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  • So where are these fluids kept? As you may remember from your anatomy and physiology classes, body fluids are divided between the intracellular and extracellular department. As you can see from the slide here, most of your body fluid is found in the intracellular department. ICF assists in cellular metabolism, and is high in potassium, phosphors, and protein.
  • The extracellular component of body fluids is about 33% of the total body fluid mass. ECF is divided into three major components: Intravascular – the fluid within the blood vessels. Plasma accounts for about half of the total blood volume of the body, Interstitial – the fluid that surrounds the cells – an example of interstitial fluid is lymph, And finally, Transcellular fluid – which is fluid found in the cerebrospinal column, pericardial envelope, synovial joints, or intraocular space
  • Let’s remember the marathon runner once again. Obviously, his output via perspiration was greater than his intake, so water was removed to keep the organs functioning from the extracellular tissues. As his water moved out of the cell, his thirst increased and the cells became dehydrated. His intracellular fluid became hypotonic, and so more anti diuretic hormone was excreted. This enabled him to initially hold on to any remaining fluid left in his body. As he continued to perspire and did not receive adequate intake, his extracellular fluid volume became more and more decreased. The adrenal glands attempted to compensate by secreting more aldosterone. Sodium reabsorption was increased by the kidneys, in the hope that more volume would be made available to the body, because water goes where sodium is. If you were able to do a physical assessment on our marathon runner at this point, what do you think he would look like?
  • What about in children? They do have further signs and symptoms that you should be aware of. These symptoms are more rapid because infants have a greater fluid mass. Does anyone remember what the fluid mass is for an infant? (75 – 80%) By the way, is dehydration the same as fluid volume deficit? Actually, it is not. Dehydration implies that there is a loss of water alone, with an increase in the sodium levels. FVD may occur alone or in combination with other imbalances. Unless other imbalances are present, the electrolyte composition is generally stable.
  • Certainly, along with physical assessment findings there is objective data to support a diagnosis of FVD. The following labs may be seen in a client experiencing fluid loss. Do any of these lab findings surprise you? Why do you suspect that there would be an increase in Hct and BUN? The BUN to Cr ratio is generally greater than 20:1 in the FVD client. The BUN is elevated due to decreased hydration and decreased renal perfusion, and will generally return to baseline after hydration occurs. Serum creatinine is also affected by dehydration, but to not as great of an extent. Additionally, the Hct is increased because the plasma volume has decreased, making the proportion appear higher than normal. You may also see some electrolyte imbalances depending on the source of the loss. K and Na imbalances are the most common
  • How is the FVD patient going to be treated? We mentioned earlier that if we don’t increase hydration, the kidneys will eventually collapse. Our main goal is to correct the fluid balance before acute renal failure sets in. Monitoring intake and output become crucial at this point. Fluids will be encouraged and given IV as necessary.
  • Why do you think we would evaluate mental status on the FVD client? Upon resolution, you would expect to see a return to baseline in your client.
  • What about the person who has too much fluid? Fluid volume excess or hypervolemia is also a major concern, as it can cause serious consequences for both adults and children. The older client is especially predisposed to developing congestive heart failure from hypervolemia. When you are thinking about FVE, think about the pizza eating example we discussed earlier. Abnormal retention of sodium, or sodium overload, causes abnormal retention of water, because water goes where sodium is. This causes the symptoms that accompanies FVE. Other than dietary indiscretions, what are some other causes of fluid overload?
  • The causes listed here are varied. Can anyone else think of other examples of causes for FVE? Can anyone explain why liver failure would cause hypervolemia? Aldosterone is being chronically stimulated in heart failure, renal disease, and in liver failure or cirrhosis. Again, as aldosterone is being produced, the renal tubules are holding on to sodium, and water is following. Tell me a bit about what you think the patient in volume overload is going to look like…
  • We had mental status changes in FVD, so why do you think you might also see mental changes in FVE? (increased fluid in the brain causes a dilution of the Hct; oxygen carrying capacity is decreased, causing alterations in mental status.)
  • Do any of these lab findings surprise you? If you were to perform a CXR, what do you think you might see at this point? (Pulmonary edema or pulmonary congestion, pleural effusion, CHF)
  • What do you think the sodium restriction should be? (1000 mg / day) What is 1000 mg? (~2-4 teaspons, or one cup of canned tomato soup) We need to take this opportunity to educate our patients about hidden sodium foods (lunchmeats) as well as salt on the table. Why do you think we would reposition every two hours if the client is bedridden? (to prevent skin breakdown – fluid is present via edema, stretching the skin tissue, making it thinner, and therefore predisposing the client to breakdown)
  • Table 14-5 in Smeltzer does provide an overview of IV solutions. Remembering back to your first year in nursing school, why are IV fluids ordered to begin with? Why do we need varying types of IV fluids? When would you expect to see isotonic solutions ordered? (with hypovolemia, resusitation, shock, DKA, metabolic alkalosis, hypercalcemia, mild Na deficiency) When would you expect to see hypotonic fluids ordered? (with hypertonic dehydration, Na and Cl depletion, gastric fluid loss – not used for third spacing shifts or with increased ICP; can cause shifts from vasculature into cells, resulting in CV collapse and increased ICP)
  • Hypertonic solutions are only used in critical situations. What is water intoxication? Can be near drowning, or someone who is severely hyponatremic. Let’s take a break here, and then come back and talk about the major electrolyte functions and their states in excess or depletion. Please return in five minutes.
  • As a reminder, table 14-6 in Smeltzer outlines briefly the major anions and cations and their resulting states. Na concentration range is 135-145. Because Na does not permeate the cell wall easily, alterations in Na account for the alterations in water or fluid balance.
  • Loss of Na can result from many things, as listed above. Let’s look at these symptoms for just a moment. Why do you think your client will experience a decreased BP? The neuro changes are generally related to cellular swelling and cerebral edema. In general, the faster the decrease in Na, the more severe the symptoms.
