Nursing 105

Essentials of Nursing Study Guide

©2018 Achieve Page 93 of 160 Hyperkalemia is due to acute or renal disease, low cardiac output states, acidosis, sodium depletion, or large muscle mass injury. • Signs and symptoms: decreased cardiac output; depression of ST segment; prolonged PR interval; tall, peaked/tented T waves; flattening and widening of P waves in severely elevated levels; abdominal cramping; nausea; diarrhea; bradycardia; apathy; confusion; muscle flaccidity, numbness of extremities • Treatment: give 10 Units of Insulin (insulin promotes shifting of potassium into the cells); glucose in the form of D50 is given after giving an insulin bolus to prevent hypoglycemia; sodium bicarbonate (allows for the exchange of intracellular hydrogen and extracellular potassium); calcium chloride to protect against the cardiotoxic effects of hyperkalemia (use calcium cautiously in patients taking Digoxin as it may cause Digoxin toxicity); Kayexalate is given orally or rectally to bind with potassium; Sorbitol is given to promote the excretion of Kayexalate from the bowel; dialysis is indicated if the cause of the hyperkalemia is refractory to initial stabilizing measures (i.e. renal failure) Hypocalcemia frequently occurs because there is a reduction in total body calcium due to increased calcium loss, altered intestinal absorption, or altered regulation by the parathyroid hormone. There is a reduction on the amount of ionized calcium available due to alkalosis. Phosphorus and calcium have a reciprocal relationship, when one rises the other falls. The two most common causes of hypocalcaemia are renal failure and pancreatitis. In acute pancreatitis, the inflamed pancreas causes a precipitation of calcium making less serum ionized calcium available for body functions. Pancreatitis also causes depressed levels of albumin causing a further fall in calcium levels. Hypomagnesaemia may also lower calcium levels as the parathyroid hormone requires magnesium to function adequately. • Risk factors: decreased ionized calcium due to alkalemia or hemodilution; increased calcium loss due to diuretics; decreased intestinal absorption due to decreased intake; impaired Vitamin D metabolism (renal failure); chronic diarrhea; post-gastrectomy; hypothyroidism; hypomagnesaemia • Signs and symptoms: numbness and tingling of fingers and lips; hyperactive reflexes; muscle cramps; tetany; convulsions; bone fractures in chronic hypocalcemia; prolonged QT interval (at risk for Torsade de Points); in severe hypocalcemia patients can develop laryngeal spasm • Treatment : treating the cause; calcium replacement; give IV calcium slowly, do not mix with phosphate or bicarbonate; watch for digoxin toxicity as calcium potentates it effects; vitamin D replacement; reduce phosphorus levels through dialysis or aluminum containing antacids; avoid hyperventilation as alkalosis causes ionized calcium levels to fall Hypercalcemia is caused by increased total calcium or increased ionized calcium. If hypercalcemia is accompanied by normal or elevated phosphate levels, calcium phosphate crystals may form and be deposited throughout the body. These crystals may form anywhere in the body causing serious damage like stroke, myocardial infarction, kidney stones, obstruction of blood flow to limbs, or mesenteric arteries. The normal serum calcium level is 8.2-10.2 mg/dl in adults, 8.6-11.2 mg/dl in children.