BRASH SYNDROME: AN UNDER RECOGNISED CAUSE OF COMPLETE HEART BLOCK IN THE ELDERLY.

Editor,

An 81 year old lady with a background of chronic kidney disease (CKD), hypertension and type two diabetes mellitus presented to Craigavon Area Hospital via ambulance as a stroke lysis call. She was dysarthric and profoundly bradycardic with an unreadable blood pressure. Following administration of 600mcg atropine a blood pressure of 100/60mmHg was obtained. An ECG demonstrated complete heart block (CHB) with a ventricular rate of 29 bpm (Figure 1). A further 1.8mg atropine did not rectify her CHB and ventricular rate remained 40bpm albeit with a satisfactory blood pressure. Dysarthria was felt to be secondary to cerebral hypoperfusion in the context of CHB and her management was deferred to the cardiology team with the assumption that she would require a pacemaker.

Figure 1

ECG demonstrating ventricular escape rhythm 29bpm without discernible atrial activity. RSR pattern with QRS 140bpm in keeping with RBBB noted in v1-3 with QRS in remaining leads noted to be relatively narrow with mild peaking of T waves noted.

An arterial gas sample was taken at this point which demonstrated elevated potassium of 8.3mmol/L. Interestingly, her ECG did not demonstrate dramatically peaked T waves as would be expected with hyperkalaemia and initially this first reading was thought to be erroneous. Repeat sampling however confirmed hyperkalaemia. Additionally, her formal laboratory biochemistry soon confirmed she was in acute on chronic renal failure with an eGFR of 12mls/min which had deteriorated from a baseline of 30mls/min. The hyperkalaemia remained refractory to conventional medical treatment and haemofiltration was commenced. Upon normalisation of serum potassium, her rhythm reverted to sinus of rate 74bpm (Figure 2). Haemofiltration was weaned over the coming days and a permanent pacemaker was not required.

Figure 2

ECG demonstrating restoration of Sinus rhythm with mildly prolonged PR interval of 240ms.

It emerged she had been taking both atenolol and Ramipril for hypertension and had recently commenced a NSAID for joint pain. This likely precipitated an acute nephrogenic insult resulting in the accumulation of atenolol causing further renal hypoperfusion and hyperkalaemia which, in synergy with B-blockade, precipitated CHB and cerebral hypoperfusion.

This case illustrates the recently coined BRASH syndrome (Bradycardia, Renal failure, AV-node blockers, Shock and Hyperkalaemia). This describes a series of events in a patient with CKD taking AV nodal blockers where an initial insult (such as dehydration or nephrotoxic medication) triggers a cascade of events where AV nodal suppression impairs the normal compensatory response to renal hypoperfusion thus causing renal decompensation resulting in worsening hyperkalaemia. The synergistic effect of hyperkalaemia and B-blockade on AV nodal function causes further decompensation resulting in a pathological downward spiral of events.1,2

This is an under-recognised cause of CHB and renal failure which may be refractory to initial conventional treatment measures. ECG changes may not be characteristic of classical hyperkalaemia, occur at lower than expected serum potassium levels and remain refractory to conventional treatment.3,4 Co-morbid elderly patients on multiple medications are at high risk of developing this syndrome therefore as physicians we must be cognisant of prescribing AV nodal blockers or indeed additional nephrotoxic agents, so as to not incite the pathological cascade of events leading to BRASH syndrome.