  • Regardless of the cause of the hyponatremia, the serum Na will be less than 135. The cell is going to swell as water is pulled in from the ECF, resulting in the increased Hct, and sometimes the increased K. Generally, urine sodium is decreased EXCEPT in cases of SIADH. In those cases, the urine Na is greater than 20 mEq/ L, and the urine specific gravity is high.
  • Again, treatment goals are to ideally restore Na to their normal range – between 135 – 145. The most effective treatment, however, is prevention. Because thirst mechanism is oftentimes altered in ill clients, our role as providers of care is to help encourage appropriate hydration in the ill client. Early detection and treatment is necessary to help avoid serious consequences.
  • Hypernatremia would result in a serum sodium greater than 145. The symptoms are generally neuro in origin, and thought to be related to the cellular shrinking as water goes to the ECF. Permanent brain damage can occur with prolonged or severe hypernatremia.
  • Thirst is the most common symptom in excessive sodium levels as desire for water is such a strong defense mechanism against hypernatremia.
  • These lab values should come as no surprise, as your patient may also be exhibiting some FVE. The kidneys are attempting to conserve water to dilute the sodium level.
  • If Na is lowered too quickly, cerebral edema may occur so caution must be taken in this area. For patients that are tube fed, generally the higher the osmolality of the feeding, the greater the need for free water replacements.
  • Under the influence of the Na / K pump, potassium is constantly moving in and out of the cell to maintain the appropriate electrical charge throughout the body. To maintain K balance, appropriate renal function must occur, as over 80% of all potassium is excreted through the kidneys.
  • Hypokalemia is actually fairly common, with GI loss being the largest reason that hypokalemia occurs. This is certainly related to the loss of K via gastric secretions, but also because the patient is predisposed to metabolic alkalosis in these cases, thus increasing the renal excretion of potassium. Additional K losses are seen with diarrhea as the intenstines can contain up to 30meq of potassium at any one time. Magnesium losses can also cause hypokalemia, and need to be corrected prior to correction of the K problem for appropriate results.
  • Severe K deficits can result in cardiac or respiratory arrest. EKG changes are frequent, with the T wave flattening in hypokalemia. The client will frequently complain of weakness and have decreased reflex action. Confusion is common in hypokalemia, as is also numbness and tingling of the extremities. Symptoms, however, do not develop until after the K generally is below 3.0. Prolonged K depletion can result in glucose intolerance. It is also important to realize that hypokalemia increases sensitivity to digitalis products.
  • Hydration may also be necessary for patients who present with hypokalemia secondary to laxative and diuretic abuse. In this case, further counselling and education may be necessary to clients regarding this risk taking behavior. Clients who are predisposed for K loss (from the use of thiazide diuretics, for example) should be educated to increase dietary consumption of K foods. Foods rich in K include fruit and fruit juices, fresh vegetables, fresh meats, chocolate and cocoa products, dried beans, coffee, tea, and dark colas, some dairy products, and eggs. IV supplementation is generally indicated for patients with severe hypokalemia. KCl is generally the most accepted and widely used additive. Although policies differ from facility to facility, if a client’s urinary output decreases to less than 20 ml / hour, the K infusion should be stopped until further evaluation can be made. Additionally, most institutions state that K can not be administered greater than 10 – 20 meq / hour.
  • In severe cases, you may note an order to administer a hypertonic glucose solution. Remember that potassium depletion depresses the release of insulin and results in glucose intolerance. If you administer a glucose solution that has an mOsm greater than serum, you will force the K out of the ECF into the serum. This is not generally performed on a routine basis. Whatever treatment options are chosen for treatment of a low K level, the nurse needs to closely monitor intake and output, EKG changes (telemetry at a minimum is a necessity), and determine bowel sounds and muscle changes with the client. Additionally, if the patient is receiving Dig products of any type, before administering any further digitalis, appropriate levels should be received. Remember, hypokalemia increases the sensitivity to digitalis.
  • Hyperkalemia is generally viewed as a K level greater than 5.3 – 5.5, depending on the lab used. Generally, hyperkalemia does not occur in clients with normal renal function. Remember, the kidney excretes approximately 80% of the K metabolized each day. Other causes of hyperkalemia would be in cases of severe trauma such as burns, crush injuries, or severe infections, or medically induced hemolysis via lysing of malignant cells via chemotherapy. Pseudohyperkalemia needs to be ruled out any time an abnormally high K level is reported. PseudohyperK is generally caused from hemolysis, either via a too tight tourniquet or leaving of the SST out in the heat after draw. Although impaired kidney function is the number one cause of hyperkalemia, patients with Addison disease or hyperaldosteronism are also at risk for an increased K, as there is inappropriate sodium regulation with these patients. Additionally, acidosis can also lead to hyperkalemia.
  • Hyperkalemia is most widely recognized by the cardiac changes it produces. On EKG, tall tented T waves are noted. This is because changes in cardiac conduction are occuring. Ventricular dysrhythmias are common. Generally, cardiac changes and manifestations begin with a K around 6 – 7, but are always present with a K level around 8.
  • In severe cases, the administration of calcium gluconate may be used. Action will occur minutes after administration, and in this case, the calcium antagonizes the K level on the heart. Other alternatives would be to utilize sodium bicarb or an insulin and glucose solution may be used. Both sodium bicarb and insulin / glucose begin to work by temporarily shifting the K into the cells. Action occurs within 30 minutes. However, these management solutions are only temporary. If patients do not return to a normal K level after drastic measures, a cation exchange solution (ie, kayexelate) or RRT must be initiated for removal of the K. Kayexelate works by binding with other cations in the GI tract. Kayexelate can not be used in someone with a paralytic ileus because perforation may occur in the gut. Moderately high K levels require patient education especially regarding diet and supplement use. Salt substitutes are commonly used for HTN treatment, but contain a high amount of K. As many HTN patients also have renal impairment, the use of salt substitutes must be immediately discontinued.
  • Normal ionized calcium is generally accepted as between 4.5 – 5.5. Ionized calcium is the only form of calcium that is physiologically relevant. Serum calcium is frequently reported and must be adjusted for albumin levels and serum proteins.
