Welcome to adult multi-professional critical care review course and my assignment within the next few minutes is related to electrolyte emergencies. I have no conflict of interest regarding to this activity and this is the outline of the few electro abnormalities we will discuss in the next few minutes. Now we know that electrolyte among electrolyte abnormalities potassium abnormalities are very common. Particularly hyperkalemia is very common with significant clinical impact. The reasons behind hyperkalemia is often due to one of these three factors. One would be increase in potassium intake in a setting of low GFR. It is very difficult to become hyperkalemic when GFR is normal or near normal. There are multiple food or other items that their intake would lead to hyperkalemia including banana, coconut juice, pika, river bed clay, burn match heads, tomato juice, avocado. Cell shift also very common among ICU patients. Non-analogic metabolic acidosis, hyperglycemia, beta blockers, digitalis, hyperkalemic periodic paralysis which is less common but very impactful on patients' signs and symptoms and also cellulitis including tumor cell lysis. However the only reason that potassium can remain elevated in a sustained fashion is decreased potassium excretion through the kidney and these patients generally have less than 40 minute equivalent of potassium excretion through daily urine and daily urine output. Although most of potassium is reabsorbed in proximal tubular cells, potassium reabsorption through proximal tubular cells is not regulated and the most of regulation of potassium happens within the collecting duct or connecting tubes by cells that are called principal cells. These cells contain several different different factions. One is a epithelial sodium channel that allows sodium to passively enter these cells and the gradient that is generated between the tubular space and intracellular space is actively generated by NAK ATPase. As sodium moves inside the cells leave chloride behind therefore it generates a negative potential and that negative potential is driving force for potassium excretion through another channels called renal artery medullary channel and this mechanism is regulated by multiple factors particularly aldosterone system. I'll show you some information. In order for sodium to be absorbed delivery of sodium to this part of nephron is very important. The higher flow is delivered to this area the higher amount of sodium can be reabsorbed. In addition in order to increase or control amount of sodium reabsorption or epithelial sodium channel there's a significant mechanism involved. First of all prostaglandins that are generated by our ketonic acids can impact renin level and renin would activate angiotensin system and angiotensin 2 via angiotensin 1 receptor can increase aldosterone. Aldosterone from the basolateral receptor can impact these cells by two different factors. First of all can result rapid increase in number of epithelial sodium channels therefore increased sodium absorption and increased potassium excretion or with continuous stimulation of these cells they can start generating more epithelial cell channels and that would result in sodium channels and that would result in hyperkalemia hypertension that we see in hyperaldosteronism. Now there are several different things that can halt this mechanism, decrease potassium excretion, lead to hyperkalemia. One is use of NSAIDs or COX-2 inhibitors that would result in suppression of prostaglandin generation therefore renin impact. Type 4 renal tubular acidosis which is hypoglycemic hyperaldosteronism would also lead to hyperkalemia from the same mechanisms. Use of medications like ACE inhibitors or angiotensin receptor blockers or spironolactone that is direct receptor blocker of aldosterone can lead to hyperkalemia through the same mechanisms. Some other medications or diseases like Addison disease or heparin can lead to the same issues by decreased effect of aldosterone and potassium excretion halts. The reason is that by lower aldosterone lower epithelial sodium channel exists therefore lower negative potential balance exists in a tubular space and that would lead to lower amount of potassium excretion therefore potassium retention and hyperkalemia. There are other factors like pseudo hyperaldosteronism type 2 or use of cyclosporine that can allow cholera to move into a basolateral space through tight junction and therefore decrease the effect of epithelial sodium channel. In addition direct epithelial channel blockers including drugs like amiloride, trimetoprim or pentamidin can lead to the same problem and finally when GFR is low or effective volume is low delivery of sodium to this part of nephron is low therefore regardless of level of aldosterone or epithelial sodium channel and amount of sodium reabsorption therefore amount of potassium excretion remains low. Now hyperkalemia could lead to muscle weakness and cardiac arrhythmias. As you well know EKG changes are very important in the setting of management of hyperkalemic patients. It could be from different ranges of peak T waves to all the way to widened QRS and sine wave that are not usually perfusing rhythms. How do we manage this setting