Chapter 24- Fluid and Electrolyte Homeostasis and Imbalances

Fluid of the body:

-Flows in arteries, veins, and lymph vessels

Body Fluids are secreted into specialized compartments:

-Joints -Cerebral ventricle -Intestinal lumen

Function of Body Fluid:

-Surrounds and permeates the cells -Lubricant and solvent for metabolic chemical reactions -Transports oxygen, nutrients, chemical messengers, and waste products to their destinations -Important in regulating body temperature

Abnormalities in Body Fluid CAN OCCUR IN:

-Volume -Concentration -Electrolyte composition of body fluid -Can cause clinical problems or death -Occur as a result of many different pathophysiologic conditions

Body Fluid:

-Pertains to water within the body and the particles dissolved in it

Extracellular Fluid:

-Contained outside the cells

Extracellular Fluid: Interstitial compartment (between cells)

-Relatively rich in sodium, chloride, bicarbonate ions, and proteins -Relatively low in potassium, magnesium, and phosphate ions

Extracellular Fluid: Vascular compartment (in blood vessels)

-Also relatively rich in proteins -Oncotic pressure

Extracellular Fluid: CT tissue

-Dense connective tissue and bone

Extracellular Fluid: Other compartments

-Synovial, cerebrospinal, GI fluids

Intracellular Fluid: Contained inside the cells

-Relatively rich in potassium and magnesium ions, inorganic and organic phosphates, and proteins -Relatively low in sodium and chloride ions

Total Body Water:

-Total of the water in all fluid compartments -Percentage of body weight that is water varies (According to a person's age) (In proportion to body fat)

Fluid Homeostasis:

-Dynamic process results from interplay of sub-processes *Fluid intake *Fluid absorption *Fluid distribution *Fluid excretion

Fluid intake:

-Fluid intake is entry of fluids into the body by any route --Healthy people ingest fluids orally *Drinking *Eating (water contained in food) --Small amount of water synthesized through cellular metabolism

Fluid intake: Influenced by?

-Habit -Social factors -Thirst triggered by: *Increased concentration of extracellular fluid *Decreased circulating blood volume *Dryness of mucous membranes of mouth *Possibly other visceral signals -In older adults, thirst diminishes; they may have insufficient fluid intake

Other Possible Routes of Fluid intake:

-Controlled by heath professionals *Intravenous intake *Intake tubes in GI tract and other body cavities *Subcutaneous tissue or bone marrow infusion *Rectal intake (tap water enema) -Accidental *Lungs (near-drowning)

Fluid Distribution: Vascular fluid distribution

-Much fluid within vascular compartments distributes into other fluid compartments -Net results of filtration across permeable capillaries (capillary forces)

Capillary forces: Move fluid from capillaries into interstitial compartment:

-Capillary hydrostatic pressure: outward push of vascular fluid against capillary walls -Interstitial fluid osmotic pressure: inward-pulling force of particles in the interstitial fluid

Capillary forces: Move fluid from interstitial compartment into capillaries:

-Capillary osmotic pressure: inward-pulling force of particles in vascular fluid -Interstitial hydrostatic pressure: outward push of interstitial fluid against outside of capillary walls

Interstitial and Intracellular Fluid Distribution:

-Fluid distribution between the vascular and interstitial compartments is net result of differences in particle concentration (osmolality) "number of particle"

Osmolality and Osmosis:

-Cell membranes are permeable to water but not to electrolytes -Water crosses the cell membrane rapidly to equalize particle concentration inside and outside the cells (osmosis)

Direction of water movement:

-Determined by the particle concentrations on the two sides of the semipermeable cell membrane -Changes in the osmolality of the interstitial and intracellular compartments control the distribution of water between them

Water movement out of cells:

-Occurs when particle concentration (osmolality) of the interstitial fluid becomes higher than the particle concentration inside cells -Water moves from the cells to the interstitial fluid to equalize the osmolality in the two compartments

Water movement into cells:

