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- 1. Fluids and Electrolytes Alteration in Fluids and Electrolytes
- 6. 80% of body weight 60 % of body weight 50 % of body weight
- 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
- 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.
- 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.
Notas del editor
- 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.