Hyperkalemia and ECG Results
Hyperkalemia is a commonly encountered metabolic abnormality in clinical practice. Several different types of drugs-most notably potassium-sparing diuretics and ACE inhibitors-can cause hyperkalemia. Renal failure is another common cause for elevated potassium levels.Characteristic ECG changes occur at various levels of hyperkalemia.
ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:
1) Early changes of hyperkalemia include peaked T-waves, shortened QT interval, and ST-segment depression.
2) These changes are followed by bundle branch block causing a uniform widening of the QRS complex. Increase in the PR interval, and decreased amplitude of the P-wave follow QRS widening.
3) These changes reverse with appropriate treatment.
4) In the absence of treatment, the P-wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows.
5) ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.
The QRS complexes begin to widen when the patient’s serum potassium level reaches about 6-6.5 mEq/L, becoming markedly slurred and abnormally winded at 10 Me/qL. The QRS complexes may widen so that they merge with the T-waves, resulting in a “sine wave” appearance. The S-segments disappear when the serum potassium level reaches 6 mEq/L and the T-waves typically become tall and peaked at this same range. The P-waves begin to flatten out and widen when a patient’s serum potassium level reaches about 6.5 mEq/L; this effect tends to disappear when levels reach 7-9 mEq/L. Sinus arrest may occur when the serum potassium level reaches about 7.5 mEq/L, and cardiac standstill or ventricular fibrillation may occur when serum levels reach 10 to 12 mEq/L. The following ECG shows tall peaked T-waves with narrow based best seen in midprecordial leads.
Hyperkalemia is a commonly encountered metabolic abnormality in clinical practice. Several different types of drugs-most notably potassium-sparing diuretics and ACE inhibitors-can cause hyperkalemia. Renal failure is another common cause for elevated potassium levels.Characteristic ECG changes occur at various levels of hyperkalemia.
ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:
1) Early changes of hyperkalemia include peaked T-waves, shortened QT interval, and ST-segment depression.
2) These changes are followed by bundle branch block causing a uniform widening of the QRS complex. Increase in the PR interval, and decreased amplitude of the P-wave follow QRS widening.
3) These changes reverse with appropriate treatment.
4) In the absence of treatment, the P-wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows.
5) ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.
The QRS complexes begin to widen when the patient’s serum potassium level reaches about 6-6.5 mEq/L, becoming markedly slurred and abnormally winded at 10 Me/qL. The QRS complexes may widen so that they merge with the T-waves, resulting in a “sine wave” appearance. The S-segments disappear when the serum potassium level reaches 6 mEq/L and the T-waves typically become tall and peaked at this same range. The P-waves begin to flatten out and widen when a patient’s serum potassium level reaches about 6.5 mEq/L; this effect tends to disappear when levels reach 7-9 mEq/L. Sinus arrest may occur when the serum potassium level reaches about 7.5 mEq/L, and cardiac standstill or ventricular fibrillation may occur when serum levels reach 10 to 12 mEq/L. The following ECG shows tall peaked T-waves with narrow based best seen in midprecordial leads.
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| ECG changes in hyperkalemia |
Changes Caused by Hypokalemia
Hypokalemia can commonly result from the loss of potassium through dehydration, vomiting,gastric suction, or excessive diuretic use. The thiazide and loop diuretics are most commonly implicated in the development of hypokalemia.The QRS complexes begin to widen when the serum potassium drops to about 3 mEq/L, the ST- segments may become depressed, and the T-waves may begin to flatten. The U-waves also begin to increase in size, becoming as tall as the T-waves. The U-waves reach “giant” size and fuse with the T-waves when the level drops to 1 mEq/L.
Calcium
Alterations in serum calcium levels may also produce serious arrhythmias, leading to alterations in ECG results. Hypocalcemia, which may be caused by loop diuretics, osteomalacia,hypoparathyroidism, or respiratory alkalosis, may produce prolongation of the ST-segment and QT interval. Hypercalcemia, caused by adrenal insufficiency, hypoparathyroidism, kidney failure, or malignancy, may also cause serious arrhythmias, especially in the presence of digitalis.
Digitalis Effect
The administration of digitalis can cause ECG changes, even when the dosage is within the recommended therapeutic range. In cases of digitalis toxicity, excitatory or inhibitory effects on the heart and its electrical conduction system may occur. Excitatory effects include various types of ventricular and supraventricular ectopy, ventricular tachycardia, and ventricular fibrillation.Inhibitory effects include sinus bradycardia and heart block. The digitalis effect produces prolonged PR intervals, depressed (scooped) ST-segments, and alterations in T-wave morphology. The following ECG shows PAT with block,one of the classic arrhythmias seen in digitalis toxicity.
