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Bradycardia: Slow heart rate? Think fast!

Hayes, Denise D. RN, CRNP, MSN

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Author Information

Denise D. Hayes is clinical editor of Nursing2004 and CriticalCareChoices2004 and an ACLS instructor.

The author has disclosed that she has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

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Abstract

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.

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What causes slow cardiac rhythms?

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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.

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Types of bradycardias

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

Sinus bradycardia originates in the SA node and is characterized by a heart rate less than 60 bpm. Remember that the normal resting heart rate in many people, including physically fit athletes, is less than 60 bpm. The key is whether the bradycardia triggers serious signs and symptoms.

Junctional escape rhythms originate in an escape or secondary pacemaker in the AV junction and produce a heart rate of 40 to 60 bpm. This type of bradycardia occurs when the rate generated by the patient's dominant or primary pacemaker (usually the SA node) decreases to the point where it's less than the rate generated by an escape pacemaker in the AV junction (AV node and bundle of His). A junctional escape rhythm can also occur when electrical impulses originating in the SA node or atria don't reach the AV junction, as in third-degree AV block.

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Ventricular escape rhythms originate in an escape pacemaker in the bundle branches, Purkinje network, or ventricular myocardium with a heart rate of less than 40 bpm. This type of bradycardia usually occurs when a patient's dominant pacemaker rate, as well as the AV junctional escape pacemaker rate, is less than the rate of the ventricular escape pacemaker. It can also occur when electrical impulses originating in the SA node, atria, and AV junction don't reach the ventricles, as in third-degree AV block.

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AV blocks generally refer to delays or interruptions of electrical impulse conduction through the AV junction. AV blocks can be classified according to either the degree or site of the block.

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Partial AV blocks include first-degree AV block, second-degree type I AV block, and second-degree type II AV block. Complete AV block is also referred to as third-degree AV block. When classified according to site, blocks can be intranodal, occurring at the level of the AV node, or infranodal, occurring below the AV node in the His-Purkinje system of the ventricles (bundle of His, bundle branches, and Purkinje network).

Along with type II second-degree AV block, third-degree AV block is considered a “red flag bradycardia” that's likely to deteriorate to ventricular asystole, even if your patient's asymptomatic.

* First-degree AV block refers to a constant delay in electrical impulse conduction from the atria to the ventricles, usually at the level of the AV node. This block is characterized by abnormally prolonged PR intervals that are usually constant; for example, a PR interval constantly greater than 0.2 second.

* The most common causes of first-degree AV block include medications that increase the refractory time of the AV node, such as calcium channel blockers, beta-blockers, and digoxin. Other causes include enhanced vagal tone, intrinsic AV nodal disease, and acute MI, especially inferior-wall MI.Some patients with a first-degree AV block have a normal heart rate. This type of AV block usually requires no treatment, but it can progress to a higher degree of AV block.

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* Second-degree AV block is a conduction disorder in which some P waves fail to conduct to the ventricle and generate a QRS complex. There are two types of this AV block.Type I second-degree AV block (also called Wenckebach or Mobitz I) refers to a progressive delay in electrical impulse conduction through the AV node, until a point is reached when conduction is completely blocked. It's characterized by a progressive prolongation or lengthening of the PR interval, causing a progressive shortening of the R-R interval until a QRS complex fails to occur after a P wave. This is referred to as a nonconducted P wave or dropped beat. Usually only a single impulse is blocked, followed by a repeat of the pattern of progressive PR lengthening and dropped beat. Type I second-degree AV block is usually transient and reversible but, like first-degree AV block, may progress to a higher degree of AV block. Common causes of this type of block include enhanced vagal tone, acute inferior-wall MI, and medications such as digoxin, beta-blockers, and calcium channel blockers.

* Type II second-degree AV block (also called Mobitz II) refers to a blocking of electrical impulse conduction at or below the level of the AV node. This type of block usually involves a complete block in one bundle branch with an intermittent block in the other bundle branch. As a result, the QRS complex typically appears abnormal. However, although rare, the block can occur at the bundle of His level, and in these cases the QRS may look normal.Type II second-degree AV block commonly occurs as a result of extensive damage to the bundle branches; for example, following an acute anteroseptal MI. Unlike type I second-degree AV block, it's characterized by the sudden, unexpected presence of a dropped beat or nonconducted P wave without prior lengthening of the PR interval. This type of block can rapidly progress to third-degree AV block and therefore is more serious than type I second-degree AV block.

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* Third-degree AV block refers to the complete interruption of electrical impulse conduction between the atria and the ventricles. This block may occur at the level of the AV node, bundle of His, or bundle branches and is characterized by atrial and ventricular rhythms that are independent of one another. This type of block may be transient and reversible or permanent (chronic).

