Bradycardia: Slow heart rate? Think fast!

Nursing,  2004  by Hayes, Denise D

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A slow heart rate can be life-threatening. Find out when to intervene-and how.

Mr. Young, 64, is admitted to your unit for treatment of worsening heart failure secondary to left ventricular systolic dysfunction. He's been experiencing increasing dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, and poor exercise tolerance. He also admits to "feeling faint off and on" over the past 2 weeks. His medications include enalapril, furosemide, carvedilol, and digoxin. He has no known drug allergies, and his medical history is significant for anteroseptal myocardial infarction (MI) and hypertension.

This morning, one of the nursing assistants calls you to assess Mr. Young after he "almost passed out" while she helped him out of bed. You enter the room and find him awake but complaining of feeling very weak. His skin is pale, cool, and diaphoretic. He's tachypneic and dyspneic; his apical heart rate is 40 beats/minute (bpm) and regular, and his BP is 70/50.

Ms. Brock, 46, is admitted to your short-procedure unit for a CT-guided percutaneous needle biopsy of a recently discovered liver mass. Her medical history is unremarkable, and she takes no medications, with the exception of over-the-counter multivitamins. During your admission assessment, you note that her heart rate is regular at 50 bpm, her BP is 110/60, and her respirations are 14 and unlabored. Her skin is warm and dry, and she denies discomfort, with the exception of feeling nervous about the biopsy scheduled for later that morning. When discussing her daily activities, she tells you that until recently, she's been an avid jogger.

Although both of these patients have heart rates less than 60 bpm (referred to as absolute bradycardia), the clinical significance and management of their slow heart rates will differ dramatically. A slow heart rate alone tells you very little about either patient. The key is to look beyond the number to see the entire picture because your nursing interventions will be guided by the severity of the clinical situation.

Besides the absolute bradycardia illustrated by these two cases, patients may also experience relative bradycardia. This means that although a patient's heart rate is above 60 bpm, he still may be experiencing serious signs and symptoms related to low cardiac output (CO). For example Mr. Collins, 49, who's been taking propranolol, becomes hypotensive because of blood loss secondary to acute gastrointestinal bleeding. In order for him to maintain an adequate CO, compensatory mechanisms normally include an increased heart rate. However, because of the beta-blocker's effects, his heart rate can't adequately increase. As a result, his heart rate relative to his BP and to the underlying cause or condition is too low. Even though Mr. Collins' heart rate is 65 bpm, he's experiencing relative bradycardia.

In clinical practice, not only must you determine if your patient is experiencing severe signs and symptoms, but you must also determine if these serious signs and symptoms result from his slow heart rate. Significant signs and symptoms of hemodynamic compromise include decreased level of consciousness, shortness of breath, chest pain (or anginal equivalent), dizziness, diaphoresis, syncope, hypotension, and pulmonary congestion. Your rapid nursing assessment and appropriate interventions in the setting of symptomatic bradycardia with a pulse may prevent further deterioration in your patient, including cardiac arrest.

What causes slow cardiac rhythms?

These abnormally slow heart rates can be caused by alterations in the ability of cardiac cells (for example, the sinoatrial [SA] node) to spontaneously generate electrical impulses (automaticity), alterations in the ability of cardiac cells (for example, the atrioventricular [AV] node) to conduct electrical impulses (conductivity), or alterations in both automaticity and conductivity.

Bradycardias can also be a result of autonomic influences; for example, increased parasympathetic or decreased sympathetic tone. Other causes include hypothermia, hypoxia, hypothyroidism, acidosis, and electrolyte imbalances such as hyperkalemia.

Bradycardias may also be induced by certain drugs, such as digoxin, beta-adrenergic blockers, or calcium channel blockers. Acute infections such as myocarditis, as well as chronic degenerative changes in the bundle branches associated with the aging process, also can cause slow heart rates in your patient.

Sinus bradycardia is often beneficial following an acute MI because it decreases myocardial oxygen demand, potentially limiting infarct size. However, once heart rate decreases CO to the point where the patient becomes symptomatic, the risk of bradycardia outweighs its benefits.

If acute MI is causing symptomatic bradycardia, the guidelines for emergency cardiac care recommend treating the original pathology (the MI) instead of bradycardia that may be caused by the MI.

Types of bradycardias

Bradycardias are a class of arrhythmias that include sinus bradycardia, junctional escape rhythms, ventricular escape rhythms, and AV blocks.