BSCN 3001 Week 1 Fluids & Electrolytes PDF

Week 1: Fluid & Electrolytes Fluid & Electrolytes: The concept Fluid and Electrolytes refers to the process of regulating the extracellular fluid volume, body fluid osmolality, and plasma concentrations of electrolytes Consequences of imbalances: ​ Impaired perfusion ​ Impaired gas exchange...

Week 1: Fluid & Electrolytes Fluid & Electrolytes: The concept Fluid and Electrolytes refers to the process of regulating the extracellular fluid volume, body fluid osmolality, and plasma concentrations of electrolytes Consequences of imbalances: ​ Impaired perfusion ​ Impaired gas exchange ​ Impaired cerebral function ​ Impaired neuromuscular function Risk factors: Vomiting, diarrhea, malabsorption, fever, inadequate or excessive intake of fluid or electrolytes, inadequate or excessive water intake, diuretics, laxatives, antacids, corticosteroids, infusion of IV fluids, blood transfusions, hemorrhage, burns, crush/head injuries, acute pancreatitis, acute kidney injury, heart failure, diabetes mellitus, cancer, chronic oliguric renal disease, chronic liver disease, chronic alcoholism, eating disorders Cause of imbalances: ​ Fluid and electrolyte output is greater than intake and absorption ​ Fluid and electrolyte output is less than intake and absorption ​ Fluid and electrolyte distribution is altered ○​ Shift of vascular fluid into the interstitial space causes edema ○​ Rapid shift of ECF into a “third space” can create ECV deficit ○​ Electrolyte shift from ECF into an electrolyte pool causes plasma electrolyte deficits ○​ Electrolyte shift from an electrolyte pool into ECF causes plasma electrolyte excesses Diagnostic: Diagnosis of ECV deficit and excess usually is made on the basis of history and clinical examination. Laboratory tests performed on blood samples provide the definitive diagnosis for osmolality and electrolyte imbalances Age-related differences: ​ Infants and Children: ○​ Neonates and infants express thirst only by crying, which requires vigilant caregivers to ensure adequate fluid intake ○​ They have a high body water percentage and more extracellular fluid (ECF) than intracellular fluid (ICF) ○​ As infants grow, the body water percentage decreases, and ICF surpasses ECF, a balance maintained throughout life ○​ Their large body and lung surface areas relative to mass result in the highest fluid exchange ratios of any age group  ○​ Neonates and infants have immature kidneys with limited reserve capacity, maturing only in childhood ​ Older adults: ○​ Older adults have a blunted thirst sensation, leading to decreased fluid intake and allowing body fluid osmolality to rise higher before thirst is triggered ○​ Their reduced lean body mass lowers the percentage of body weight that is water compared to younger individuals ○​ While their kidneys remain functional without renal disease, aging reduces renal reserve due to a natural decline in nephron numbers Prevention: ​ Primary: Primary prevention of fluid and electrolyte imbalances is based on the principle that intake must balance output to maintain optimal fluid and electrolyte balance ○​ Ex: Teaching people to replace body fluid output from vomiting or diarrhea with Na+-containing fluid can prevent ECV deficit, teaching physically active individuals optimal fluid replacement during and after exercise can prevent both ECV deficit and hyponatremia ​ Secondary: Screening to detect disrupted fluid and electrolyte balance is not performed in the general population except as part of a routine physical exam that would include assessment for physical signs of ECV excess or deficit and standard laboratory tests including measurement of serum Na+, K+, and Ca2+ levels IV Fluids: ​ Hypotonic: A hypotonic solution provides more water than electrolytes, diluting the ECF ○​ 0.45% NS: Provides free water in addition to Na+ and Cl-, used to replace hypotonic fluid losses, used as maintenance solution (although it does not replace daily losses of other electrolytes), provides no calories ​ Isotonic: Administration of an isotonic solution expands only the ECF ○​ 0.9% NS: Used to expand intravascular volume and replace extracellular fluid losses, only solution that may be administered with blood products, contains Na+ and Cl − in excess of plasma levels, does not provide free water, calories, other electrolytes, may cause intravascular overload or hyperchloremic acidosis ○​ 5% dextrose in water: Provides free water necessary for renal excretion of solutes, used to replace water losses and treat hypernatremia, provides 170 cal/L, does not provide any electrolytes  ○​ 5% in 0.225% dextrose in saline: Provides Na+, Cl −, and free water, used to replace hypotonic losses and treat hypernatremia, provides 170 cal/L ○​ Ringer’s solution: Similar in composition to plasma except that it has excess Cl −, no Mg2+, and no HCO3 −, does not provide free water or calories, used to expand the intravascular volume and replace