Unit 3 A

Unit 3 A - Fluid and Electrolyte Fluid Balance Balance...

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Unformatted text preview: Fluid and Electrolyte Fluid Balance Balance Objectives Objectives Describe clinical manifestations associated with alterations in fluid balance. Describe common electrolyte disturbances and associated clinical manifestations. Distribution of Body Fluids Distribution Total body water: 60% of body weight (adult); 75­80%(infant) Higher body fat lower total body water ICF: 2/3 of body fluid located in the cell ECF: 1/3 of body fluid located outside the cell. • Interstitial fluid (space between cells and outside of blood vessels • Intravascular: (plasma) • Others: examples: pleural, CSF, synovial, pericardial fluid Intake and Output (Adults) Intake Daily INTAKE OUTPUT DRINKING 1400-1800 ml URINE 1400-1800 ml FOOD 700-1000 ml STOOL 100 ml OXIDATION 300-400 ml SKIN 300-500 ml (insensible water loss) Total: 2400-3200 LUNGS 300-400 ml (insensible water loss) Total: 2400-3200 Fluid Movement Between Compartments Compartments Diffusion • Movement of solutes down a concentration gradient Osmosis • Movement of water which follows Na+ Fluid Movement between Capillaries and Interstitial spaces Capillaries Capillary hydrostatic pressure is the primary force for fluid movement out of the arteriolar end of the capillary and into the interstitial space. At the venous end, capillary oncotic pressure (from plasma proteins) attracts water back into the vascular space. Interstitial hydrostatic pressure promotes the movement of fluid and proteins into the lymphatics. Interstitial oncotic pressure accounts for the movement of fluid between the interstitial space and the intracellular space. Normally intracellular and extracellular fluid osmotic pressures are equal (280 to 294 mOsm) and water is equally distributed between the interstitial and intracellular compartments. Regulation of Water Balance Regulation ADH: Antidiuretic Hormone ADH secreted:↑ plasma osmolality or ↓blood volume or ↓ blood pressure Osmoreceptors in hypothalamus: stimulated by ↑ osmolality causing thirst Volume sensitive receptors (R and L atria, thoracic vessels.) and Baroreceptors(in aorta, PA, and carotid sinus) stimulate ADH release Sodium Regulation Sodium Renal Tubular reabsorption Aldosterone: secreted by the adrenal cortex when: • Blood volume is low and Na + is low or K+ is high • Increases the reabsorption of Na+ and H2O and K+ excretion in urine. Low circulating blood volume and blood pressure activate the renin-angiotensinaldosterone system Natriuretic Hormones lowers blood pressure pressure Tonicity Tonicity Alterations in Water and Sodium Balance Isotonic Alterations Isotonic TBW changes are proportional to electrolyte TBW changes changes Osomolality remains in the normal range Isotonic fluid losses due to: • • • Hemorrhage Excessive wound drainage Excessive diaphoresis Symptoms: • Weight loss, dry skin and mucous membranes, poor skin turgor, decreased urine output, (S/S of hypovolemia: tachycardia, flat neck veins, BP may ↓ can lead to hypovolemic shock.) Isotonic Fluid Excess Isotonic Hypervolemia Causes: • • • Excessive administration of IV fluids ↑ secretion of aldosterone Medications: cortisone • • • • • Weight gain Distended neck veins (+JVD) Hemodilution → decreased Hct. and plasma proteins ↑ blood pressure Severe cases: edema, pulmonary edema and death Symptoms Hypertonic Alterations Hypertonic (Serum osmolality > 294m0sm) Causes: • ↑ concentration of ECF Na+ concentration • ECF fluid deficit ECF hypertonicity attracts water from the IC space → ICF dehydration. Primary increase in ECF Na++ → S/S of Primary hypervolemia (due to osmotic attraction) hypervolemia Hypertonic state due to water loss → Hypertonic hypovolemia Hypotonic Alterations Hypotonic Osmolality is < normal Osmolality (<280mOsm) (<280mOsm) Causes • Hyponatremia • Water excess Lead to cellular swelling (cellular edema) Symptoms • If Na+ ↓:Hypovolemia due to movement of water into the cell, decreases plasma volume • Water excess: ICF and ECF are