Trandate

Slow down and learn which drugs can decrease heart rate and threaten your patients cardiac output

Carlo Johnson, 52, is admitted to the telemetry unit after a fainting episode. When you assess him, he's hemodynamically stable, and the cardiac monitor shows third-degree heart block with a ventricular response of 40 to 50 beats/minute. Mr. Johnson takes several medications, including diltiazem (Cardizem CD) for hypertension, fluoxetine (Prozac) for depression, and cimetidine (Tagamet) for gastroesophageal reflux disease. Some drugs, such as the ones Mr. Johnson is taking, can cause cardiac arrhythmias in certain situations or when taken in excessive amounts. Before we review those that pose a risk, lets take a closer look at bradycardia.

Bradycardia and cardiac output

Bradycardia is a broad term that indicates a heart rate under 60 beats/minute. It encompasses the following arrhythmias:

* Sinus bradycardia occurs when the heart's normal pacemaker, the sinoatrial (SA) node, generates fewer than 60 impulses/minute. As long as the patient's blood pressure (BP) and cardiac output are adequate, sinus bradycardia doesn't pose a problem. Some patients receive cardiac medications to induce sinus bradycardia in order to decrease the heart's workload.

* A functional rhythm can occur if the SA node fails to fire and the atrioventricular (AV) node, the heart's secondary pacemaker, takes over to fire 40 to 60 impulses/minute.

* An AV heart block occurs if impulses have difficulty getting through the AV junction, which acts as the gatekeeper between the atria and the ventricles.

A heart block usually decreases ventricular respouse, often to less than 60 beats/minute.

* An idioventricular rhythm occurs when both the SA node and the AV node fail to initiate an impulse and the pacemaker cells of the ventricles take over. By far the least efficient pacemaker cells, they typically generate 20 to 40 impulses/minute.

If bradycardia doesn't cause signs and symptoms, the patient may not require treatment. But if it significandy reduces cardiac output, your patient will need treatment to restore hemodynamic stability. (To learn more about the role of heart rate, see What Determines Cardiac Output?)

When your patient's cardiac output is reduced, he may develop syncope, light-headedness, diaphoresis, chest pain, decreased BP, dyspnea, dizziness, fatigue, or palpitations. Your assessments may reveal signs of fluid retention, such as neck vein distension, crackles in his lungs, or an S3 heart sound due to fluid overload.

Now let's look at drugs that could affect cardiac output by decreasing heart rate.

Cardiac drugs that pose a risk

Cardiovascular medications that may trigger bradycardia include calcium channel blockers, betablockers, alpha/beta-adrenergic blockers, and digoxin.

Calcium channel blockers. Used to treat hypertension, arrhythmias, and angina, calcium channel blockers work by preventing calcium from entering cells through the slow calcium channels in the heart and blood vessels. This decreases contraction and causes vasodilation to decrease BP and relieve cardiac vasospasm.

Some calcium channel blockers, such as verapamil and diltiazem, affect the heart more than the vasculature to influence impulse conduction and decrease heart rate. Decreasing stimulation of the SA node limits the number of spontaneous impulses generated and slows impulse conduction through the AV node to decrease ventricular response. As a result, the patient is at risk for sinus bradycardia, functional rhythms, and second- and third-degree heart blocks.

Methods to combat bradycardia: If the patient is symptomatic, atropine and possibly a temporary transcutaneous pacemaker to increase heart rate; if symptoms are ongoing, possibly a temporary transvenous pacemaker.

Beta-blockers. Beta-receptor antagonists, better known as beta-blockers, combat hypertension, angina, cardiac arrhythmias, and myocardial infarction. Agents such as metoprolol (Lopressor) and atenolol (Tenormin) decrease heart rate and myocardial contractility by blocking epinephrine stimulation at betareceptor sites to decrease myocardial oxygen consumption and the hearts workload. Beta-blockers consist of two types: cardioselective agents block beta-receptors only in the heart; nonselective agents block beta-receptors in the heart, lungs, and vascular smooth muscle.

Methods to combat bradycardia: Dose adjustment of the beta-blocker (typically all that's needed); atropine or temporary transcutaneous pacing if the patient is hemodynamically unstable.

Alpha/beta-adrenergic blockers. Medications such as labetalol (Trandate) and carvedilol (Coreg) block both alpha- and beta-receptor sites to combat hypertension. (Carvedilol is also used for heart failure.) Blocking alpha-receptors on vascular smooth muscle causes vasodilation. A patient who's taking an alpha/beta-blocker has a risk of bradycardia, including heart blocks.

