this lecture is part one over the concept of fluid and electrolytes we will begin with a review of anatomy and physiology a solvent is the water portion of body fluids solute refers to particles dissolved in the solvent of body fluids electrolytes also called ions are solute particles that express an overall electrical charge this electrical charge can be either positive or negative body fluids deliver dissolved nutrients and electrolytes to all organs tissues and cells this maintains the volume of fluid and the electrolyte composition of the major fluid spaces or compartments within the normal range this is critical for optimal body function fluid and electrolyte balance is the regulation of body fluid volume osmalerity and composition as well as the regulation of electrolytes by the process of filtration diffusion osmosis and selective excretion although it is easier to understand how body water and individual electrolytes are regulated remember these substances and their regulation are interrelated and that control actions usually occur simultaneously the processes involved in fluid and electrolyte balance are never truly separate body fluid is divided into two main compartments or spaces we have the fluid outside of the cells which is called extracellular fluid and the fluid inside the cells which is called intracellular fluid the extra cellular fluid space is about 1/3 or about 15 L of the total body water the extracellular fluid includes interstitial fluid which is fluid between cells this is also sometimes referred to as the third space we also have blood lymph bone and connective tissue water as well as transcellular fluids that make up the extracellular fluid transcellular fluids include cerebral spinal fluid synenovial fluid peritineal fluid as well as plural fluid intracellular fluid is about 2/3 or 25 L of the total body water intracellular fluid remember is the fluid inside of the cells filtration is the movement of fluid or water through a cell or blood vessel membrane because of hydrostatic pressure differences on both sides of the membrane an example of this is blood pressure diffusion is the movement of particles across a permeable membrane from an area of higher particle concentration to an area of lower particle concentration this is also referred to as down a concentration difference or gradient an example of this is the transport of most electrolytes and other particles through the cell membrane some membranes unlike capillary membranes are selective for which particles can diffuse they permit diffusion of some particles but not others osmosis is the movement of water through a semi-permeable membrane to achieve an equilibrium of osmarity the normal osmalerity value for plasma and other body fluids ranges from 270 to about 300 the body functions best when the osmalerity of all body fluid spaces is closer to 300 when all fluids have this solute concentration the fluids are isoic or isotonic also referred to as normatonic to each other osmalerity is the number of millles in a liter of solution osmolality is the number of millles in a kilogram of solution in human physiology osmalerity and osmolality are generally considered the same different types of fluids fluids that have the solute particle concentration within the normal range for human body fluids are called isoosmotic or isotonic fluids hyperossmotic or hypertonic fluids are fluids with an osmarity greater than 300 these fluids have a greater osmotic pressure than do isoosmotic fluids and tend to pull water from the isoosmotic fluid space into the hyperosmotic fluid space until an osmotic balance occurs hypoosmotic or hypotonic fluids are fluids with an osmolerity that is less than 270 hypoaller fluids have a lower osmotic pressure than isosmotic fluids and water is pulled from the hypoatic fluid space into the isoosmotic fluid spaces of the interstitial and intracellular fluids as a result the interstatial and intracellular fluid volumes expand and the plasma shrinks an example of hypotonic IV fluid would be 0.45% saline fluid balance is linked to and affected by electrolyte balance remember electrolytes are dissolved substances that express an electrical charge most of the common blood electrolytes are mineral elements cations ions are positively charged electrolytes and annions are negatively charged electrolytes body fluids are electrically neutral which means that the number of positive ions is balanced by an equal number of negative ions most ions have different concentrations in the extracellular fluid and in the intracellular fluid this concentration difference helps maintain membrane excitability and allows nerve impulse transmission the normal ranges of blood electrolytes are narrow so even small changes in these levels can cause major problems there are three hormones to help control fluid and electrolyte balance these are aldoststerone antidiuretic hormone or ADH and nitriotic peptide aldoststerone is secreted by the adrenal cortex whenever sodium levels and the extracellular or ECF fluid are low aldoststerone prevents both water and sodium