A 32 year old male with a history of chemotherapy-induced cardiomyopathy on furosemide and chronic tachycardia on metoprolol presents as an outside hospital transfer for possible heart failure.
On arrival here, BP is 110/70, HR 140, sat 99%.
On exam he is sitting comfortably in the stretcher without respiratory distress or lower extremity edema.
Bedside ultrasound, however, shows dilated atria and ventricles, severely decreased EF, and a plethoric IVC without respiratory variation. He has diffuse B lines.
Further history and workup is concerning for CHF exacerbation. In the ED, his HR has remained in the 140’s…
Beta blocker use in heart failure:
Beta blockers are well known to reduce mortality in heart failure by preventing detrimental effects of catecholamine stimulation including elevated heart rate, increased myocardial energy demands and adverse remodeling. However, when used in acute heart failure exacerbation, beta blockers may lead to hemodynamic collapse.
There are three key questions to ask yourself before administering beta blocker therapy in the ED in CHF:
- Is my patient stable or unstable?
- Is my patient severely overloaded or only mild to moderately overloaded?
- Is my patient showing evidence of hypoperfusion?
- For unstable patients, patients with severe volume overload, or patients with evidence of hypoperfusion: withhold beta blockers.
- For stable patients, patients with only mild to moderate overload, and patients with no evidence of hypotension or hypoperfusion: beta blockers may be given at home dose or ½ of home dose cautiously.
Support for the continuation of beta blockers in stable CHF exacerbations comes from the OPTIMIZE-HF program and the Italian Survey on Acute Heart Failure. Withdrawal of beta blocker therapy was associated with increased mortality, as compared to continuation of such therapy. Also, the American College of Cardiology/American Heart Association guidelines recommend continuing the beta blocker if the exacerbation is primarily secondary to fluid overload without hemodynamic instability.
Of note, these guidelines/recommendations are for patients that are already on beta blockers. It is not recommended to start a beta blocker naïve patient on beta blockers during their exacerbation in the ED.
It is critical to recognize that most of these recommendations and guidelines do not refer to addressing the patient’s state on initial ED presentation. On initial presentation, it is important to consider whether or not a patient’s tachycardia is a compensatory response required to maintain their pressure in a severe exacerbation. Only after a thorough assessment and workup, once it is determined that the patient is stable and the exacerbation is mild, is it appropriate to consider resuming beta blocker therapy.
The patient received metoprolol for HR remaining in the 140’s, as he had missed his home dose that day, had a stable blood pressure, and had unclear severity of fluid overload. However, within 30 minutes of receiving metoprolol, his HR decreased to the 100’s from 140 and his blood pressure dropped to the 70’s systolic. The patient ultimately required inotropic support and diuresis in the ICU.
The bottom line:
The case above demonstrates how tenuous patients with congestive heart failure can be. A seemingly stable patient can quickly flip into cardiogenic shock if the severity of the heart failure exacerbation is underestimated. In the ED, physicians often have only a brief snapshot of a patient, and it can be difficult to accurately assess a patient’s degree of clinical decompensation from baseline. Beta blockers reduce long term mortality and can safely be given in a non-severe exacerbation, but in most CHF exacerbations in the ED they should be withheld as their short term efficacy is questionable. Withholding them in the ED can prevent accidental loss of the patient’s compensatory sympathetic drive in an exacerbation. Allow the inpatient team to assess the patient’s trajectory and administer beta blockers if needed.
The featured image for this post was taken from Wikimedia Commons. The original author is James Heilman, MD.