in a setting of significant hyperkalemia? In order to establish myocardial cell membrane we have a few options. One is calcium that doesn't change the potassium level however decreases threshold potential for cardiac myocytes. We need to inject the calcium over 10 minutes and repeat it in 5 minutes. Duration of action is usually not longer than 30 to 60 minutes so it's only a temporizing measure. It is important to know in a setting of ditch toxicity using IV calcium should be very done with a lot of caution. In addition among patients who have end-stage kidney disease therefore very high phosphorus level regardless of the amount of calcium we deliver as calcium phosphorus rapidly precipitates in tissues we may not be able to see the benefit therefore calcium is only preserved in ESRD patients at a time that the QRS widening is noted. Hypertonic saline is also used. Hypertonic saline would be used in hyponatremic hyperkalemic patients and there is no change in potassium level but stabilizes myocardial membrane therefore decreases rate of arrhythmias. Now the second strategy is to ship potassium inside the cells. The most effective way is to use glucose and insulin and by that we can decrease potassium by about 0.6 millimole per liter for about 15 minutes again another temporizing measure. These can be followed by a D5W chaser in order to avoid hypoglycemia. Insulin infusion over course of time can maintain a potassium level low inside the cells for about 90 minutes and then effect of it disappears therefore elimination of potassium from body would become extremely important. Now bicarbonate has been used in a form of bolus it doesn't have much effect among patients with MSH kidney disease and 4-hour infusion would result in modest decrease in potassium level. Another strategy is using a beta-2 adrenergic agonist like Albuterol that maximum effect has been reported between 30 to 60 minutes of prescription. IV infusion or inhalation forms have been used. The problem with these medications is that 40% of patients are resistant to the effect of beta-2 adrenergic agonist therefore has to be used as a secondary agent. But the most important part of management of hyperkalemia is elimination which has to happen with one of these two strategies. We can increase potassium extrusion through the bowel or increase potassium extrusion through kidney or dialysis. There are several different ways that we can increase potassium extrusion through the bowel. Coyexalate, Pateromer, Sodium Zirconium, Cyclosilicate are resins that are able to bind with chelate potassium inside the bowel and increases elimination through the bowel. The problem with Coyexalate which is the most commonly used resin is that amount of data that shows that in a randomized trial that shows it decreases potassium doesn't exist and therefore is very scarce and therefore the efficacy of it is not very clear. However, there are a growing number of patients with a report of necrotizing enterocolitis particularly in elderly population that they are dealing with decreased effective blood volume. Now Pateromer and Sodium Zirconium Cyclosilicate, there are two new resins. Pateromer is calcium potassium exchanger and the Sodium Zirconium is sodium proton potassium exchanger are rather effective and they can bring potassium down for within 12 to 24 hours after prescription by increased elimination through the bowel. The effect of them in ICU for rapid decrease in potassium however is not studied. Now the most important aspects of management would be elimination with diuretics or dialysis. Diuretics, any type of diuretics can potentially increase potassium elimination outside of spironolactone, amiloratrion, those that decrease the effect of aldosterone on principal cells. Loop diuretics, Vidor-Vidar thyroid diuretics have been shown to be very effective in decreasing potassium. Regardless of GFR, if we can increase flow into the collecting duct, there is a flow dependent potassium channel in collecting ducts that allow potassium excretion, therefore by increasing flow rate into the kidney we can eliminate potassium more efficiently. And finally dialysis is a very efficient way of decreasing potassium. Potassium can decrease by one millimole per liter in the first hour of dialysis. This rate decreases over the course of time, however is very effective. Obviously potassium can rebound after dialysis stops, therefore a measurement of potassium four to six hours after end of dialysis may be necessary for particularly for patients who have increased total body potassium. Now switching gears to sodium. Hyponatremia is one of another type of electrode abnormalities that we commonly encounter in ICU. Symptoms and signs, a lot of these patients are asymptomatic, but the decreasing incidence has been seen with higher severity all the way to coma, seizure, and increased intracranial hypertension. It is not uncommon, a number of patients that develop this hyponatremia among ICU patients is rather very common, and it has significant impact on the outcome. Both hyponatremia and hyponatremia are associated with higher risk of mortality among our patients. Now we have to kind of define how we can approach it, however before we do that we need