167Case 36 Features of Hypokalemia

Table 36.2: Causes of hypokalemia

•   Body fluid loss

There are several causes of hypokalemia which have been enlisted in Table 36.2. True loss of potassium is due to vomiting, diarrhea, naso-gastric suction and diuretic therapy (see Table 36.2). Redistribution of potassium occurs in metabolic alkalosis (intracellular shift) and with beta-agonist or insulin therapy. Hypokalemia is a feature of cortisol excess due to Cushing’s disease or steroid therapy as well as a feature of hyperaldosteronism in Conn’s syndrome.

Genetic causes of hypokalemia are Type 2 renal tubular acidosis (RTA-2) and hypokalemic periodic paralysis. Typical clinical features of hypokalemia are fatigue and leg cramps. In severe cases, neuromuscular paralysis and cardiac arrhythmias may occur. In cardiac patients on diuretic treatment, hypokalemia aggravates digitalis toxicity and increases the likelihood of serious ventricular arrhythmias.

In our case, the hypokalemia was multi-factorial. Firstly, the patient was prescribed a diuretic for his hypertension. Secondly, he was using an inhaled beta-agonist for asthma, which is known to cause hypokalemia. Finally, he had a recent episode of gastro-enteritis, which might have caused substantial loss of potassium from his body.

CLINICAL DISCUSSION

The ECG is sometimes helpful in the diagnosis of an electrolyte abnormality, even before the blood biochemistry results from the laboratory are available. Variation in the blood levels of potassium and calcium are mainly responsible for these ECG changes. Hypokalemia causes pseudo-prolongation of the Q-T interval, at the expense of the T wave. Hypocalcemia causes true prolongation of the Q-T interval, with true lengthening of the S-T segment.

168 Section 11 Typical ECG Abnormalities

Table 36.3: Management of hypokalemia

•   Potassium replacement Dietary supplements Oral K preparations Intravenous infusion

•   Treatment of the cause Anti-emetics

Anti-diarrheals Diuretic withdrawal

MANAGEMENT ISSUES

Management of hypokalemia includes potassium replacement and correction of the underlying cause (Table 36.3). Potassium can be replaced through dietary supplementation of potassium-rich foods. Oral proprietary supplements of potassium citrate can also be prescribed. If potassium deficiency is severe or if the patient is vomiting, potassium chloride is administered as an intravenous infusion. Generally, potassium deficiency is more severe, if there is true loss of body fluids than if there is only a transcellular shift of potassium.

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C A S E

37 Features of

Hyperkalemia

CASE PRESENTATION

A 64-year old woman was wheeled into the emergency room, with generalized weakness and shortness of breath of one week duration. She also complained of swelling around the eyes and over the feet, loss of appetite and occasional vomiting.

The lady was a known case of diabetes mellitus since 25 years and systemic hypertension for the last 12 years. She sustained an anterior wall myocardial infarction four years back, for which she was thrombolysed. At that time, coronary angiography showed triple-vessel disease, but she declined a revascularization procedure. Her serum creatinine value was found to be high and therefore, she was switched over from oral antidiabetic drugs to insulin therapy. The patient also underwent laser photocoagulation for proliferative retinopathy, one year back. She was presently undergoing maintenance hemodialysis, thrice a week.

On examination, the patient was drowsy, disoriented and obviously dyspneic.

The complexion was pale and sallow with dry skin that bore marks of pruritus.

There was periorbital puffiness and pitting edema over the ankles and lower legs.

The neck veins were engorged but there was no cyanosis or icterus. The pulse rate was 92 beats/min. with a BP of 160/94 mm Hg. The precordium was unremarkable and the apex beat was displaced to the left. The S₁ was normal with a loud A₂ and a S₃ sound in early diastole. An ejection murmur was audible along the left sternal border. No pericardial friction rub was audible. There were bilateral basilar rales over the lung fields. An ECG was obtained (Fig. 37.1) following which she was immediately given an injection. Her laboratory reports were Hemoglobin 9.2 g/dL% Urine sugar +1 albumin +2, Glucose 144 mg/dl, Urea 124 mg/dl, Creatinine 5.2 mg/dl, Sodium 129 mEq/L, Potassium 6.8 mEq/L and Calcium 7.4 mg%.

Figure 37.1: ECG showing tall T waves with flat P waves

170 Section 11 Typical ECG Abnormalities

Table 37.1: ECG features of progressive hyperkalemia A. Serum K>6.8 mEq/L tall T waves;

short Q-T interval B. Serum K>8.4 mEq/L (A) plus flat P waves;

prolonged P-R interval C. Serum K>9.1 mEq/L (B) plus wide QRS complex;

A-V block and arrhythmias

The ECG features of hyperkalemia depend upon its severity (Fig. 37.2). When the serum level exceeds 6.8 mEq/L, tall T waves and short Q-T interval are seen.

When it exceeds 8.4 mEq/L, additionally the P wave gets flattened and the P-R interval gets prolonged. At a serum level which is in excess of 9.1 mEq/L, the QRS complex also becomes wide and ventricular arrhythmias occur (Table 37.1).

Figure 37.2: ECG features of progressively increasing hyperkalemia

ECG INTERPRETATION

The ECG showed normal sinus rhythm. The P wave was flattened and the P-R interval was prolonged. There were no significant Q waves and the S-T segment was isoelectric. The T wave was upright, tall and peaked. The Q-T interval was short. These findings are consistent with the diagnosis of hyperkalemia. A T-wave that exceeds a voltage of 5 mm in the standard leads and 10 mm in the precordial leads is considered tall. Besides hyperkalemia, causes of tall T wave are myocardial ischemia and the hyperacute phase of myocardial infarction. The T wave of hyperkalemia is tall, peaked symmetrical and has a narrow base, the so called ‘tented’ T wave. The Q-T interval is short. On the other hand, the T wave of coronary insufficiency is tall but broad-based and the Q-T interval is prolonged.

The normal Q-T interval is 0.39 + 0.04 sec. and ranges from 0.35 to 0.43 sec. A Q-T interval measuring less than 0.35 sec is considered short. Besides hyperkalemia, causes of short Q-T interval are hypercalcemia and digitalis toxicity.

Hyperkalemia shortens the Q-T interval and is associated with tall T waves, wide QRS complexes and diminished P waves. Hypercalcemia also shortens the Q-T interval but there are no changes in the morphology of the QRS deflection. The proximal limb of the T-wave has an abrupt upslope to its peak.

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