loss antidiuretic hormone or ADH also referred to as vasopressin is released from the posterior pituitary gland in responses to changes in blood osmalerity increased blood osmalerity especially an increase in the level of plasma sodium results in a slight shrinkage of these cells and triggers ADH release from the posterior pituitary gland because the action of ADH retains just water it only indirectly regulates electrolyte retention or excretion nitriotic peptides are hormones secreted by special cells that line both the atria and ventricles of the heart the peptides secreted by the heart ventricular cells is known as brain nitriotic peptide these peptides are secreted in response to increased blood volume and blood pressure which stress the heart tissue the most important body fluids to keep in balance for optimal function are the blood or plasma volume and the fluid inside the cells the intracellular fluid changes in these volumes especially decreases can lead to poor organ profusion and cellular dysfunction maintaining blood volume at a sufficient level for blood pressure to remain high enough to ensure adequate profusion is critical for life because the kidney is a major regulator of water and sodium balance to maintain blood pressure and profusion to all tissues and organs the kidneys monitor blood pressure blood volume blood oxygen levels and blood osmarity this is spec specific to sodium concentration when the kidneys sense that any one of these parameters is getting low they begin to secrete a substance called rein that sets into motion a group of hormonal and blood vessel responses to ensure that blood pressure is raised back up to normal the triggering event for renan secretion is any change in the blood indicating that perfusion is at risk low blood pressure is a triggering event because it reduces perfusion to tissues and organs anything that reduces blood volume such as dehydration or hemorrhage anything that decreases the blood volume below a critical level always lowers blood pressure low blood oxygen levels are also triggering events when there is not enough oxygen in the blood it can't supply the oxygen needed to the tissues and organs a low blood sodium level could also be a triggering event because sodium and water are closely linked remember where sodium goes water follows so anything that causes the blood to have too little sodium prevents water from staying in the blood the result is going to be low blood volume with low blood pressure and this will lead to poor tissue perfusion age gender and the amount of fat affect the amount and distribution of body fluids an older adult has less total body water than a younger adult an adult who is obese has less total water than a lean adult of the same weight because fat cells contain almost no water older adults are at risk for fluid and electrolyte imbalances as a result of age related organ changes be sure to always ask older adults which drugs they take because older adults are more likely to be taking drugs that affect fluid and electrolyte balance age related changes in fluid balance include the loss of skin elasticity decreased tur and decreased oil production they also have a decrease in the glomearilla filtration rate this causes poor excretion of waste products so metabolism of medications is not as efficient this is why older adults often have to have reduced dosages of medications to prevent toxicity as they are not able to metabolize medications as quickly they also have a decreased concentrating capacity which increase water loss and therefore increase the risk of dehydration decreased muscle mass and a reduced thirst reflex are also issues that can cause them to have an increased risk of dehydration adrenal atrophy is another issue that occurs which affects the ability to regulate sodium and potassium although all electrolytes play a role in homeostasis the more critical ones are sodium potassium calcium and magnesium many of the same control mechanisms that regulate fluid balance are also critical for regulating the balance of these important electrolytes the normal plasma level of sodium is 136 to 145 sodium levels and movement influence water balance the extracellular sodium level determines whether water is retained excreted or moved from one fluid space to another changes in plasma sodium levels seriously change fluid volume and the distribution of other electrolytes normal plasma level of potassium is 3.5 to 5 mill equivalents per liter the normal intracellular fluid potassium level is about 150 millle equivalents per liter keeping this large difference in potassium concentration between the ICF and the ECF is critical for excitable tissues to be able to depolarize and generate action potentials because sodium levels in the blood and interstitial fluid are so low even small changes can produce a significant effect almost all foods contain potassium it is highest in meat fish and many but not all vegetables and fruits it is lowest in eggs bread and cereal grains fruits such as watermelon oranges and bananas should be limited or avoided in a