increased, S/S of hypervolemia and water intoxication (confusion, convulsions, weakness, nausea, muscle twitching, HA) Edema Excessive fluid accumulation in the interstitial spaces interstitial What causes edema? • Increased capillary hydrostatic pressure Due to venous obstruction, Na+ and H20 retention, thrombophlebitis, hepatic obstruction, restrictive clothing, prolonged standing • Lowered plasma oncotic pressure Liver disease, protein calorie malnutrition, kidney disease, excess wound drainage, burns Edema (cont) Edema • Increased capillary membrane permeability Trauma, burns, neoplasm, allergic reactions • Lymphatic channel obstruction Blocked lymphatic channels lead to lymphedema Types of Edema Types Localized Edema: Site of trauma or related organ (pulmonary, cerebral, pleural effusions, pericardial effusion etc) Generalized Edema: uniform distribution of fluid in the interstitial spaces, also called anasarca Dependent Edema: fluid in gravity­dependent areas such as the feet or lower legs from standing. Pitting edema: skin over edematous area “pits” when pressure is applied. Clinical Presentation Clinical Weight gain Swelling of affected area Sometimes associated with weeping (weeping edema) Impairs wound healing (edema impedes the transport of nutrients from the capillaries to the wound bed) “Third­spacing”: term used to refer to edema (fluid in the third or interstitial space) Types of Edema Types Pedal Edema Anasarca (pathguy.com) Lymphedema amylhwilliams.com Water Deficit Water Dehydration: water and sodium loss (isotonic) Pure water loss: hypertonic dehydration (rare) Causes: • hyperventilation (fever), • increased renal clearance of free water due to impaired renal function • inability to concentrate urine as in diabetes insipidus (decreased ADH) Water Excess Water Causes: Compulsive water intake Acute renal failure Severe CHF Liver disease Decrease urinary output (renal disease or ↓renal blood flow • Tap water enemas • All produce a hypoosmolar state. • SIADH: due to ↓renal excretion of water • • • • • Symptoms: confusion, convulsions, weakness, nausea, muscle twitching, HA, weight gain Alterations in Sodium Balance Alterations *Primary Cation in the ECF* Hypernatremia (Na+ >147mOsm/L) • Gain in sodium or net loss of H20 Intracellular Dehydration (fluid shifts to the ECF resulting hypervolemia and hyperosmolality of the ECF) • Causes: Hypertonic saline administration Hyperaldosteronism (Cushings) ↑ ACTH → ↑ aldosterone Hypernatremia with water deficit: fever, respiratory infections(↑ resp. rate), diabetes insipidus, diabetes mellitus (hyperglycemia), polyuria, diaphoresis, diarrhea, poor water intake Hyponatremia Hyponatremia Serum Sodium < 135m0sm/L Cause hypoosmolality with movement of water into the cells Causes: • Pure sodium losses: vomiting, diarrhea, GI suctioning, diuretics • Dilutional hyponatremia: Proportion of TBW to total body Na+ is excessive. Causes: IV dextrose 5% for fluid replacement, large fluid intake, • Hypoosmolar hyponatremia: severe CHF, acute renal failure, cirrhosis lead to impaired excretion of water • Hyperosmolar hyponatremia: hyperproteinemia, hyperlipidemia, hyperglycemia. Water is displaced by lipids or proteins thus decrease sodium levels. Hyperglycemia increases the osmolality of ECF thus diluting sodium concentration. Hypernatremia • • • • • • • Thirst Fever Dry mucous membranes Restlessness Muscle twitching Hyperreflexia Convulsions Hyponatremia • Lethargy • Confusion • Apprehension • Depressed reflexes • Seizures • Coma Dilutional hyponatremia: symptoms of fluid overload (weight gain, edema, ascites and +JVD) Chloride Chloride (Cl-)major anion in the ECF Transport of chloride is passive and follows the active transport of sodium. Increases/decreases in Chloride are proportional to increases/decreases in sodium. Inversely proportional to HC03­ concentration. Hyperchloremia Hyperchloremia Causes: •Elevate sodium levels (hypernatremia) -Decreased bicarb levels (metabolic acidosis) Hypochloremia Causes: •Hyponatremia •Metabolic alkalosis •Vomiting •Diuretics •Cystic