Alterations in Fluid and Electrolytes PDF

Alterations in Fluid and Electrolytes Learning Objectives Name the fluid compartments and sub- Describe imbalances of fluid homeostasis and compartments of the body, and the relative their consequences. amount of body fluid in each....

Alterations in Fluid and Electrolytes Learning Objectives Name the fluid compartments and sub- Describe imbalances of fluid homeostasis and compartments of the body, and the relative their consequences. amount of body fluid in each. Identify the mechanisms regulating sodium Describe the mechanisms of fluid movement balance of the body fluids. between fluid compartments. Examine the mechanisms regulating potassium, Identify the routes of water intake and output to calcium, and phosphate balance of the body and from the body. fluids. Explain the thirst mechanism and mechanism of Discuss the mechanisms regulating anions in the cessation of thirst. body fluids. Indicate how shifts in water output by the body Describe the pathophysiology of diabetes occur, and how the body compensates for such insipidus. shifts. Discuss the pathophysiology of the syndrome of Discuss the activity of antidiuretic hormone. inappropriate ADH (SIADH). Fluids, Ions, Nonelectrolytes, and Electrolytes Body fluids Ions Nonelectrolytes Electrolytes  Functions of Body Fluids Transport gases, nutrients, and wastes Help generate the electrical activity needed to power body functions Take part in the transformation of food into energy Maintain the overall function of the body  Distribution of Body Fluids Intracellular Compartment (ICF) Consists of fluid contained within all of the billions of cells in the body Larger of the two compartments, with approximately two thirds of the body water in healthy adults High concentration of K+ Extracellular Compartment (ECF) Contains the remaining one third of body water Contains all the fluids outside the cells, including that in the interstitial or tissue spaces and blood vessels High concentration of Na+ Composition of the ECF, Plasma, and Interstitial Fluids Large amounts of sodium and chloride Moderate amounts of bicarbonate Small quantities of potassium, magnesium, calcium, and phosphate Composition of the ICF Almost no calcium Small amounts of sodium, chloride, bicarbonate, and phosphate Moderate amounts of magnesium Large amounts of potassium (hypo/hyperkalemia) Located between capillary and cell Separates cells from surrounding cells Hydrostatic pressure and osmotic pressure= blood pressure Diffusion and Osmosis Concentration Gradient Difference in concentration over a distance Diffusion The movement of charged or uncharged particles along a concentration gradient from an area of higher concentration to one of lower concentration O2 high to low and CO2 low to high Alveoli has high O2 when you breathe in and low in blood stream CO2 is high concentration in blood streams but low in alveoli Osmosis The movement of water across a semipermeable membrane from the side of the membrane with the lesser number of particles and greater concentration of water to the side with the greater number of particles and lesser concentration of water Tonicity The tension or effect that the effective osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane Solutions can be classified according to whether or not they cause cells to shrink: Isotonic: neither shrink nor swell (wanted) when solution and cell have same concentration Hypotonic: swell Hypertonic: shrink How much fluid is circulating  Mechanisms Protecting Extracellular Fluid Volume Alterations in Hemodynamic Variables Vasoconstriction and an increase in heart rate - how fast you get more blood back, quicker Alterations in Sodium and Water Balance Isotonic contraction or expansion of ECF volume - concentration and expansion have to do with tonicity Hypotonic dilution or hypertonic concentration of extracellular sodium brought about by changes in extracellular water - whether too hypo or hyper it will make a difference on how much blood we have circulating When sick and vomiting losing fluid you do not die immediately because your body knows how to compensate by altering hemodynamics and sending a signals to constrict blood vessel. When it constricts blood vessels get more blood back to the heart  Edema Accumulation of fluid in extracellular space Pitting edema ( when you push down there is a pit) Indentation is made and the “pit” persists after pressure is released and you determine by how many mm you push in Non-pitting edema Indentation is made, but the “pit” does NOT persist after pressure is released Example- fracture ankle Brawny edema Example- peripheral vascular disease- lousy blood flow A form of non-pitting edema Skin becomes harder and thicker (skin and tissue are chronically deprived of O2 because of lack of blood flow) The lack of blood flow causes Red or dark discoloration along the affected limb, warm to the touch The affected part also displays significant swelling and may be warm to the touch  Edema Formation The physiologic mechanisms that contribute to edema include factors that: Localized edema (in a specific site) Increase the capillary filtration pressure General edema (people with heart - capillaries are increased from surgery, injury, failure or edema all over inflammation, pushing out hydrostatic pressure, more likely to leak out higher pressure Dependent edema ( sitting for a long Decrease the capillary colloidal osmotic pressure time legs start to swell and common - one of primary proteins in blood steam is albumin. in older people) Albumin can fall for any reason like poor nutritional status or