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Chapter: Medical Surgical Nursing: Fluid and Electrolytes: Balance and Distribution

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Potassium Excess (Hyperkalemia)

Hyperkalemia (greater-than-normal serum potassium concentra-tion) seldom occurs in patients with normal renal function.

POTASSIUM EXCESS (HYPERKALEMIA)

Hyperkalemia (greater-than-normal serum potassium concentra-tion) seldom occurs in patients with normal renal function. Like hypokalemia, hyperkalemia is often due to iatrogenic (treatment-induced) causes. Although less common than hypokalemia, hyper-kalemia is usually more dangerous because cardiac arrest is more frequently associated with high serum potassium levels.

 

A variation of hyperkalemia, pseudohyperkalemia has a num-ber of causes The most common causes are the use of a tight tourniquet around an exercising extremity while drawing a blood sample and hemolysis of the sample before analysis. Other causes include marked leukocytosis (white blood cell count exceeding 200,000) or thrombocytosis (platelet count exceeding 1 million), drawing blood above a site where potassium is infusing, and fa-milial pseudohyperkalemia, where potassium leaks out of the red blood cells while the blood is awaiting analysis. Failure to be aware of these causes of pseudohyperkalemia can lead to aggressive treat-ment of a nonexistent hyperkalemia, resulting in serious lower-ing of serum potassium levels. Thus, measurements of grossly elevated levels should be verified.

 

The major cause of hyperkalemia is decreased renal excretion of potassium. Thus, significant hyperkalemia is commonly seen in patients with untreated renal failure, particularly those in whom potassium levels rise as a result of infection or excessive in-take of potassium in food or medications. In addition, patients with hypoaldosteronism and Addison’s disease are at risk for hyperkalemia because these conditions are characterized by defi-cient adrenal hormones, leading to sodium loss and potassium retention.

 

Medications have been identified as a probable contributing factor in more than 60% of hyperkalemic episodes. Medications commonly implicated are potassium chloride, heparin, ACE in-hibitors, captopril, NSAIDs, and potassium-sparing diuretics. In most such cases, potassium regulation is compromised by renal insufficiency (Perazella, 2000).

 

Although a high intake of potassium can cause severe hyper-kalemia in patients with impaired renal function, hyperkalemia rarely occurs in people with normal renal function. For all pa-tients, however, improper use of potassium supplements predis-poses them to hyperkalemia, especially when salt substitutes are used. Not all patients receiving potassium-losing diuretics require potassium supplements, and patients receiving potassium-conserving diuretics should not receive supplements.

In acidosis, potassium moves out of the cells into the ECF. This occurs as hydrogen ions enter the cells, a process that buffers the pH of the ECF. An elevated extracellular potassium level should be anticipated when extensive tissue trauma has occurred, as in burns, crushing injuries, or severe infections. Similarly, it can occur with lysis of malignant cells after chemotherapy.

Clinical Manifestations

The most important consequence of hyperkalemia is its effect on the myocardium. Cardiac effects of an elevated serum potassium level are usually not significant below a concentration of 7 mEq/L (7 mmol/L), but they are almost always present when the level is 8 mEq/L (8 mmol/L) or greater. As the plasma potassium level rises, disturbances in cardiac conduction occur. The earliest changes, often occurring at a serum potassium level greater than 6 mEq/L (6 mmol/L), are peaked, narrow T waves; ST-segment depres-sion; and a shortened QT interval. If the serum potassium level continues to rise, the PR interval becomes prolonged and is fol-lowed by disappearance of the P waves. Finally, there is decom-position and prolongation of the QRS complex (see Fig. 14-5). Ventricular dysrhythmias and cardiac arrest may occur at any point in this progression.


 

Severe hyperkalemia causes skeletal muscle weakness and even paralysis, related to a depolarization block in muscle. Similarly, ventricular conduction is slowed. Although hyperkalemia has marked effects on the peripheral nervous system, it has little effect on the central nervous system. Rapidly ascending muscular weak-ness leading to flaccid quadriplegia has been reported in patients with very high serum potassium levels. Paralysis of respiratory and speech muscles can also occur. Additionally, GI manifestations, such as nausea, intermittent intestinal colic, and diarrhea, may occur in hyperkalemic patients.

Assessment and Diagnostic Findings

Serum potassium levels and ECG changes are crucial to the diag-nosis of hyperkalemia, as discussed above. Arterial blood gas analy-sis may reveal metabolic acidosis; in many cases, hyperkalemia occurs with acidosis.

Medical Management

An immediate ECG should be obtained to detect changes. Shortened repolarization and peaked T waves are seen initially.

It is prudent as well to obtain a repeat serum potassium level from a vein without an IV infusion containing potassium to verify results.

 

In nonacute situations, restriction of dietary potassium and potassium-containing medications may suffice. For example, elim-inating the use of potassium-containing salt substitutes in the pa-tient taking a potassium-conserving diuretic may be all that is needed to deal with mild hyperkalemia.

