Fluid and Electrolyte Imbalances PDF

Care of the Clients with FLUID AND ELECTROLYTE Imbalances “Many of life’s failures are people who did not realize how close they were to success when they gave up.” – Thomas Edison  OBJECTIVES At the end of the topic the students will able to understand and familiarize the Flui...

Care of the Clients with FLUID AND ELECTROLYTE Imbalances “Many of life’s failures are people who did not realize how close they were to success when they gave up.” – Thomas Edison  OBJECTIVES At the end of the topic the students will able to understand and familiarize the Fluid Imbalances, Electrolyte Imbalances and the Respiratory Acid- Base Imbalances  CONTENT ▪ Fluid Imbalances ▪ Electrolyte Imbalances ▪ Respiratory Acid-Base Imbalances  Fluid Imbalances 1. Hyperosmolar Imbalance (Dehydration) Dehydration is water loss without corresponding loss of sodium. This causes shifting of fluids from the ICF to ECF. The cells shrink. There is sodium excess or water deficit. The initial manifestation of dehydration is thirst. The most objective indicator of dehydration is weight loss, next is decreased urine output.  Fluid Imbalances The vital sign changes in dehydration are as The other signs and follows: symptoms of dehydration Body Temperature are as follows: Pulse rate Dry mouth and throat (tachycardia) Warm, flushed, dry skin Respiratory rate Soft, sunken eyeballs (tachypnea) Dark, concentrated urine Blood pressure Altered LOC (hypotension due to Increased hematocrit, BUN, decreased plasma serum electrolyte levels. volume)  Fluid Imbalances Collaborative management for dehydration are as follows: Fluid replacement. Oral care for dry mouth and throat. Safety measures for altered level of consciousness. Identify and treat underlying cause, e.g., enteral feedings, renal failure, diabetes mellitus (DM).  Fluid Imbalances 2. Hyposmolar imbalance (Water Intoxication) This causes shifting of fluids from the ECF to ICF. The cells swell. There is sodium deficit or water excess. The most dangerous effect of water intoxication is increased ICP. The clinical manifestations of water intoxication are as follows: Changes in mental status, e.g., confusion, incoordination, convulsions. Sudden weight gain Peripheral edema  Fluid Imbalances Collaborative management for water intoxication include the following: Fluid restriction. Administration of diuretics as prescribed. Infusion of hypertonic saline per IV. Promote safety. Assess neurologic status. Identify and treat underlying cause, e.g., excess intake of electrolyte - free fluid, repeated tap water enema, SIADH, sodium deficit.  Fluid Imbalances 3. Isotonic Volume Deficit (ECF Volume Deficit) There is water and electrolyte loss. The clinical manifestations of ECF volume deficit are as follows: Weight loss Oliguria, urine specific gravity is high Dry mucous membrane of the mouth Poor skin turgor (not an accurate indicator among elderly because their skin is normally wrinkled) Postural hypotension Tachycardia, tachypnea  Fluid Imbalances Collaborative management for ECF volume deficit Administer fluids with sodium (e.g., Lactated Ringer's solution, NaCl 0.9%). Meticulous oral care. Promote safety. Identify the correct underlying cause, e.g., hemorrhage. Profuse sweating, vomiting, diarrhea, draining intestinal fistulas, colostomies.  Fluid Imbalances 4. Isotonic Volume Excess (ECF volume excess) It is also known as edema or over hydration. Edema is the accumulation of fluids in the interstitial spaces. Edema occurs due to the following: Increased capillary hydrostatic pressure, e.g., administration of large volumes of IV fluids. Decreased colloidal osmotic pressure (C.O.P.) or oncotic pressure (O.P.), e.g., hypoalbuminemia.  Fluid Imbalances Increased capillary permeability, e.g., damage to blood vessels in burns; vasodilation due to inflammation and release of histamine. Lymphatic obstruction, e.g. removal of lymph nodes in mastectomy, malignant metastasis. Sodium and water excess, e.g., congestive heart failure (CHF), renal failure, hypersecretion of aldosterone.  Fluid Imbalances The clinical manifestations of edema are as follows: Weight gain - is the best indicator of edema. Dependent edema - sacral area, ankles and feet. Tight, smooth, shiny skin. Cool, pale skin. This is due to poor circulation in the area. Therefore, the area is prone to pressure sure. Neck vein engorgement. Weeping edema - fluid leaks out of the pores when skin is pressed. Clothing and shoes feel tight. Pleural effusion, pericardial effusion, ascites.  