  • Both hypocalcemia and hypercalcemia are fairly common because so many factors influence Ca regulation. Ca is required for bone and teeth strength and density, blood coagulation, and nerve contraction. Ca is absorbed and utilized in the presence of vitamin d, and is controlled by PTH.
  • Hypocalcemia is generally seen in patients with removal of the parathyroid gland, or with patients who have any type of radical neck surgery. Additionally, in clients with low Mg levels, low levels of Ca would be common. In the presence of an elevated PO4 level, lower levels of Ca would be seen. This is common in renal failure or insufficiency as there is an inverse relationship between the two electrolytes. Citrated blood (such as exchange transfusions) may result in a decreased Ca level, but this is usually transient in nature. Finally, if the Vit D is not being absorbed, Ca production would be lower. Clients with osteoporosis will generally have a normal serum ionized Ca, but have a total body Ca deficit. Bed ridden clients are also at risk for bone loss via hypocalcemia and bone resorption.
  • Tetany is the most common sign of decreased calcium. Chvostek sign – abnormal spasm of the facial muscle elicited by light taps on the facial nerve – sign of tetany Trousseau sign – carpal spasm induced by inflating BP cuff on upper arm to pressure exceeding systolic BP for 3 minutes – sign of tetany. Tetany refers to the entire symptom complex related to nerve excitability. In severe cases, seizures may occur.
  • Treatment for mild hypocalcemia include change in dietary patterns. Severe cases of hypocalcemia can be life threatening and require IV administration of Ca. Ca gluconate is is generally used, as it is less tissue irritating that calcium chloride. IV calcium needs to be administered in D5w via slow IVP or with a pump. Skin sloughing and tissue necrosis can occur with infiltration, so care must be taken. Effects of calcium are similar to Digoxin – can lead to toxicity, and thus the client must have a dig level performed during therapy. Additionally, it is important to correct other electrolyte disturbances such as PO4 and Mg, and possibly institute Vit D therapy to help aid in absorption in the gut of Ca. In all cases of hypocalcemia, seizure precautions must be instituted for the safety of the client
  • Severe hyperCa is a very dangerous imbalance, and has greater than a 50% mortality rate if not treated promptly. The most common causes of hyperCa are malignancy, bone mobilization, and increased PTH. These are generally seen in CKD patients.
  • Generally, s/sx of hyperCa are directly related to the level of elevation. Cardiac standstill can and does occur when the serum Ca level falls below 18 mg / dl. S/sx such as anorexia, constipation, and muscle weakness are generally thought to be directly related to decreased tone in smooth muscles and the reduction in neuromuscular excitability
  • Hypercalcemic crisis is an emergency frequently resulting in death if not treated promptly. Levels of 8-9 meq/ l or a serum Ca greater than 17 mg / dl that occurred rapidly are indicative of hypercalcemic crisis. Azotemia – excessive amounts of nitrogenous waste products in the blood
  • Treatment for hyperCa is listed on this slide. For patients with Cancer, the use of corticosteroids and mithramycin help decrease bone turnover, but do need to be used cautiously. Calcitonin – hormone secreted by thyroid gland to decrease calcium levels If possible, fluids administered orally should contain Na, as sodium helps aid in the removal of Ca. Pts are encouraged to drink 3-4 liters per day.
  • Mg plays a great role in electrolyte balance as it is the second most abundant intracellular cation. As Mg plays a role in nerve conduction, Mg affects the cardiovascular system peripherally by producing vasodilation. Mg is also thought to decrease total peripheral resistance.
  • Mg levels are similar to Ca in that they should be evaluated in conjunction with albumin leels. Low serum albumin levels decrease total Mg.
  • HypoMg is a common imbalance in ill patients. You may initially see hypoMg in clients withdrawing from ETOH, or with administration of tube feedings or TPN. Mg is absorbed in the small bowel, so any changes in the bowel can cause hypoMg. In ETOH withdrawal cases, serum Mg should be checked on a regular basis, generally every 2 days.
  • Babinski – dorsiflexion of big toe with extension and fanning of other toes You will note that many of these sx are familiar, and mimic Ca issues.
  • Diarrhea is a common side effect of increased dietary Mg. TPN clients require Mg added to the feedings. Boluses of Mg too rapidly can cause cardiac arrest
  • Swallow reflex affected by jerking movements – test w/ water prior to food or meds Teaching / counselling important
  • Can appear falsely elevated with hemolyzed specimens. Respiratory center is depressed when Mg is greater than 10. Death can occur when hyperMg is not treated.
  • Do not administer Mg to renal impaired clients. Vent support and IV Ca is indicated for emergencies. Dialysis can reduce Mg levels within 2-4 hours. In pts with nl renal function, loop diuretics with half strength NaCl enhances Mg excretion.
  • 85% of PO4 is located in bones and teeth, with 14% in soft tissue, and less than 1% in ECF. PO4 levels decrease with age.
  • Sx appear to result from impaired cell energy (low PO4 causes ATP deficiency) and / or impaired o2 delivery to tissues. Hypoxia can occur from the low delivery of O2 to peripheral tissues, resulting in an increase in resp rate. This may lead to resp alkalosis, which causes PO4 to move into the cell, and making the hypoPO4 even worse. It is also believed the hypoPO4 predisposes individuals to infection.
  • IV PO4 is indicated with severe hypoPO4, when the PO4 level falls below 1.
  • Primary complication is metastatic calcification.
  • Education is key, and requires constant reinforcement. Calcification can occur when Ca x PO4 product is greater than 70.

