Electrolytes Imbalances PDF

ELECTROLYTES IMBALANCES ELECTROLYTES IMBALANCES LEARNING OBJECTIVES: In this chapter, we were able to learn ways to assess a patient’s fluid status ways to identify patients at risk for fluid imbalances signs and symptoms of fluid imbala...

ELECTROLYTES IMBALANCES ELECTROLYTES IMBALANCES LEARNING OBJECTIVES: In this chapter, we were able to learn ways to assess a patient’s fluid status ways to identify patients at risk for fluid imbalances signs and symptoms of fluid imbalances teaching tips for patients with fluid imbalances tips for ensuring proper documentation of fluid imbalances. ELECTROLYTES IMBALANCES Magnesium Imbalances Normal serum magnesium Magnesium (Mg++) is an level is 1.8 to 2.6 mg/dL abundant intracellular (0.74 to 1.07 mmol/L) cation. It acts as an activator for Mg+ many intracellular enzyme systems and plays a role in both carbohydrate and protein metabolism ELECTROLYTES IMBALANCES Normally, the gastrointestinal (GI) and urinary systems regulate magnesium through absorption, excretion, and retention—that is, through dietary intake and output in urine and feces. The body tries to adjust to if the serum if the any change in magnesium magnesium Most healthy people can get all the the level drops level rises magnesium they need by eating a magnesium well-balanced diet that includes level. the GI tract magnesium-rich foods. the GI tract may absorb excretes more chocolate (especially dark chocolate) more in the feces dry beans and peas magnesium green, leafy vegetables the kidneys meats the kidneys excrete the nuts conserve excess in the magnesium seafood urine whole grains. ELECTROLYTES IMBALANCES HYPOMAGNESEMIA ( a serum magnesium (Mg2+) level Mg+ below 1.8 mEq/L or 0.74 mmol/L.) Frequently associated with hypokalemia and hypocalcemia. Magnesium is similar to calcium in two aspects: (1) it is the ionized fraction of magnesium that is primarily involved in neuromuscular activity (2) magnesium levels should be evaluated in combination with albumin levels ELECTROLYTES IMBALANCES FACTORS Mg+ GI TRACT LOSS (nasogastric suction, fluid from the lower GI tract has a higher diarrhea, or fistulas) concentration of magnesium than fluid from the upper tract, losses from diarrhea and intestinal fistulas are more likely to induce magnesium deficit than are those from gastric suction DISRUPTION IN SMALL BOWEL The distal small bowel is the major site of FUNCTION (e.g., intestinal resection magnesium absorption or inflammatory bowel disease) CHRONIC ALCOHOL ABUSE causes the urinary system to excrete more magnesium than normal. Alcoholics can also lose magnesium through poor intestinal absorption or from frequent or prolonged vomiting. Patients receiving prolonged I.V. Feedings contain little magnesium supplement FLUID THERAPY, TOTAL PARENTERAL NUTRITION (TPN), OR ENTERAL FEEDING FORMULAS Use of AMPHOTERICIN B, Drugs that can boost excretion of magnesium in the CISPLATIN, CYCLOSPORINE, urine PENTAMIDINE ISETHIONATE, OR AMINOGLYCOSIDE ANTIBIOTICS, ELECTROLYTES IMBALANCES Normally, if the Mg+ serum Hypomagnesemia occur magnesium level causing an increased drops membrane excitability accompanied by serum The body will compensate by calcium and potassium moving imbalances. magnesium out of the cells FACTORS the GI tract may absorb more Excitable membranes, magnesium especially nerve cell membranes, may depolarize the kidneys spontaneously conserve magnesium ELECTROLYTES IMBALANCES Increasing depolarization Mg+ of cell membrane Cardiovascular changes when serum magnesium levels are low, intracellular potassium levels are also low alter the resting membrane potential in cardiac muscle cells shortening the ST segment, prolonging the PR and QRS intervals, and triggering ectopic beats risk for hypertension, atherosclerosis, hypertrophic left ventricle, and a variety of dysrhythmias ELECTROLYTES IMBALANCES Mg+ Increasing depolarization of cell The patient has hyperactive deep tendon reflexes, numbness and tingling, and painful muscle contractions. Decreased levels increase Positive