MedElevator
Войти в исследования The Canadian veterinary journal = La revue veterinaire canadienne · 2026
Emergency management of hyperkalemia in dogs and cats - Part 1: Pathophysiology and etiology.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Iimori Yasumasa, Johnson Paula A, Thomovsky Elizabeth J, Brooks Aimee C, Aghili Ana
Аннотация
OBJECTIVE: Hyperkalemia is a frequent, life-threatening emergency in dogs and cats. It disrupts neuromuscular function and cardiac conduction. Clinicians need a clear physiologic framework to recognize risk and act quickly.
ANIMALS AND PROCEDURE: Part 1 of this 2-part review explains potassium homeostasis and the main causes of hyperkalemia in small animals. The article draws on peer-reviewed veterinary studies and core physiology, with direct patient-side relevance.
RESULTS: Most body potassium is intracellular; small extracellular shifts alter membrane excitability and electrocardiogram patterns. Two systems control plasma potassium: transcellular control through insulin, β2-adrenergic tone, and acid-base effects; and renal control through filtration, distal sodium delivery, tubular flow, and mineralocorticoid effect. Common clinical causes include decreased renal excretion (feline urethral obstruction, oligoanuric acute kidney injury, canine hypoadrenocorticism); transcellular shifts from intracellular to extracellular spaces (diabetic ketoacidosis, mineral metabolic acidosis, extensive tissue injury); increased intake or iatrogenic load when excretion is limited (potassium chloride in IV fluids, older stored blood, drugs that reduce aldosterone effect or distal sodium delivery); and pseudohyperkalemia due to sample factors (hemolysis, marked thrombocytosis or leukocytosis, anticoagulant contamination).
CONCLUSION AND CLINICAL RELEVANCE: Evaluate hyperkalemia in the full clinical context. In dogs, common causes include hypoadrenocorticism, acute kidney injury, and urinary tract obstruction or rupture. In cats, urethral obstruction and advanced renal failure predominate, whereas iatrogenic potassium load and severe metabolic acidosis are additional concerns. A firm grasp of both pathophysiology and etiology improves differential diagnosis and early decisions. Part 2 of this review will build on this foundation and outline diagnosis and treatment.
ANIMALS AND PROCEDURE: Part 1 of this 2-part review explains potassium homeostasis and the main causes of hyperkalemia in small animals. The article draws on peer-reviewed veterinary studies and core physiology, with direct patient-side relevance.
RESULTS: Most body potassium is intracellular; small extracellular shifts alter membrane excitability and electrocardiogram patterns. Two systems control plasma potassium: transcellular control through insulin, β2-adrenergic tone, and acid-base effects; and renal control through filtration, distal sodium delivery, tubular flow, and mineralocorticoid effect. Common clinical causes include decreased renal excretion (feline urethral obstruction, oligoanuric acute kidney injury, canine hypoadrenocorticism); transcellular shifts from intracellular to extracellular spaces (diabetic ketoacidosis, mineral metabolic acidosis, extensive tissue injury); increased intake or iatrogenic load when excretion is limited (potassium chloride in IV fluids, older stored blood, drugs that reduce aldosterone effect or distal sodium delivery); and pseudohyperkalemia due to sample factors (hemolysis, marked thrombocytosis or leukocytosis, anticoagulant contamination).
CONCLUSION AND CLINICAL RELEVANCE: Evaluate hyperkalemia in the full clinical context. In dogs, common causes include hypoadrenocorticism, acute kidney injury, and urinary tract obstruction or rupture. In cats, urethral obstruction and advanced renal failure predominate, whereas iatrogenic potassium load and severe metabolic acidosis are additional concerns. A firm grasp of both pathophysiology and etiology improves differential diagnosis and early decisions. Part 2 of this review will build on this foundation and outline diagnosis and treatment.