Fluid Imbalances Collaborative management for edema include the following: Sodium and fluid restriction. Diuretics High protein diet (except in renal failure and liver cirrhosis. The diet in renal failure is low protein to reduce formation of urea and nitrogenous waste products. The diet in liver cirrhosis is low protein to reduce ammonia formation).  Fluid Imbalances Elevate edematous body parts. To promote venous return (except in CHF (congestive heart failure). In CHF, the legs are not elevated even if they are edematous to prevent increase in preload). Protect edematous body parts from prolonged pressure, injury, extremes of heat and cold. The area is susceptible to pressure sore, trauma and infection. Keep the skin dry and well - lubricated. To maintain skin integrity. Administer diuretics as ordered. To promote excretion of sodium and water. Regulate intravenous fluids accurately. To prevent fluid overload. Electrolyte Imbalances 1. Sodium Imbalances 2. Potassium Imbalances 3. Calcium Imbalances 4. Magnesium Imbalances  Electrolyte Imbalances 1. Sodium Imbalances A. Hyponatremia (Sodium deficit) It is caused by sodium loss or water excess. The causes of hyponatremia: diuretics, low sodium diet, decreased aldosterone section (Addison’s disease), edema, ascites, burns, diaphoresis.  Electrolyte Imbalances The clinical manifestations of hyponatremia are as follows: (These are due to decreased ECF volume and increased ICF volume) Headache Muscle weakness, fatigue and apathy Anorexia, nausea and vomiting Abdominal cramps Weight loss Postural hypotension Seizures, coma  Electrolyte Imbalances Collaborative management for hyponatremia include the following: Administer NaCL 0.9% per IV, plasma expanders (e.g., hetastarch). To prevent shock. Sodium - rich foods in diet. Safety precautions, e.g., use of side rails, supervision of ambulation.  Electrolyte Imbalances B. Hypernatremia (Sodium excess, edema) Sodium and water excess results to edema. The causes of hypernatremia are as follows: hyperventilation and diarrhea (more water is lost than sodium); high sodium intake, sodium tablets, water deprivation.  Electrolyte Imbalances The clinical manifestations of hypernatremia are as follows: (These are due to increased ECF volume and decreased ICF volume, ICF dehydration) Extreme thirst Dry, sticky mucous membrane Oliguria Firm, rubbery tissue turgor Red, dry, swollen tongue Restlessness, tachycardia, fatigue Disorientation, hallucination  Electrolyte Imbalances Collaborative management for hypernatremia include the following: Monitor intake and output. Restrict sodium in diet. Increase oral fluids or administer D5W per IV as prescribed. Administer diuretics as prescribed. Dialysis as indicated. Promote safety, monitor behavior changes.  Electrolyte Imbalances 2. Potassium Imbalances A. Hypokalemia (Potassium deficit) The causes of hypokalemia are as follows: decreased food and fluid intake (starvation); increased loss of potassium (hypersecretion of aldosterone, gastrointestinal losses, potassium - wasting diuretics); shifting of potassium into cells (treatment of DKA, metabolic alkalosis).  Electrolyte Imbalances The clinical manifestations of hypokalemia are as follows: (These are due to decreased neuromuscular irritability). Gastrointestinal Tract: anorexia, nausea and vomiting, abdominal distention, paralytic ileus. Central Nervous System: lethargy, diminished deep tendon reflexes, confusion, mental depression. Muscles: weakness, fatigue, leg cramps, flaccid paralysis, weakness of respiratory muscles, respiratory arrest. Cardiovascular System: hypotension, dysrhythmias, myocardial damage, cardiac arrest. Kidneys: water loss, thirst, renal damage  Electrolyte Imbalances ECG Changes in hypokalemia ST Segment depression Flattened T-wave Presence of U-wave Ventricular dysrhythmias (e.g., PVCs) Bradycardia Enhanced digitalis effect  Electrolyte Imbalances Collaborative management for hypokalemia include the following: a. Include potassium - rich foods in the diet, e.g., banana, dried fruits, orange, raw carrot, raw tomato, baked potato, melon (cantaloupe), watermelon. b. Fresh fruit in general, have high potassium content except apple. NURSE ALERT Administer potassium supplement (Potassium Chloride) per slow IV drip. NEVER administer Potassium Chloride (KCI) per IV push or direct IV. This may cause dysrhythmias and cardiac arrest. KCI is never given unless there is urine output of 30 mls/hour. "No Pee, No K+" This is to prevent renal damage. KCI supplements added to IV solutions should never exceed 60m Eq/L. The preferred level is 40m Eq/L.  