Chvostek and membrane impulse transmission Trousseau signs may be Neuromuscular changes from nerve to nerve or present because from nerve to skeletal hypomagnesemia may muscle. occur with hypocalcemia The patient may have tetany and seizures as hypomagnesemia worsens Source: https://www.youtube.com/watch? v=3PILgkVKlAg&pp=ygUgaHlwZXJhY3RpdmUgZGVlcCB0ZW5kb24gcmVmbGV4ZXM%3D ELECTROLYTES IMBALANCES Mg+ Increasing depolarization of cell Reduced motility, anorexia, nausea, constipation, and abdominal membrane distention are Magnesium is not decreased intestinal common. Intestinal changes able to absorb by smooth muscle the GI tract contraction A paralytic ileus may occur when hypomagnesemia is severe. ELECTROLYTES IMBALANCES Mg+ Instruct patient to consume foods rich in can be corrected by Mg such as green leafy vegetables, beans, diet alone lentils, white potatoes, wheat bran, dry roasted almonds, and peanut butter Mild magnesium MEDICAL MANAGEMENT Magnesium salts can be deficiency given orally in an oxide or gluconate form to replace continuous losses but can produce diarrhea Vital signs must be assessed frequently during magnesium Administer administration magnesium in the Patient receiving IV solution to Monitoring urine parenteral nutrition prevent output before and Shows how Mg++ hypomagnesemia after Magnesium is excreted administration ELECTROLYTES IMBALANCES NURSING MANAGEMENT Assess the patient’s mental status and report changes. Check the patient for dysphagia before he’s given food, oral fluids, or oral medications. Hypomagnesemia may impair his ability to swallow. Monitor the patient’s respiratory status. A magnesium deficiency can cause laryngeal stridor and compromise the airway. Institute seizure precautions. If a seizure occurs, report the type of seizure, its length, and the patient’s behavior during the seizure. Reorient him as needed. Connect your patient to a cardiac monitor if his magnesium level is below 1 mEq/L ELECTROLYTES IMBALANCES Mg+ FACTORS HYPERMAGNESEMIA (serum magnesium level KIDNEY INJURY As kidney function declines, magnesium levels higher than 2.6 mg/dL [1.07 rise since there is no magnesium regulatory mmol/L]) system other than urinary secretion UNTREATED DKA catabolism causes the release of cellular magnesium that cannot be excreted because of profound fluid volume depletion and resulting oliguria a rare electrolyte abnormality, because the EXCESSIVE USE OF Excessive use decreases GI motility causing kidneys efficiently excrete MAGNESIUM- decreased elimination of magnesium or its magnesium BASED ANTACIDS increased absorption due to intestinal OR LAXATIVES hypomotility from any cause can contribute to AND hypermagnesemia MEDICATIONS ELECTROLYTES IMBALANCES Mg+ Hypermagnesemia Normally, if there is causes reduced an increase Mg level membrane in the body excitability FACTORS the kidneys can rapidly reduce the Symptoms are amount of excess usually not apparent magnesium , especially if the until serum excess is from food magnesium levels sources exceed 4 mEq/L (1.6 mmol/L) ELECTROLYTES IMBALANCES Reduced membrane excitability Mg+ Cardiovascular Central nervous changes system ECG changes show bradycardia, a prolonged PR depressed nerve peripheral interval with a impulse vasodilation, and widened QRS transmission hypotension complex. Patients may be Bradycardia can drowsy or lethargic. be severe, and Coma may occur if the cardiac arrest is imbalance is prolonged possible. or severe Hypotension is also severe, with a diastolic pressure lower than normal. ELECTROLYTES IMBALANCES Chart to compare total serum magnesium levels Reduced membrane with the typical signs and symptoms that excitability Mg+ mayappear. 3 mEq/L Feelings of warmth Flushed appearance Mild hypotension Nausea and vomiting Neuromuscular 4 mEq/L Facial paresthesia changes Diminished DTR Muscle weakness 5 mEq/L D r o w s i n e s s E C G c ha n g e s B r a d yc a r d i a reduced or absent Wo r s e ni n g hyp o t e n s i o n deep tendon reflexes. 