Transcript

  • 1. Fluids and Electrolytes Alteration in Fluids and Electrolytes
  • 2. Terms
    • Osmosis
      • movement of water across cell membranes from less concentrated to more concentrated
    • Solutes
      • substances dissolved in a liquid
    • Osmolality
      • the concentration within a fluid
  • 3. Terms
    • Diffusion
      • movement of molecules in liquids from an area of higher concentration to lower concentration
    • Filtration
      • fluid and solutes move together across a membrane from area of higher pressure to one of lower pressure
    • Active Transport
      • substance moves across cell membranes from less concentrated solution to more concentrated - requires a carrier
  • 4. Homeostasis
    • A delicate balance of fluids, electrolytes, and acids and bases is required to maintain good health.
    • This balance is called Homeostasis.
  • 5. Body Fluid and Electrolyte Compartments
    • Approximately 60% of a typical adult’s weight consists of fluid (water and electrolytes).
    • Factors Influence the amount of Body Fluid
        • Age
        • Gender
        • Body Fat
  • 6. 80% of body weight 60 % of body weight 50 % of body weight
  • 7. Compartments of Body Fluid
    • Intracellular Space- 70%
        • Approximately two-third of the body, located in the skeletal muscle mass.
        • Fluid within the cells themselves
        • Provide nutrients for metabolism:
        • High in K, Po4, protein
        • Moderate levels of Mg, So4
        • Assists in cellular metabolism
  • 8. Compartments of Body Fluid
    • Extracellular Space
        • Intravascular fluid- blood plasma
        • Interstitial fluid (tissue fluid)- ex. lymph
        • Transcellular fluid- ex. Cerebrospinal, pericardial, synovial, intraocular and pleural fluids, sweats and digestive secretions
  • 9.
    • Electrolytes in body fluids are active chemicals
    • Cations- carry positive charges
    • Anions- carry negative charges
    • Major Cations in body fluid:
    • sodium
    • potassium
    • calcium
    • magnesium
    • hydrogen
    • Major Anions in body fluid:
    • chloride
    • bicarbonate
    • phosphate
    • sulfate
    • proteinate
  • 10. Approximate Major Electrolyte Content in Body Fluid Electrolytes MEQ/L Extracellular Fluid (Plasma) Cations Sodium (Na) 142 Potassium (K) 5 Calcium (C ++) 5 Magnesium (Mg++) 2 Total Cations 154 Electrolytes MEQ/L Extracellular Fluid (Plasma) Anions Chloride (Cl-) 103 Bicarbonate (HCO3-) 26 Phosphate (HPO4-) 2 Sulfate (SO4-) 1 Organic Acids 5 Proteinate 17 Total Anions 154
  • 11. Approximate Major Electrolyte Content in Body Fluid Electrolytes MEQ/L Intracellular Fluid Cations Potassium (K+) 150 Magnesium (Mg++) 40 Sodium (Na+) 10 Total Cations 200 Electrolytes MEQ/L Intracellular Fluid Anions Phosphates and Sulfates 150 Bicarbonate (HCO3-) 10 Proteinate 40 Total Anions 200
  • 12. Functionsof Electrolytes
    • Promote neuromuscular irritability
    • Maintain body fluid volume and osmolality
    • Distribute body water between fluid compartments
    • Regulate acid base balance
  • 13. Average Daily Intake and Output in an Adult Intake Output Oral Liquids 1,300 mL Urine 1,500 mL Water in Food 1,000 mL Stool 200 mL Water Poroduce by Metabolism 300 mL Insensible Lungs 300 mL skin 600 mL Total Gain 2,600 mL Total Loss 2,600 mL
  • 14. Falling Systemic Blood Pressure/ Volume Reduces Filtrate Volume or Solute content in Renal Tubules JG Cells of Kidney Renin Angiotensin II Formed in Blood Baroreceptors in Blood Vessels Sympathetic Nervous System Systemic Arterioles Vasoconstriction Peripheral Resistance Hypothalamic Osmoreceptors Posterior Pituitary ADH (antidiuretic hormone Collecting Ducts of Kidneys Water Reabsorption
  • 15. Systemic Arterioles Vasoconstriction Peripheral Resistance Adrenal Cortex Aldosterone Kidney Tubules Na Reabsorption (and Water Absorption) Blood Volume Rising Blood Pressure
  • 16. Regulation of Body Fluid Compartments When two different solutions are separated by a membrane that is impermeable to the dissolved substances, fluid shifts through te membrane from region of low concentration to the region of high solute concentration until the solutions are of equal concentration; this diffusion of water caused by a fluid concentration gradient is known as OSMOSIS
  • 17. Regulation of Body Fluid Compartments Diffusion- is the normal tendency of a substance to move from an area of higher concentration to one of lower concentration . It occurs through the random movement of ions and molecules. Example of diffusion are the exchange of oxygen and carbon dioxide between the pulmonary capillaries and alveoli and the tendency of sodium to move from the ECF compartment, where the sodium concentration is high, to the ICF where its concentration is low.
  • 18.  
  • 19. Laboratory Tests for Evaluating Fluid Status
    • Osmolality - reflects the concentration of fluid that affects the movement of water between fluid compartments by osmosis.
      • measures the solute concentration per kilogram in blood and urine.
      • measure of a solution’s ability to create osmotic pressure and affect the movement of water.
      • Serum osmolality- primarily reflects the concentration of Sodium
      • Normal Serum Osmolality- 280 to 300 mOsm/kg
      • Urine osmolality- is determined by urea, creatinine and uric acid. – most reliable of urine concentration.
      • Normal Urine Osmolality- 250 to 900 mOsm/kg
      • mOsm/kg
  • 20. Laboratory Tests for Evaluating Fluid Status
    • Osmolarity - describes the concentration of solutions, is measured in milliosmoles per liter (mOsm/L).
    • Urine Specific Gravity - measures the kidney’s ability to excrete or conserve water.
      • Normal range- 1.010 to 1.025
  • 21. Laboratory Tests for Evaluating Fluid Status
    • Blood Urea Notrogen (BUN) - is made up of urea, an end product of metabolism of protein by the liver. Amino acid breakdown produces large amounts of amonia molecules, which are absorbed into the bloodstream. Amonia molecules are converted to urea and excreted in the urine.
