Unusual Cause of Cardiac Arrest

A patient in their 40s with a history of remote coronary artery bypass grafting, heart failure with reduced ejection fraction, and poorly controlled insulin-dependent diabetes was admitted to the cardiac intensive care unit with acute decompensated heart failure. The patient’s baseline electrocardiogram (ECG) demonstrated normal sinus rhythm, with normal PR and QRS intervals at 132 and 82 milliseconds, respectively. With poor response to intravenous (IV) diuretics, the patient underwent right heart cardiac catheterization, which demonstrated a low cardiac index, high left ventricular filling pressure, and elevated systemic vascular resistance. The patient’s outpatient use of metoprolol was discontinued, and IV dobutamine (5.0 μg/kg/min) was initiated with continuing aggressive IV diuresis. While defecating on the bedside commode, the patient became lightheaded and unresponsive. The patient’s pulse was barely palpable, and the ECG rhythm showed bradycardia (Figure).

Figure. Electrocardiogram (ECG) Rhythm.

The patient’s ECG rhythm is shown before using the bedside commode (A), after developing unresponsiveness during defecation (B), and 1 minute after developing the unresponsiveness (C). After developing unresponsiveness during defecation, the initial ECG rhythm demonstrated an ectopic atrial rhythm, with an atrial cycle length (CL) of 920 milliseconds and prolonged PR interval (240 ms) (A). The rhythm progressed to 2:1 atrioventricular block 25 seconds later (B). One minute later, the patient developed sinus bradycardia (atrial CL, 1320 ms) with complete heart block (C). The recorded ECG shows a few different letters on each QRS wave, such as “N”, “?”, or “M.” These are associated with the setting of our telemetry machine but did not mean any specific information.

Questions: What is your diagnosis? How would you treat this patient’s condition?

Interpretation

A detailed analysis of the ECG rhythm elucidates a plausible mechanism of the cardiac arrest. After the patient developed new unresponsiveness, the initial ECG rhythm demonstrated ectopic atrial rhythm, with an atrial cycle length (CL) of 920 milliseconds and a prolonged PR interval (240 ms) (Figure, A). The rhythm progressed to 2:1 atrioventricular block 25 seconds later (Figure, B). One minute later, the patient developed sinus bradycardia (atrial CL, 1320 ms) with complete heart block (Figure, C). The ECG analysis demonstrated a simultaneous slowing of the patient’s sinus rate and atrioventricular conduction. This suggests a central mechanism, such as an increase in the parasympathetic tone during defecation, rather than a structural abnormality of the conduction system.¹

Clinical Course

A transient increase in the junctional escape rhythm (CL, 1880 ms) was observed with IV atropine, 0.5 mg, but the rhythm subsequently led to asystole. Despite multiple attempts of resuscitations, the patient died.

Discussion

Defecation is a known cause of syncope, and a structurally normal heart generally tolerates the exaggerated parasympathetic tone. By contrast, patients with advanced cardiomyopathy and poor cardiac reserve may have difficulty compensating for the negative chronotropic and dromotropic effects during defecation. Defecation-induced cardiac arrest has been reported for a long time, but the mechanism has not been fully elucidated.² We are aware of only 1 case that showed ECG rhythms with complete heart block during defecation, but the mechanism was not discussed.³ We believe that the present case provides important insights into the pathophysiology of defecation-induced bradyarrhythmia.

During defecation in healthy individuals, sitting or squatting reduces the venous return to the heart owing to the shifting of blood from the thorax to the lower trunk, and the fluid shift decreases cardiac output.^4–6 Arterial baroreceptors sense the reduced cardiac output, and the sympathetic efferent reflex compensates hemodynamics.^4–6 It is suggested that defecation syncope is associated with abnormal responses to the physiologic compensation.^4–6 While the sympathetic efferent reflex is activated, cardiac mechanoreceptors (C-fiber) undergo inappropriate stimulation in the setting of sympathetically mediated hypercontractility of the volume-depleted ventricle.^4–6 The afferent C-fiber signal activates vasodepressor neurons in medulla, and the generated parasympathetic reflex causes sympathetic withdrawal.^4–6 These reflexes result in negative chronotropic, dromotropic, and inotropic effects, as well as an inability to maintain vascular tone during defecation.^4–6 Allan et al⁷ showed that patients with recurrent defecation syncope had predominantly significant sympathetic dysfunction and concomitant parasympathetic abnormalities.

Fisher-Hubbard et al⁸ estimated the outpatient incidence of defecation-induced cardiac arrests as 2.3% to 7.4% in patients with cardiovascular disease. Kiyohara et al⁹ identified that 4.6% of out-of-hospital cardiac arrest occurred inside the restroom, and the number of patients with the initial shockable rhythm was 5.2%. Based on these studies, it is suggestive that one of the unrecognized causes of sudden cardiac death in patients with heart failure is defecation-induced bradyarrhythmia.

To prevent defecation-induced syncope and sudden death, it is important to avoid constipation with lifestyle modifications and the use of laxatives. Also, the squatting position has been suggested to decrease straining during defecation by straightening the rectoanal angle, as opposed to the sitting posture.^2,3 The current guideline recommends IV atropine as the first-line agent for symptomatic bradycardia.¹⁰ However, given that cardiac reserve is limited in patients with advanced cardiomyopathy, epinephrine may be a better choice than atropine to provide positive chronotropic, dromotropic, and inotropic effects, as well as vasoconstrictive properties, in the setting of defecation-induced bradyarrhythmia. If patients face impending pulseless electrical activity or asystole secondary to defecation-induced bradyarrhythmia like the patient in this article, epinephrine should be considered as the first-line agent.

Take-Home Points.

• Defecation-induced cardiac arrest is an unrecognized cause of sudden cardiac death in patients with cardiomyopathy and poor cardiac reserve.

• The suggestive mechanism is an increase in parasympathetic tone and sympathetic withdrawal, which leads to bradyarrhythmia (negative chronotropic and dromotropic effects) and hypotension (vasodilatation).

• Defecation-induced syncope and sudden death are potentially preventable.

• Atropine should not be the first choice.

• Epinephrine is probably a better choice than atropine because it can provide positive chronotropic and inotropic effects as well as vasoconstrictive properties.