We present a case of intraoperative paradoxical bradycardia following administration of epinephrine. This phenomenon is counterintuitive to the cardiovascular effects typically observed. Recognition of this potential hemodynamic effect can help the pediatric anesthesiologist promptly treat an unfavorable decrease in heart rate.
An eight-day old, 0.65kg male neonate prematurely born at 25 weeks via emergency Cesarean section for pre-eclampsia and non-reassuring fetal heart rate presented with pneumoperitoneum and suspected perforated bowel. He arrived intubated for emergent exploratory laparotomy. As the case progressed, mean arterial pressure (MAP) had decreased below 10% of starting values, and infusions of normal saline (12mL total) and pRBC (10 mL/kg) were started in efforts to improve the blood pressure. Heart rate remained stable in low 180’s. Calcium (6mg) was given which transiently improved MAP. The MAP continued to deteriorate with no change in heart rate. Epinephrine 0.5mcg was administered when the systolic blood pressure was in the mid 30s. The heart rate immediately dropped to 61 with an increase in the systolic blood pressure to 55-60 mmHg; CPR was immediately started to ensure adequate cardiac output along with 100% oxygen. Within one minute, the heart rate improved to 108 and the systolic blood pressure had increased into the 70s (43). The procedure concluded soon afterward without further derangement of vitals.
One explanation for bradycardia following exogenous epinephrine includes medication error. It was confirmed postoperatively that the medication that induced profound bradycardia in this case was indeed epinephrine and at the correct dilution, with an administered dose of 0.5 mcg. Most case reports of incorrect epinephrine dosing are based on overdose with subsequent hypertension and tachyarrythmias, not paradoxical bradycardia (1).
Another possibility is reflex bradycardia from a sudden increase in alpha agonism, systemic vascular resistance, and baroreceptor-mediated suppression of sympathetic tone on sinoatrial node automaticity (2). A gradient of receptor agonism occurs along the spectrum of plasma epinephrine levels with dynamic receptor activation. Low dose epinephrine is mostly beta active, with beta-2 mediated vasodilation as well as beta-1 increase in myocardial contractility. Alpha activation increases at higher doses. Typical doses of exogenous epinephrine exceed this varying receptor response and simultaneously stimulate alpha as well as beta receptors, causing vasoconstriction and increased heart rate/contractility, respectively (3).
A third differential for bradycardia would be Bezold-Jarish reflex (BJR). The combination of peripheral vasodilation, subsequent venous pooling and an under-filled left ventricle, in addition to hypercontractility, can result in the (BJR). Inhibition of sympathetic tone and augmented parasympathetic influence on the heart induces profound bradycardia; this is in direct response to signaling from intramyocardial mechanoreceptors that sense the hypercontractility of a relatively empty ventricle. (4, 5, 6).
The most likely explanation in this case is reflex bradycardia because the blood pressure increased with the drop in heart rate and further increased once cardiac output increased with the increase in heart rate. Familiarity with this phenomenon of paradoxical bradycardia following a low dose of epinephrine can accelerate recognition and successful clinical management.
