The Canadian veterinary journal = La revue veterinaire canadienne · 2026
Emergency management of hyperkalemia in dogs and cats - Part 2: Diagnosis and treatment.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Iimori Yasumasa, Johnson Paula A, Thomovsky Elizabeth J, Brooks Aimee C, Aghili Ana
Аннотация
OBJECTIVE: Hyperkalemia in dogs and cats can cause rapid cardiac and neuromuscular compromise. Fast recognition, ECG-guided stabilization, and cause-directed therapy improve survival.
ANIMALS AND PROCEDURE: Part 2 of this 2-part review gives a patient-side approach for recognition, confirmation, and emergency treatment of hyperkalemia. It integrates current veterinary evidence and core physiology into step-by-step guidance for ECG interpretation, point-of-care testing, drug selection, and monitoring. It also maps 1st-hour priorities to common etiologies such as urethral obstruction and hypoadrenocorticism.
RESULTS: Immediate cardioprotection with intravenous calcium treats cardiotoxicity. Potassium decreases rapidly with regular insulin plus dextrose, β2 agonists serve as adjuncts, and bicarbonate is reserved for severe acidemia. Potassium elimination follows with balanced crystalloids and, when needed, renal replacement therapy. After initial stabilization, durable correction depends on identifying and treating the underlying cause and removing excess potassium from the body. Close glucose surveillance prevents late hypoglycemia after insulin. For urethral obstruction, prompt unblocking and fluids often normalize potassium with little need for repeat shifting drugs. For Addisonian crisis, fluids and glucocorticoids correct the driver while potassium decreases.
CONCLUSION AND CLINICAL RELEVANCE: Use a consistent sequence: Verify true hyperkalemia, protect the heart, shift potassium, remove potassium, and fix the cause. Pair ECG findings with serum potassium concentrations to guide action, since ECG stages do not always match absolute potassium concentrations. This approach helps emergency clinicians stabilize patients quickly and avoid relapse. Part 1 of this review covered homeostasis and causes, whereas Part 2 delivers diagnostic and treatment approaches.
ANIMALS AND PROCEDURE: Part 2 of this 2-part review gives a patient-side approach for recognition, confirmation, and emergency treatment of hyperkalemia. It integrates current veterinary evidence and core physiology into step-by-step guidance for ECG interpretation, point-of-care testing, drug selection, and monitoring. It also maps 1st-hour priorities to common etiologies such as urethral obstruction and hypoadrenocorticism.
RESULTS: Immediate cardioprotection with intravenous calcium treats cardiotoxicity. Potassium decreases rapidly with regular insulin plus dextrose, β2 agonists serve as adjuncts, and bicarbonate is reserved for severe acidemia. Potassium elimination follows with balanced crystalloids and, when needed, renal replacement therapy. After initial stabilization, durable correction depends on identifying and treating the underlying cause and removing excess potassium from the body. Close glucose surveillance prevents late hypoglycemia after insulin. For urethral obstruction, prompt unblocking and fluids often normalize potassium with little need for repeat shifting drugs. For Addisonian crisis, fluids and glucocorticoids correct the driver while potassium decreases.
CONCLUSION AND CLINICAL RELEVANCE: Use a consistent sequence: Verify true hyperkalemia, protect the heart, shift potassium, remove potassium, and fix the cause. Pair ECG findings with serum potassium concentrations to guide action, since ECG stages do not always match absolute potassium concentrations. This approach helps emergency clinicians stabilize patients quickly and avoid relapse. Part 1 of this review covered homeostasis and causes, whereas Part 2 delivers diagnostic and treatment approaches.