fibrosis Potassium Potassium *Chief cation of the ICF* 3.5-5.0mEq/L Responsible for regulation of ICF osmolality and fluid balance Required for glycogen and glucose deposition in skeletal/liver cells Maintains the resting membrane potential Kidney is the responsible for K+ regulation. Changes in the rate of flow through the kidneys influences K+ level in urine. Changes in pH (H+ ion concentration) affect K+ balance Aldosterone plays a role in K+ regulation by increasing secretion of K+ if serum K+ is elevated Insulin stimulates Na+/K+ ATPase pump moving K+ back into the cells. Used to treat hyperkalemia Causes: Hypokalemia Hypokalemia K+ < 3.5mEq/L • GI disorders Diarrhea Intestinal tube drainage Fistula Laxative abuse • Renal excretion Potassium wasting diuretics Excessive aldosterone secretion. Primary hyperaldosteronism Magnesium deficits • K+ shifts to the ECF from ICF with urinary loss of K+ DKA • Shift of ECF K+ into the cell Metabolic alkalosis Respiratory alkalosis Insulin administration Hyperkalemia Hyperkalemia Serum K+ > 5.0mEq/L Causes • • • • • Renal Failure Increased K+ intake: accidental ingestion Stored blood transfusion K+ IV administration K+ shifts to the ECF • • • • • Cell trauma; surgery, injury, burns DKA­acidosis Hypoxia: decrease effectiveness of cell membrane transport Decreased renal excretion Addison’s disease: decreased aldosterone production/secretion Potassium­sparing diuretics Hypokalemia • Neuromuscular depression: Skelatal muscle weakness Smooth muscle atony Cardiac arrythmias (change in membrane excitability); sinus bradycardia, A­V blocks; depressed ST segment, peaked p waves • Carbohydrate metabolism­decreases insulin secretion Hyperkalemia • Early: Neuromuscular irritability Restlessness Abdominal cramping Diarrhea • Severe: Muscle weakness Loss of muscle tone Paralysis • EKG changes: V. fibrillation, cardiac arrest Calcium Calcium Necessary for nerve transmission, bone structure, cofactor for blood clotting, contraction of muscles Serum Ca++ bound to plasma proteins and ionized Ca++ is free. Ionized Ca++ is physiologically more important Vit D is necessary to absorb Ca++ Excess phosphate blocks the absorption of Ca+ + causing hypocalcemia Parathyroid hormone (PTH) produced by the parathyroid gland pulls Ca++ from bones to regulate serum Ca++ Hypercalcemia: >10­ 12mg/dl • Causes: Hyperparathroidism • Malignant tumors: cancer cells release substances that remove Ca++ from the bones into the serum, therefore, patients are at risk for fractures, (pathologic fractures) (calcium is in the plasma and not the bone where it belongs) • Non­specific fatigue, weakness, lethargy, anorexia • Extremely high levels of Ca++ in blood can cause cardiac arrhythmias Hypocalcemia: < 8.5 mg/dl Hypoparathyroidism, Vit. D deficiency, S/S: muscle twitching, tremors, paresthesia (tingling) Trousseau’s sign= obstruct blood flow to hand for 3 min, observe for spasms Chvostek’s sign= tap facial nerve in front of ear and look for spasm/twitching Hyperphosphatemia Hyperphosphatemia Hypophosphatemia Serum phosphate >4.5 mg/dl Causes: •Laxative use •Chemotherapy •Renal failure Serum phosphate <2.0 mg/dl Causes: •Decreased absorption in gut due to Vitamin D deficiency •Excess renal excretion Clinical manifestations •Same as hypocalcemia Clinical manifestations: Decreased energy metabolism Altered nerve and muscle function. Hypermagnesemia Hypermagnesemia Serum magnesium >2.5 mEq/L Causes Hypomagnesemia Serum magnesium <1.5 mEq/L Causes • • • • • • • Renal failure • Antacid use Clinical manifestations • • • • • • Nausea, vomiting Respiratory depression Hypotension Bradycardia Loss of DTR Muscle weakness Malnutrition Malabsorption Alcoholism Renal tubule dysfunction Diuretic use Diabetes mellitus • • • • • Depression Increased reflexes Convulsions Irritability Tetany Clinical manifestations ...
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This note was uploaded on 03/07/2012 for the course 830 201 taught by Professor Leyton during the Fall '08 term at Rutgers.

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