Arrhythmia potassium

The major objective of drug therapy in the alcohol withdrawal period is prevention of seizures, delirium, and arrhythmias. Potassium, magnesium, and phosphate balance should be restored as rapidly as is consistent with renal function. Thiamine therapy is initiated in all cases. Persons in mild alcohol withdrawal do not need any other pharmacologic assistance. 

Be especially alert for potassium depletion in patients taking digoxin (cardiac arrhythmias). Potassium supplements are frequently ordered. 

One of the major side effects of using a loop diuretic Is excessive excretion of electrolytes. Including potassium Ions. Loss of potassium can eventually lead to hypokalemia (low blood potassium), and hypokalemia alone can lead to the development of cardiac arrhythmias. Potassium loss, however, also potentiates the actions of digitalis (cardiac sodlum-potassium-adenosine triphosphatase Inhibition) and can lead to digitalis-induced cardiac arrhythmias as well. Hypokalemia can be treated/prevented by the use of potassium supplements or the use of a potassiumsparing diuretic (e.g., triamterene and amiloride). Because potassium-sparing diuretics are weakly basic drugs, they do not alter the active secretion of loop diuretics. 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

No significant interactions have been reported when tiie expectorants are used as directed. The exception is iodine products. Lithium and other antithyroid drug may potentiate the hypotliyroid effects of these drug if used concurrently with iodine products. When potassium-containing medications and potassium-sparing diuretics are administered with iodine products, the patient may experience hypokalemia, cardiac arrhythmias, or cardiac arrest. Thyroid function tests may also be altered by iodine... 

The most common imbalances are a loss of potassium and water. Other electrolytes, namely magnesium, sodium, and chlorides, are also lost. When too much potassium is lost, hypokalemia (low blood potassium) occurs (see Home Care Checklist Preventing Potassium Imbalances). In certain patients, such as those also receiving a digitalis glycoside or those who currently have a cardiac arrhythmia, hypokalemia has the potential to create a mo re serious arrhythmia Hypokalemia is... 

Adverse reactions observed with the administration of terbutaline include nervousness, restlessness, tremor, headache, anxiety, hypertension, hypokalemia (low serum potassium), arrhythmias, and palpitations. A serious, but rare, adverse reaction is pulmonary edema... 

To reduce mortality, administration of an aldosterone antagonist, either eplerenone or spironolactone, should be considered within the first 2 weeks following MI in all patients who are already receiving an ACE inhibitor (or ARB) and have an EF of equal to or less than 40% and either heart failure symptoms or diagnosis of diabetes mellitus.3 Aldosterone plays an important role in heart failure and in MI because it promotes vascular and myocardial fibrosis, endothelial dysfunction, hypertension, left ventricular hypertrophy, sodium retention, potassium and magnesium loss, and arrhythmias. Aldosterone antagonists have been shown in experimental and human studies to attenuate these adverse effects.70 Spironolactone decreases all-cause mortality in patients with stable, severe heart failure.71... 

Hyperkalemia is defined as a serum potassium concentration greater than 5 mEq/L (5 mmol/L). Manifestations of hyperkalemia include muscle weakness, paresthesias, hypotension, ECG changes (e.g., peaked T waves, shortened QT intervals, and wide QRS complexes), cardiac arrhythmias, and a decreased pH. Causes of hyperkalemia fall into three broad categories (1) increased potassium intake (2) decreased potassium excretion and (3) potassium release from the intracellular space. 

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

Calcium administration rapidly reverses ECG manifestations and arrhythmias, but it does not lower serum potassium concentrations. Calcium is short acting and therefore must be repeated if signs or symptoms recur. 

W., Keating, M.T. and Goldstein, S.A. (1999) MiRPl forms IKr potassium channels with HERG and is associated with cardiac arrhythmia. Cell, 97, 175-187. 

Sanguinetti, M.C., Jiang, C., Curran, M.E. and Keating, M.T. (1995) A mechanistic linkbetween an inherited and an acquired cardiac arrhythmia HERG encodes the Iki potassium channel. Cell, 81, 299-307. 

Sanguinetti, M.C. and Tristani-Firouzi, M. (2006) hERG potassium channels and cardiac arrhythmia. Nature, 440, 463 69. 

Maintenance dose 0.125-0.25 mg PO/IV qd low potassium or magnesium levels potentiate toxicity reduce dose in renal failure toxicity indicated by nausea, headache, visual disturbances (yellow-green halos), ventricular arrhythmias. Quinidine, verapamil, and amiodarone elevate digoxin level. 

Prevention of potassium depletion when dietary intake is inadequate in the following conditions Patients receiving digitalis and diuretics for CHF significant cardiac arrhythmias hepatic cirrhosis with ascites states of aldosterone excess with normal renal function potassium-losing nephropathy certain diarrheal states. 

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