when someone isn’t able to take in adequate nutrients Increase capillary permeability - leaky capillaries Decreased lymphatic flow - due to lack of lymph drainage -can be damaged, blocked, or surgically removed, fluid is staying in interstitial fluid  Methods for Assessing Edema Daily weight Visual assessment Measurement of the affected part Application of finger pressure to assess for pitting edema 1. what does it look like 2. press for pit 3. you measure in mm 4. continue to look for difference  Physiologic Mechanisms Assisting in Regulating Body Water Thirst Mechanism Primarily a regulator of water intake - if you are thirsty, you are already dehydrated, and you body is telling you to intake more fluids The elderly have an intrinsic defect in the thirst mechanism resulting in decreased fluid intake - older peoples thirst mechanism does not work right, therefore more likely to be dehydrated quicker ADH (antidiuretic hormone) Your body holds on to more water as a result of the hormone A regulator of water output Both mechanisms respond to an increase in extracellular osmolality and a decrease in volume Extracellular osmolality keeps body in check by showing how concentrated ECF is. If too concentrated, it will send feedback to the rest of the body and the pituitary gland says it needs more water  Water and Na+ Balance There are pressure sensors in the vasculature (blood vessels) as an early indication that something is wrong Baroreceptors regulate effective volume. Gain Modulating sympathetic nervous system outflow and ADH secretion Water (holding onto more water or drinking - sends feedback signals through sympathetic nervous system, tells pituitary when more) to secrete ADH Oral intake and metabolism of nutrients (eating Atrial Natriuretic Peptide (ANP) foods high in sodium) Na+ Secretes when you have a reduction in ECF- which increases renal sodium excretion Sensible Loss (can be measured) Causes a reduction in extracellular fluid (ECF) volume by increasing renal sodium Kidneys ( by measuring urine) excretion Gastrointestinal tract ( by measuring what Renin-Angiotensin-Aldosterone System (RAAS) comes out of GI system) Angiotensin II Insensible Loss (cannot be measured) Aldosterone (most powerful) Skin (sweat) Aldosterone promotes reabsorption of sodium and water into the body Lungs (exhale water vapor) Secreted to make RAAS) Regulators of Sodium If kidneys know to hold on to sodium, it will hold onto water too The kidney is the main regulator of sodium. -sensitive to blood pressure, it will retain sodium when arterial pressure is down Monitors arterial pressure; retains sodium when arterial pressure is decreased; and eliminates it when arterial pressure is increased The rate is coordinated by the sympathetic nervous system and the renin–angiotensin– aldosterone system (RAAS). Atrial natriuretic peptide (ANP) may also regulate sodium excretion by the kidney. Normal serum sodium 135 to 145 milliequivalents per liter (mEq/L) Assessment of Body Fluid Loss History of conditions that predispose to sodium and water losses, weight loss, and observations of altered physiologic function indicative of decreased fluid volume - look for a condition that means they are losing fluid Heart rate (tachycardia- high heart rate) Blood pressure Postural hypotension Venous volume/filling - veins are very distensible and gravity has an effect on them Capillary refill rate - assess the speed at which blood returns to the capillaries in the skin after pressure is applied, -detect changes in blood flow - normal time is 5L. Per day Craving for ice water Excessive urine output >30-40 L per day Urine is color of water Diagnosis labs reflect dilution Serum sodium >145 Urine specific gravity 48 hours May be asymptomatic even with Na 48 hours Rate of correction should not exceed 8-12 mmol/L to avoid cerebral demyelination syndrome Treatment of Choice: Fluid restriction 800 – 1000 mL/day Usually will correct itself within a few days  Complications Of Treatment Central Pontine Cause not known, but Myelinolysis: related to the rate of Spastic quadriparesis correction of hyponatremia Pseudobulbar palsy How long patient was Spastic paralysis of larynx hyponatremic (related to how and pharynx fast) Airway occlusion = EMERGENCY How big the change in serum Na+ Treatment Complications Those at highest risk for CPM: Alcoholics Malnourished Elderly women on thiazides Hypokalemic (low K+) Potassium Distribution and Regulation High concentration of potassium in the intracellular compartment Normal serum potassium (extracellular compartment) 3.5 to 5.0 mEq/L Body stores of potassium are related to body size and muscle mass. - the more muscular= more K+ in cell Is normally derived from dietary sources Plasma potassium is regulated through two mechanisms: Renal mechanisms that conserve or eliminate potassium (outside of kidney) A transcellular shift between the ICF and ECF compartments  Abnormal Potassium Hypokalemia refers to a decrease in plasma potassium levels below 3.5 mEq/L 1. Inadequate intake 2. Excessive gastrointestinal, renal, and skin losses - not taking in enough, or losing too much 3. Redistribution between the ICF and ECF compartments Hyperkalemia refers to an increase in plasma levels of potassium in excess of 5.0 mEq/L 1. Decreased renal elimination - not eliminating through kidney 2. Excessively rapid administration -giving too fasts 3. Movement of potassium from the ICF to ECF compartment  Diagnosis and Treatment of Potassium Disorders Diagnosis is based on complete history, physical examination to detect muscle weakness and signs of volume depletion, plasma potassium levels, and ECG findings. -ECG- is it affecting Treatment Sodium bicarbonate will cause K+ to move ICF. (medications) Insulin will decrease ECF K+ concentration. Curtailing intake or absorption, increasing renal excretion, and increasing cellular uptake - dietary modifications Vitamin D, Calcitonin, and Parathyroid Hormone Calcium, phosphate, and magnesium Normal serum calcium level is 8.5 to are the major divalent cations in the 10.2 mg/dL body. Vitamin D acts to sustain normal plasma levels of calcium and phosphate by increasing their absorption from the intestine. Calcitonin acts on the kidney and bone to remove calcium from the extracellular circulation.