7 mEq/L Loss DTR 8 mEq/L Respiratory compromise 12 H e a r t b l o c k Voluntary skeletal mEq/L F l a c c i d p a r a l ys i s muscle contractions C o ma become progressively 15 Respiratory arrest weaker and finally mEq/L stop. ELECTROLYTES IMBALANCES MEDICAL MANAGEMENT Patient with respiratory Patient with patients with Severe depression or adequate renal kidney injury hypermagnesemia defective cardiac function conduction ventilatory support Administration of all parenteral and and IV elemental loop diuretics (e.g., avoiding the oral magnesium calcium as a furosemide) and administration of salts are magnesium sodium chloride or magnesium discontinued antagonist are lactated Ringer’s IV indicated solution enhances hemodialysis with a magnesium IV calcium magnesium-free excretion antagonizes the dialysate can cardiovascular and reduce the serum neuromuscular magnesium to a effects of safe level within magnesium hours ELECTROLYTES IMBALANCES NURSING MANAGEMENT Monitor your patient’s vital signs frequently. Stay especially alert for hypotension, bradycardia, and respiratory depression—indicators of hypermagnesemia. Assess the patient’s neuromuscular system, including DTRs and muscle strength Monitor serum electrolyte levels and other laboratory test results that reflect renal function, such as blood urea nitrogen and creatinine levels. Monitor the patient for hypocalcemia, which may accompany hypermagnesemia, because a low serum calcium level suppresses PTH secretion Evaluate the patient for changes in mental status. If the patient’s LOC decreases, institute safety measures. Reorient the patient if he’s confused. Prepare the patient for continuous cardiac monitoring. Assess ECG tracings for pertinent changes. ELECTROLYTES IMBALANCES Chloride Imbalances Normal serum Chloride (Cl−) is chloride level is 97 the major anion of to 107 mEq/L (97 the ECF to 107 mmol/L compartment. Chloride is It maintains cellular Chloride travels produced in the integrity by providing with positively stomach, where it water balance and charged sodium combines with maintains acid–base and work together hydrogen to form balance to form CSF. hydrochloric acid. CI- Chloride assists in maintaining acid–base balance and works as a buffer in the exchange of oxygen and CO2 in RBCs ELECTROLYTES IMBALANCES Normally, most chloride is absorbed in the intestines, with only a small portion lost in feces Acid-base balance Dietary sources of chloride include: canned vegetables eggs When chloride levels fresh fruits and vegetables, decrease, the kidneys retain especially high concentration in bicarbonate and bicarbonate levels increase. tomatoes, celery, lettuce, and olives milk processed meats When chloride levels salty foods increase, the kidneys excrete table or sea salt. bicarbonate and bicarbonate levels decrease ELECTROLYTES IMBALANCES FACTORS HYPOCHOLEREMIA (a serum chloride level below 97 REDUCED CHLORIDE occur in infants being fed chloride- mEq/L (97 mmol/L). INTAKE deficient formula and in people on salt- restricted diets Excessive chloride Severe vomiting can cause a loss of When serum chloride levels drop, losses (prolonged hydrochloric acid from the stomach, an levels of sodium, potassium, vomiting, diarrhea, acid deficit in the body, and calcium, and other electrolytes may severe subsequent metabolic alkalosis also be affected. diaphoresis, burns, Addison’s disease, Any prolonged and untreated gastric surgery, hyperchloremic state can result in a Here’s how hypochloremia can nasogastric (NG) state of hyperchloremic alkalosis. suctioning, and other GI lead to hyperchloremic metabolic tube drainage) alkalosis. HCO C NaHCO3 pH 3 l Kidneys retain Excess HCO3 ions raises NG suctioning HCO3 ions sodium and pH level and leads to can deplete Cl accumulate in the bicarbonate ions to hyperchloremic metabolic ELECTROLYTES IMBALANCES The kidneys are responsible for the Hypochloremia maintenance of total chloride balance Can cause sodium and The nerves also FACTORS potassium become more deficiency or excitable When chloride levels metabolic decrease, the kidneys alkalosis retain bicarbonate