        • Normal BUN- 10 to 20 mg/dL (3.5 to 7 mmol/L)
        • Factors that Increase BUN include:
        • Decrease Renal Function
        • GI Bleeding
        • Dehydration
        • Increase Protein Intake
        • Fever
        • Sepsis
  • 22. Laboratory Tests for Evaluating Fluid Status
        • Factors that Decrease BUN:
        • End Stage Liver Disease
        • Low Protein Intake
        • Starvation
        • Any condition that results in expanded fluid volume
        • Example Pregnancy
    • Creatinine - end product of muscle metabolism. Better indicator of Renal Function.
        • Normal Serum Creatinine- 0.7 to 1.5 mg/dL
        • Serum Creatinine levels increases when renal function decreases,
  • 23. Laboratory Tests for Evaluating Fluid Status
    • Hematocrit - measures the volume percentage of RBC in whole blood.
          • Normal value:
          • Male- 44 % to 52 %
          • Female- 39 % to 47 %
          • Increase Hct: Dehydration and Polycythemia
          • Decrease Hct: Overhydration and anemia
    • Urine Sodium - values change with sodium intake and the status of fluid volume.
          • Normal Urine Sodium levels: 50 to 220 mEq/24h
          • used to assess volume status and are useful in the diagnosis of hyponatremia and acute renal failure.
  • 24. Routes of Gains and Losses
    • Drinking
    • Eating
    • Parenteral Route
    • Enteral Feeding
    KIDNEYS the usual daily urine in the adult is 1 to 2 L. A general rule is that the output is approximately 1 mL of urine per kilogram of body weight per hour in all age groups.
  • 25. Routes of Gains and Losses LUNGS lungs normally eliminate water vapor (insensible loss) at rate of approximately 400mL everyday. . SKIN Sensible perspiration refers to visible water and electrolyte loss through the skin (sweating). Continuous water loss by evaporation occurs through the skin as insensible perspiration, a nonvisible form of water loss.
  • 26. Routes of Gains and Losses GI TRACT the usual loss through the GIT is only 100 to 200 mL daily, even through approximately 8 L of fluid circulates through the GI system every 24 hours. Because the bulk of fluid is reabsorbed in the small intestine, diarrhea and fistulas cause larger losses. In healthy people, the daily average intake and output of water are approximately equal.
  • 27. Homeostatic Mechanism
    • Kidney Functions
      • vital to the regulation of fluid and electrolyte balance.
      • kidneys normally filter 170 L of plasma every day in the adult. While excreting only 1.5 L of urine.
      • Major functions of the kidneys in maintaining normal fluid balance include following:
      • Regulation of ECF volume and osmolality by selective retention and excretion of body fluids.
  • 28. Homeostatic Mechanism
      • Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances.
      • Regulation of pH of the ECF by retention of hydrogen ions
      • Excretion of metabolic wastes and toxic substances
    • Heart and Bood Vessel Functions
      • the pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for urine formation.
      • failure of this pumping action interferes with renal perfusion and thus with water and electrolyte regulation.
  • 29. Homeostatic Mechanism
    • Lung Functions
        • also vital in maintaining homeostasis.
        • through exhalation, the lungs remove approximately 300 mL of water daily in the normal adult.
        • also have a major role in maintaining acid-base balance.
        • changes from normal aging result in decreased respiratory function causing increased difficulty in pH regulation in older adults with major illness or trauma.
  • 30. Homeostatic Mechanism
    • Pituitary Functions
        • the hypothalamus manufactures ADH, which is stored in the posterior pituitary gland and released as needed. ADH sometimes called the water-conserving hormone because it causes the body to retain water.
        • functions of ADH include maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume.
  • 31. Homeostatic Mechanism
    • Adrenal Functions
        • Aldosterone, a mineralococticoid secreted by the zona glomerulosa (outer zone) of the adrenal cortex, has profound effect on fluid balance.
        • increased secretion of aldosterone causes sodium retention (and thus water retention) and potassium loss.
        • conversely, decreased secretion of aldosterone causes sodium and water loss and potassium retention.
        • Cortisol, another adrenocortical hormone, has only a fraction of the mineralocorticoid potency of aldosterone. When secreted in large quantities, however, it can also produce sodium retention and fluid retention and potassium deficit.
  • 32. Homeostatic Mechanism
        • Parathyroid Functions
        • embedded in the thyroid gland, regulated calcium and phosphate balance by means of parathyroid hormone (PTH).
        • PTH influences bone resorption, calcium absorption from the intestines, and calcium reabsorption from the renal tubules.
  • 33. Other Mechanism
    • Baroreceptors
        • are small nerve receptors that detect changes in pressure within blood vessels and transmit this information to the central nervous system .
        • responsible for monitoring the circulating volume, and they regulate sympathetic and parasympathetic neural activity as well as endocrine activities .
        • Low- pressure baroreceptor- located in the cardiac atria, particularly the left atrium.
        • High- pressure baroreceptor- nerve endings in the aortic arch and in the cardiac sinus. Also located in the afferent arteriole of the juxtaglomerular apparatus of the nephrons.
  • 34. Other Mechanism
        • As arterial pressure decreases, baroreceptors transmit fewer impulses from the carotid sinuses and the aortic arch to the vasomotor center.
        • A decrease in impulses stimulates the sympathetic nervous system and inhibits the parasympathetic nervous system.
        • The outcome is an increase in cardiac rate, conduction and contractility and in circulating blood volume.
        • Sympathetic stimulation constrict renal arterioles; this increases the release of aldosterone, decreases glomerular filtration, and increases sodium and water reabsorption.
  • 35. Other Mechanism
    • Renin-Angiotensin- Aldosterone System
        • is an enzyme that converts angiotensinogen, an inactive substance formed by the liver, into angiotensin 1.
        • renin is released by the juxtaglomerular cells of the kidneys in response to decreased renal perfusion.
        • Angiotensin-Converting Enzyme (ACE) converts angiotensin 1 to Angiotensin II.