client following a low potassium diet about 80% of potassium is removed from the body by the kidney kidney excretion of potassium is enhanced by aldoststerone the normal plasma levels of calcium are 9 to 10.5 mg per decaler this mineral is important for maintaining bone strength and density activating enzymes allowing skeletal and cardiac muscle contraction controlling nerve impulse transmission and enhancing blood clotting calcium enters the body by dietary intake and absorption through the intestinal tract absorption of dietary calcium requires the active form of vitamin D some foods that are rich in calcium include dairy fortified orange juice canned salmon broccoli and spinach most body calcium is stored in the bone matrix rather than in the any fluid compartment when more calcium is needed parathyroid hormone is released from the parathyroid glands normal plasma levels of magnesium are 1.3 to 2.1 melee equivalents per liter magnesium is an ion that is stored mostly in bones and cartilage little magnesium is present in the blood like potassium and calcium the intracellular fluid has more magnesium this mineral has more functions inside the cells than in the blood it is important for skeletal muscle contraction carbohydrate metabolism the generation of energy stores vitamin activation blood coagulation and cell growth adequate amounts of intracellular magnesium are particularly essential for the health and maintenance of cardiac muscle within cells and blood magnesium levels are related to the levels of potassium and calcium and help maintain proper balance of these two electrolytes this slide shows a laboratory profile for fluid and electrolyte assessment please review this laboratory profile as you begin to study electrolytes and the different imbalances that may occur portion of our lecture we will discuss electrolyte imbalances in more detail hyponetriia is an electrolyte imbalance when the serum sodium level drops below 136 mill equivalents per liter sodium imbalances often occur along with a fluid imbalance because the same hormones regulate both sodium and water balance with hyponetriia the osmolerity of the ECF is lower than that of the ICF as a result water moves into the cell causing swelling cerebral changes are the most obvious problems of hyponetriia behavioral changes result from cerebral edema and increased incraanial pressure it is important to closely observe and document the patients behavior level of consciousness and cognition a sudden onset of acute confusion or increased confusion is often seen in older adults who have low serum sodium levels when sodium levels become very low seizures coma or even death may occur neuromuscular changes are seen as general muscle weakness the nurse should assess the patients neuromuscular status during each nursing shift for changes from baseline deep tendon reflexes diminish and muscle weakness is worse in the legs and arms it is important to assess both muscle strength and deep tendon reflex responses if muscle weakness is present immediately check respiratory effectiveness because ventilation depends on adequate strength of respiratory muscles many conditions and drugs can lead to hyponetriia a common cause of low sodium levels is the prolonged use and overuse of diuretics especially in older adults when these drugs are used to manage fluid overload sodium is lost along with water hyponetriia can result from the loss of total body sodium the movement of sodium from blood to other fluid spaces or the dilution of serum sodium from excessive water in the plasma it is important to determine the cause of the low sodium level to plan appropriate management interventions with drug therapy and nutrition therapy are used to restore serum sodium levels to normal and prevent complications from fluid overload or a too rapid change in the serum sodium level a serious complication that may occur is sodium if sodium is replaced too rapidly is called osmotic demisination syndrome the rapid correction causes the brain cells to shrink at an accelerated rate leading to damage or destruction of the myelin sheath that insulates nerve fibers in the brain this demyelination can result in severe and potentially permanent neurological deficits or even death to prevent this complication chronic hyponetriia should be corrected gradually and carefully under medical supervision the priorities for nursing care of the patient with hyponetriia are to monitor the patients response to therapy and prevent hyponetriia and fluid overload drug therapy involves reducing the doses of any drugs that increase sodium loss such as most diuretics when hyponetriia occurs with a fluid deficit IV infusions of 0.9% normal saline is prescribed to restore both sodium and fluid volume when hyponetriia occurs with fluid excess drug therapy includes drugs that promote the excretion of water rather than sodium such as vasopressin receptor antagonist like convan or tolvapan please make drug cards on both of these medications drug therapy for hyponetriia caused by inappropriate secretion of antidiuretic hormone ADH may include