Why the study?
Anti-arrhythmic medications used to control common arrhythmias in critically ill patients can cause bradycardia and haemodynamic compromise, whereas paced atrial rhythm may help treat bradycardia, prevent arrhythmias, and support cardiac output.
Does atrial pacing suppress ventricular arrhythmias and prevent bradycardia in critically ill patients?
Does atrial pacing suppress ventricular arrhythmias and prevent bradycardia in critically ill patients?
Atrial pacing can effectively suppress ventricular ectopy and sustained arrhythmias in critically ill patients while preventing hemodynamically compromising bradycardia.
May support atrial pacing for bradycardia in select critically ill patients; hypothesis-generating and requires prospective validation.
Background: Atrial and ventricular arrhythmias are common in the critically ill due to a variety of factors including sepsis, myocardial ischaemia, renal dysfunction, and electrolyte disturbances. Anti-arrhythmic medications can be useful to control arrhythmias but can result in bradycardia and haemodynamic compromise. A paced atrial rhythm alongside normal atrioventricular conduction can be helpful to treat bradycardia, prevent arrhythmias, and support cardiac output. Case summary: A 55-year-old gentleman with pseudomonas pneumonia, respiratory failure necessitating mechanical haemodynamic support, and subsequent coronary ischaemia presented to the intensive care unit. Paroxysms of atrial fibrillation and ventricular arrhythmias caused haemodynamic embarrassment and presented an ongoing clinical challenge as anti-arrhythmic medications resulted in bradycardia and Torsade de Pointes. Atrial pacing mediated intrinsic conduction via the His-Purkinje system inhibited ventricular ectopy and further arrhythmia breaking the tachycardia-bradycardia cycle; this stabilized the patient, facilitated ongoing intensive therapy unit care and promoted recovery. Conclusion: Atrial pacing mediated intrinsic conduction via the His-Purkinje system is an effective approach to suppress ventricular ectopy and sustained arrhythmias whilst protecting the patient from haemodynamically compromising bradycardia.
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Riad et al. (2022) studied this question.
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