to be able to calculate and measure osmolarity and tonicity. Osmolarity obviously can be measured and has to be measured, as unknown osms may be present in the plasma, also could be calculated using the formula of twice as sodium, glucose divided by 18, BUN divided by 2.8, and ethanol divided by 4.6, could provide us some understanding of what the plasma osmolarity is. However, as urea is not effective osm, in order to calculate effective serum tonicity, we need to measure serum osmolarity and subtract BUN, serum urea level, which is twice as much as BUN, from the measure serum osmolarity in order to calculate tonicity. Now the first step in approaching hyponatremic patients is to identify the tonicity or osmolarity of these patients. If serum tonicity is very high, diseases like a high osmolar load like hyperglycemia, glycerotoxicity, mannitol prescriptions should be suspected. If tonicity is normal between 280 to 295, then pseudo hyponatremia should be considered, including marked hyperlipidemia or hyperproteinemia, including multiple myeloma. The most common type of hyponatremia, however, is when serum tonicity is very low, less than 280 milliosm per kilogram. And these are true hyponatremia, and traditionally we have approached them based on the volume balance, effective circulating volume of high, normal, and low. High includes differential diagnosis of condensate heart failure, cirrhosis, nephrosis. Normal effective circulating volume is most commonly seen in SIADH, however, patients with hypothyroidism and hypodermalism could also suffer from the same path. And low effective circulating volume is due to volume loss through the kidney or outside of the kidney, which could be diagnosed by measurement of urine sodium. Now, to describe hyponatremia, there are several different types. Hypovolemic hyponatremia, usually sodium and salt both decrease, however, the loss of water is less than loss of sodium. This happens in a setting of diarrhea, vomiting, dehydration, and malnutrition. In euvolemic hyponatremia, pre-water increases and sodium does not change. This is at the time we have thyroid disease, SIADH, or primary pyelodipsia. In hypervolemic hyponatremia, we have increase in water and sodium level, however, water increases more than sodium level in a setting of CHF, cirrhosis, or nephrosis. Now, in true hyponatremia, urine osmolarity can help us to understand approach significantly better. So, when we have urine osmolarity less than 100 mOz per kg, means that the amount of free water that is excreted through the kidney is tremendously high, yet a patient is hyponatremic, primary pyelodipsia should be considered. It means the kidney is doing the right thing, however, cannot catch up with the demand that patients have. Also, recent osmosis should be suspected. If urine osmolarity is more than 100 mOz, however, decreased water excretion should be suspected. In a setting of hypothyroidism, adrenal insufficiency, or based on the urine sodium level, we can reach a differential diagnosis in next slide set. Again, when we have true hyponatremia with urine osmolarity more than 100 mOz per liter, we measure urine sodium. If urine sodium is low, hypovolemia should be suspected, dehydration, or decreased effective blood volume, a setting of heart failure, cirrhosis, nephrotic syndrome should be considered. If urine sodium is high, and then diseases like SIADH syndrome, inappropriate ADH secretion, recent osmostat, and renal salt basting should be considered. The difference between SIADH and renal salt basting are very subtle. In SIADH, usually sodium's urethra level is normal, and fractional excretion of urethra is low. While in renal salt basting, serum urethra level is low, and fractional excretion of urethra is within normal range. Now, what if the urine sodium is in gray zone of 20 to 40 mOz per liter? In that case, we can use a saline load test to give this patient 2 liters per day for two days of normal saline. If changes in serum sodium is more than 5 mOz per liter, hypovolemia should be suspected. If the change is less than 5 mOz per liter, then reset osmostat, SIADH should be suspected. Now, receiving hyposmolar fluid intake could potentially lead to hyponatremia. Mostly, these are hydrogenic in a setting of bladder irrigation or uterine irrigation, and a frosting tube insertion and irrigation, and CVVHD with distilled water could lead to hyponatremia, and 25% human albumin diluted in sterile water could lead to hyposmolar fluid intake that leads to hyponatremia. Fresh water drowning that has been seen in animal models could also have been reported as a cause of hyposmolar fluid intake that lead to hyponatremia. Now, response to hyponatremia are several. In acute hyponatremia, sodium and potassium shift out of cells, and therefore generate equilibration of osmolarity across the cell membranes. In chronic setting, however, loss of intracellular organic osms leads to a equilibration of osmolarity between inside and outside of cells. It takes five to seven days for that loss of intracellular organic osms to return to normal. Therefore, hyponatremia should be corrected slowly within five to seven days, particularly in very severe cases in the chronic setting. Particularly, oligodendrocytes