lithium and demy cycllosin the nurse should assess the patient hourly for signs of excessive fluid loss potassium loss and increased sodium levels nutrition therapy can also help restore sodium balance in mild cases of hyponetriia therapy involves increasing oral sodium intake and restricting oral fluid intake collaborate with the registered dietician nutritionist or RDN to teach the patient about which flu foods to increase in the diet fluid restriction may be needed long-term when chronic fluid overload is the cause of the hyponetriia or when kidney fluid excretion is impaired listed here are the actual and relative common causes of hyponetriia the signs and symptoms of hyponetriia are caused by its effects on excitable cellular activity the cells especially affected in addition to cerebral and neuromuscular cells are cells that perform intestinal smooth muscle and cardiovascular functions intestinal changes include increased motility causing nausea and vomiting and diarrhea assess the GI system by listening to bowel sounds and observing stools bow sounds are hyperactive and bowel movements are frequent and watery patients will usually also complain of abdominal cramping cardiovascular changes are seen as changes in cardiac output the cardiac responses to hyponetriia with hypoalmia include a rapid weak thready pulse peripheral pulses are difficult to palpate and are easily blocked blood pressure is decreased and the patient may have severe orthostatic hypotension leading to lightadedness or dizziness the central venus pressure is low when hyponetriia occurs with hypervalmia which is fluid overload cardiac changes include a full or bounding pulse with normal or high blood pressure peripheral pulses are full and difficult to block however they may not be palpable if edema is present hyperatriia is a serum sodium level over 145 mill equivalents per liter when serum sodium levels are high severe cellular dehydration with cellular shrinkage occurs eventually the dehydrated excitable tissues may no longer be able to respond to stimuli symptoms of hyperetriia vary with the severity of sodium imbalance and whether a fluid imbalance is also present changes are first seen in excitable membrane activity especially nerve skeletal muscle and cardiac function nervous system changes start with altered cerebral function assess the patients mental status for attention span and cognitive function in hyponetriia with normal or decreased fluid volumes the patient may have a short attention span and be restless agitated or confused skeletal muscle changes vary with the degree and stage of sodium increase mild rises in the early stages cause muscle twitching and irregular muscle contractions as hyponetriia continues to worsen the muscles and nerves are less able to respond to a stimulus and muscles become progressively weaker in later stages the deep tendon reflexes are reduced or absent cardiovascular changes include decreased contractility because the high sodium levels slow the movement of calcium into the heart cells which is needed for effective cardiac contraction measure blood pressure and the rate and quality of the apical and peripheral pulses the patient will likely have tacicardia they will also usually have increased thirst it is important that drug and nutrition therapies are used to prevent further sodium increases and to decrease high serum sodium levels nursing care priorities for the patient with hyponetriia include monitoring and res the response to therapy and ensuring patient safety by preventing hyponetriia and dehydration drug therapy is used to restore fluid balance when hyperonetriia is caused by fluid loss hyperonatriia caused by reduced kidney sodium excretion requires drug therapy with diuretics that promote sodium loss such as fioamide or bumanadide assess the patient hourly for indications of excessive losses of fluid sodium or potassium i would also recommend that you make a drug card on fioamide nutrition therapy to prevent or correct mild hyperetreia involves ensuring adequate water intake especially among older adults dietary sodium restriction may be needed to prevent sodium excess when kidneys present a problem listed here are the actual and relative causes of hyperatriia you will want to review these as you study for the exam hypocalemia is a serum potassium level that falls below 3.5 mill equivalents per liter this imbalance can be life-threatening because every body system is affected gradual potassium loss may have no symptoms until the loss is extreme rapid reduction of serum potassium levels causes dramatic changes in function interventions for hypocalemia focus on preventing potassium loss increasing serum potassium levels and ensuring patient safety drug and nutrition therapies help restore normal serum potassium levels the priorities for nursing care of the patient with hypocalemia are to ensure adequate gas exchange prevent patient falls prevent injury from potassium administration and monitor the patients response to therapy potassium is a severe tissue irritant and is never given by IM or subcutaneous