conditions that and bicarbonate affect acid-base levels increase. or electrolyte balance ELECTROLYTES IMBALANCES Hypochloremia Cardiovascular Neuromuscular Intestinal changes changes changes Decreases the activity of CI Hyperexcitability Metabolic channels in the of muscles alkalosis heart Cardiac tetany, As chloride decreases (usually because of arrhythmic hyperactive volume depletion), the kidney retains attacks such as DTRs, weakness, sodium and bicarbonate ions to balance the myocardial twitching, and loss. Bicarbonate accumulates in the ECF, ischemia muscle cramps which raises the pH Hand tremors, muscle twitching, numbness or tingling in the face, hands or feet ELECTROLYTES IMBALANCES MEDICAL MANAGEMENT Normal saline (0.9% sodium chloride) or half-strength Patient is Metabolic saline (0.45% sodium receiving a alkalosis chloride) solution is given by diuretic IV to replace the chloride. it may be Ammonium chloride, an discontinued or acidifying IV agent may another diuretic administer prescribed This agent is metabolized by the liver, and its effects last for about 3 days. Its use should be avoided in patients with impaired liver or renal function  ELECTROLYTES IMBALANCES NURSING MANAGEMENT Monitor cardiac Monitor and Monitor level of Monitor vital rhythm record serum signs, If the patient is consciousness because electrolyte especially alert and can (LOC), muscle hypokalemia levels, respiratory rate swallow without strength, and may be present especially and pattern, difficulty movement. with chloride, and observe for hypochloremia. sodium, worsening potassium, and offer foods high respiratory Have bicarbonate. in chloride, function. emergency assess arterial such as tomato equipment blood gas juice or salty handy in case (ABG) results broth. the patient’s for acid-base condition imbalance. deteriorates.  FACTORS ELECTROLYTES IMBALANCES INCREASED INTAKE OF can cause hyperchloremia, especially CHLORIDE ( in the form if water loss from the body occurs of sodium chloride) simultaneously. The water loss raises the chloride level even more. HYPERCHOLEREMIA ANASTOMOSES of the Increased chloride absorption by the serum level of chloride exceeds ureter and intestines bowel 107 mEq/L (107 mmol/L) dehydration, renal tubular Metabolic acidosis = most likely acidosis, diabetes caused insipidus, renal failure, by a loss of bicarbonate ions by the respiratory kidneys or GI tract thus a alkalosis, salicylate corresponding increase in chloride Hypernatremia, bicarbonate loss, toxicity, ions also occurs and metabolic acidosis can occur hyperparathyroidism, with high chloride levels.. hyperaldosteronism, and hypernatremia direct ingestion of cause chloride retention can lead to ammonium chloride or hyperchloremia other drugs that contain chloride Ion exchange resins cause chloride to be exchanged for ELECTROLYTES IMBALANCES The kidneys are responsible for the Hyperchloremia maintenance of total chloride balance Chloride and bicarbonate have an inverse FACTORS Maybe associated relationship, so an excess with hypernatremia of chloride ions may be linked to a decrease in When chloride levels bicarbonate increase, the kidneys excrete bicarbonate and bicarbonate Metabolic acidosis levels decrease  ELECTROLYTES IMBALANCES Hyperchloremia Untreated acidosis major indications are essentially those of (hyperchloremic Hypernatremia metabolic acidosis metabolic acidosis) can lead to tachypnea, lethargy, thirst, arrhythmias, weakness, dehydration, decreased cardiac hypotension diminished fluid retention output, a further cognitive ability, and deep, decrease in LOC, rapid respirations and even coma (Kussmaul’s respirations) dyspnea, tachycardia, hypertension, or pitting edema— signs of hypernatremia and hypervolemia ELECTROLYTES IMBALANCES MEDICAL MANAGEMENT Hypotonic IV Lactated Ringer’s solutions may be IV sodium Sodium, chloride, and solution may be given to restore bicarbonate fluids are restricted prescribed balance. To convert lactate to To increase bicarbonate in the bicarbonate levels, liver, which increases which