Electrolyte Imbalances The rate of IV administration of KCI should not exceed 10 to 20m Eq/hour to prevent hyperkalemia and cardiac arrest. When given IV, potassium may cause pain in the area of the vein where it is entering. c. Administer potassium - sparing diuretics as prescribed (e.g., Aldactone (Spironolactone). High Impact Concepts: Hypokalemia is characterized by decreased neuromuscular irritability. In hypokalemia, "Everything is low and slow."  Electrolyte Imbalances B. Hyperkalemia (Potassium excess) The causes of hyperkalemia: excess dietary intake of potassium - rich foods, excess parenteral administration of potassium; decreased excretion of potassium (potassium - sparing diuretics, renal failure, adrenal insufficiency); shifting of potassium out of cells (extensive trauma, crushing injuries, metabolic acidosis).  Electrolyte Imbalances The clinical manifestations of hyperkalemia are as follows: (These are due to increased neuromuscular irritability). Gastrointestinal Tract: nausea, vomiting, diarrhea, colic. Central Nervous System: numbness, tingling. Muscles: irritability (early), weakness (late), flaccid paralysis. Cardiovascular System: ventricular fibrillation, cardiac arrest. Kidneys: oliguria, anuria  Electrolyte Imbalances Collaborative management for hyperkalemia include the following: Low potassium diet. Dextrose 10% in water with regular insulin per IV as prescribed. Potassium attaches to glucose. Then, insulin transports glucose with attached potassium into the cells. This lowers serum potassium levels. Polysterene sulfonate (exchange resin kayexalate) by mouth or per enema as prescribed. Sodium ions exchange with potassium ions in the G.I. tract. This prevents absorption of potassium. The exchange resin kayexalate with attached potassium is excreted via the feces.  Electrolyte Imbalances Calcium gluconate per IV as prescribed. This is the antidote for hyperkalemia. Dialysis as indicated. Common clinical manifestation of hypokalemia High Impact Concepts: and hyperkalemia: Hyperkalemia is characterized Anorexia by increased neuromuscular Nausea and Vomiting irritability. Muscle weakness "Everything is high and fast." Fatigue (The major route of excretion Dysrhythmias of potassium are the Renal Damage kidneys). Paralysis  Electrolyte Imbalances 3. Calcium Imbalances A. Hypocalcemia The causes of hypocalcemia are as follows: decreased ionized calcium (large blood transfusions with citrated blood; alkalosis); excess loss of calcium (renal disease; draining fistulas); inadequate dietary intake of calcium - rich foods; decreased calcium absorption (decreased vitamin hypoparathyroidism; hyperthyroidism; hypergmagnesemia).  Electrolyte Imbalances The clinical manifestations of hypocalcemia are as follows: (These are due to increased cell membrane permeability result to increased neuromuscular irritability). Central nervous system: tingling, convulsions Gastrointestinal Tract: increased peristalsis, nausea vomiting, diarrhea. Muscles: muscle spasm, tetany (Chvostek's sign Trousseau's sign). Cardiovascular System: dysrhythmias, cardiac arrest. Other signs and symptoms: Bones: osteoporosis, fracture. These are due to calcium deposited into the bones.  Electrolyte Imbalances Collaborative management for hypocalcemia are as follows: High calcium diet. Oral calcium salts as prescribed. Vitamin D and parathormone supplements as ordered. Amphogel (Albumin hydroxide) as prescribed. This is a phosphate-binder. As it lowers phosphate levels, calcium levels will increase. Calcium gluconate 10% per IV as prescribed. This is indicated if hypocalcemia is severe. Promote safety. Seizures may occur. Protect from trauma. To prevent fracture. Monitor breathing. Laryngospasm may occur  Electrolyte Imbalances High Impact Concepts: To remember signs and symptoms of hypocalcemia. Hypocalcemia: Increased cell membrane permeability Increased neuromuscular irritability “Everything is high and fast, EXCEPT BP”  Electrolyte Imbalances Hypercalcemia The causes of hypercalcemia are as follows: calcium loss from bones (immobilization; carcinoma with bone metastases); excessive intake of calcium (high calcium diet, calcium containing antacids); hyperparathyroidism; hypervitaminosis D; steroid therapy.  