All of the following are the electrocardiographic features of severe hyperkalemia except.
1. Peaked T waves.
2. Presence of U waves.
3. Sine wave pattern.
4. Loss of P waves.
2. Presence of U waves.
Harrison 15th Edition Chapter 49 and Page 1269
Hyperkalemia, defined as a plasma K+ concentration 5.0 mmol/L, occurs as a result of either K+ release from cells or decreased renal loss. Increased K+ intake is rarely the sole cause of hyperkalemia since the phenomenon of potassium adaptation ensures rapid K+ excretion in response to increases in dietary consumption.
The earliest electrocardiographic changes include increased T-wave amplitude, or peaked T waves. More severe degrees of hyperkalemia result in a prolonged PR interval and QRS duration, atrioventricular conduction delay, and loss of P waves. Progressive widening of the QRS complex and merging with the T wave produces a sinewave pattern. The terminal event is usually ventricular fibrillation or asystole.
1. Peaked T waves is seen.
2. Presence of U waves is not seen.
3. Sine wave pattern is seen.
4. Loss of P waves is seen.
Iatrogenic hyperkalemia may result from overzealous parenteral K+ replacement or in patients with renal insufficiency.
Pseudohyperkalemia represents an artificially elevated plasma K+ concentration due to K+ movement out of cells immediately prior to or following venipuncture. Contributing factors include prolonged use of a tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis. The latter two result in an elevated serum K+ concentration due to release of intracellular K+ following clot formation. Pseudohyperkalemia should be suspected in an otherwise asymptomatic patient with no obvious underlying cause. If proper venipuncture technique is used and a plasma (not serum) K+ concentration is measured, it should be normal.
Gordon's syndrome is a rare condition characterized by hyperkalemia, metabolic acidosis, and a normal GFR. These patients are usually volume-expanded with suppressed renin and aldosterone levels as well as refractory to the kaliuretic effect of exogenous mineralocorticoids. It has been suggested that these findings could all be accounted for by increased distal Cl- reabsorption (electroneutral Na+ reabsorption), also referred to as a Cl- shunt. A similar mechanism may be partially responsible for the hyperkalemia associated with cyclosporine nephrotoxicity. Hyperkalemic distal (type 4) RTA may be due to either hypoaldosteronism or a Cl- shunt (aldosterone-resistant).
Source of this Question: RxPG AIPG 2004
Author : Dr. J. Mariano Anto Bruno Mascarenhas
Publisher: Jaypee Brothers Medical Publishers, India
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