injection tissues damaged by potassium can become necrotic causing loss of function and requiring surgery iv potassium solutions irritate veins and cause phobitis check the order carefully to ensure that the patient receives the correct amount of potassium it is also important to make sure that you assess the IV site hourly and ask the patient about any burning or pain at the site if infiltration of a solution containing potassium occurs stop the IV solution immediately remove the Venus access and notify the healthc care care provider document these actions and provide complete description of the photograph of the IV site here are actual and relative common causes of hypocalemia actual potassium depletion occurs when potassium loss is excessive or when potassium intake is inadequate to match normal potassium loss relative hypocalemia occurs when total body potassium levels are normal but the potassium distribution between fluid spaces is abnormal or diluted by excess water this can also occur during rapid infusions of insulin because this drug increases the activity of the sodium potassium pump forcing more blood potassium into the cells in the ICF and ECF potassium levels are linked to that of magnesium low blood levels of magnesium are often accompanied by hypocalemia when we are per performing an assessment on a patient with hypocalemia there are several things to consider and many cues to recognize age is important because urine concentrating ability decreases with aging which increases potassium loss older adults are more likely to use drugs that lead to potassium loss such as diuretics drugs especially diuretics corticosteroids and beta adinuric agonist or antagonists can increase kidney potassium loss diseases of the adrenal glands and kidneys can also lead to potassium loss it is also important to assess the respiratory status of a patient with hypocalemia at least every 2 hours because respiratory insufficiency and cardiac dysriythmias are major causes of death from hypocalemia muscularkeletal changes include skeletal muscle weakness a stronger stimulus is needed to begin muscle contraction patients may be too weak to stand hand grasps are weak and deep tendon reflexes are reduced severe hypocalemia causes flaccid paralysis so assess for muscle weakness and the patients ability to perform ADLs cardiovascular changes often present with an irregular heartbeat caused by dysriythmia be sure to palpate the peripheral pulses in hypocalemia the pulse is usually thready and weak palpation is difficult and the pulse is easily blocked pulse rate ranges vary from very slow to very rapid and is often irregular due to dysriythmia neurologic changes from hypocalemia include altered mental status the patient may have short-term irritability and anxiety followed by lethargy that progresses to acute confusion and coma as hypocalemia progresses intestinal changes also occur with hypocalemia because GI smooth muscle contractions are decreased which leads to decreased paristalsis bowel sounds are hypoactive nausea vomiting constipation and abdominal distension are common observe for abdominal distension and oscultate for bowel sounds in all four abdominal quadrants severe hypocalemia can cause the absence of parasolsis leading to paralytic ilas is a serium potassium level higher than 5 mill equivalents per liter the heart is very sensitive to serum potassium increases hypercalemia interferes with electrical conduction leading to heart block and ventricular fibrillation the problems that occur with hypercalemia are related to how rapidly ECF potassium levels increase a sudden rise in potassium causes severe problems at serum levels between 6 and 7 mill equivalents per liter when serium potassium rises slowly problems may not occur until potassium levels reach 8 mill equivalents per liter or higher hypercalemia is rare in people with normal kidney function most cases of hypercalemia occur in patients undergoing medical treatment the greatest risk for exists for chronically ill patients debilitated patients older adults and those taking potassium sparing diuretics interventions for hyperc calalemia focus on reducing the serum potassium level preventing reoccurrences and ensuring patient safety drug therapy is key the priorities for nursing care of the patient with hypercalemia are assessment for cardiac complications placing the client on a cardiac monitor is the number one priority because a patient with an elevated potassium has a risk for cardiac dysriythmias in order for the nurse to detect these abnormalities the nurse would need to place the cardiac patient on cardiac monitors prevention of falls and monitoring of the patients response to therapy and healthcare teaching are also important nursing interventions drug therapy can restore potassium balance by enhancing potassium excretion and promoting the movement of potassium from the ECF into the cells the oral drug patterr binds with potassium in the GI tract and decreases its absorption stop potassium containing infusions and keep the IV access open withhold oral potassium supplements