extracellular fluid losses ○​ Lactated Ringer’s (Hartmann’s) solution: Similar in composition to normal plasma except does not contain Mg2+, used to treat losses from burns and lower GI tract, may be used to treat mild metabolic acidosis but should not be used to treat lactic acidosis, does not provide free water or calories ​ Hypertonic: A hypertonic solution initially raises the osmolality of ECF and expands it ○​ 10% dextrose in water: Provides free water only, no electrolytes, provides 340 cal/L ○​ 3.0% NS: Used to treat symptomatic hyponatremia, must be administered slowly and with extreme caution because it may cause dangerous intravascular volume overload and pulmonary edema ○​ 5% in 0.45% dextrose in saline: Same as 0.45% NaCl except provides 170 cal/L ○​ 5% in 0.9% dextrose in saline: Same as 0.9% NaCl except provides 170 cal/L ECV Deficit (Too Little Extracellular Volume) ​ Causes: Lack of sodium & water, vomiting, acute/chronic diarrhea (laxative use), draining GI fistula, gastric suction, or intestinal decompression, hemorrhage or burns, overuse of diuretics, lack of aldosterone (adrenal insufficiency, Addison disease), acute intestinal obstruction, ascites that develop rapidly ​ Manifestations: Sudden weight loss, skin tenting, dry mucous membranes, vascular underload: rapid thready pulse, postural BP drop w/ concurrent HR increase, lightheadedness, flat neck veins when supine, oliguria, syncope, circulatory shock if severe ​ Treatment: ○​ The goal of treatment for fluid volume deficit is to correct the underlying cause and to replace both water and electrolytes. Balanced IV solutions, such as lactated Ringer’s solution, are usually given. Isotonic NaCl is used when rapid volume replacement is indicated. Blood is administered when volume loss is caused by blood loss ECV Excess (Too Much Extracellular Volume)  ​ Causes: Excessive IV infusions of Na+-containing isotonic solution (0.9% NaCl, Ringer), high oral intake of salty foods and water w/ renal retention of sodium and water, oliguria, aldosterone excess, high levels of glucocorticoids ​ Manifestations: Sudden weight gain, dependent edema, vascular overload: bounding pulse, distended neck veins when upright, dyspnea, pulmonary edema if severe ​ Treatment: ○​ The goal of treatment for fluid volume excess is removal of sodium and water without producing abnormal changes in the electrolyte composition or osmolality of ECF. The primary cause must be identified and treated. IV therapy is usually not indicated for this type of fluid imbalance. Diuretics and fluid restriction are the primary forms of therapy. Restriction of sodium intake may also be indicated. If the fluid excess leads to ascites or pleural effusion, an abdominal paracentesis or thoracentesis may be necessary Hyponatremia (Body Fluids Too Dilute; Osmolality Too Low) ​ Causes: Excess amount of IV 5% dextrose in water infusion, rapid oral ingestion of massive amounts of water (abuse, club initiation, psychiatric disorder), overuse of tap water enemas or hypotonic irrigating solution, vomiting/diarrhea, excessive ADH ○​ Na+ excretion increased with renal problems, NG suction (GI system rich in sodium), vomiting, diuretics, sweating, diarrhea, decreased secretion of aldosterone (wasting sodium) ○​ Overload of fluid with congestive heart failure, hypotonic fluids infusions, renal failure (dilutes sodium) ○​ Na+ intake low through low salt diets or nothing by mouth ○​ Antidiuretic hormone over secreted **SIADH (syndrome of inappropriate antidiuretic hormone secretion…remembers retains water in the body and this dilutes sodium) ​ Manifestations: Impaired cerebral function: decreased LOC, nausea, seizures, if severe; serum sodium 145mEq/L ○​ Fatigue ○​ Restless, really agitated (confused….central nervous system changes) ○​ Increased reflexes (progress to seizures and coma) ○​ Extreme thirst (*big sign) ○​ Decreased urine output, dry mouth/skin ​ Normal lab values: 136–145mmol/L ​ Treatment: ○​ Overall Goal: Address the underlying cause, whether it is water loss or sodium gain ○​ Treatment of Water Deficit: ​ Fluid Replacement: Administer fluids orally or via IV using isotonic solutions (e.g., 0.9% sodium chloride) to restore hydration and balance ○​ Treatment of Sodium Excess: ​ Dilution: Use salt-free IV fluids, such as 5% dextrose in water, to lower sodium concentration ​ Excretion: Administer diuretics to promote sodium removal from the body ​ Dietary Management: Restrict sodium intake to prevent further imbalance  ○​ Preventive Measures for Vulnerable Patients: ​ Older Adults and Cognitively Impaired Individuals: Monitor fluid intake and output carefully ​ Routine Hydration: Include regular administration of oral fluids as part of their care plan to prevent dehydration and hypernatremia ​ Nursing Interventions ○​ Restrict sodium intake! Know foods high in salt such as bacon, butter, canned food, cheese, hot dogs, lunch meat, processed food, and table salt ○​ Keep