Case Report

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American Journal of Emergency Medicine

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Complication after treatment for resistant supraventricular tachycardia: the Bezold-Jarisch reflex?

Abstract

The Bezold-Jarisch reflex may become clinically relevant in times of profound relative hypovolemia. This results in uncoupled cardio inhibition leading to the triad of hypotension, bradycardia and vasodilation.

A previously healthy 16-year-old male presented to the pediatric emergency department with a 1-day history of palpitations, nausea, vomiting and fatigue. He denied chest pain or dizziness. He had one previous episode of palpitations two weeks prior that self-resolved within one to two hours. Physical examination revealed an afebrile patient with a heart rate of 246 beats per minute (bpm), respiratory rate 22 per minute, oxygen saturations 97% on room air, and blood pressure of 110/50 mmHg. The remainder of the examination was unremarkable. His chest was clear to auscultation with audible first and second heart sounds and no detected murmur. Electrocardiogram revealed an accelerated ventricular rate with a constant R-R interval and no discernible P-waves consistent with supraventricular tachy- cardia (SVT).

A 0.9% normal saline bolus of one liter was initiated, and Vagal maneuvers were attempted without successful return of normal sinus rhythm (NSR). Intravenous adenosine was administered three times (6 mg, 12 mg, and 12 mg) with no return to NSR. In consultation with the attending pediatric cardiologist, an intrave- nous (IV) esmolol infusion was administered at 150 ug/kg per minute and increased incrementally to ug/kg per minute, but return to NSR was unsuccessful. The patient was subsequently prepared for electrical cardioversion for prolonged refractory SVT. After the esmolol was discontinued, pre-sedation vitals were: HR 180 bpm and blood pressure 96/51 mmHg. Procedural sedation consisted of

IV fentanyl and IV midazolam. Three minutes following the administration of sedative medications, the patient suddenly became bradycardic with a monitored heart rate of 45 bpm without a pulse. Cardiopulmonary resuscitation was initiated, and epineph- rine was administered. Two minutes later, peripheral pulses were palpated and cardiopulmonary resuscitation was discontinued. The electrocardiogram documented a sinus rhythm of 90 bpm with a blood pressure of 90/70 mmHg.

In light of the abrupt onset of symptoms and the clinical scenario, an uncoupled Bezold-Jarisch reflex was presumed.

? Financial Disclosure: None.

Normally, cardiovascular reflexes aid in the maintenance of cardiac function. These reflexes rely on various receptors that respond to pressure changes in different areas of the cardiovascular system [1]. One type of receptor in the walls of the ventricles is related to the cardio-inhibitory Bezold-Jarisch reflex (BJR). This was first described in 1867 by von Bezold and Hirt [2] after injection of veratrum alkaloids caused marked hypotension and bradycardia associated with apnea. This was later confirmed by Jarisch in the 1950s [3]. In 1947, Dawes et al [4], discovered that the reflex apnea was mechanically separate from the hemodynamic changes. Today, the BJR refers to the triad of hypotension, bradycardia and vasodilation [1,5].

The receptors for the BJR have very low basal firing rate in the absence of stimulation. When stimulated, the afferent fibers travel up the nonmyelinated vagal fibers and result in vasomotor center inhibition. This results in bradycardia, decreased sympathetic output resulting in decreased peripheral vascular resistance and subsequent hypotension [1].

In general, it is believed that the dominant controller of blood pressure is not the BJR reflex, but the baroreceptor reflexes. The high-pressure receptors in the carotid and aortic bodies stimulate the afferent Hering and vagus nerves to the medulla, resulting in increased efferent vagal firing, and decreased Sympathetic nerve activity. This results in an abrupt decrease in heart rate, blood pressure, contractility and total peripheral resistance. Conversely, low-pressure receptors that are of the atrial stretch type detect increase blood volume returning to the atria, resulting in a net increase in heart rate and contractility. Also, stretch receptors in the same location at the endocardium result in the release of atrial natriuretic factor promoting diuresis and natriuresis. However, the reaction of veratrum alkaloids producing marked clinical symptoms suggests that under certain circumstances, this relationship can become uncoupled, resulting in dominant BJR activity [1].

The most common clinical scenario where this uncoupling can occur is with profound hypovolemia. In most cases of hypovolemia, the BJR reflex would be decreased resulting in protective increased blood pressure. In some instances profound hypovolemia, resulting in hypotension may result in paradoxical bradycardia. Activation of the BJR reflex may explain this scenario. In animal models in cats with severe blood loss, increased firing of cardio-inhibitory receptors has been recorded [6]. The vigorous contraction of an empty ventricle can lead to the trigger of the BJR reflex. In humans, a sudden decrease of peripheral resistance coupled with decreased venous return triggers bradycardia presumably to preserve cardiac filling. There may be evidence that this activation

0735-6757/$ - see front matter (C) 2013

may help preserve diastolic filling in times of decreased venous return [7].

Recognition of this reflex highlights the importance of volume assessment and resuscitation in patients with marked hypovolemia. In our patient, the vomiting preceding the visit causing a volume contracted state, medications used prior to cardioversion, and possible upright positioning of the patient may have been factors leading to BJR activation.

Restoration of venous return as preload to the heart is urgent for management of BJR effects [8]. This may be accomplished by fluid administration, positioning (head-down tilt or leg elevation), anti- cholinergic medications and sympathomimetic drugs.

Thankfully, our patient had a Full recovery (be more specific). It is important for clinicians to recognize that patients with arrhythmias such as SVT as in our patient, or other conditions leading to marked relative hypovolemia may be at risk of an uncoupled BJR event, and the anticipation and prevention, as well as rapid recognition and prompt management is crucial.

Rodrick Lim MD

Departments of Paediatrics and Medicine, Schulich School of Medicine

at the University of Western Ontario Children‘s Hospital at London Health Sciences Centre

London, ON, Canada N6C 2V5 Children‘s Health Research Institute

Children‘s Hospital at London Health Sciences Centre

London, ON, Canada N6C 2V5 E-mail address: [email protected]

Jennifer Kilgar MD Stanley Cayo MD Krista Helleman MD

Naveen Poonai MSc, MD

Departments of Paediatrics and Medicine

Schulich School of Medicine at the University of Western Ontario

Children‘s Hospital at London Health Sciences Centre

London, ON, Canada, N6C 2V5

http://dx.doi.org/10.1016/j.ajem.2013.05.030

References

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