        • Angiotensin II, with its vasoconstrictor properties, increases arterial perfusion pressure and stimulates thirst.
        • As the sympathetic nervous system is stimulated, aldosterone is released in response to an increased release of renin.
        • Aldosterone is a volume regulator and is also released as serum potassium increases, serum sodium decreases, or adrenocorticotropic hormone increases.
  • 36. Other Mechanism
    • ADH and Thirst
        • important roles in maintaining sodium concentration and oral intake of fluids.
        • Oral intake is controlled by the thirst center located in the hypothalamus.
        • as serum concentration or osmolality increases or blood volume decreases, neuron in the hypothalamus are stimulated by intracellular dehydration; thirst then occurs, and the person increases oral intake of fluids.
        • water excretion is controlled by ADH, aldosterone, and basoreceptors
        • Absence or presence of ADH is the most significant factor in determining whether the urine that is excreted is concentrated or dilute.
  • 37. Other Mechanism
    • Osmoreceptors
        • Located on the surfaceof the hypothalamus, osmoreceptors sense changes in sodium concentration.
        • as osmotic pressure increases,the neurons become dehydrated and quickly release impulses to the posterior pituitary, which increases the release of ADH. ADH travels in the blood to the kidneys, where it alters permeability to water, causing increased reabsorption of water and decreased urine output.
        • The retained water dilutes the ECF and returns its concentration to normal. Restoration of normal osmotic pressure provides feedback to the osmoreceptors to inhibit further ADH release.
  • 38.
    • Release of Atrial Natriuretic Peptide
        • ANP is released by cardiac cells in the atria of the heart in response to increased atrial pressure.
        • any disorder that results in volume expansion or increased cardiac filling pressure will increase the release of ANP.
        • action of ANP is the direct opposite of the renin-angiotensin- aldosterone system and decrease blood pressure and volume.
        • ANP measured in plasma is normally 20 to 70 pg/mL.
        • this level increases in acute heart failure, paroxysmal atrial tachycardia, hyperthyroidism, subarachnoid hemorrhage, and small cell lung cancer.
        • the level decreases in chronic heart failure and with the use of medications such as urea (ureaphil) and prazosin (minipress).
  • 39. Fluid Volume Deficit
    • HYPOVELIMIA
    • FVD occurs when loss of extracellular fluid volume exceeds the intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids, so that the ratio of serum electrolytes to water remains the same.
    • Abnormally low volume of body fluid in intravascular and/or interstitial compartments
    • Causes
      • Vomiting
      • Diarrhea
      • Fever
      • Excess sweating
      • Burns
      • Diabetes insipidus
      • Uncontrolled diabetes mellitus
  • 40. Fluid Volume Deficit
    • What happens
      • Output > Intake -> Water extracted from ECF
        • ECF hypertonic (water moves out of cell -> cell dehydration) + osmotic pressure increased (stimulates thirst preceptor in hypothalamus)
        • ICF hypotonic with decreased osmotic pressure -> posterior pituitary secretes more ADH
        • Decreased ECF volume -> adrenal glands secrete Aldosterone
  • 41. Signs & Symptoms
    • Acute weight loss
    • Decreased skin turgor
    • Oliguria
    • Concentrated urine
    • Weak, rapid pulse
    • Capillary filling time elongated
    • Decreased BP
    • Increased pulse
    • Sensations of thirst, weakness, dizziness, muscle cramps
  • 42. Significant Points
    • Dehydration – one of most common disturbances in infants and children
    • Additional S/S
      • Sunken eyeballs
      • Depressed fontanels
      • Significant wt loss
  • 43. Laboratory
    • Increased HCT
    • Increased BUN out of proportion to Creatinine
    • High serum osmolality
    • Increased urine osmolality
    • Increased specific gravity
    • Decreased urine volume, dark color
  • 44. Intervention
    • Major goal prevent or correct abnormal fluid volume status before ARF occurs
    • Encourage fluids
    • IV fluids
      • Isotonic solutions (0.9% NS or LR) until BP back to normal, then hypotonic (0.45% NS)
    • Monitor I & O at least every 8 hrs
    • Check urine specific gravity and urine concentration
    • daily weights
    • Check skin turgor
  • 45. Intervention
    • Monitor skin turgor
    • Monitor VS and mental status
    • Evaluation
      • Normal skin turgor, increased UOP with normal specific gravity, normal VS, clear sensorium, good oral intake of fluids
  • 46. Fluid Volume Excess
    • Hypervolemia
    • Isotonic expansion of ECF caused by abnormal retention of water and sodium
    • Fluid moves out of ECF into cells and cells swell
  • 47. Causes
    • Cardiovascular – Heart failure
    • Urinary – Renal failure
    • Hepatic – Liver failure, cirrhosis
    • Other – Cancer, thrombus, PVD, drug therapy (i.e., corticosteriods), high sodium intake, protein malnutrition
  • 48. Clinical Manifestation
    • Physical assessment
      • Weight gain
      • Distended neck veins
      • Periorbital edema, pitting edema
      • Adventitious lung sounds (mainly crackles)
      • Dyspnea
      • Mental status changes
      • Generalized or dependent edema
  • 49. Clinical Manifestation
    • VS
      • High CVP/PAWP
      • ↑ cardiac output
    • Lab data
      • ↓ Hct (dilutional)
      • Low serum osmolality
      • Low specific gravity
      • ↓ BUN (dilutional)
    • Radiography
      • Pulmonary vascular congestion
      • Pleural effusion
      • Pericardial effusion
      • Ascites
