SAN FRANCISCO — The increased use of β-blockers may be contributing to a proportionate increase in pulseless electrical activity in cardiac arrest, Dr. Scott Youngquist reported in a poster presented at the 12th International Conference on Emergency Medicine.
His retrospective study concluded that patients whose presenting rhythm was pulseless electrical activity (PEA) were five times as likely to be taking a β-blocker as those presenting with ventricular fibrillation—a finding that raises questions about the presumed causes and treatment of PEA arrest.
“We know that β-blockers prevent patients from going into ventricular fibrillation,” Dr. Youngquist said in an interview. “But patients who have [ventricular fibrillation] as a presenting rhythm in cardiac arrest can often be shocked back into a normal rhythm. Unfortunately, there's often not much you can do for someone in PEA. The outcome is usually very poor. Furthermore, β-blockade may thwart the one medication we have: epinephrine.”
Both β-blocker use and presenting PEA in cardiac arrest have increased over the past 20 years, said Dr. Youngquist, now at the University of Utah, Salt Lake City. β-Blockers are now the fourth most-commonly prescribed medication for hypertension, and about 60% of post-MI patients at all hospitals are discharged on β-blockers.
At the same time, however, PEA has gone up as well. In the 1980s and 1990s, ventricular fibrillation (VF) accounted for up to 60% of all out-of-hospital cardiac arrests in the United States. Now, VF accounts for only about 25% of arrests, Dr. Youngquist said, and the reason is unclear.
Dr. Youngquist and his colleagues theorized that the temporal association between the two trends might be more than coincidental. They performed a chart review of 478 out-of-hospital cardiac arrests that presented to Harbor-UCLA Medical Center, Los Angeles, from 2001 to 2006. Most of the patients (59%) were male; the median age was 70 years.
The researchers excluded the records of patients for whom β-blocker status was unknown and for those who arrived in asystole, leaving them with a final cohort of 179; 100 (56%) of these presented with PEA and 79 (44%) with VF. Overall, 65 (36%) were taking β-blockers and 114 (64%) were not.
Significantly more patients presenting with PEA than VF were on β-blockers at the time of their arrest (49% vs. 20%). In a univariate analysis, patients taking a β-blocker were almost four times as likely to present with PEA as they were to present with ventricular fibrillation. After adjustment for misclassification of β-blocker use, confounding, and random error, the odds ratio rose to five.
Although the results are interesting, they raise as many questions as they answer. However, “if larger studies confirm this, they may suggest that we need to change the way we treat the patient in PEA,” Dr. Youngquist said.
For example, glucagon is typically used to reverse a β-blocker overdose, he added, and there are some animal studies that suggest glucagon also may be useful in treating PEA.