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* Third-degree AV block associated with normal QRS complexes and a heart rate of 40 to 60 bpm (junctional escape rhythm) may be transient and reversible and is commonly due to complete block at the level of the AV node. This type of AV block may be secondary to an acute inferior-wall MI and usually is associated with a more favorable prognosis than a third-degree AV block below the level of the AV node and with a ventricular escape rhythm (wide and bizarre-appearing QRS complexes and a heart rate of 30 to 40 bpm or less). A ventricular escape rhythm is commonly due to complete block involving both bundle branches (for example, following an acute anteroseptal MI) and indicates extensive infranodal conduction system disease.

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See The Brady Bunch: ECG Clues to Slow Rhythms for a summary of the similarities and differences of bradycardias.

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Dealing with bradycardia

To care for a patient with bradycardia who isn't in cardiac arrest, follow the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Here's how you'd use these guidelines to intervene for Ms. Brock and Mr. Young.

After obtaining a 12-lead electrocardiogram (ECG) on Ms. Brock, the cardiologist identifies her cardiac rhythm as sinus bradycardia. A physical assessment reveals no serious signs or symptoms related to her bradycardia, and the cardiologist orders no treatment for her asymptomatic bradycardia. You communicate the assessment findings to the radiology nurse who'll be caring for Ms. Brock during her biopsy, which will be guided by computed tomography.

Ms. Brock tolerates the biopsy well without complications and is discharged later that day.

Mr. Young, however, presents a much different situation. Keep in mind that the initial stabilization of a patient with symptomatic bradycardia usually isn't difficult. Check his responsiveness and remember your ABCs. While the nursing assistant calls for additional help, you assess Mr. Young's level of consciousness. Although he responds to his name, he's lethargic and breathing spontaneously but rapidly, at 26 respirations/minute and labored. His carotid pulse is readily palpable, but slow and regular. You call a code because of the possibility of cardiopulmonary arrest.

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The code team arrives with emergency equipment, including the crash cart and monitor/defibrillator. You place Mr. Young in a supine position because of his hypotension, and a respiratory therapist supports his airway and provides supplemental oxygen.

Another nurse inserts a large-bore intravenous (I.V.) line in Mr. Young's antecubital vein and starts an infusion of 0.9% sodium chloride solution. You connect Mr. Young to the cardiac monitor while another staff member connects him to the pulse oximeter and automatic noninvasive BP machine. His BP is 70/50, and his heart rate is 40 bpm. The physician identifies his cardiac rhythm as a junctional escape rhythm.

The physician completes a brief, targeted history and focused physical examination and considers possible treatable causes for the bradycardia. Meanwhile, you prepare to administer 0.5 mg of I.V. atropine and ask one of your colleagues to get the transcutaneous pacemaker from the crash cart.

The physician orders a dopamine infusion in case Mr. Young's heart rate doesn't respond adequately to atropine and transcutaneous pacing (TCP) and also orders a stat 12-lead ECG, portable chest X-ray, and arterial blood gas analysis.

Because Mr. Young is experiencing serious signs and symptoms secondary to his bradycardia, and his 12-lead ECG shows no signs of an acute MI, atropine is the initial drug of choice. Classified as a parasympatholytic or anticholinergic, atropine can restore normal SA nodal automaticity (increasing sinus node rate) and AV nodal conductivity through its direct vagolytic action. It's the initial drug of choice to treat symptomatic bradycardia in patients with a pulse. But because areas of the heart that aren't innervated by the vagus nerve won't respond to atropine, this drug isn't indicated for type II second-degree AV block or third-degree AV block. Also, denervated transplanted hearts won't respond to atropine, so immediately use pacing or catecholamine infusion (such as epinephrine) or both.

When used to treat bradycardia during a suspected acute MI, atropine may actually worsen ischemia or cause tachyarrhythmias including ventricular tachycardia and ventricular fibrillation.

In a non-cardiac-arrest situation, administer atropine I.V. push in doses of 0.5 to 1 mg, repeating the doses at 3- to 5-minute intervals until the patient's heart rate increases or signs and symptoms of hemodynamic compromise are resolved. The maximum dose (total vagal blockade) of atropine is 0.04 mg/kg of body weight. Remember that doses less than 0.5 mg in adults may result in a paradoxical bradycardia, which could further compromise your patient and trigger cardiac arrest.

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Following a total dose of 2 mg of I.V. atropine (Mr. Young weighs 154 pounds [70 kg]), his ventricular rate increases slightly to 50 bpm, with minimal improvement in his signs and symptoms. He remains in a junctional escape rhythm.