  • 50. Intervention
    • Sodium restriction (foods/water high in sodium)
    • Fluid restriction, if necessary
    • Closely monitor IVF
    • If dyspnea or orthopnea > Semi-Fowler’s
    • Strict I & O, lung sounds, daily weight, degree of edema, reposition q 2 hr
    • Promote rest and diuresis
  • 51. IV Fluid Replacement
    • IV Fluid to manage fluid volume imbalances
    • Isotonic fluids (approximate normal serum plasma)
      • Rapid ECF expansion needed
      • D 5 W, NS, LR
    • Hypotonic fluids
      • Treatment of cellular dehydration
      • .45% NS, .2% NS, 2.5% dextrose
  • 52. IV Fluid Replacement
    • Hypertonic
      • Treatment of water intoxication
      • D 5 ½ NS, D 10 W, 3% NS
      • Shifts fluids from ICF & ECF to intravascular component – expands blood volume
      • Now can be removed by kidneys
  • 53. Sodium
    • Normal 135-145 mEq/L
    • Major cation in ECF
    • Regulates voltage of action potential; transmission of impulses in nerve and muscle fibers, one of main factors in determining ECF volume
    • Elderly at risk
    • Helps maintain acid-base balance
  • 54. Hyponatremia
    • Results from excess Na loss or water gain
      • GI losses, diuretic therapy, severe renal dysfunction, severe diaphoresis, DKA, unregulated production of ADH associated with cerebral trauma, narcotic use, lung cancer, some drugs
    • Clinical manifestations
      • ↓ BP, confusion, headache, lethargy, seizures, decreased muscle tone, muscle twitching and tremors, vomiting, diarrhea, and cramps
  • 55. Assessment
    • Labs
      • Increased HCT, K
      • Decreased Na, Cl, Bicarbonate, UOP with low Na and Cl concentration
      • Urine specific gravity ↓ 1.010
  • 56. Treatment
    • Interventions
      • Mild
        • Water restriction if water retention problem
        • Increase Na in foods if loss of Na
      • Moderate
        • IV 0.9% NS, 0.45% NS, LR
      • Severe
        • 3% NS – short-term therapy in ICU setting
  • 57. Hypernatremia
    • Gain of Na in excess of water or loss of water in excess of Na
    • Causes
      • Deprivation of water; hypertonic tube feedings without water supplements, watery diarrhea, greatly increased insensible water loss, renal failure, inadequate blood circulation to kidneys, use of large doses of adrenal corticoids, excess sodium intake
  • 58. Hypernatremia
    • Early: Generalized muscle weakness, faintness, muscle fatigue, HA
    • Moderate: Confusion, thirst
    • Late: Edema, restlessness, thirst, hyperreflexia, muscle twitching, irritability, seizures, possible coma
    • Severe: Permanent brain damage, hypertension, tachycardia, N & V
  • 59. Labs
    • Increased serum Na
    • Increased serum osmolality
    • Increased urine specific gravity
  • 60. Treatment
    • Free water to replace ECF volume
    • Gradual lowering with hypotonic saline
      • Decrease by no more than 2 mEq/L/hr
    • Offer fluids at regular intervals
    • Supplement tube feedings with free water
    • Teach about foods, medications high in Na
    • Treat underlying problem
  • 61. Potassium
    • Normal 3.5-5.5 mEq/L
    • Major ICF cation
    • Vital in maintaining normal cardiac and neuromuscular function, influences nerve impulse conduction, important in CHO metabolism, helps maintain acid-base balance, control fluid movement in and out of cells by osmosis
  • 62. Hypo kalemia
    • Serum potassium level below 3.5 mEq/L
    • Causes
      • Loss of GI secretions
      • Excessive renal excretion of K
      • Movement of K into the cells (DKA)
      • Prolonged fluid administration without K supplementation
      • Diuretics (some)
  • 63. Signs/Symptoms
    • Skeletal muscle weakness, ↓ smooth muscle function, ↓ DTR’s
    • ↓ BP, EKG changes, possible cardiac arrest
    • N/V, paralytic ileus, diarrhea
    • Metabolic alkalosis
    • Mental depression and confusion
  • 64. Treatment
    • Hydrate if low urine output
    • Oral replacement through high K diet
    • IV supplementation
      • No more than 10 mEq/hr; for child 2-4 mEq/kg/24 h
      • No more than 40 mEq/L
  • 65. Treatment
    • Hypertonic glucose solution
    • Monitor
      • I & O
      • Bowel sounds
      • VS, cardiac rhythm
      • Muscle strength
      • Digoxin level if necessary
  • 66. Hyper kalemia
    • Serum potassium level above 5.3 mEq/L
    • Causes
      • Excessive K intake (IV or PO) especially in renal failure
      • Tissue trauma
      • Acidosis
      • Catabolic state
  • 67. Signs/Symptoms
    • ECG changes – tachycardia to bradycardia to possible cardiac arrest
      • Tall, tented T waves
    • Cardiac arrhythmias
    • Muscle weakness, paralysis, paresthesia of tongue, face, hands, and feet, N/V, cramping, diarrhea, metabolic acidosis
  • 68. Treatment
    • 10% Calcium gluconate
    • Sodium bicarbonate
    • 50% glucose solution
    • Kayexalate PO or PR
    • Stop K supplements and avoid K in foods, fluids, salt substitutes
  • 69. Calcium
    • Normal 4.5-5.5 mEq/L
    • 99% of Ca in bones, other 1% in ECF and soft tissues
    • Total Calcium – bound to protein – levels influenced by nutritional state
    • Ionized Calcium – used in physiologic activities – crucial for neuromuscular activity
  • 70. Calcium
    • Required for blood coagulation, neuromuscular contraction, enzymatic activity, and strength and durability of bones and teeth
    • Nerve cell membranes less excitable with enough calcium
    • Ca absorption and concentration influenced by Vit D, calcitriol (active form of Vitamin D), PTH, calcitonin, serum concentration of Ca and Phos
  • 71. Causes of Hypo calcemia
    • Most common – depressed function or surgical removal of the parathyroid gland
    • Hypomagnesemia
    • Hyperphosphatemia
    • Administration of large quantities of stored blood (preserved with citrate)