and collaborate with the registered dietitionian nutritionist to ensure that a potassium restricted diet is prescribed and then help the client select foods low in potassium increasing potassium excretion helps reduce hypercalemia if kidney function is normal potassium excreting diuretics are then prescribed when kidney problems exist more invasive interventions may be needed potassium movement into the cells is enhanced by insulin insulin increases the activity of the sodium potassium pumps which move potassium from the ECF into the cell iv fluids containing glucose and insulin may be ordered to help decrease serum potassium levels cardiac monitoring allows for the early recognition of dysriythmias and other symptoms of hypercalemia on cardiac muscle a nursing safety priority is to assess anyone who has or is at risk for hypercalemia to recognize cardiac changes if the patient's heart rate falls below 60 beats per minute or if the T-waves become spiked both of which accompany hypercalemia respond by notifying the rapid response team health teaching is key to the prevention of hypercalemia and the early detection of complications the teaching plan includes diet drugs and the recognition of indicators of hypercalemia listed here are actual and relative common causes of hyperc calalemia when recognizing cues during an assessment age is important because kidney function decreases with aging ask about kidney disease diabetes molitus any recent or medical or surgical treatments and urine output including the frequency and amount of voidings you'll also want to ask about drug use particularly potassium sparing diuretics angiotensin converting enzyme inhibitors and angotensin receptor blockers also be sure to obtain a nutrition history to determine the intake of potassium richch foods and the use of salt substitutes which contain potassium ask whether the patient has had any palpitations skipped heartbeats or other cardiac irregularities muscle twitching leg weakness or unusual ting tingling or numbness in the hands feet or face you'll also want to ask about any recent changes in bowel habits especially diarrhea cardiovascular changes are the most severe problems from hypercalemia and are the most common cause of death in patients with hypercalemia cardiac symptoms include brady cardia hypotension and ECG changes of tall peak T- waves prolonged PR intervals flat or absent P waves and wide QRS complexes arhrhythmias or extra beats may also appear complete heart block asy and ventricular fibrillation are life-threatening complications that may occur with severe hypercalemia neuromuscular changes with hypercalemia may also occur and they have two phases skeletal muscles twitch in the early stages of hypercalemia and the patient may be aware of tingling and burning sensations followed by numbness in the hands and feet and around the mouth this is referred to as paristhesia as hypercalemia worsens muscle weakness occurs followed by flaccid paralysis the weakness moves up from the hands and feet and first affects the muscles of the arms and legs respiratory muscles are not affected until serum potassium levels reach lethal levels intestinal changes may also occur and include increased motility with diarrhea and hyperactive bowel sounds bowel movements are frequent and watery laboratory data confirms hypercalemia if it is caused by dehydration levels of other electrolytes hematocrit and hemoglobin will also be elevated hypercalemia caused by kidney failure occurs with elevated serum creatinin levels as well as decreased blood pH and normal or low hematocrit and hemoglobin levels hypocalcemia is a total serum calcium level that drops below 9 milligrams per decaler acute hypocalcemia results in the rapid onset of life-threatening symptoms chronic hypocalcemia occurs slowly over time and excitable membrane symptoms may not be severe because the body has adjusted to the gradual reduction of serum calcium levels interventions focus on restoring normal calcium levels and preventing complications these include drug therapy nutrition therapy a reduction in environmental stimuli and prevention of injury patient safety during the restoration of serum calcium levels is a nursing care priority drug therapy includes direct calcium replacement this can be done either oral or IV and drugs that enhance the absorption of calcium such as vitamin D when neuromuscular symptoms are troublesome drugs that decrease nerve and muscle responses may also be used nutrition therapy involves a calciumrich diet for patients with mild hypocalcemia and for those who are at continuing risk for hypocalcemia collaborate with the registered dietitian nutritionist to help the patient select calciumrich foods environmental ma management for safety is needed because the excitable membranes of the nervous system and the skeletal system are overstimulated in hypocalcemia reduce stimulation by keeping the room quiet limiting visitors adjusting the lighting and using a soft voice injuryrevention strategies are needed because the patient with long-standing calcium loss may have