leads to the the bicarbonate level renal excretion of and corrects the chloride ions acidosis. ELECTROLYTES IMBALANCES NURSING MANAGEMENT Assessment findings related to respiratory, Monitoring vital signs, neurologic, and cardiac The nurse educates the ABG values, and I&O is systems are documented, patient about the diet that important and changes are should be followed discussed with the primary provider. to assess the patient’s to manage status and the hyperchloremia and effectiveness of maintain adequate treatment. hydration. ELECTROLYTES IMBALANCES Phosphorus Imbalances Normal serum Phosphorus is essential to the phosphorus level is function of muscle and RBCs; It provides 2.7 to 4.5 mg/dL the formation of adenosine structural support (0.87 to 1.45 triphosphate (ATP) and of 2,3- to bones and teeth. mmol/L) in adults diphosphoglycerate the primary facilitates the anion of the release of oxygen ICF from hemoglobin maintaining acid–base balance, as well as the nervous system HPO4- intermediary metabolism of carbohydrate, protein, and fat ELECTROLYTES IMBALANCES Hod does body regulated phosphorus Major dietary sources of phosphorus include: Parathyroid dairy products, such as milk GI tract Kidneys gland and cheese dried beans The kidneys eggs phosphorus is readily excrete about absorbed through the controls hormonal fish 90% of gastrointestinal (GI) regulation of nuts and seeds phosphorus as tract, with the amount they regulate phosphorus levels organ meats, such as brain absorbed proportional to serum levels. by affecting the and liver the amount ingested. activity of poultry parathyroid whole grains hormone (PTH) Most ingested phosphorus is absorbed through the jejunum.  FACTORS ELECTROLYTES IMBALANCES Chronic diarrhea, GI malabsorption of phosphate Crohn’s disease, or celiac disease Vitamin D deficit Vitamin D regulates intestinal absorption of calcium and phosphate ion; therefore, a deficiency of vitamin D can cause both decreased calcium and phosphorus levels High intake of antacids Excess phosphorus binding by antacids may decrease the phosphorus available from the diet to an amount lower than HYPOPHOSPHATEMIA required to maintain serum phosphorus a value below 2.7 mg/dL (0.87 balance mmol/L) Administration of Feeding a patient who is nutritionally calories to patients who deprived stimulates a large insulin have had severe protein– release that can cause shift of phosphate calorie malnutrition from the extracellular to the intracellular compartment. Hyperparathyroidism cause increased urinary losses of phosphorus leading to hypophosphatemia Respiratory alkalosis cause a decrease in phosphorus in the commonly caused by bloodstream because of an intracellular shift extreme hyperventilation of phosphorus  HYPOPHOSPHATEMIA ELECTROLYTES IMBALANCES Mild to moderate Severe hypophosphatemia hypophosphatemia doesn’t are apparent in many organ usually cause symptoms. systems Musculoskeletal changes Deficiency of ATP Muscle damage may develop as the ATP level in the muscle tissue declines. Muscle weakness, diplopia weakened Altered muscle (double vision), malaise, respiratory cell activity and anorexia muscles and poor contractility of the rhabdomyolysis diaphragm. (skeletal muscle destruction) Respiratory Muscle enzymes such as failure creatine kinase are Respirations may appear released from the cells into shallow and ineffective. In the extracellular later stages, the patient Loss of bonefluid. may be cyanotic. density, osteomalacia (softening of the bones) Pain and bone fracture is present ELECTROLYTES IMBALANCES HYPOPHOSPHATEMIA Severe hypophosphatemia are apparent in many organ systems Deficiency of ATP decrease cell energy metabolism Cardiovascular Central nervous changes changes the patient may develop hypotension paresthesia, irritability, apprehension, and low cardiac output. memory loss, and confusion. Severe hypophosphatemia The neurologic effects of may lead to cardiomyopathy, hypophosphatemia may progress to which treatment can reverse seizures or coma. more susceptible to infection