 

Prevention of serious hyperkalemia by the administration, either orally or by retention enema, of cation exchange resins (eg, Kayexalate) may be necessary in patients with renal impairment. Cation exchange resins cannot be used if the patient has a para-lytic ileus because intestinal perforation can occur. Kayexalate can bind with other cations in the GI tract and contribute to the de-velopment of hypomagnesemia and hypocalcemia; it may also cause sodium retention and fluid overload (Karch, 2002).

 

EMERGENCY PHARMACOLOGIC THERAPY

 

When serum potassium levels are dangerously elevated, it may be necessary to administer IV calcium gluconate. Within minutes after administration, calcium antagonizes the action of hyper-kalemia on the heart. Infusion of calcium does not reduce the serum potassium concentration but immediately antagonizes the adverse cardiac conduction abnormalities. Calcium chloride and calcium gluconate are not interchangeable: calcium gluconate con-tains 4.5 mEq of calcium and calcium chloride contains 13.6 mEq of calcium; therefore, caution must be used.

 

Monitoring the blood pressure is essential to detect hypoten-sion, which may result from the rapid IV administration of cal-cium gluconate. The ECG should be continuously monitored during administration; the appearance of bradycardia is an indi-cation to stop the infusion. The myocardial protective effects of calcium are transient, lasting about 30 minutes. Extra caution is required if the patient has been “digitalized” (received accelerated dosages of a digitalis-based cardiac glycoside to reach a desired serum digitalis level rapidly) because parenteral administration of calcium sensitizes the heart to digitalis and may precipitate digi-talis toxicity.

 

IV administration of sodium bicarbonate may be necessary to alkalinize the plasma and cause a temporary shift of potassium into the cells. Also, sodium bicarbonate furnishes sodium to an-tagonize the cardiac effects of potassium. Effects of this therapy begin within 30 to 60 minutes and may persist for hours; how-ever, they are temporary.

 

IV administration of regular insulin and a hypertonic dextrose solution causes a temporary shift of potassium into the cells. Glu-cose and insulin therapy has an onset of action within 30 minutes and lasts for several hours.

 

Beta-2 agonists also move potassium into the cells and may be used in the absence of ischemic cardiac disease. These stop-gap measures only temporarily protect the patient from hyper-kalemia. If the hyperkalemic condition is not transient, actual removal of potassium from the body is required; this may be ac-complished by using cation exchange resins, peritoneal dialysis, hemodialysis or other forms of renal replacement therapy.

 

Nursing Management

 

Patients at risk for potassium excess, for example those with renal failure, should be identified so they can be monitored closely for signs of hyperkalemia. The nurse observes for signs of muscle weakness and dysrhythmias. The presence of paresthesias is noted, as are GI symptoms such as nausea and intestinal colic. For patients at risk, serum potassium levels are measured periodically.Elevated serum potassium levels may be erroneous; thus, highly abnormal levels should always be verified. To avoid false reports of hyperkalemia, prolonged use of a tourniquet while drawing the blood sample is avoided, and the patient is cautioned not to ex-ercise the extremity immediately before the blood sample is ob-tained. The blood sample is delivered to the laboratory as soon as possible, because hemolysis of the sample results in a falsely ele-vated serum potassium level.

 

PREVENTING HYPERKALEMIA

 

Measures are taken to prevent hyperkalemia in patients at risk, when possible, by encouraging the patient to adhere to the pre-scribed potassium restriction. Potassium-rich foods to be avoided include coffee, cocoa, tea, dried fruits, dried beans, and whole-grain breads. Milk and eggs also contain substantial amounts of potassium. Conversely, foods with minimal potassium content include butter, margarine, cranberry juice or sauce, ginger ale, gumdrops or jellybeans, hard candy, root beer, sugar, and honey.

 

CORRECTING HYPERKALEMIA

 

As stated earlier, it is possible to exceed the tolerance for potas-sium in any person if it is administered rapidly by the IV route. Therefore, great care should be taken to monitor potassium so-lutions closely, paying close attention to the solution’s concen-tration and rate of administration. When potassium is added to parenteral solutions, the potassium is mixed with the fluid by in-verting the bottle several times. Potassium chloride should never be added to a hanging bottle because the potassium might be ad-ministered as a bolus (potassium chloride is heavy and settles to the bottom of the container).

 

It is important to caution patients to use salt substitutes spar-ingly if they are taking other supplementary forms of potassium or potassium-conserving diuretics. Also, potassium-conserving diuretics, such as spironolactone (Aldactone), triamterene (Dyre-nium), and amiloride (Midamor); potassium supplements; and salt substitutes should not be administered to patients with renal dys-function. Most salt substitutes contain approximately 50–60 mEq of potassium per teaspoon.

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