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LUKE 1:
Electrolyte Imbalances : K+ Imbalances
Na+ is the major intracellular electrolyte
- 98% of body’s K is INSIDE cell
- 2% is in ECF (important in neuromuscular function) K+ influences both skeletal and cardiac muscle activity Ex. Alterations in its concentration = change in myocardial irritability and rhythm Under Na+K+ pump = K+ is constantly moving in and out of cells Normal Serum K+ Concentration = 3.5 - 5 mEq/L K+ imbalances are associated with: a. Various disease b. Injuries c. Medications (NSAIDs & ACEI) d. Acid-base imbalance To maintain K+ balance: renal system MUST function (80% of K+ is excreted daily, by way of kidneys; 20% is lost through bowel and sweat) Kidney - regulate K+ balance by adjusting the amount of K+ excreted in urine INCREASE K+ = INCREASED K+ LEVEL IN RENAL TUBULAR CELL Concentration Gradient occurs, favoring the movement of K+ into renal tubule and excretion of K+ in urine = Increased aldosterone d/t excretion of K+ by kidney (kidney DOES NOT conserve K+) = K+ may still be lost in urine in presence of K+ deficit
Potassium Deficit (Hypokalemia)
Serum K+ level < 3.5 mEq/L (3.5 mmol/L) May occur in px w/ normal K+ stores; when alkalosis is present - temporary shift of Serum K+ into cells occurs
Pathophysiology:
Clinical Manifestation
Can result in widespread derangements in physiologic function Severe hypokalemia - can cause death through: Cardiac or respiratory arrest Clinical signs - develop when K+ level < 3 mEq/L Can lead ti inability of kidneys to concentrate urine = dilute urine = Polyuria, nuctoria and excessive thirst K+ depletion - suppresses the release of insulin = glucose intolerance
Assessment and Diagnostic Findings:
Serum K+ concentration < lower limit of normal ECG : flat T waves/inverted T waves/both (ischemia); depressed ST segments Contributing Factors: Potassium-losing diuretics a. Thiazide diuretics b. Loop diuretics Corticosteroids Na penicillin Carbenicillin Amphotercin B GI loss of K+ (common cause) Vomiting and Gastric suction K+ is lost when gastric fluid is lost; K+ is lost through kidneys in response to metabolic acidosis Relatively large amounts of K+ are contained in intestinal fluids, K+ deficit occurs frequently w/ DIARRHEA - may contain as much as 30 mEq/L of K+ Prolonged Intestinal suctioning Recent ileostomy Villous^ adenoma^ -^ tumor^ of^ intestinal^ tract characterized by excretion of K+ rich mucus Hyperaldosteronism Increases renal K+ wasting = severe K+ depletion i. Primary Hyperaldosteronism - seen in px w/ adrenal adenomas ii. Secondary Hyperaldosteronism - occur in px w/ cirrhosis, nephrotic syndrome, heart failure, or malignant HPN Risk Factors: Px^ w/^ persistent^ insulin^ hypersecretion Insulin promotes entry of K+ into skeletal muscle and hepatic cells (case in px receiving high-carbohydrate parenteral nutrition Px who do not eat normal diet for prolonged period a. Older people and Px with alcoholism or anorexia nervosa b. People with bulimia (d/t): a) Self-induced vomiting b) Misuse of laxative, diuretics, and Enemas Magnesium Depletion HYPOKALEMIA S/Sx: Fatigue Anorexia Nause and Vomiting Muscle Weakness Polyuria Decreased bowel mtility Ventricular asystole/fibrilation Paresthesias Leg cramps ↓BP Ileus, abdominal distention Hypoactive reflexes ECG: flattened T waves, Prominent U waves, ST depression, Prolonged PR
LUKE 1: Effect of potassium on the electrocardiogram (ECG). a. Normal tracing. b. Hypokalemia : serum potassium level below normal. Left : Flattening of the T wave and the appearance of a U wave. Right : Further flattening with prominent U wave. c. Hyperkalemia : serum potassium level above normal. Left : Moderate elevation with wide, at P wave; wide QRS complex; and peaked T wave. Right : ECG changes seen with extreme potassium elevation: widening of QRS complex and absence of P wave. Elevated U wave - specific to hypokalemia Hypokalemia - increases sensitivity to digitalis (predisposing px to digitalis toxicity at lower digitalis level) K+ loss - evident from Hx; IF cause of loss is UNCLEAR - 24-hr urinary K+ excretion test is performed (distinguish between renal & extrarenal loss ) Urinary K+ excretion > 20 mEq/day with HYPOKALEMIA = renal K+ loss is the cause.