Electrolyte Imbalances The clinical manifestations of hypercalcemia are as follows: (These are due to decreased cell membrane permeability that result to decreased neuromuscular irritability). Central nervous system: diminished deep-tendon reflexes, lethargy, coma. Gastrointestinal Tract: decreased peristalsis (constipation, paralytic ileus). Muscles: muscle fatigue, hypotonia. Cardiovascular System: depressed electrical activity (dysrhythmias), cardiac arrest. Other signs and symptoms: Bones: osteoporosis, fracture. Kidneys: polyuria, dehydration, stones, renal damage.  Electrolyte Imbalances Collaborative management for hypercalcemia include the following: Increase fluid intake (3 to 4 day L/day). To prevent dehydration due to polyuria and to prevent renal stone formation. Provide acid-ash fruit juices (cranberry juice and prune juice) and vitamin C. To acidify urine and prevent renal stone formation. Protect the client from injury. To prevent fracture. Administer Normal Saline (NaCI 0.9%) per IV as prescribed. Sodium promotes calcium excretion. Mithracin (Mithramycin). To reduce serum calcium levels.  Electrolyte Imbalances High Impact Concepts: To remember the signs and symptoms of hypercalcemia. Hypercalcemia: Decreased cell membrane permeability Decreased neuromuscular irritability "Everything is low and slow, EXCEPT BP."  Electrolyte Imbalances 4. Magnesium Imbalances A. Hypomagnesemia The causes of hypomagnesemia: prolonged malnutrition or starvation; malabsorption syndromes, hypercalcemia, alcohol withdrawal syndromes, draining fistulas.  Electrolyte Imbalances The clinical manifestations of hypomagnesemia are as follows: (Note: Magnesium inhibits acetylcholine release. Therefore, in hypomagnesemia, there is increased acetylcholine release). Central Nervous System: convulsions, paresthesia, tremors, ataxia. Mental changes: agitation, depression, confusion Muscles: cramps, spasticity, tetany. Cardiovascular System: tachycardia, hypertension, dysrhythmias.  Electrolyte Imbalances Collaborative management for hypomagnesemia include the following: Provide foods rich in magnesium, e.g., meat, milk, fruits, green vegetables, whole grain cereals, nuts, sea foods. Promote safety, protect the client from injury. Monitor client for laryngeal stridor. This indicates airway obstruction. Administer magnesium supplement oral or parenteral as prescribed.  Electrolyte Imbalances High Impact Concepts: To remember signs and symptoms of hypomagnesemia: Hypomagnesemia Increased acetycholine release Increased neuromuscular irritability "Everything is high and fast, EXCEPT BP." Electrolyte Imbalances B. Hypermagnesemia The causes of hypermagnesemia: excessive intake of magnesium - containing antacids, renal failure, diabetic ketoacidosis.  Electrolyte Imbalances The clinical manifestations of hypermagnesemia are as follows: (Note: Magnesium inhibits acetylcholine release. Therefore, in hypermagnesemia, there is decreased acetylcholine release). Decreased BP Thirst, nausea and vomiting Drowsiness Diminished or loss of deep tendon reflexes.  Electrolyte Imbalances Collaborative management for hypermagnesemia include the following: Calcium gluconate per IV as prescribed. Calcium antagonizes magnesium. Dialysis if the client has renal failure. Correct underlying cause.  Electrolyte Imbalances High Impact Concepts: To remember signs and symptoms of hypermagnesemia: Hypermagnesemia Decreased acetylcholine release Decreased neuromuscular irritability "Everything is low and slow, EXCEPT BP." Respiratory Acid-Base Imbalances Metabolic Acidosis (Bicarbonate Deficit) Results from abnormal accumulation of fixed acids or loss of base. The clinical manifestations of metabolic acidosis are as follows: headache; mental dullness; Kussmaul's breathing (deep, rapid breathing which is an attempt to blow off potassium excess (hyperkalemia). Respiratory Acid-Base Imbalances Collaborative management for metabolic acidosis include thefollowing: Maintain good respiratory function. Fluid replacement. Water loss may result from hyperventilation.o Protect the client from injury. Risk for injury related to mental duliness. Restore electrolyte balance, specifically potassium. Administer Sodium Bicarbonate per IV as prescribed. Identify and treat underlying cause, e.g., renal failure, DM,starvation ketoacidosis, shock, chronic diarrhea, ASA  Respiratory Acid-Base Imbalances 2. Metabolic Alkalosis (Bicarbonate Excess) Results from loss of hydrogen ions or addition of base to body fluids. The clinical manifestations of metabolic alkalosis are as follows: hypoventilation (the body's attempt to conserve CO2) mental confusion; dizziness; numbness and tingling of fingers and toes, muscle twitching, tetany and seizures (these are due to hypokalemia because alkalosis damages ionized calcium); potassium deficit(hypokalemia).  