because of the effect of low levels of ATP results in decreased function of WBCs ELECTROLYTES IMBALANCES HYPOPHOSPHATEMIA Severe hypophosphatemia are apparent in many organ systems A drop in production of 2,3-DPG causes a decrease in oxygen delivery to tissues Cardiovascular changes less oxygen is delivered to changes in the structure and the myocardium, which function of RBCs can cause chest pain. hemolytic anemia ELECTROLYTES IMBALANCES MEDICAL MANAGEMEN T severe mild to moderate hypophosphatemia or hypophosphatemia a nonfunctioning GI tract, During infusions, diet high in phosphorus- I.V. watch for signs of rich foods, such as eggs, phosphorus hypocalcemia, nuts, whole grains, organ replacement hyperphosphatemia meats, fish, poultry, and milk products I.V. I.V. sodium potassium phosphate Oral supplements phosphate include Neutra-Phos and Neutra-Phos-K Potassium phosphate requires slow administration can cause tissue sloughing ELECTROLYTES IMBALANCES NURSING MANAGEMEN T Assess the Assess the Monitor the patient Administer Monitor vital patient’s level patient’s frequently for prescribed signs. of temperature at evidence of phosphorus consciousness least every 4 decreasing supplements and neurologic hours. Check WBC muscle strength,. Remember, status each counts. such as weak hypophosphatemi hand grasps or Keep in mind time you check Follow strict that oral a can lead to his vital signs. sterile slurred speech, respiratory failure, and document supplements technique in may cause low cardiac changing your findings output, confusion, regularly diarrhea. dressings. seizures, or coma. To improve Report signs their taste, of infection. mix them with juice. Vitamin D may also be ordered with the oral phosphate supplements to increase ELECTROLYTES IMBALANCES FACTORS kidney injury diminishes urinary phosphate excretion Conditions such as Cellular destruction causes a shift of excessive vitamin D phosphate from the intracellular to intake, administration of extracellular space total parenteral nutrition, HYPERPHOSPHATEMIA chemotherapy for a serum phosphorus level neoplastic disease, that exceeds 4.5 mg/dL (1.45hypoparathyroidism, mmol/L) pseudohypoparathyroidism , metabolic or respiratory acidosis, DKA, acute hemolysis, high phosphate intake, profound muscle necrosis, and increased phosphorus absorption Hypoparathyroidism causes hyperphosphatemia by failure of the kidneys to inhibit renal reabsorption of phosphate. ELECTROLYTES IMBALANCES HYPERPHOSPHATEMIA a high serum phosphorus level tends to cause a low serum calcium concentration causes neuromuscular major long- short-term irritability and muscle term consequence spasms consequence When phosphorus levels rise, tetany (severe phosphorus binds with calcium, muscle forming an insoluble compound cramping) called calcium phosphate Organ dysfunction can result when calcium phosphate precipitates, or is deposited, in the heart, lungs, kidneys, or other soft tissues (calcification) patient may experience arrhythmias, an irregular heart rate, and decreased urine output. ELECTROLYTES IMBALANCES MEDICAL MANAGEMENT Therapeutic severe measures a patient with hyperphosphate include reducing diabetes mia dietary intake of phosphorus and eliminating the Administering use of insulin causes proximal hemodialysis or I.V. saline phosphorus- phosphorus to diuretics such as peritoneal solution based laxatives shift back into acetazolamide dialysis and enemas. the cells, which can result in decreased serum phosphorus to promote to increase levels renal excretion renal excretion of phosphorus of phosphorus ELECTROLYTES IMBALANCES NURSING MANAGEMENT Notify the Watch for signs and practitioner if you symptoms of detect signs or Give antacids with hypocalcemia, such symptoms of meals to increase Monitor vital signs. as paresthesia in the calcification, including their effectiveness in fingers or around the oliguria, visual binding phosphorus mouth, hyperactive impairment, reflexes, or muscle conjunctivitis, cramps. irregular heart rate or palpitations, and papular eruptions