When beta-blockers aren't the drug of choice

Nursing, Oct 1996 by Holcomb, Susan Simmons

Can you recognize when therapy goes awry?

Earlier today, Mrs. Elbert, 82, was admitted to your hospital's telemetry unit with a diagnosis of aortic stenosis and coronary artery disease (CAD). She's scheduled for a cardiac catheterization in the morning as part of an evaluation to plan her treatment.

Last month, Mrs. Elbert had an anterior wall myocardial infarction (MI), which was treated with thrombolytic therapy. At the time, she was taking nifedipine (Procardia XL), 60 mg once a day, for hypertension. Her physician switched her to the beta-blocker atenolol (Tenormin), 50 mg once a day, because of the benefits beta-blockers offer during the acute period of an MI and for the first 3 months afterward (see The Case for Using BetaBlockers after an MI).

Mrs. Elbert's other medications include nitroglycerin 0.2 mg patch; aspirin, 81 mg daily; and furosemide (Lasix), 20 mg daily.

The monitor technician notifies the nurse that Mrs. Elbert has had two episodes of sinus arrest lasting 2.3 seconds (shown below) and 3 seconds. Sinus arrest is a prolonged failure of the sinoatrial (SA) node to initiate an impulse. When mapping out the P-P or R-R intervals, you'll find more than one PQRST complex missing. Note the length of the arrest in seconds because prolonged and frequent episodes can lead to decreased cardiac output, hypotension, dizziness, and syncope.

The nurse places Mrs. Elbert on oxygen at 2 liters/minute by nasal cannula, per unit protocol. After assessing Mrs. Elbert and obtaining a stat 12-lead electrocardiogram (ECG), she notifies the cardiologist. She reports that Mrs. Elbert's vital signs are stable and that she has no shortness of breath (her Spo2 is 97%), chest pain, or light-headedness while on bed rest.

The 12-lead ECG confirms sinus rhythm with first-degree atrioventricular (AV) block (the PR interval is longer than 0.2 second) and occasional sinus arrests, 2 to 3 seconds long.

The physician decides to move Mrs. Elbert to the intensive care unit (ICU) for closer observation. He also discontinues the atenolol, which he believes may have caused her AV block. He switches her to captopril (Capoten), 12.5 mg every eight hours. He tells her she may need a permanent pacemaker if her abnormal rhythm continues or worsens.

DISTINGUISHING HEART BLOCKS

After Mrs. Elbert has spent 4 uneventful hours in the ICU, you hear her monitor alarm and notice the rhythm shown below. You identify it as second-degree AV block with 2:1 conduction. In this rhythm, conduction from the SA node is intermittently blocked at the AV junction and can't reach the ventricles. Mrs. Elbert's 2:1 conduction pattern means that every other SA node impulse is blocked; these blocked impulses appear on the ECG as P waves not followed by QRS complexes. When an impulse is able to complete the pathway, normal-looking sinus complexes are formed with a constant PR interval.

In second-degree AV block with 2:1 conduction, P waves and QRS complexes are regular. In type I second-degree AV block, the QRS complex is usually within normal limits; in type II, it's wide.

Second-degree AV block with 2:1 conduction is dangerous because it can progress to complete heart block or the ratio of nonconducted beats to conducted beats may increase. In either situation, the ventricular rate and cardiac output could drop dangerously.

Beta-blockers and calcium channel blockers can cause second-degree AV block. Other causes include CAD, anterior and inferior wall MI, acute myocarditis, and valvular heart disease.

ASSESSING YOUR PATIENT

After hearing the alarm, you immediately go to Mrs. Elbert's bedside to assess her airway, breathing, and circulation. She has no complaints of chest pain or shortness of breath, but admits to feeling slightly weak and light-headed. Her blood pressure is 160/90 with a ventricular rate of 36 to 42, and her Spo2 is 97%.

She's stable for the moment, so you obtain a stat 12-lead ECG and page her cardiologist. (Had Mrs. Elbert been more symptomatic with her bradycardic rhythm, you would have continued to follow the advanced cardiac life support bradycardia algorithm.)

The ECG confirms the rhythm findings, but doesn't show any acute changes that suggest myocardial ischemia. When the physician calls, he decides to reschedule Mrs. Elbert's cardiac catheterization for this afternoon and insert a temporary transvenous pacemaker because of her unstable rhythm.

During the cardiac catheterization, Mrs. Elbert's physician finds a left anterior descending lesion and proximal circumflex lesion; both vessels are almost 90% occluded. Her aortic stenosis is mild and doesn't require further intervention. She returns to the ICU with a temporary transvenous pacemaker.

The day after her cardiac catheterization, Mrs. Elbert spontaneously converts to sinus rhythm with a rate of 70. The rest of the day is uneventful.

Two days later (after the atenolol has cleared and her rhythm is under control), she undergoes percutaneous coronary angioplasty to unblock her diseased coronary arteries. The next day, the angioplasty sheaths and temporary transvenous pacemaker are removed. She has no further AV blocks and is soon discharged home.