brittle fragile bones that fracture easily despite causing little pain when lifting or moving a patient with fragile bones use a lift sheet rather than pulling the patient observe for normal range of joint motion and for any unusual surface bumps or depressions over bony areas that may indicate a bone fracture here are the actual and relative common causes of hypocalcemia it's important to assess the nutrition history for the risk a person has of hypocalcemia ask patients about their intake of dairy products and whether they are taking a calcium supplement regularly one indicator of hypocalcemia is a report of frequent painful muscle spasms usually in the thigh calf or foot during rest or sleep also ask about a history of recent orthopedic surgery or bone healing thyroid surgery therapeutic irradiation of the upper middle chest and neck area or a recent anterior neck injury also increase the risk for hypocalcemia most symptoms of acute hypocalcemia are caused by overstimulation of nerves and muscles neuromuscular changes often occur first in the hands and feet paristhesas occur at first with sensations of tingling and numbness if hypocalcemia continues or worsens muscle twitching or painful cramps and spasms occur tingling may also affect the lips nose and ears these problems may signal the onset of neuromuscular overstimulation and tetany cardiovascular changes involve heart rate as well as ECG changes the heart may be either slower or slightly faster than normal with a weak thready pulse severe hypocalcemia causes severe hypotension and ECG changes of a prolonged ST interval and a prolonged QT interval intestinal changes include increased paristalsic activity assess the abdomen for hyperactive bowel sounds the patient may report painful abdominal cramping and diarrhea skeletal changes are also common with chronic hypocalcemia calcium leaves bone storage sites causing a loss of bone density or osteoporosis the bones are less dense more brittle and fragile and may break easily with slight trauma vertebra become more compact and the spine may bend forward leading to an overall loss of height ask about changes in height and any unexplained bone pain observe for spinal curvatures and any unusual bumps or protrusions in bones that may indicate old fractures you'll also want to assess for hypocalcemia by testing for tresel and schwastc signs to test for a trical sign place a blood pressure cuff around the arm inflate the cuff to greater than the patient's systolic pressure and keep the cuff inflated for 1 to four minutes under these hypo hypoxic conditions a positive tercal sign occurs when the hand and fingers go into spasm and palmer flexion as shown in the picture here to check forc sign tap the face just below and in front of the ear to trigger facial twitching on one side of the mouth nose and cheek calcemia is a total serum calcium level above 10.5 mgs per decaler even small increases above normal have severe effects and all systems are affected the signs and symptoms of hypercalcemia are related to its severity and how quickly the imbalance occurred the patient with mild but rapidly occurring calcium excess often has more severe problems than the patient whose imbalance is severe but has developed slowly cardiovascular changes are the most serious and life-threatening problems of hypercalcemia mild hypercalcemia at first causes increased heart rate and blood pressure however severe or prolonged calcium imbalance depresses electrical conduction and slows the heart rate it is important to measure the pulse rate and blood pressure and observe for indications of poor profusion such as cyanosis and palar you'll also want to examine EC ECG tracings for dysriythmias especially a shortened QT interval hypercalcemia allows blood clots to form more easily whenever blood flow is slow or impaired blood clotting is more likely in the lower legs pelvic region areas where blood flow is blocked by internal or external constrictions and areas where Venus obstruction occurs you'll want to assess for slowed or impaired profusion measure and record calf circumferences with a soft tape measure you also want to assess the feet for temperature color and capillary refill to determine profusion to and from an area high levels of serum calcium may also lead to kidney stone formation neuromuscular changes include severe muscle weakness and decreased deep tendon reflexes without paristhesia the patient may be confused and lethargic as well intestinal changes are first reflected as decrease in paristalsis constipation anorexia and nausea vomiting abdominal distension and pain are common bow sounds are hypoactive or absent assess abdominal size by measuring measuring abdominal girth with a soft tape measure in a line circling the abdomen at the umbilicus interventions for hypercalcemia focus on reducing serum calcium levels through drug therapy rehydration and depending on the cause and severity dialysis cardiac monitoring is also important drug therapy involves the prevention of increases in calcium as well as drugs to lower calcium levels iv solutions