulation from the atria, the AV node is forced to protect the ventricular pumping mechanism by conducting only a portion of the impulses through to the ventricles, giving rise to an irregular rhythm. Because of this, there is no observable pattern to the ventricular impulses, which occur at irregular intervals and rates. So to put it all together, the EKG tracing in atrial fibrillation shows an uneven baseline with no identifiable P waves, and an irregularly irregular QRS pattern.2

    An additional concern with atrial fibrillation is the loss of atrial kick or normal atrial contraction. In normal sinus conduction, the atria and the ventricles fill with blood when they are in the resting phase known as diastole. When the atria are stimulated to contract—the phase known as systole—the blood is forced into the ventricles to help fill them up prior to ventricular systole and ejection from the heart. This final squeeze of blood moving from the atria into the ventricles is known as atrial kick. With atrial fibrillation, since the atria do not contract as a unit, atrial kick is lost, along with the additional stroke volume that it normally generates. This loss can decrease cardiac output by 20% to 30%.2

    RISK FACTORS/CAUSES As people age, the risk for developing atrial fibrillation increases—from less than 1% in individuals under 60 years old to more than 6% in individuals over 80 years old. Men tend to have a higher risk of developing atrial fibrillation than women, and at an earlier age. Atrial fibrillation often is associated with myocardial infarction, especially an anterior wall infarct. Individuals with a history of hypertension or heart failure are also at a greater risk for developing atrial fibrillation.2

    Other risk factors for atrial fibrillation include diabetes, coronary heart disease, mitral valve disease, atrial septal defect, alcohol excess, and hyperthyroidism.

    SIGNS AND SYMPTOMS Patients diagnosed with atrial fibrillation may present with signs and symptoms rang-ing from being completely asympto-matic to dangerously hemodynamically unstable. Signs and symptoms associated with atrial fibrillation include palpitations, anxiety, fatigue, malaise, exercise intolerance, and nausea. Dyspnea, dizziness, syncope, hypotension, chest pain, diaphoresis, and, in some cases, confusion and altered mental status are common. When patients exhibit signs of hemodynamic compromise, immediately implement adequate perfusion care procedures as outlined on your unit.2

    TREATMENT Atrial fibrillation treatment includes chemical or electrical cardioversion, anticoagulation, and ventricular rate control. Further treatment also may include catheter ablation with radiofrequency energy and possible surgery to maintain therapeutic goals. These goals are designed to maximize the cardiac potential of the heart, and include restoring the cardiac conduction pattern to a normal sinus rhythm and/or maintaining the ventricular rate to less than 100 beats per minute, decreasing symptoms associated with atrial fibrillation, and preventing potential complications such as thromboembolism, cerebrovascular accident (CVA), and tachycardia-associated myocardiopathy.4 Cardioversion typically treats new-onset atrial fibrillation, when the arrhythmia occurred within 48 hours.5 Another reason to cardiovert is if the patient is having symptoms, such as dizziness and weakness, from atrial fibrillation.