Hypokalemia can commonly result from the loss of potassium through dehydration, vomiting,gastric suction, or excessive diuretic use. The thiazide and loop diuretics are most commonly implicated in the development of hypokalemia.The QRS complexes begin to widen when the serum potassium drops to about 3 mEq/L, the ST- segments may become depressed, and the T-waves may begin to flatten. The U-waves also begin to increase in size, becoming as tall as the T-waves. The U-waves reach “giant” size and fuse with the T-waves when the level drops to 1 mEq/L.
Calcium
Alterations in serum calcium levels may also produce serious arrhythmias, leading to alterations in ECG results. Hypocalcemia, which may be caused by loop diuretics, osteomalacia,hypoparathyroidism, or respiratory alkalosis, may produce prolongation of the ST-segment and QT interval. Hypercalcemia, caused by adrenal insufficiency, hypoparathyroidism, kidney failure, or malignancy, may also cause serious arrhythmias, especially in the presence of digitalis.
Digitalis Effect
The administration of digitalis can cause ECG changes, even when the dosage is within the recommended therapeutic range. In cases of digitalis toxicity, excitatory or inhibitory effects on the heart and its electrical conduction system may occur. Excitatory effects include various types of ventricular and supraventricular ectopy, ventricular tachycardia, and ventricular fibrillation.Inhibitory effects include sinus bradycardia and heart block. The digitalis effect produces prolonged PR intervals, depressed (scooped) ST-segments, and alterations in T-wave morphology. The following ECG shows PAT with block,one of the classic arrhythmias seen in digitalis toxicity.
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| Atrial Tachycardia, 2:1AV block |
P henothiazines
The electrophysiological properties of phenothiazines are comparable to those of the Class I a antiarrhythmic-quinidine. Numerous ECG aberrations may be induced by these agents, including changes in the morphology of the T-wave, prolongation of the QT interval, and accentuation of the U-wave.“These repolarization abnormalities occur more frequently with thioridizine than with chlorpromazine, and even less so with trifluoperazine,” wrote Symanski and Gettes in the February 1993 issue of Drugs. “Supraventricular and ventricular tachycardias have been reported in patients receiving high doses of phenothiazines. Even with standard clinical dosages (100-400 mg/day), thioridazine causes minimal prolongation of the QT interval, reduction of T-wave amplitude, and prominent U-waves in nearly 50 per cent of patients.”
Antidepressants
At either therapeutic or toxic dosages, tricyclic and tetracyclic antidepressants can produce a number of effects on the ECG. ECG Changes produced by TCAs occur in about 20 per cent of patients receiving therapeutic dosages and include an increase in heart rate, prolongation of the PR interval, intraventricular conduction disturbances, increase in QTc interval, and flattening of T-waves. Factors such as the specific agent, plasma drug concentration, duration of therapy, age of the patient, and degree of underlying cardiovascular disease all play a role in the severity and frequency of these effects. While the risk of ventricular arrhythmia has been shown to correlate poorly with serum TCA concentrations, the electrocardiogram may still be a useful tool in detecting patients with suspected TCA overdose.
Antihistamines
Stimulation of histamine receptors (H 1 and H 2 ), which are located in both the atrial and ventricular myocardium and on epicardial coronary arteries, may also produce changes on the ECG. Stimulation of the H 2 receptors in the atrial and ventricular myocardium raises intracellular concentrations of cAMP by activating adenylate cyclase and phosphorylase, resulting in enhanced inotropic and chronotropic effects. Thus, the blocking of H 2 receptors by the H 2 antagonists may result in bradyarrhythmias, as noted in several case reports in which cimetidine and ranitidine have been implicated as rare causes of sinus bradycardia and heart block. The risk of these complications appears to be greater with long-term therapy and among elderly individuals.
The newer, long-acting, nonsedating antihistamines such as terfenadine and astemizole can pose a threat of cardiotoxicity. Rare reactions have occurred when blood levels of these agents become elevated due to either overdose or inhibition of their metabolism when given concomitantly with other agents (erythromycin, ketoconazole, or, as has been recently reported, grapefruit juice) affecting the same CP450 isozyme.
The disturbance in cardiac conduction is thought to be caused by these agents’ ability to block the potassium channel in the myocardial cell membrane, which affects cardiac repolarization. Thus, the effect on the ECG is prolongation of the QT interval, which may lead to torsade de pointes(see glossary). Studies to date have found no similar threat of cardiotoxicity with loratidine and cetirizine.
Other Drug Influences
The electrocardiographic effects of catecholamines, including agents such as dopamine and epinephrine, can be problematic to predict, since these agents have numerous effects on the heart.Catecholamines affect the currents that regulate repolarization of individual cells and fibers, and also can affect the heart rate, blood pressure, and serum potassium levels.