- - activates vitamin D -vitamin D has to be activated by the kidney to be available to the body Mechanisms Regulating Calcium, Phosphate and Magnesium Balance Calcium, phosphate, and magnesium are the major divalent cations in the body. They are Ingested in the diet then Absorbed from the intestine then Filtered in the glomerulus of the kidney then Reabsorbed in the renal tubules then Eliminated in the urine Calcium Gain and Loss Gains Losses Dietary dairy foods When dietary intake (and calcium Parathyroid Hormone (PTH) and vitamin absorption) is less than intestinal D stimulate calcium reabsorption in this secretion segment of the nephron. - too much through intestine - in the kidney  Causes and Symptoms of Hypocalcemia Causes Symptoms Impaired ability to mobilize calcium from bone Chvostek’s and Trousseau’s Sign stores Caused by increased neuromuscular Abnormal losses of calcium from the kidney excitability (hyperactive) Increased protein binding or chelation such that Cardiovascular effect greater proportions of calcium are in the Nerve cells less sensitive to stimuli nonionized form - chelation- not available to the body Soft tissue sequestration Hypocalcemia: Chvostek’s Sign & Trousseau’s Sign Causes and Symptoms of Hypercalcemia Increased intestinal absorption Symptoms Excessive vitamin D and calcium Changes in neural excitability Milk-alkali syndrome Almost always caused by taking too many Alterations in smooth and calcium supplements cardiac muscle function Increased bone resorption Exposure of the kidneys to high  Parathyroid hormone concentrations of calcium Malignant neoplasms Prolonged immobilization Decreased elimination Thiazide, lithium therapy - from medications Role of Phosphate in the Body Plays a major role in bone formation Serves as an acid–base buffer in the Essential to certain metabolic processes: extracellular fluid and in the renal excretion of hydrogen ions The formation of ATP and the enzymes needed for metabolism of glucose, fat, and Necessary for delivery of oxygen by protein - for normal cell metabolism the red blood cells A necessary component of several vital Needed for normal function of other parts of the cell blood cells Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell White blood cells and platelets membrane Normal serum phosphate 2.8 to 4.5 mg/dL  Role of Phosphate in the Body Serves as an acid–base buffer in the extracellular fluid and in the renal excretion of hydrogen ions Necessary for delivery of oxygen by the red blood cells Needed for normal function of other blood cells White blood cells and platelets Common Causes of Hypophosphatemia and Hyperphosphatemia Hypophosphatemia Hyperphosphatemia Depletion of phosphate because of From failure of the kidneys insufficient intestinal absorption to excrete excess phosphate Trans-compartmental shifts Rapid redistribution of Increased renal losses intracellular phosphate to the ECF compartment Excessive intake of phosphate Magnesium Balance Essential to all reactions that require ATP Regulation at the kidney level Magnesium absorption in the thick ascending loop of Henle is the positive voltage gradient created in the tubular lumen by the Na+-K+-2Cl− co-transporter system Ingested in the diet Absorbed from the intestine Excreted by the kidneys Normal serum magnesium 1.8 to 2.6 mEq/L  Manifestations of Hypomagnesemia Laboratory Values Serum magnesium level less than 1.8 mg/dL Neuromuscular Manifestations Personality change, athetoid or choreiform movements, nystagmus, tetany, positive Babinski, Chvostek, Trousseau signs Cardiovascular Manifestations Tachycardia, hypertension, cardiac dysrhythmias You want negative Babinski on 24 + month old (toes curl) You want positive Babinski in babies (toes fan out) Athetoid and Choreiform Movements Nystagmus -involuntary movement of the eyes Causes of Hypermagnesemia Excessive Intake Intravenous administration of magnesium for treatment of preeclampsia - oral anti-acids Excessive use of oral magnesium-containing medications Decreased Excretion Kidney disease Acute renal failure  Signs & Symptoms of Hypermagnesemia Usually do not appear Depressed respiration & apnea unless Mg >2 mmol/L (5 - can be from too much magnesium mg/dL) Hypotension Depressed mental status Bradycardia Disappearance of deep tendon reflexes Complete heart block & Muscular weakness cardiac arrest Paralysis ECG abnormalities Drowsiness Seizures PRACTICE QUESTION A patient has been excessively vomiting for several days. Why would the patient experience hypokalemia? a) Potassium excreted through the vomitus b) Inability to consume foods high in potassium c) Extracellular potassium is being pushed inside the cells d) Excessive muscle contraction while vomiting pushes potassium back into the cells PRACTICE QUESTION Stimulation of the facial nerve via the masseter muscle causes twitching of the nose/lips in hypocalcemia is known as? a) Trousseau's Sign b) Chvostek's Sign c) Homan's Sign d) Goodell's Sign