containing calcium such as ringer lactate are stopped oral drugs containing calcium or vitamin D are discontinued fluid volume replacement can help restore normal serum calcium levels iv normal saline at 0.9% sodium chloride is usually given because sodium increases kidney excretion of calcium thioide diuretics are discontinued and replaced with diuretics that enhance the excretion of calcium such as fioamide drugs to prevent hypercalcemia include agents that inhibit calcium reabsorption such as phosphorus calcetonin and bifphosphonates cardiac monitoring of patients with hypercalcemia is needed to identify dysriythmias and decrease cardiac output compare recent ECG tracings with the patients baseline readings especially look for changes in the T-waves and the QT interval as well as changes in rate and rhythm listed here are both actual and relative common causes of hypercalcemia please review these as you are studying and preparing for your exam magnesmia is a serum magnesium level that falls below 1.3 mill equivalents per liter it is most often caused by a decrease in the absorption of dietary magnesium often related to alcoholism or increased kidney magnesium excretion there are two major causes of hypomagnesmia which are inadequate intake and the use of lube or thioide diuretics cardiovascular changes associated with this condition are serious low magnesium levels increase the risk for hypertension atherosclerosis hypertrophic left ventricle and a variety of dysriythmias the dysriythmias include premature contractions atrial fibrillation ventricular fibrillation and long QT intervals neuromuscular changes are caused by increased nerve impulse transmission normally magnesium inhibits nerve impulse transmission at synapse areas decreased levels increase impulse transmission from nerve to nerve or from nerve to skeletal muscle the patient has hyperactive deep tendon reflexes numbness and tingling and painful muscle contractions intestinal changes are from decreased intestinal smooth muscle contraction reduced motility anorexia nausea constipation and abdominal distension are all common a paralytic ilas may also occur when hypommagnesmia is severe interventions aim to correct the imbalance and manage a specific problem that caused it in addition because hypocalcemia often occurs with hypomagn magnesmia interventions also aim to restore normal serum calcium levels drugs that promote magnesium loss such as high ceiling loop diuretics osmotic diuretics and amoglycoside antibiotics and drugs containing phosphorus are discontinued magnesium is replaced intravenously with magnesium sulfate when hypommagnesmia is severe when ad administering introvenous magnesium sulfate it is crucial to monitor the patients deep tendon reflexes at least hourly the assessment helps to evaluate the effectiveness of the magnesium therapy and prevents potential complications of excessive magnesium levels which can cause respiratory depression and paralysis the other options while important are not directly related to monitoring for complications of intravenous magnesium therapy if hypocalcemia is also present drug therapy to increase serum calcium levels is also prescribed hyper magnesmia is a serum magnesium level that rises above 2.1 mill equivalents per liter this condition is rare in the absence of magnesium administration or kidney failure symptoms of hypermagnesmia are usually not apparent until serum magnesium levels exceed 4 mill equivalents per liter cardiac changes include radicardia peripheral vasoddilation and hypotension these problems become more severe as serum magnesium levels increase ecg changes show a prolonged PR interval with a widened QRS complex and an increase in QT interval brady cardia can be severe and cardia cardiac arrest is possible hypotension is also severe with a diastolic pressure lower than normal patients with severe hypermagnesmia are in grave danger of cardiac arrest central nervous system changes also result from depressed nerve impulse transmission patients may be drowsy or even lethargic coma may occur if the imbalance is prolonged or severe neuromuscular changes include reduced or absent deep tendon reflexes voluntary skeletal muscle contractions become progressively weaker and finally stop hypermagnesmia has no direct effect on the lungs however when the respiratory muscles are weak respiratory insufficiency can lead to respiratory failure and death interventions focus on reducing the serum level and correcting the underlying problem that caused the imbalance all oral and parental magnesium is discontinued when kidney failure is not present giving magnesiumfree IV fluids can reduce serum magnesium levels high ceiling loop diuretics such as fioamide can further reduce serum magnesium levels when cardiac problems are severe giving calcium may reverse the cardiac effects of hypermagnesmia this table shows the common causes of both hypomagnesmia and hypermagnesmia please review these as you are going through your study guide and preparing for our exam this concludes part one of the lecture over fluid and electrolytes