are very sensitive to this osmotic stress. They can potentially change their function quickly or get injured quickly by rapid changes in sodium level, particularly in chronic setting. So when we look into normal brain with normal osmolarity, by immediate effect of hypotonic state, there is a water gain that results in hyposmolarity in the brain. Rapid adaptation by removal of sodium and potassium from intracellular space to outside of cells, the degradation starts. Now, slow adaptation would lead to loss of organic osmolides that would lead to sensitivity of rapid response to correction. So if correction happens in a slow fashion and normal brain function osmolarity happens, however rapid correction of sodium would potentially lead to osmotic demyelination and that leads to significant neuro deficits. So in management of hyponatremia, correction rate should be very limited. 0.5 millikilopal per liter per hour until patient is asymptomatic. So if patients are symptomatic, they have coma, seizure, or a significant neurologic deficit, then rapid correction is recommended and the rate should be about 0.5 millikilopal per liter per hour. However, following resolution of symptoms, the rate of correction should slow down. These are not the targets but the ceilings of correction. So in the first 24 hours, 6 to 8 millikilopal, and in the first 48 hours, up to 18 millikilopal is allowed for sodium to increase. In animal studies, they've been reported that there is a benefit in re-lowering sodium if sodium correction is fast. So if by chance sodium correction is faster than the target, the limits that I just mentioned, we can dilute blood again with prescription of free water or other strategies that I alluded to in later slides. Now among patients who are volume contracted, when crystalloids are delivered, there is significant suppression of ADH and that would lead to significant rapid correction of sodium. Often patients that are dehydrated and volume contracted, they also have hyponatremia that is not chronic. Although a slow correction of sodium among those patients are also recommended. Among patients with normal volume or those who are volume overloaded, free water restriction alone in majority of patients can lead to improvement in sodium and there is no recommendation for IV or oral salt intake among these patients. So we have to, in a management strategy, we have to try to limit conditions that increase ADH level, including dehydration, to avoid dehydration, controlling nausea and vomiting, controlling pain, avoiding opioids. And we also need to watch for dramatic increase in rate of correction. One other factor that is extremely common among adult ICU population, particularly among elderly, is amount of daily solute excretion. Normally within American diet, in normal adults, we generate about 5 to 10 milliosm per day, which would be about 600 to 900 milliosm per day is generated, therefore need to be excreted. Now if we consider that maximum dilution ability of kidney is about 60 milliosm per liter, if we take 900 milliosm per day, we can drink about 11 to 12 liters of fluid and dilute it to 65 milliosm per liter in a urine and be not hyponatremic. However, if we drink more than that limit, additional water does not be excreted from the body, therefore leads to hyponatremia. If intake of ozones is only 600 milliosm per day, that limit would decrease to about 6 liters. And among patients who receive very small amount of solutes a day, low salt diets, tea and toast diets, beer potomania patients, elderly population that are all malnourished and do not take enough amount of protein, they usually fall in this category. Among those patients, only 4 liters is a limit before they start becoming hyponatremic. Now this is at the time that urine can be diluted to the maximum of 65 milliosm. However, among those who cannot dilute their urine to 65 milliosm, which only happens in normal kidney function, that limit is significantly more limited. So just imagine that they cannot dilute their urine to less than 120 milliosm per liter due to chronic kidney disease or acute kidney injury or due to tubular damage, they only can drink about 1 liter before they retain extra water. So, osmolar intake excretion is very important. Now, where are these ozones coming? Urea generation from protein metabolism, including internal sources, which is about 50 to 100 millimoles per day by protein catabolism, and external sources from protein intake, 10 gram protein, would lead to 50 millimoles of urea. In addition to dietary sodium and potassium, these are the major ozone intake that would lead to 6 to 900 milliosm per day of osmolar excretion. Now, a few words on urea and hyponatremia. Urea recently has been added to the artillery of treatment options for hyponatremia. When we deliver urea in a form of medication to these patients, urea as ineffective ozone incorporates in total body water very quickly. However, blood-brain barrier is resistant into passage of urea, therefore generates a slight osmolarity gradient around the blood-brain barrier and removes the water from the brain, lead to rapid correction of neuro-deficits among patients who are very hyponatremic. With that, while sodium