Respiratory Acid-Base Imbalances Collaborative management for metabolic alkalosis include the following: Maintain good respiratory function. Protect the client from injury. Seizures may occur. NaCI or Ammonium Chloride oral intravenous. Diamox (Acerazolamide). This is carbonic anhydrase inhibitor that increases excretion of biocarbonate by the kidneys. Identify and treat underlying cause, e.g., excessive intake of sodium bicarbonate or baking soda, vomiting, gastric suctioning, intestinal fistulas.  RESPIRATORY ACIDOSIS (Carbonic Acid Excess) Failure of the respiratory system to remove CO2 from body fluids as fast as it is produced in the tissues Causes:  Assessment in Respiratory Acidosis Hyperpnea (increased RR (respiratory rate) and depth) Headaches, restlessness Drowsiness, confusion Diaphoresis Ventricular fibrillation Cyanosis (hypoxia) Late: confusion, drowsiness, coma Potassium excess (hyperkalemia) Nursing Interventions in Respiratory Acidosis Bronchodilators Postural drainage Chest clapping Na Bicarbonate for ventricular fibrillation or potassium excess Respiratory Alkalosis (Carbonic Acid Deficit) Loss of CO2 from the lungs at a faster rate than it is produced in the tissue Causes:  Assessment in Respiratory Alkalosis Lightheadedness Numbness or tingling of fingers or toes Late: tetany convulsions Hyperpnea (increased RR and dept) Potassium deficit (hypokalemia) Nursing interventions in Respiratory Alkalosis Treat underlying conditions Metabolic Acidosis (Biocarbonate Deficit) Abnormal accumulation of fixed acids or loss of base. Causers:  Assessment in Metabolic Acidosis Headache Mental dullness Kussmaul's respiration (attempt to blow off) Potassium excess Nursing Intervention in Metabolic Acidosis Treatment of underlying conditions and restoration of electrolyte balance Na Biocarbonate IV Maintain respiratory function Fluid replacement, measure I and O Protect from injury  Assessment in Metabolic Acidosis Headache Mental dullness Kussmaul's respiration (attempt to blow off) Potassium excess Nursing Intervention in Metabolic Acidosis Treatment of underlying conditions and restoration of electrolyte balance Na Biocarbonate IV Maintain respiratory function Fluid replacement, measure I and O Protect from injury   Assessment in Metabolic Alkalosis Depressed breathing (toconserve CO₂) Mental confusion Nausea and vomiting Dizziness Numbness and tingling of fingers or toes Muscle twitching Late: tetany, convulsions Potassium deficits Dysthythmias: tachycardia Headache Mental dullness Nursing Interventions in Metabolic Alkalosis NaCl or Ammonium Chloride oral or IV Carbonic Anhydrase Inhibitor (Diamox) To increase excretion of bicarbonate by the kidneys Maintain good respiratory function Protect from injury  Magnesium (Mg) Administer Mg (in solution) slowly to prevent hot or flushed feeling. Hypomagnesemia + Digoxin = Digitalis Toxicity Administer calcium gluconate for hypermagnesemia. Nutritional Support For continuous enteral feeding, check residual feeding every 2 to 4hours. If more than 50 mls., stop infusion for 30 minutes to 1 hour. Then recheck. For TPN, to prevent air embolism, teach client to do Valsalva's maneuver when changing infusion bags and tubing Hyperglycemia may be transient. Insulin may be added to the TPN solution as prescribed. Hyperglycemia may also occur when infusion rate for TPN is too rapid. Monitor the client's body weight, body temperature, I and O, and blood glucose. The body weight is the best indicator of nutritional status.  The most common complication of TPN infusion is infection, especially at the insertion site of TPN catheter. Change TPN solution and tubing every 24 hours Do not draw blood, give medications, or check CVP via TPN line. Administer D10W if TPN infusion is interrupted or for 12 to 24 hours after TPN therapy is discontinued. To prevent hypoglycemia.    THE END!!!