-Occurs when the osmolality of the interstitial fluid becomes lower than the osmolality of the intracellular fluid -Water moves from the interstitial compartment to the intracellular compartment to equalize the osmolality

Fluid Excretion occurs through:

-Urinary tract (largest volume excreted) -Bowels (normal bowel function) (Increases with diarrhea) -Lungs (Exhalation) -Skin (Visible sweat) (Insensible perspiration)

Urine Amount of fluid excreted in the urine is controlled primarily by:

-Hormones *Antidiuretic hormone (ADH) *Aldosterone (Slat water hormone) *Natriuretic peptides (ANP and BNP)(ANP-elevated blood pressure helps get rid of salt; BNP-cardiac pathological instances) *Other minor hormones

Secretion and Release of ADH:

-Synthesized by cells in the supraoptic and paraventricular nuclei of the hypothalamus -Release of ADH occurs from the posterior pituitary gland -Factors that increase release of ADH into the blood include increased osmolality (concentration) of the extracellular fluid, decreased circulating fluid volume, pain, nausea, and physiologic and psychological stressors endurance training .

Functions of ADH:

-Causes reabsorption of water, which: *Decreases urine volume *Makes urine more concentrated *Decreases fluid excretion *concentrates the urine thus decreasing fluid excretion -If ADH release is decreased, result is large dilute urine volume *Decreased osmolality of extracellular fluid *Ethanol intake

Aldosterone:

-Synthesized and secreted by cells in the adrenal cortex -Major stimulus for its release *Angiotensin I --From the rennin-angiotensin system --Activated by decreased circulating blood volume and increased concentration of potassium ions in the plasma

Function of Aldosterone:

-Causes renal tubules to reabsorb sodium and water (saline) -Decreases fluid excretion, although by different mechanism than ADH -When more aldosterone is secreted, urine volume is smaller; decreased secretion of aldosterone causes a larger urine volume

Comparison of ADH and Aldosterone:

-ADH is the tap water hormone *Causes the kidneys to reabsorb water *Renal reabsorption of water due to ADH makes a smaller volume of more concentrated urine -Aldosterone is the saltwater hormone *Causes the kidneys to reabsorb sodium and water *Renal reabsorption of sodium and water due to aldosterone makes a smaller volume of urine

ANP:

-Normally secreted from cells in the heart when the atria are stretched

BNP:

-B-type natriuretic peptide -Released from ventricular cells when ventricular diastolic pressure -Increases abnormally, as in heart failure

Function of ANP and BNP

-Promote fluid excretion in the urine by: *Causing natriuresis (sodium excretion in the urine) *Sodium excretion is accompanied by water excretion

Regulation of NPs

-When vascular volume increases: *Heart is stretched *More NPs released to cause renal excretion of the excess -When vascular volume is decreased: *Heart is less stretched *Fewer NPs released *Kidneys excreted less fluid -NPs oppose the action of aldosterone, but they are not as strong as aldosterone

Adequate Urine Volume highly dependent on:

-Adequate blood pressure to perfuse the kidneys -Glomerular filtration rate (GFR)

Abnormal Fluid Loss:

-May be a significant factor in disturbing fluid status

Abnormal Fluid Loss: Types of abnormal fluid loss:

-Emesis -Tubes in the GI tract or other body cavities -Hemorrhage -Drainage from fistulas, wounds, or open skin, burns -Paracentesis

Categories of Fluid Imbalances:

-Extracellular (saline) imbalances -Imbalances of body fluid (water) concentration -Extracellular and body fluid imbalances can occur simultaneously (both volume and serum sodium concentration are abnormal)

Extracellular Fluid Imbalances:

-Too much or too little extracellular fluid -Involve a change in the amount or volume of extracellular fluid -Also termed saline imbalances because they are disorders of isotonic slat water (in the same concentration as the normal plasma concentration) -May lead to hypovolemic shock, which can be fatal if not treated effectively (fluid replacement)

Volume Deficit:

-Caused by removal of a sodium-containing fluid from the body -Decrease in saline in the same concentration as normal extracellular -Condition sometimes termed saline deficit