level does not change as urea is distributed across the total body water, plasma osmolarity rapidly increases, and that would, by about 20 milliosm per liter, that would be in the first hour of your delivery, and that would lead to improvement in neuroscience and symptoms. After a first hour of delivery of urea, urea starts showing in the urine. In a normal kidney, that load of 30 gram usually is completely excreted in urine in about 12 hours or so. By entering in the urine, free water can move with the kidney, through the kidney, can move water, and that would lead to increased water excretion. As water continues to be excreted through the kidney, plasma sodium level starts increasing, and that is the mechanism that would lead to increasing plasma sodium after delivery of urea as a medication. Indeed, in a recent study, retrospective analysis of UPMC, University of Pittsburgh Medical Center, in 2016-2017, all patients who had sodium level less than 135 and received at least one dose of urea, they found 58 patients, average age of 68 year old, and 81% had SIADH. 25% of these patients only received urea to manage their hyponatremia. What they found was sodium level increased from average of 124 to 131. One patient did not tolerate urea, and there was no report of overcorrection among this patient population. And among those 24 patients, 24% of patients who only received urea as a treatment option, they tried to match these patients with those who did not receive urea. And as you see, among those patients who received urea, the 12 patients, increasing serum sodium within 24 hours was about 2.5 milliequivalent per liter, and final serum sodium more than 135 was observing about 33%, one-third of patients. While those who did not receive urea, sodium in the first 24 hour actually decreased, and the number of patients who achieved sodium more than 135 was only 8%, and statistically significant difference from the previous group. Now the problem among patients who do not receive a lot of osmolar intake and retain volume because kidney does not have ability to pass additional free water is that when we deliver IV fluids including normal saline or other crystalloids, banana bag that includes other electrolytes or vitamins, electrolyte replacement antibiotics, and food, we deliver enough amount of osmolar load to these patients, they can pass the retained free water very quickly, and that would lead to rapid correction of sodium. Therefore, patients who are malnourished, the patients who have beer-potomania, tea and toast diet, and they generally come in a malnourished fashion, if they receive these substances, they can correct their sodium very quickly, particularly if urine output increases rapidly. In this kind of condition, we need to replace free water with oral or IV free water or use DD-AVP in order to mimic high ADH level, avoid rapid decline in total body water, therefore rapid correction of hyponatremia. There are also diuretics that can impact sodium level, thiazide diuretics, effect is in distal convoluted tubule, they decrease urine diluting capacity, therefore they decrease free water excretion, and they may lead to hyponatremia. In comparison with loop diuretics that they work in thick ascending loop of Henle, they decrease diluting and concentrating ability of the kidney, and they increase free water excretion, therefore they are used for patients with hyponatremia. Now, there are also a new class of medications including VATANS, and we know that VATANS or ADH blockers, ADH or vasopressin generally activates V2 receptors at basolateral surface of tubular cells in a distal part of collecting duct, and that would activate adenyl cyclase and generate cyclic AMP, which activates protein kinase A, and that would lead to phosphorylation of aquaporin 2, leads to connection of aquaporin 2 to the urine space, and make your cell membrane very permeable to water. Therefore, ADH is able to increase free water reabsorption from collecting duct. Now, VATANS, they block the V2 receptor, and therefore block this mechanism, and because of that they let free water to be extruded through the kidney, therefore sodium be corrected. There are several different VATANS that are generally called aquaeretics. 12-VATAN is more available and rather very expensive among patients who have failed to respond to any other strategy they could be potentially used. Few words on hyponatremia, excessive sodium intake, pure water loss, or loss of water more than sodium are the reasons for hyponatremia. When we deliver a lot of bicarbonate and saline, in particular in surgical setting, we see rapid increase in their sodium level. Seawater intoxication is another reason. Pure free water loss is in a setting of lack of access to water, all ICU patients, those who are bedridden, or those who are on coma. And lots of water more than sodium seen in several different settings. GI loss in vomiting, diarrhea, kidney loss in diabetes insipidus, hypercalcemia, hypokalemia, drugs like alcohol, lithium, phenytoin, propoxifen, and skin loss through excessive sweating or burn, and perturbing dialysis all can lead to hyponatremia. Symptoms of hyponatremia changes based on osmolarity among these patients. When osmolarity