ECG in hyperkalemia

Electrocardiographic signs and cardiac risks

The primary threat to a patient's life in acute kidney injury is hyperkalemia. The impaired electrolyte excretion has a direct toxic effect on the conduction system and myocardium. On the electrocardiogram, this condition manifests with a specific and very early pattern: a tall, peaked T wave is registered.

As serum potassium concentration rises, severe rhythm disturbances develop. The patient experiences bradycardia, and various intracardiac blocks form. A critical increase in electrolyte levels leads to fatal consequences: there is a high risk of sudden death due to ventricular fibrillation or hyperkalemic cardiac arrest (asystole). This is precisely why continuous ECG monitoring is absolutely essential in the acute phase of kidney injury.

Etiology and pathogenesis of potassium accumulation

The rapid development of hyperkalemia is based on necrotic nephrosis — a severe kidney injury with destruction and necrosis of the tubular epithelium. This condition serves as the morphological substrate of the "shock kidney" syndrome.

The causes of such massive damage include:

• Ischemia (against the background of hypovolemia or any type of shock).
• Exogenous and endogenous toxins (including the development of hepatorenal syndrome).
• Medications (e.g., analgesics capable of causing papillary necrosis).
• Infectious processes (acute pyelonephritis).
• Pigments (in massive hemolysis or rhabdomyolysis).

The pathogenesis of hyperkalemia is inextricably linked to the mechanism of renal structural damage. The impact of shock or toxin causes hypercatecholaminemia, which leads to a sharp spasm of renal vessels and ischemia of the cortex. The epithelium of the convoluted tubules undergoes necrosis. Desquamated dead cells form casts that obstruct the tubular lumen. As a result, intratubular pressure rises rapidly, "back-leakage" of the filtrate into the blood occurs, and glomerular filtration drops catastrophically.

Stages of development and clinical presentation

Hyperkalemia and the tall T wave on the ECG clearly manifest in the second, oligoanuric stage of necrotic nephrosis. It occurs after the initial (shock) stage, which lasts from several hours to two days.

During this period, there is a sharp drop in diuresis — oliguria develops (output of less than 400 ml of urine per day) or complete anuria. Against the background of the peak of renal tissue necrosis, severe homeostasis disorders rapidly progress:

1. Azotemia occurs (accumulation of nitrogenous waste products).
2. Metabolic acidosis and hyperchloremia develop.
3. Hyperhydration forms.

Clinically, this manifests as acute uremic syndrome. The patient experiences pronounced adynamia, nausea, and vomiting. From the gastrointestinal tract, abdominal pain and hepatomegaly are noted. Neurological symptoms include muscle twitching and drowsiness, which can progress to uremic coma. Due to metabolic acidosis and early pulmonary edema (which is clearly detected radiologically), the patient experiences severe shortness of breath.

Morphological changes and outcomes

Macroscopically, the kidneys in hyperkalemia and necrotic nephrosis appear enlarged and swollen. The cortex is pale and ischemic, whereas the medullary pyramids are markedly congested and dark red in color. In papillary necrosis, the papillae become gray-yellow, resembling an infarct zone.

The microscopic picture depends on the underlying cause. In toxic damage, continuous necrosis of the convoluted tubule epithelium is observed, but the basement membrane remains intact. In ischemic damage, necrosis is focal and accompanied by rupture of basement membranes — tubulorrhexis. Coagulative necrosis forms in the papillae, surrounded by a demarcation leukocyte rim.

It is the integrity of the basement membrane that determines the outcome of the disease and the chances of resolving hyperkalemia. If the membrane is intact, complete recovery with epithelial regeneration is possible (the process goes through the polyuric stage, where the risk of hypokalemia arises, and ends with a recovery stage lasting up to 1 year). With tubulorrhexis, full regeneration is impossible, and the process progresses to nephrosclerosis and chronic kidney disease. In the worst case, death occurs from uremic coma or hyperkalemic cardiac arrest.

Class and exam questions

What else to study on this topic

• Pathogenesis of the "shock kidney" syndrome and the role of hypercatecholaminemia
• Mechanisms of metabolic acidosis and hyperchloremia development in oliguria
• Macro- and microscopic picture of necrotic nephrosis (ischemic and toxic variants)
• Polyuric stage: risks of hypokalemia, isosthenuria, and dehydration
• Acute uremic syndrome: neurological and gastroenterological manifestations

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