Poster Presentation ESA-SRB-ANZOS 2025 in conjunction with ENSA

A "K"-ritical Situation: Unmasking Primary Hyperaldosteronism After Cardiac Arrest  (128455)

Sarah C Brennan 1 2 , Mark Swyak 3 , Ravinay Bhindi 4 , Roderick J Clifton-Bligh 1 5
  1. Department of Diabetes & Endocrinology,, Royal North Shore Hospital, Sydney, NSW, Australia
  2. School of Life & Environmental Sciences, University of Sydney, Camperdown, NSW, Australia
  3. Department of Endocrine Surgery, Royal North Shore Hospital, St Leonards, NSW, Australia
  4. Department of Cardiology, Royal North Shore Hospital, St Leonards, NSW, Australia
  5. Faculty of Medicine & Health, University of Sydney, Camperdown, NSW, Australia

Background: Primary hyperaldosteronism (PHA) is a common cause of secondary hypertension, typically presenting with hypertension and hypokalaemia. Excess aldosterone causes direct cardiovascular toxicity through structural and functional cardiac changes, increasing arrhythmia risk [1]. However, sudden cardiac arrest as the initial presentation is exceptionally rare [2]. 

Case Presentation: A 71-year-old male with well-controlled hypertension, atrial fibrillation, and dyslipidaemia presented with sudden cardiac arrest due to ventricular fibrillation requiring extensive resuscitation. Post-resuscitation investigations revealed profound hypokalaemia (initial K 7.8 mmol/L, rapidly dropping to 1.9 mmol/L), necessitating aggressive potassium replacement (up to 550 mmol/24 hours). Cardiac catheterisation showed unobstructed coronaries. Renal workup demonstrated potassium wasting (TTKG 9), prompting PHA investigation despite reasonably controlled blood pressure. Biochemical testing revealed elevated aldosterone (720 pmol/L), suppressed renin (<2 mIU/L), and ARR >360. Saline suppression test was positive. CT imaging identified a 15mm left adrenal adenoma, with adrenal venous sampling confirming lateralised aldosterone production. The patient underwent successful left adrenalectomy. 

Clinical Significance: This case demonstrates the critical importance of investigating secondary causes of hypokalaemia in life-threatening arrhythmias. While hypokalaemia is a recognised PHA complication, its severity and presentation with sudden cardiac arrest were unusual. The patient's underlying chronic hypokalaemia (historical outpatient K 3.0-3.2 mmol/L) likely predisposed to acute decompensation. Post-adrenalectomy, complete normalisation of blood pressure occurred, allowing cessation of all antihypertensive medications. 

Conclusion: PHA should be considered in patients with profound, refractory hypokalaemia presenting with life-threatening arrhythmias, even without severe hypertension. Early diagnosis and targeted surgical intervention can achieve complete resolution of biochemical abnormalities and hypertension [3], emphasising the importance of recognising this potentially curable cause of secondary hypertension. 

  1. Monticone, S., et al., Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. Lancet Diabetes Endocrinol, 2018. 6(1): p. 41-50.
  2. Funder, J.W., et al., The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab, 2016. 101(5): p. 1889-916.
  3. Rossi, G.P., et al., Long-term control of arterial hypertension and regression of left ventricular hypertrophy with treatment of primary aldosteronism. Hypertension, 2013. 62(1): p. 62-9.