Medical Management:
a. Increased Intake in daily diet or by Oral K+ supplements for deficiencies b. IV replacement therapy
- IF hypokalemia cannot be prevented by conventional measures
- K+ loss MUST be corrected daily; administration of 40- mEq/day (adult IF there are no abnormal losses of K+) c. Diet containing sufficient K+ - Dietary intake in average adult = 50-100 mEq/day Foods high in K+ : fruits & vegetables, legumes, whole grains, milk, and meat Salt substitutes = 50-60 mEq of K+/teaspoon; may be sufficient to prevent hypokalemia IV route - mandatory for px with severe hypokalemia (serum K+ level = 2 mEq/L) KCL - usually used to correct K+ deficit CH3CO2K (potassium acetate) & KH2PO4 (potassium phosphate) may be prescribed
Nursing Management:
Monitor for early presence of Hypokalemia (px at risk) Signals that warrants the need so assess serum potassium concentration: a. Fatigue b. Anorexia c. Muscle Weakness d. Decreased Bowel Motility e. Parethesias f. Dysrhythmias ECG - may provide useful information Ex. Px receiving digitalis who are at risk for K+ deficiency should be monitored closely for signs of digitalis toxicity (hypokalemia potentiates the action of digitalis)
Preventing Hypokalemia:
Encourage px at risk to eat foods rich in K+ (when diet allows) Source of K+ a. Fruit juices and bananas b. Melon c. Citrus fruits d. Fresh and frozen vegetables e. Lean meats f. Milk g. Whole grains IF hypokalemia is caused by laxatives/diuretics - px education may help alleviate the problem Part of health Hx and assessment SHOULD be directed at identifying problems amenable to prevention through education Careful monitoring of fluid I&O (40 mEq of K+ is lost qLiter of urine output) Monitor ECG for changes Check arterial blood gas values for elevated bicarbonate and pH levels
Correcting Hypokalemia:
Mild to moderate hypokalemia - PO; oral K+ supplements are absorbed well CARE - should be exercised when administering K+ (older adults who have lower lean body mass and total body K+ levels = lower K+ requirements) K+ may be retained more readly in OLDER PX - renal f(x) is loss with advancing years
Administering Intravenous K+
Administered ONLY after adequate urine output has been established DECREASE in urine volume <20mL/hr for 2 consecutive hours - indication to STOP K+ infusion until situation is evaluated K+ is excreted by kidneys; when Oliguria occurs = K+ administration can cause Serum K+ concentration to RISE dangerously Administration is done w/ extreme caution using Infusion pump (px monitored by continuous ECG) Caution mus be used when selecting premixed soln’ of IV fluid containing KCL (concentration ranges from 10- mEQ/L) Renal Function - monitored through BUN and Creatinine levels and Urine output (px receiving K+ replacement) Monitor for S of worsening Hypo/hyperkalemia (“)
LUKE 1: Minutes after administration, Ca antagonizes action of hyperkalemia on heart BUT does NOT reduce serum K+ concentration CaCl = 13.6 mEq of Ca; Ca Gluconate = 4.5 mEq of Ca; NOT INTERCHANGEABLE Myocardial protective effects of Ca last about 30 minutes Monitor BP to detect hypotension, may result from rapid IV administration of Ca gluconate Monitor ECG - appearance of bradycardia is an indication to STOP the infusion Extra caution in px that has been digitalized (received accelerated dosages of digitalis-based cardiac glycoside to reach desired serum digitalis level rapidly); parenteral administration of Ca sensitizes heart to digitalis and may precipitate digitalis toxicity IV administration of Na bicarbonate (severe metabolic acidosis) - to alkalinize plasma, shift K+ INTO cells, and furnish Na to antagonize cardiac effects of K+ (effects begin with 30 to 60 minutes, persist for hours, temporary) Circulatory Overload & hypernatremia can occur when large amounts of hypertonic Na bicarbonate are given Should be guided by bicarbonate concentration ir calculated base deficit obtained from blood gas analysis or laboratory measurement IV administration of regular Insulin and hypertonic dextrose solution - causes temporary shift of K+ INTO cells Onset of action within 30 minutes, lasts for several hours Loop diuretics (Furosemide [Lasix]) - increase excretion of H2O by inhibiting Na, K, and Chloride reabsorption in ascending loop of Henle and distal renal tubule Beta-2 agonist (albuterol [Proventil, Ventolin]) - highly effective in decreasing K+, can cause tachycardia and chest discomfort Move K+ INTO cells, may be used in absence of ischemic cardiac disease Their use is a stopgap measure that only temporarily protects the px from hyperkalemia Actual removal of K+ in body (cation exchange resins, peritoneal dialysis, hemodialysis or other renal replacement therapy) - used if Hyperkalemic condition is NOT transient
Nursing Management
Identify and closely monitor px at risk for K+ excess for signs of hyperkalemia Monitor and observe I&O, signs of muscle weakness and dysrhythmias V/s, apical pulse should be taken Note presence of Paresthesias and GI symptoms (nausea, and intestinal colic) Monitor BUN, creatinine, glucose, and arterial blood gas values in px at risk for developing hyperkalemia
Preventing Hyperkalema
Encourage px to adhere to precribed K+ restriction - to prevent hyperkalemia in px at risk K+ rich foods (to be avoided) a. Fruits and vegetables b. Legumes c. Whole-grain breads d. Lean meat e. Milk f. Eggs g. Coffee h. Tea i. cocoa Food w/ minimal K+ content a. Butter b. Margarine c. Cranberry juice or sauce d. Ginger ale e. Gumdrops or jellybeans f. Hard cadny g. Root beer h. Sugar i. Honey
Correcting Hyperkalemia
Administer and Monitor K+ solutions CLOSELY (esp concentrations and rate of administration) Caution px to use sal substitutes sparingly if they are taking other supplementary forms of K+ or potassium-conserving diuretics DO NOT ADMINISTER : Potassium-conserving diuretics (spironolactone [Aldactone], triamterene [Dyrenium], amiloride [Midamor]) potassium supplements, and salt substitutes in px with renal dysfunction