ECG changes caused by catecholamines are influenced by the route and rate of administration, as well as the dosage. For example, subcutaneous administration of epinephrine produces only sinus tachycardia and occasional premature beats. However, when administered intravenously,epinephrine may cause a variety of repolarization abnormalities, including ST changes.Intravenous infusion of isoprenaline (isoproterenol), to give another example, may cause inversion of T-waves.As more and more elderly nursing home residents are treated with a variety of pharmacological agents that affect membrane function and myocardial cells, the ECG is becoming a useful tool for monitoring drug effects and toxicities-not only for the physician, but for the entire interdisciplinary care team, including the consultant pharmacist. An appreciation of the information contained in the ECG printout is an essential component in the continuing effort to provide the best in comprehensive patient care.
The electrophysiological properties of phenothiazines are comparable to those of the Class I a antiarrhythmic-quinidine. Numerous ECG aberrations may be induced by these agents, including changes in the morphology of the T-wave, prolongation of the QT interval, and accentuation of the U-wave.“These repolarization abnormalities occur more frequently with thioridizine than with chlorpromazine, and even less so with trifluoperazine,” wrote Symanski and Gettes in the February 1993 issue of Drugs. “Supraventricular and ventricular tachycardias have been reported in patients receiving high doses of phenothiazines. Even with standard clinical dosages (100-400 mg/day), thioridazine causes minimal prolongation of the QT interval, reduction of T-wave amplitude, and prominent U-waves in nearly 50 per cent of patients.”
Antidepressants
At either therapeutic or toxic dosages, tricyclic and tetracyclic antidepressants can produce a number of effects on the ECG. ECG Changes produced by TCAs occur in about 20 per cent of patients receiving therapeutic dosages and include an increase in heart rate, prolongation of the PR interval, intraventricular conduction disturbances, increase in QTc interval, and flattening of T-waves. Factors such as the specific agent, plasma drug concentration, duration of therapy, age of the patient, and degree of underlying cardiovascular disease all play a role in the severity and frequency of these effects. While the risk of ventricular arrhythmia has been shown to correlate poorly with serum TCA concentrations, the electrocardiogram may still be a useful tool in detecting patients with suspected TCA overdose.
Antihistamines
Stimulation of histamine receptors (H 1 and H 2 ), which are located in both the atrial and ventricular myocardium and on epicardial coronary arteries, may also produce changes on the ECG. Stimulation of the H 2 receptors in the atrial and ventricular myocardium raises intracellular concentrations of cAMP by activating adenylate cyclase and phosphorylase, resulting in enhanced inotropic and chronotropic effects. Thus, the blocking of H 2 receptors by the H 2 antagonists may result in bradyarrhythmias, as noted in several case reports in which cimetidine and ranitidine have been implicated as rare causes of sinus bradycardia and heart block. The risk of these complications appears to be greater with long-term therapy and among elderly individuals.
The newer, long-acting, nonsedating antihistamines such as terfenadine and astemizole can pose a threat of cardiotoxicity. Rare reactions have occurred when blood levels of these agents become elevated due to either overdose or inhibition of their metabolism when given concomitantly with other agents (erythromycin, ketoconazole, or, as has been recently reported, grapefruit juice) affecting the same CP450 isozyme.
The disturbance in cardiac conduction is thought to be caused by these agents’ ability to block the potassium channel in the myocardial cell membrane, which affects cardiac repolarization. Thus, the effect on the ECG is prolongation of the QT interval, which may lead to torsade de pointes(see glossary). Studies to date have found no similar threat of cardiotoxicity with loratidine and cetirizine.
Other Drug Influences
The electrocardiographic effects of catecholamines, including agents such as dopamine and epinephrine, can be problematic to predict, since these agents have numerous effects on the heart.Catecholamines affect the currents that regulate repolarization of individual cells and fibers, and also can affect the heart rate, blood pressure, and serum potassium levels.
ECG changes caused by catecholamines are influenced by the route and rate of administration, as well as the dosage. For example, subcutaneous administration of epinephrine produces only sinus tachycardia and occasional premature beats. However, when administered intravenously,epinephrine may cause a variety of repolarization abnormalities, including ST changes.Intravenous infusion of isoprenaline (isoproterenol), to give another example, may cause inversion of T-waves.As more and more elderly nursing home residents are treated with a variety of pharmacological agents that affect membrane function and myocardial cells, the ECG is becoming a useful tool for monitoring drug effects and toxicities-not only for the physician, but for the entire interdisciplinary care team, including the consultant pharmacist. An appreciation of the information contained in the ECG printout is an essential component in the continuing effort to provide the best in comprehensive patient care.
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