Hypokalemia, a common electrolyte disorder, is frequently observed in hospitalized patients, affecting up to 20% of them. The primary causes of hypokalemia include the use of diuretic medications, secret vomiting (such as in bulimia), and severe diarrhea. Another cause is Gitelman syndrome, which is a genetic defect in the Na+/Cl- symporter found in the apical membrane of distal tubule cells (refer to Chapter 36 for more details). On the other hand, hyperkalemia, another prevalent electrolyte disorder, occurs in 1% to 10% of hospitalized patients. It is often seen in individuals with renal failure, those taking medications like angiotensin-converting enzyme (ACE) inhibitors and K+-sparing diuretics, people with high blood sugar (hyperglycemia), and the elderly. Pseudohyperkalemia, which falsely raises plasma [K+] levels, can occur due to the traumatic lysis of red blood cells during blood drawing. Red blood cells contain K+ and their rupture releases K+ into the plasma, artificially elevating its concentration.

The maintenance of a large concentration difference of K+ across cell membranes (approximately 146 mEq/L) is facilitated by the Na+,K+-ATPase. This gradient of [K+] is crucial in various aspects such as maintaining the resting membrane potential in skeletal muscle (as shown in Fig. 36.1) and the function of nerve and muscle cells, including cardiac, skeletal, and smooth muscle cells. It plays a vital role in the excitability and contractility of these cells.

To prevent any adverse effects on the electrical activity of the heart and other excitable tissues, the rapid uptake of K+ into cells occurs within minutes. The kidneys also play a role in excreting K+. Both hypokalemia and hyperkalemia can lead to cardiac arrhythmias. The electrocardiogram (ECG) provides a quick and efficient method for monitoring the heart's electrical activity and assessing whether changes in plasma [K+] affect excitable cells. In contrast, measuring plasma [K+] in a clinical laboratory requires a blood sample and may not yield immediate results.

Hyperkalemia is initially indicated by tall, thin T waves on the ECG. Further elevation of plasma [K+] results in the prolongation of the PR interval, depression of the ST segment, and lengthening of the QRS interval on the ECG. As plasma [K+] approaches 10 mEq/L, the P wave disappears, the QRS interval broadens, the ECG takes on a sine wave appearance, and the ventricles fibrillate (displaying rapid, uncoordinated muscle contractions). On the other hand, hypokalemia prolongs the QT interval, inverts the T wave, and decreases the ST segment on the ECG.
Hypokalemia is one of the most common electrolyte disorders in clinical practice and can be observed in as many as 20% of hospitalized patients. The most frequent causes of hypokalemia include administration of diuretic drugs, surreptitious vomiting (e.g., bulimia), and severe diarrhea. Gitelman syndrome (a genetic defect in the Na+/ Cl− symporter in the apical membrane of distal tubule cells) also causes hypokalemia (see Chapter 36). Hyperkalemia is also a common electrolyte disorder and is seen in 1% to 10% of hospitalized patients. Hyperkalemia often occurs in patients with renal failure, in patients taking drugs such as angiotensin-converting enzyme (ACE) inhibitors and K+-sparing diuretics, in patients with hyperglycemia (i.e., high blood sugar), and in the elderly. Pseudohyperkalemia, a falsely high plasma [K+], is caused by traumatic lysis of red blood cells during blood drawing. Red blood cells, like all cells, contain K+ , and lysis of red blood cells releases K+ into plasma, thereby artificially elevating plasma [K+].
The large concentration difference of K+ across cell membranes (≈146 mEq/L) is maintained by the operation of Na+,K+-ATPase. This [K+] gradient is important in • Fig. 36.2 Electrocardiographs from individuals with varying plasma • Fig. 36.1 Effects of variations in plasma [K+] on resting membrane potential of skeletal muscle. Hyperkalemia causes membrane potential to become less negative, which decreases excitability by inactivating the fast Na+ channels responsible for the depolarizing phase of the action potential. Hypokalemia hyperpolarizes the membrane potential and thereby reduces excitability because a larger stimulus is required to depolarize the membrane potential to the threshold potential. Resting indicates “normal” resting membrane potential. Normal threshold indicates the membrane threshold potential.
maintaining the potential difference across cell membranes. Thus K+ is critical for the excitability of nerve and muscle cells, as well as for the contractility of cardiac, skeletal, and smooth muscle cells (
Fig. 36.1 [K+]. See text for details. (Modified from Barker L et al. Principles of Ambulatory Medicine. 5th ed. Baltimore: Williams & Wilkins; 1999.)
This rise in plasma [K+], which could have deleterious effects on the electrical activity of the heart and other excitable tissues, is prevented by the rapid (minutes) uptake of K+ into cells. Because excretion of K+ by the kidneys
Cardiac arrhythmias are produced by both hypokalemia and hyperkalemia. The electrocardiogram (ECG;
Fig. 36.2 ) monitors the electrical activity of the heart and is a fast and easy way to determine whether changes in plasma [K+] influence the heart and other excitable cells. In contrast, measurement of plasma [K+] by the clinical laboratory requires a blood sample, and values are often not immediately available. The first sign of hyperkalemia is the appearance of tall, thin T waves on the ECG. Further increases in plasma [K+] prolong the PR interval, depress the ST segment, and lengthen the QRS interval of the ECG. Finally, as plasma [K+] approaches 10 mEq/L, the P wave disappears, the QRS interval broadens, the ECG appears as a sine wave, and the ventricles fibrillate (i.e., manifest rapid, uncoordinated contractions of muscle fibers). Hypokalemia prolongs the QT interval, inverts the T wave, and lowers the ST segment of the ECG.