Etiology (the causes) of volume deficit:

-Removal of a sodium-containing fluid from the extracellular compartment *Usually fluids is removed from body *In some instances, fluid is sequestered in a "third space" in the body, outside the extracellular compartment "fluid where it is not supposed to be" (Example: ascites, fluid in the peritoneal cavity) (If this develops rapidly, may deplete extracellular volume)

Clinical Manifestation of volume deficit:

-Sudden weight loss -Postural blood pressure decrease with concurrent increased heart rate -Flat neck veins (or veins collapsing with inspiration) when a patient is supine -Prolonged small vein filling time -Prolonged capillary refill time -Lightheadedness -Dizziness -Syncope -Oliguria or small volume of concentrated urine (if kidneys are responding normally)

Other Clinical Manifestations of volume deficit:

-Decreased skin turgor -Dryness of oral mucous membrane between cheek and gum -Hard stool -Soft sunken eyeball -Longitudinal furrows in the tongue -Absence of tears and sweat (In infants - Fontanel may be sunken, neck veins are not reliably assessed in infants)

Weight loss:

-Sudden weight loss is a sensitive measure of ECV deficit *One litter of saline weight 1kg *A person who loses 1kg in 24 hours has excreted 1L of fluid or loss it through an abnormal route

Third Space Sequestration:

-EVC deficit may occur without a weight loss if fluid is sequestered in a third space somewhere in the body, as with ascites or intestinal obstruction -Can be detected with shifts in orthostatic blood pressure (different pressure siting and standing up)

Extracellular Volume Excess:

-Opposite of extracellular volume deficit -Amount of extracellular fluid is abnormally increased -Vascular and interstitial areas have too much fluid

Uncomplicated ECV Excess:

-Concentration of extracellular fluid is normal -Excessive amount of that fluid is present

Etiology (the causes) of volume excess:

-Caused by addition or retention of isotonic saline; sometimes termed saline excess -Hormone aldosterone causes kidneys to retain saline; therefore, ECV excess may be caused by conditions that involve excessive aldosterone secretion (Compensatory mechanism that can accompany chronic heart failure)

Causes of Extracellular Fluid Volume Excess:

-Excessive intravenous infusion of sodium-containing isotonic solutions *Normal saline -0.9% sodium chloride *Ringer injection *Lactated Ringer injection -Renal retention of sodium and water *Primary hyperaldosteronism *Chronic heart failure *Cirrhosis *Acute glomerulonephritis *Chronic renal failure *Cushing disease *Corticosteroid therapy

Clinical Manifestations of Extracellular Volume Excess:

-Sudden weight gain: a sensitive measure of extracellular volume excess -Manifestation of circulatory overload *Bounding pulse *Neck venin distention in upright position *Crackles in dependent portions of lungs *dyspnea *Orthopnea *Edema *If advanced, frothy sputum of pulmonary edema *In infant (Bulging fontanel, Assessment of neck veins is not effective in infants)

Body Fluid Concentration:

-Imbalances of body fluid concentration are disorders of concentration and not amount of extracellular fluid -Also called water imbalances *Serum sodium concentration reflects osmolality of blood *Recognized by abnormal serum sodium concentration

Hyponatremia

-A serum sodium concentration below the lower limit of normal -When present the extracellular fluid contains relatively too much water for the amount of sodium ions present -Extracellular fluid is more dilute than normal

Etiology of Hyponatremia

-Factors that produce a relative excess of water in proportion to salt in the extracellular fluid -Because serum sodium concentrations reflects the osmolality of the blood, reduced serum sodium indicates that extracellular fluid has a reduced osmolality; it is too dilute -Also called: *Hypotonic syndorme *Hypo-osmolality *Water intoxication

Etiology of Excess Water in Extracellular Fluid:

-Excessive intravenous infusion of 5% dextrose in water (D5W) -Hypotonic irrigating solutions -Tap water enemas -Psychogenic polydipsia (compulsive water drinking) -Forced excessive water ingestion (child abuse or club initiation) -Excessive beer ingestion (beer potomania) -Near-drowning in fresh water -Selective serotonin reuptake inhibitors (SSRIs) -Loss of relatively more salt than water -Diuretics, especially thiazides -Salt-wasting renal disease -Replacement of water but not salt lost through emesis, diarrhea, gastric suction, diaphoresis, or burns -Abnormal concentration of extracellular fluid -Results when normal proportion of salt to water in extracellular fluid is disrupted (gain of relatively more water than salt) -ADH elevation *Causes kidneys to retain excessive amounts of water (a gain of water relative to salt)

Causes of ADH Elevation

-The syndrome of inappropriate secretion of ADH (SIADH) -Ectopic synthesis *For example, small cell (oat cell) carcinoma is a type of lung tumor that frequently synthesizes and releases ADH -Physical or psychological stressors *Pain, nausea, other symptoms

Clinical Manifestations: Mild central nervous system dysfunction: Severe central nervous system dysfunction:

-Malaise, anorexia, nausea, vomiting, headache -Confusion, lethargy, seizures, coma, fatal cerebral herniation

Hyprenatremia:

-Serum sodium concentration above upper limit of normal -Extracellular fluid contains relatively too little water for the amount of sodium ions present; it is too concentrated -Also called *Water deficit *Hypertonic syndrome *Hypersomolality

Etiology of Hyprenatremia: Gian of more slat than water:

-Gain of more salt than water *Inadequately dilution concentrated tube feedings

• Intravenous infusion of hypertonic solution

• Near-drowning in saltwater *Overuse of salt tablets *Food intake with reduced fluid intake *Difficulty swallowing fluids *No access to water *Inability to respond to thirst

Etiology of Hyprenatremia: Loss of more water than slat:

-Loss of more water than salt *Diabetes insipidus (deficient antidiuretic hormone) *Tube feeding (causes obligate water loss in urine) *Osmotic diuresis *Prolonged emesis, diarrhea or diaphoresis without water replacement

clinical Manifestations of Hyprenatremia: Mild: Severe:

-Mild *Thirst *Oliguria *Confusion *Lethargy -Severe *Seizures *Coma *Death

Clinical Dehydration:

-Combination of two fluid disorders *Extracellular volume deficit *Hypernatremia *Too small a volume of fluid in the extracellular compartments and too-concentrated body fluids

Dehydration Etiology:

-Vomiting -Diarrhea -Knowledge deficit about salt and fluid replacement

Dehydration Clinical Manifestations:

-Sudden weight loss -Postural blood pressure decrease with concurrent increased heart rate -Light head ness, dizziness, or syncope on standing -Flat neck veins that collapse during inspiration (older children and adults) -Sunken fontanel (infants) -Rapid, thready pulse -Prolonged small-vein filling time -Prolonged capillary refill time -Decreased skin turgor -Dryness of oral mucous membranes -Absence of sweat and tears -Hard stools -Soft, sunken eyeballs -Longitudinal furrows in the tongue -Thirst -Increased serum sodium concentration -Confusion, lethargy -Coma -Hypovolemic shock

Edema:

Edema: Excess fluid interstitial compartment -May be a manifestation of excess extracellular fluid volume -May also arise from other mechanisms *Increased capillary hydrostatic pressure *Increased interstitial fluid osmotic pressure *Blockage of lymphatic drainage *Decreased capillary osmotic pressure

Blockage of Lymphatic Drainage: Caused by:

*Tumor *Parasites *Fibrosis from radiation therapy *Surgical removal of lymph nodes -Edema is frequently localized

Principles of Electrolyte Homeostasis: Electrolytes:

-Ionized salts dissolved in water -Most clinically important *Sodium *Potassium *Calcium *Magnesium *Chloride *Bicarbonate *Phosphate

Electrolyte: Dynamic control

-Concentration of an electrolyte is plasma is different from its concentration in the cell -For body function, electrolyte concentration must be normal in both the plasma and in the cells -Control of electrolyte levels is dynamic *If intake of specific electrolyte increases, excretion of that electrolyte may increase to normalize plasma levels *Similarly, if electrolyte intake decreases, electrolyte may be redistributed into the plasma to maintain normal plasma level.