Unfortunately, within a few minutes, his heart rate drops to 30 bpm and his clinical status deteriorates further. Looking at the cardiac monitor, you note that Mr. Young is now in third-degree AV block. As discussed earlier, third-degree AV block is characterized by a complete lack of conduction of electrical impulses through the AV node, bundle of His, and bundle branches. As a result, the atria and ventricles contract independently of each other, a condition called AV dissociation. New, symptomatic complete heart block requires emergency cardiac pacing.

Although sometimes not as readily available as atropine, TCP is indicated for all symptomatic bradycardias, especially if atropine may be contraindicated because of a higher-level AV block or myocardial ischemia. In fact, TCP should supersede atropine if your patient is severely bradycardic and critically unstable.

In certain clinical settings where atropine may not be indicated for symptomatic bradycardias, TCP should be considered a first-line intervention. Transcutaneous pacing also is useful for “standby pacing” for clinically stable patients who are considered at risk for developing hemodynamically compromising bradycardias, especially those with myocardial ischemia or infarction.

In Mr. Young's case, because of the ease and speed of application, the initial pacing method of choice is transcutaneous. (See The Pros and Cons of TCP for more on this method.) Most conventional monitor/defibrillators have built-in TCP capabilities.

You quickly attach the pacing electrodes to Mr. Young's anterior chest wall and prepare to use TCP as a therapeutic bridge device until transvenous pacing is possible. Connecting Mr. Young to the transcutaneous pacer by external adhesive pads allows him to be paced as well as defibrillated if necessary. The pacing option typically provides both fixed (asynchronous) and demand (synchronous) pacing modes. Usually when the pacer is turned on, a preset rate, output setting, and mode are activated. These programmed settings can be easily adjusted according to your patient's clinical status.

After both electrical and mechanical capture are verified, Mr. Young improves dramatically. His heart rate is now 70 bpm, and his BP is gradually increasing to 110/60.

Because it's not unusual for patients to experience discomfort with each transcutaneously paced beat, assess Mr. Young's need for cautious analgesia or sedation or both. Prepare to transfer him to the coronary care unit for more therapy, including a transvenous pacemaker.

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What would you have done if TCP hadn't been successful or if it weren't available and the bradycardia didn't respond to atropine? A dopamine infusion is usually indicated as a pharmacologic therapeutic bridge to transvenous pacing. Dopamine, a catecholamine, is a precursor of norepinephrine, which has a strong sympathetic action on the heart and peripheral blood vessels.

The usual dosage for symptomatic bradycardia is 5 to 20 mcg/kg/minute. Start at 5 mcg/kg/minute and quickly increase the dose if hypotension is associated with the bradycardia. Dopamine at 5- to 10-mcg/kg/minute doses enhances myocardial contractility and increases heart rate, BP, and CO. At doses of 10 to 20 mcg/kg/minute, it causes peripheral arterial and venous constriction and is used to treat hypotension with signs and symptoms of shock. Dopamine is contraindicated in hypovolemic patients until after volume replacement.

If your patient is experiencing severe bradycardia with hypotension, or if higher doses of dopamine aren't working, the drug of choice is epinephrine as an infusion at a recommended dosage of 2 to 10 mcg/minute.

Although isoproterenol is also classified as a catecholamine, use it with extreme caution because of the risk of peripheral vasodilation and increased myocardial oxygen consumption, which would only further compromise your patient. In patients with symptomatic bradycardia (except those with denervated transplanted hearts), isoproterenol at doses of 2 to 10 mcg/minute should be cautiously considered only after your patient fails to respond to atropine, TCP, dopamine, and epinephrine or as a temporizing measure until TCP or transvenous pacing is available. See Which Drug to Use to Treat Symptomatic Bradycardia for more information.

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Back up to speed

By being able to recognize various bradycardias and knowing how to manage them appropriately, you may be able to protect your patient from further hemodynamic compromise, including cardiac arrest.

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The pros and cons of TCP

Advantages

* Least invasive pacing method

* Can be quickly instituted at the patient's bedside

* No vascular puncture required

* No fluoroscopic guidance required

* Easily instituted by trained nonphysician health care providers

* Can pace and defibrillate through the same cutaneous electrodes

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Disadvantages

* Pacemaker may fire but heart may not contract (non-capture).

* Treatment may mask underlying treatable ventricular fibrillation, although this is rare because of advances made in transcutaneous pacing (TCP) technology

* Prolonged TCP may cause tissue damage.

* Chest wall contractions may be painful, requiring analgesia or sedation.

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SELECTED REFERENCES

Braunwald, E. (ed): Heart Disease: A Textbook of Cardiovascular Medicine, 6th edition. Philadelphia, Pa., W.B. Saunders Co., 2001.

Huszar, R.: Basic Dysrhythmias: Interpretation and Management, 3rd edition. St. Louis, Mo., Mosby, Inc., 2001.

International Consensus on Science: “Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation. 102(8, Suppl 1):I-1–I-384, August 22, 2000.

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