is between 350 to 375, patients are restless and irritable, all the way to osmolarity of more than 430 milliaosm per liter which could lead to seizure and death. In a recent study of rapid versus slow correction of hyponatremia, as you can see among patients who were enrolled in a large data set, on admission had a sodium level of more than 155 millimoles per liter, and 122 on admission, 327 within the hospital, they compared rapid correction of more than 0.5 millimoles per liter per hour versus less than 0.5 millimoles per liter per hour. As you can see, there was no difference in 30-day mortality among this patient population after rapid versus slow correction, and zero cases of cerebral edema seizure was noted. So, unlike hyponatremia, the rate of correction should be slow, and in hyponatremia we can expedite the correction, however, with a lot of caution. It is more and more apparent that hyponatremia for more than three days would potentially lead to higher mortality among patients that are critically ill, so avoiding hyponatremia and treating hyponatremia in more rapid correction of more than 0.5 liter per liter per hour may be recommended. A few words on calcium. Hypercalcemia could be associated with different signs and symptoms. In mild hypercalcemia, often patients are asymptomatic and may have polydipsia polyurea. In severe hypercalcemia could lead to coma or cardiac arrest. In order to manage hypercalcemia, we need to decrease calcium reabsorption from proximal tubular cells, and in order to do that, we need to send a message to a kidney that there is a significant volume overload. Therefore, paralyze proximal tubular cells in order to reabsorb calcium. Following that step, we need to eliminate reabsorption of calcium in distal nephron by uvulamic force diuresis. When patients are well hydrated and volume is repleted, use of fluorescemide or other loop diuretics along with isotonic crystalloids could potentially lead to increased elimination of calcium. If all of these fail, hemodialysis is a very good modality in removal of calcium. A few words on magnesium. Hypermagnesium is seen in cell shift, in the setting of acute pancreatitis, catecholamine treatment, ethanol abuse, hungry bone syndrome, chelation with post-surgical free fatty acids, phosgarnet or transfusion, GI loss through decreased intake in starvation or decreased absorption in laxative abuse or chronic diarrhea or short bowel syndrome, and renal loss which could be acquired through TCATS and then loop of Henle defect, use of diuretics or RTAs, ethanol, increased calcium, decreased phosphorus volume expansion, nephrotoxins, ATN recovery, all the way to primary magnesium reabsorption defects due to genetic or acquired deficiencies. Now consequences of hypomagnesemia is very significant. Metabolically, they can cause refractory hypokalemia and hypercalcemia. In cardiovascular system, it can lead to arrhythmia, prolonged QTC, hypertension, coronary spasm, and sudden death. In CNS, it can result in depression all the way to coma. In neuromuscular, it can cause neuropathy, tremor, myoclonus, wussexine, tetanus, weakness, and paresthesia that we need to be aware of. For treatment of hypomagnesemia outside of resolution of underlying source, if that is possible, is IV or oral replacement. In IV replacement, slow infusion is very important. So obviously if you are dealing with a torso out patient, giving a bowl of magnesium is recommended. However, if you are trying to replace magnesium on patients with hypomagnesemia, then slow infusion is very important because if you increase plasma magnesium level really high to higher level, amount of excretion through the kidney increases. The faster you deliver magnesium, the more magnesium is excreted through the kidney. So usually, one gram over six hours would have significant more efficacy. Even with that slow rate, 50% of that magnesium is lost in urine. Oral replacement is another route. Amiluride that decreases sodium absorption collecting, therefore increases magnesium reabsorption and calcitriol by increasing GI absorption would help in management of hypomagnesemia. Hypomagnesemia has been seen in multiple settings, including decreased kidney excretion in a setting of low GFR and receiving milk alkali, tissue injuries like burn, hyperparathyroidism, Addison's disease, theophylline, lithium toxicity, familial hypocalcemia, hypocalceric hypocalcemia, and then high intake including dead seawater, preeclampsia, that is iatrogenic, and magnesium-containing animals. Symptoms can be from asymptomatic to very high levels, deep tendon reflexes could be completely absent, all the way to respiratory failure, heart block, and cardiac arrest. In EKG changes, when patients are hypermagnesemic, PR is prolonged, QRS duration increases, and the QT interval also increases. In management, we have to stop the source, we need to increase GFR significantly by hydration or euvolemic forced diuresis, dialysis could be used to remove magnesium, and also IV calcium to stabilize membranes could be potentially used. With that, I thank you for your attention.

electrolyte emergencies

hyperkalemia

hyponatremia

hypercalcemia

hypomagnesemia

treatment options

management strategies