Maintenance of Electrolyte Concentrations: 4 processes responsible

-Electrolyte intake -Electrolyte absorption -Electrolyte distribution -Electrolyte excretion *Processes work together to maintain dynamic control of electrolyte within normal limits

Electrolyte Intake:

-Intake normally occurs orally, through food and drink -Other routes *Oral medications (magnesium antacids) *Intravenous fluids *Nutritional solutions *Blood transfusions *Administration of the electrolyte magnesium *Tubes into body cavities (Nasogastric and GI feeding tube) *Near-drowning in saltwater

Electrolyte Absorption:

-Essentially if electrolyte is to be useful metabolically -Depends on other factors *Concentration gradients to much to little *Binding proteins (may increase or decease absorption) *pH of intestinal content *Medications *Surgical removal of portions of GI tract

Electrolyte Distribution:

-Influenced primary by hormones *Epinephrine *Insulin *Parathyroid hormone -Certain medications also influence electrolyte distribution -Electrolyte movement may be rapid *Shift of electrolytes from extracellular fluid into the electrolyte pools decreases the plasma electrolyte concentration *Shift of electrolyte from an electrolyte pool into the extracellular fluid increases the plasma electrolyte concentration

Electrolyte Excretion:

-Occurs through urine, feces, sweat -Influenced by hormones *Other factors --Rate of renal tubular fluid flow --Medications --Diarrhea --Vomiting

Electrolyte Loss Through Abnormal Routes:

-Exit of electrolyte from the body through routes other than urine, feces, sweat -May be controllable or may result from therapeutic procedures -Alters electrolyte homeostasis -Examples *Vomiting *Nasogastric suction *Paracentesis *Hemodialysis *Wound drainage *Fistula drainage

Electrolyte Imbalances:

-Common in many people pathophysiologic conditions -May be total body imbalances or may be imbalance in distribution within compartments

Electrolyte Imbalances: Excess:

-Excess may be caused by: *Increased intake *Increased absorption *Shift into extracellular fluid

Electrolyte Imbalances: Deficit:

-Deficit may be caused by: *Decreased intake *Decreased absorption *Increased excretion *Loss through abnormal route

Plasma Potassium:

-Normal concentration of potassium ions in serum is 3.5 to 5 mEq/L (may vary slightly with different laboratories) *Higer in neonates (an infant less than four weeks old)

Hypokalemia:

-Decreased potassium ion concentration in extracellular fluid -Does not necessarily denote decrease in total body potassium -May coexist with: *Total body potassium deficit *Total body potassium excess *Normal total body potassium ion concentration

Hypokalemia: Etiology:

-Decreased intake -Increased excretion

Decreased Potassium Intake:

-Anorexia -NPO (nothing by mouth) orders and intravenous solutions without potassium -Fasting -Unbalanced diet

Shift of Potassium from Extracellular Fluid to Cells:

-Alkalosis -Rapid correction of acidosis -Excess insulin (during total parenteral nutrition) -Excess B-adrenergic stimulation -Hypokalemic familial periodic paralysis

Increased Potassium Excretion Through Normal Routes: Renal Route:

-Potassium-wasting diuretics -Corticosteroid therapy -Cushing disease -Hyperaldosteronism -Excessive ingestion of black licorice (glycyrrhizin) -Hypomagnesemia -Parenteral carbenicillin or similar agents -Amphotericin B, cisplatin, and many other drugs -Fecal route *Diarrhea (includes laxative abuse) -Skin route *Excessive diaphoresis

Loss of Potassium Through Abnormal routes:

-Emesis -Gastric suction -Fistula drainage

Clinical Manifestations of loss of Potassium:

-Altered smooth, skeletal, cardiac muscle function *Abdominal symptoms --Distention --Diminished bowel sounds --Paralytic ileus *Skeletal muscle symtoms --Bilateral muscle weakness; usually begins in legs --Respiration paralysis *Cardiac muscle cell hyperpolarization --Ectopic beats --Alterations in conduction --Dysrhythmias may be severe enough to cause sudden cardiac death *Polyuria

Hyperkalemia:

-Rise of serum potassium ion concentration in the extracellular fluid -Level above 5mEq/L (depending on lab) -Because most potassium ions are inside cells, total body potassium may be increased or decreased depending on cause

Hyperkalemia: Etiology:

-Increased potassium intake -Shift of potassium from cells to extracellular fluid -Decreased potassium excretion

Increased Potassium intake:

-Excessive or too-rapid intravenous potassium infusion -Insufficiently mixed intravenous potassium -Large transfusion of stored blood -Massive doses of potassium penicillin G

Shift of Potassium from Cells to Extracellular Fluid:

-Acidosis caused by nonorganic acids -Insufficient insulin -Crushing injury -Cytotoxic drugs (tumor lysis syndrome) -Hyperkalemic periodic paralysis -B-Adrenergic blockade and prolonged strenuous exercise

Decreased Potassium Excretion:

-Oliguria (such as in hypovolemia or renal failure) -Potassium-sparring diuretics -Adrenal insufficiency -Renin-deficient states -Drugs that reduce aldosterone effects *Angiotensin-converting enzymes (ACE) inhibitors *Angiotensin-II receptor antagonists *Selective aldosterone blockers -Nephrotoxic drugs

Clinical Manifestations of Decreased Potassium Excretion:

-Muscle dysfunction *Early, mild --Intestinal cramping, diarrhea *Late, more severe --Muscle weakness: ascending, beginning in lower extremities -Cardiac dysrhythmias and even cardiac arrest *Don't have right resting membrane potential

Potassium Adaptation:

-Patients who have chronic renal failure often undergo potassium adaptation *Therefore, relatively mild symptoms at high plasma potassium concentrations -Mechanisms *Increased aldosterone levels *Shift of potassium excretion by colon *Shift in potassium ions from extracellular fluid into cells

Plasma Calcium:

-Present in three forms *Calcium ions bond to plasma proteins (such as albumin) *Bound to small organic ions (such as citrate) *Unbound -Only free ionized calcium is physiologically active

Hypocalcemia:

-Serum calcium concentration drops below the lower limit of normal -Fraction of unbound ionized calcium in the blood drops by more calcium binding to plasma proteins or other organic ions *The total serum calcium may be normal *Ionized hypocalcemia is present and may cause signs and symptoms

Hypocalcemia: Etiology:

-Decreased calcium intake or absorption -Decreased physiologic availability of calcium -Increased calcium excretion through normal routes

Decreased Calcium Intake or Absorption:

-Diet with insufficient calcium and vitamin D -Chronic kidney disease (deficient activated vitamin D) -Excessive dietary phytates or oxalates -Steatorrhea -Pancreatitis -Chronic diarrhea (includes laxative abuse) -Malabsorption syndromes

Increased Calcium Excretion Through Normal Routes:

-Steatorrhea (excess fat in feces) -Pancreatitis

Clinical Manifestations: Hypocalcemia

-Alternation in normal neuromuscular excitability resulting in: *Positive Trousseau sign *Positive Chvostek sign -Paresthesias -Muscle twitching and cramping -Hyperactive reflexces -Carpal spasm -Pedal spasm -Tetany -Laryngospasm -Seizures -Cardiac dysrhythmias

Hypercalcemia: Increased calcium intake or absorption:

*Milk-alkali syndorme *Vitamin D overdose (includes shark cartilage supplements)

Hypercalcemia: Shift of calcium from bone to extracellular fluid:

-Hyperparathyroidism -Immobilization -Paget disease -Bone tumors -Multiple myeloma -Leukemia -Non osseous malignancies that produce bone-resorbing factors