    • Renal insufficiency
    • ↓ absorption of Vitamin D from intestines
  • 72. Signs/Symptoms
    • Abdominal and/or extremity cramping
    • Tingling and numbness
    • Positive Chvostek or Trousseau signs
    • Tetany; hyperactive reflexes
    • Irritability, reduced cognitive ability, seizures
    • Prolonged QT on ECG, hypotension, decreased myocardial contractility
    • Abnormal clotting
  • 73. Treatment
    • High calcium diet or oral calcium salts (mild) - √ formulas for calcium content
    • IV calcium as 10% calcium chloride or 10% calcium gluconate – give with caution
    • Close monitoring of serum Ca and digitalis levels
    • ↓ Phosphorus levels ↑ Magnesium levels
    • Vitamin D therapy
  • 74. Hyper calcemia
    • Causes
      • Mobilization of Ca from bone
      • Malignancy
      • Hyperparathyroidism
      • Immobilization – causes bone loss
      • Thiazide diuretics
      • Thyrotoxicosis
      • Excessive ingestion of Ca or Vit D
  • 75. Signs/Symptoms
    • Anorexia, constipation
    • Generalized muscle weakness, lethargy, loss of muscle tone, ataxia
    • Depression, fatigue, confusion, coma
    • Dysrhythmias and heart block
    • Deep bone pain and demineralization
    • Polyuria & predisposes to renal calculi
    • Pathologic bone fractures
  • 76. Hypercalcemic Crisis
    • Emergency – level of 8-9 mEq/L
    • Intractable nausea, dehydration, stupor, coma, azotemia, hypokalemia, hypomagnesemia, hypernatremia
    • High mortality rate from cardiac arrest
  • 77. Treatment
    • NS IV – match infusion rate to amount of UOP
    • I&O hourlyLoop diuretics
    • Corticosteroids and Mithramycin in cancer clients
    • Phosphorus and/or calcitonin
    • Encourage fluids
    • Keep urine acid
  • 78. Magnesium
    • Normal 1.5 to 2.5 mEq/L
    • Ensures K and Na transport across cell membrane
    • Important in CHO and protein metabolism
    • Plays significant role in nerve cell conduction
    • Important in transmitting CNS messages and maintaining neuromuscular activity
  • 79. Magnesium
    • Causes vasodilatation
    • Decreases peripheral vascular resistance
    • Balance - closely related to K and Ca balance
    • Intracellular compartment electrolyte
    • Hypomagnesemia - < 1.5 mEq/L
    • Hypermagnesemia - > 2.5 mEq/L
  • 80. Hypo magnesemia
    • Causes
      • Decreased intake or decreased absorption or excessive loss through urinary or bowel elimination
      • Acute pancreatitis, starvation, malabsorption syndrome, chronic alcoholism, burns, prolonged hyperalimentation without adequate Mg
      • Hypoparathyroidism with hypocalcemia
      • Diuretic therapy
  • 81. Signs/Symptoms
    • Tremors, tetany, ↑ reflexes, paresthesias of feet and legs, convulsions
    • Positive Babinski, Chvostek and Trousseau signs
    • Personality changes with agitation, depression or confusion, hallucinations
    • ECG changes (PVC’S, V-tach and V-fib)
  • 82. Treatment
    • Mild
      • Diet – Best sources are unprocessed cereal grains, nuts, legumes, green leafy vegetables, dairy products, dried fruits, meat, fish
      • Magnesium salts
    • More severe
      • MgSO4 IM
      • MgSO4 IV slowly
  • 83. Treatment
    • Monitor Mg q 12 hr
    • Monitor VS, knee reflexes
    • Precautions for seizures/confusion
    • Check swallow reflex
  • 84. Hypermagnesemia
    • Most common cause is renal failure, especially if taking large amounts of Mg-containing antacids or cathartics; DKA with severe water loss
    • Signs and symptoms
      • Hypotension, drowsiness, absent DTRs, respiratory depression, coma, cardiac arrest
      • ECG – Bradycardia, CHB, cardiac arrest, tall T waves
  • 85. Treatment
    • Withhold Mg-containing products
    • Calcium chloride or gluconate IV for acute symptoms
    • IV hydration and diuretics
    • Monitor VS, LOC
    • Check patellar reflexes
  • 86. Phosphorous
    • Normal 2.5-4.5 mg/dL
    • Intracellular mineral
    • Essential to tissue oxygenation, normal CNS function and movement of glucose into cells, assists in regulation of Ca and maintenance of acid-base balance
    • Influenced by parathyroid hormone and has inverse relationship to Calcium
  • 87. Hypophosphotemia
    • Causes
      • Malnutrition
      • Hyperparathyroidism
      • Certain renal tubular defects
      • Metabolic acidosis (esp. DKA)
      • Disorders causing hypercalcemia
  • 88. Signs/Symptoms
    • Impaired cardiac function
    • Poor tissue oxygenation
    • Muscle fatigue and weakness
    • N/V, anorexia
    • Disorientation, seizures, coma
  • 89. Treatment
    • Closely monitor and correct imbalances
      • Adequate amounts of Phos
      • Recommended dietary allowance for formula-fed infants 300 mg Phos/day for 1 st 6 mos. and 500 mg per day for latter ½ of first year
      • 1:1 ratio Phos and Ca recommended dietary allowance. Exception is infants, whose Ca requirements is 400 mg/day for 1 st 6 mos and 500 mg/day for next 6 months
  • 90. Treatment
    • Treatment of moderate to severe deficiency
      • Oral or IV phosphate (do not exceed rate of 10 mEq/h)
      • Identify clients at risk for disorder and monitor
      • Prevent infections
      • Monitor levels during treatment
  • 91. Hyperphosphatemia
    • Causes
      • Chronic renal failure (most common)
      • Hyperthyroidism, hypoparathyroidism
      • Severe catabolic states
      • Conditions causing hypocalcemia
  • 92. Signs/Symptoms
    • Muscle cramping and weakness
    • ↑ HR
    • Diarrhea, abdominal cramping, and nausea
  • 93. Treatment
    • Prevention is the goal
    • Restrict phosphate-containing foods
    • Administer phosphate-binding agents
    • Diuretics
    • Treat cause
    • Treatment may need to focus on correcting calcium levels