patient safe because they will be confused and agitated ○​ Doctor may order to give isotonic or hypotonic solutions such as 0.45% NS (which is hypotonic and most commonly used). Give hypotonic fluids slowly because brain tissue is at risk due to the shifting of fluids back into the cell (remember the cell is dehydrated with hypernatremia) and the patient is at risk for cerebral edema. In other words, the cell can lyse if fluids are administered too quickly ○​ Educate patient and family about sign and symptoms of high sodium level and proper foods to eat Hypokalemia (Plasma K+ Deficit) ​ Causes: Prolonged anorexia or diet lacking potassium, no oral intake plus IV solutions not containing potassium, vomiting, acute/chronic diarrhea, use of K+-wasting diuretics or drugs that increase renal K+ excretion, excessive aldosterone (large amounts of black licorice, cirrhosis, chronic heart failure, primary hyperaldosteronism), high levels of glucocorticoids (Cushing disease, corticosteroid therapy), alkalosis, excessive insulin ○​ Drugs (laxatives, diuretics, corticosteroids) ○​ Inadequate consumption of Potassium (NPO, anorexia) ○​ Too much water intake (dilutes the potassium) ○​ Cushing’s Syndrome (during this condition the adrenal glands produce excessive amounts of cortisol (if cortisol levels are excessive enough, they will start to affect the action of the Na+/K+ pump which will have properties like aldosterone and cause the body to retain sodium/water but waste potassium)…hence hypokalemia ○​ Heavy Fluid Loss (NG suction, vomiting, diarrhea, wound drainage, sweating) ​ Manifestations: Bilateral ascending flaccid muscle weakness, abdominal distention, constipation, postural hypotension, polyuria, cardiac dysrhythmias, decreased bowel sounds; serum potassium 5.0mEq/L ○​ Muscle weakness ○​ Urine production little or none (renal failure) ○​ Respiratory failure (due to the decreased ability to use breathing muscles or seizures develop) ○​ Decreased cardiac contractility (weak pulse, low blood pressure) ○​ Early signs of muscle twitches/cramps…late profound weakness, flaccid ○​ Rhythm changes: Tall peaked T waves, flat p waves, Widened QRS and prolonged PR interval ​ Normal lab values: 3.5–5.1mmol/L ​ Treatment: ○​ Eliminating oral and parenteral potassium intake ○​ Increasing elimination of potassium. This is accomplished with diuretics, dialysis, and use of ion-exchange resins such as sodium polystyrene sulphonate (Kayexalate). Increased fluid intake can enhance renal potassium elimination. ○​ Forcing potassium from the ECF to the ICF. This is accomplished by administration of IV insulin (along with glucose so that the patient does not become hypoglycemic) or by administration of IV sodium bicarbonate in the correction of acidosis. In rare cases, a β-adrenergic agonist (e.g., epinephrine) is administered. ○​ Reversing the membrane effects of the elevated ECF potassium by administering calcium gluconate intravenously. Calcium ion can immediately reverse the effect of the depolarization on cell excitability. ​ Nursing Interventions ○​ Monitor cardiac, respiratory, neuromuscular, renal, and GI status ○​ Stop IV potassium if running and hold any PO potassium supplements ○​ Initiate potassium restricted diet and remember foods that are high in potassium  ○​ Prepare a patient ready for dialysis. Most patients are renal patients who get dialysis regularly and will have high potassium. ○​ Kayexalate is sometimes ordered and given PO or via enema. This drug promotes GI sodium absorption which causes potassium excretion. ○​ Doctor may order potassium wasting drugs like Lasix or Hydrochlorothiazide ○​ Administer a hypertonic solution of glucose and regular insulin to pull the potassium into the cell Hypomagnesemia (Plasma Mg2+ Deficit) ​ Causes: Diet lacking magnesium, poor magnesium absorption, prolonged vomiting, steatorrhea, use of diuretics or other drugs that increase urinary magnesium, large load of citrate from massive blood transfusion, alkalosis ○​ Limited intake Mg+ (starvation) ○​ Other electrolyte issues are associated with a low Mg. level like hypOkalemia, hypOcalcemia)…it’s important to note that hypercalcemia can lead to a low magnesium level because a high calcium level causes the kidneys to not reabsorb magnesium (hence dropping the levels). ○​ Wasting Magnesium kidneys (loop and thiazide diuretics & cyclosporine…stimulates the kidneys to waste Mag) ○​ Malabsorption issues (Crohn’s, Celiac, proton-pump inhibitors drugs “Prilosec, Nexium, Protonix”…drug family ending in “prazole” Omeprazole, diarrhea/vomiting) ○​ Alcohol (due to poor dietary intake, alcohol stimulates the kidneys to excreted mag, acute pancreatitis) ○​ Glycemic issues (Diabetic Ketoacidosis, insulin administration) ​ Manifestations: Increased neuromuscular excitability: positive Chvostek & Trousseau signs, insomnia, hyperactive reflexes, muscle cramps & twitching, nystagmus, tetany, cardiac dysrhythmias; serum magnesium