Methods to combat bradycardia: Decreased dosage for asymptomatic bradycardia; atropine if the patient is symptomatic; possibly a temporary transcutaneous pacemaker if the symptoms are severe.

Cardiac glycoside (digoxin). Indicated for heart failure, atrial fibrillation, and atrial flutter, digoxin is a positive inotrope, meaning it increases the force and velocity of myocardial contraction. It depresses the SA node and slows conduction through the AV node. If the patient's digoxin level becomes toxic, he'll develop severe bradycardia and his PR interval will prolong-a combination that could lead to advanced heart block.

Methods to combat bradycardia: Discontinuing the drug; atropine if the patient becomes symptomatic; possibly a temporary transcutaneous pacemaker. For life-threatening toxicity, digoxin immune FAB (Digibind) to inactivate circulating digoxin.

Noncardiac drugs that pose a risk

Certain drugs given for noncardiac conditions can pose similar risks for developing bradycardia. They include histamine^sub 2^ (H^sub 2^) blockers, lithium, certain antidepressants, and neuromuscular blockers.

H^sub 2^ blockers. The H^sub 2^ blockers cimetidine (Tagamet) and famotidine (Pepcid) decrease acid production and are used to treat gastrointestinal ulcers, esophagitis, and gastric esophageal reflux disease. They work by inhibiting histamine at the Hz receptors on parietal cells and on the vascular endothelium. In rare cases, patients receiving cimetidine or famotidine rapidly by intravenous (I.V.) push have developed sinus bradycardia and AV block.

Method to combat bradycardia: Prevention by following the manufacturer's instructions for administering these medications I.V.

Lithium. Used to control mania, lithium can lead to dysfunction of the sinus node, causing sinus bradycardia and possibly syncope. However, patients whose serum lithium level is less than 1.5 mEq/liter seldom have adverse reactions.

Methods to combat bradycardia: Monitoring for decreased heart rate; warning the patient to report any episodes of light-headedness, dizziness, or fainting; reducing the dosage or discontinuing the drug.

Antidepressants. Tricyclic antidepressants (TCAs) such as amitriptyline have been known to slow intraventricular conduction, which is manifested by prolonged PR, QRS, and QT intervals. And reports have been increasing that chronic treatment with selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, can cause arrhythmias. Adverse reactions are rare but significant.

Method to combat bradycardia: Close monitoring of patients with a history of cardiac disease who take TCAs or SSRIs.

Neuromuscular blockers. Rapid-acting neuromuscular blockers such as succinylcholine are commonly used as a paralyzing agent during tracheal intubation. They stimulate both the autonomic ganglia and muscarinic receptors and may cause changes in cardiac rhythm, including bradycardia.

Method to combat bradycardia: An anticholinergic agent, such as atropine.

Teach caution

Any one of Mr. Johnson's medications-or a combination-could have decreased his heart rate and caused his syncope. To protect a patient who's taking a drug that could cause bradycardia, teach him the signs and symptoms. Tell him how to monitor his pulse rate and when to call the primary care provider to report a problem.

With a solid understanding of which drugs can trigger bradycardia, you can help ward off problems and protect your patient if one develops.

SELECTED REFERENCES

2001 Mosby's Guide, 11th edition. St. Louis, Mo., Harcourt Health, 2001. Drug Facts and Comparisons. St. Louis, Mo., Facts and Comparisons, Inc., 2001.

Fisher, D.: "Clinical Pharmacology of Neuromuscular Agents," American Journal of Health System Pharmacists. 56(Suppl.): S4-S9 1, June 1, 1999.

Pacher, R, et al.: "Speculation on Difference between Tricyclic and Selective Reuptake Inhibitor Antidepressants on Their Cardiac Effects. Is There Any?" Current Medical Chemistry. 6(6):469-480, June 1999. Roth, L.: Mosby's Nursing Drug Reference. St. Louis, Mo., Mosby, Inc., 2002.

ANNEMARIE PALATNIK, RN, CS, MSN, AND ROSEMARY KATES, RN, CCRN, BSN

AnneMarie Palatnik is a clinical nurse specialist at Our Lady of Lourdes Medical Center and teaches pharmacology at Our Lady of Lourdes School of Nursing, both in Camden, NJ. Rosemary Kates is a clinical educator at Our Lady of Lourdes Medical Center.

Copyright Springhouse Corporation Aug 2002
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