Management of Electrolyte Abnormalities

For Elective Surgery, what is the:
1. Highest acceptable Sodium Concentration
2. Lowest acceptable Sodium Concentration
Click the card to flip 👆
1 / 128
Terms in this set (128)
1. A patient is hypotensive and/or hypovolemic
2. Renin is secreted from the kidneys
3. Renin converts angiotensinogen to angiotensin I
4. ACE (angiotensin converting enzyme) converts angiotensin I to angiotensin II
The ACE enzyme is produced in the lungs
5. Angiotensin II increases blood pressure in 2 ways:
-5a. Direct vasoconstriction
-5b. Causes release of aldosterone & ADH
6. Aldosterone & ADH cause sodium & water reabsorption
****Definite Test Topic**** What is Aldosterone released in response to?Decreased Blood Volume****Definite Test Topic**** What are the TWO general ways that Aldosterone responds to decreases in blood volume?-Aldosterone increases: 1. Sodium AND 2. Water reabsorption****Definite Test Topic**** What are the FOUR specific ways that Aldosterone effects the body?1. Plasma sodium concentration INCREASES -Sodium reabsorption thus appears to be greater than water reabsorption 2. Blood volume increases 3. HCO3- increases (possible metabolic alkalosis) -HCO3- reabsorption also thus appears to be greater than water reabsorption 4. Plasma potassium concentration decreases -Because of this, hyperkalemia can actually stimulate aldosterone secretion****Definite Test Topic**** What is ADH/Vasopressin released in response to?1. Decreased Blood Volume 2. Increase in Plasma Sodium ConcentrationWhat general effect does ADH have on the body?ADH Increases water reabsorptionWhat are the TWO effects that ADH has in response to decreased BP/Blood volume?1. Blood volume increases 2. Plasma sodium concentration decreasesWhat TWO effects would inhibition of ADH have on the body? Provide some examples of what conditions could inhibit ADH secretion?-Inhibition of ADH (SIADH, central diabetes insipidus, etc) will cause a: 1. Lower blood volume 2. Increased plasma sodium concentrationWhat is the name of the drug that is a form of synthetic ADH?DDAVPWhat drug antagonizes ADH?DemeclocyclineWhat are the THREE hormones produced by the Adrenal Cortex, their corresponding drug class, and what zone of the cortex their produced in?1. Aldosterone -Mineralocorticoid -Zona Glomerulosa 2. Cortisol -Glucocorticoids -Zona Fasciculata 3. Androgens -Androgens -Zona ReticularisHow does Cushing's Disease affect the Adrenal Cortex?These patients have a hyperactive adrenal cortex****100% Test Question**** The chronically high levels of what TWO hormones is a characteristic of Cushing's Disease?1. Aldosterone 2. Glucocorticoids (Cortisol) -Cortisol is the primary hormone associated with Cushing's****100% Test Question**** The chronically high levels of Aldosterone with Cushing's Disease can have what FOUR effects?1. Increased blood volume -Therefore, sometimes diuretics are prescribed to patients with Cushing's disease 2. Hypernatremia 3. Hypokalemia 4. Metabolic alkalosis****100% Test Question**** Patient's with Cushing's Disease have chronically high levels of cortisol, which can have what effect?Can lead to HyperglycemiaPatients who have adrenal insufficiency typically have what disease?Addison's DiseasePatient's with Addison's Disease have chronically Low levels of what hormones?Cortisol and AldosteronePatient's with Addison's Disease have chronically Lower levels of what TWO hormones? Which one is primarily responsible for the condition, and the defining feature of this syndrome?1. Chronically low levels of Cortisol and usually also Aldosterone 2. Low cortisol levels are the defining feature of this conditionThe chronically high levels of Aldosterone with Addison's Disease can have what FOUR effects?1. Hypovolemia 2. Hyponatremia 3. Hyperkalemia 4. Metabolic AcidosisPatient's with Addison's Disease have chronically Low levels of cortisol and steroids, which can have what effect?Can lead to hypoglycemiaWhat is the PRIMARY hormonal imbalance that characterizes Addison's Disease?Decreased Cortisol LevelsWhat are the TWO other names for Hyperaldosteronism?1. Primary Aldosteronism 2. Conn's SyndromeHyperaldosteronism is characterized by: 1. Increased Concentration of what drug 2. Normal Concentration of what drug1. Increased Aldosterone concentration 2. Normal Cortisol LevelsWhat effect does Hyperaldosteronism have on sodium and water reabsorption?Leads to increased water and sodium reabsorptionWhat are the THREE clinical manifestations (in terms of electrolyte abnormalities) of Hyperaldosteronism?1. Hypokalemia -Potassium is excreted when sodium is reabsorbed 2. Hypernatremia 3. Increased blood volume & blood pressure (possible HTN) -Treated with potassium sparing diuretics****100% will be tested on the differential symptoms, hormone levels, etc for Hyperaldosteronism, Hypoaldosteronism, Addison's, and Cushing's Disease****Hypoaldosteronism is characterized by: 1. Decreased Concentration of what drug 2. Normal Concentration of what drug1. Decreased Aldosterone 2. Normal CortisolThe decreased aldosterone concentrations but normal cortisol levels that occur with Hypoaldosteronism have what effect on water and sodium excretion?Leads to water and sodium excretionHypoaldosteronism is often a result of what?Renal failureWhat are the TWO clinical manifestations (in terms of electrolyte imbalances) of Hypoaldosteronism?1. Hyponatremia 2. Hyperkalemia -Potassium is reabsorbed when sodium is excreted -Renal failure is thus a cause of hyperkalemiaHypoaldosteronism can cause what ionic imbalance in the body? Explain why/how this happens?1. Hypoaldosteronism can cause Hyperkalemia 2. Hyperkalemia is caused by the increased reabsorption of K+ -The increase in K+ is a result of the Increased excretion of Na+ (as a result of decreased aldosterone secretion) -Because K+ is reabsorbed when sodium is excreted, the increased Na+ excretion results in increased reabsorption of K+, thus causing HyperkalemiaWhat is the normal Na+ [ ]?135-145mEq/LWhat Na+ concentration would indicate Hypernatremia?This is defined as a sodium concentration >145mEq/LWhat are the TWO causes of Hypernatremia?1. An increase in total body sodium 2. Water loss -Diabetes insipidus, etcWhat are the SIX symptoms of Hypernatremia?1. Brain cells shrink -Leads to possible seizures, coma, etc 2. MAC requirements are INCREASED 3. HTN 4. Hyperreflexia and possible weakness 5. Potentiate the effects of muscle relaxants 6. No effect on the ECG -"Hypernatremia does not cause any significant changes on the ECG"True or False: Hypernatremia often causes potentially dangerous arrhythmias?False -"Hypernatremia does not cause any significant changes on the ECG"What are the FOUR considerations for treatment of Hypernatremia?1. Hypernatremia must be treated slowly 2. A water deficit exists in all cases of hypernatremia 3. In order to treat hypernatremia, the anesthetist simply needs to replace the water deficit with a hypotonic IV fluid 4. In addition to the fluids, a loop diuretic may also be givenWhy must Hypernatremia be treated slowly?If treated too rapidly, it can cause seizures, cerebral edema, and even deathWhy is there always a water deficit with Hypernatremia?-The water deficit is proportional to the sodium concentration -The higher the sodium concentration, the higher the water deficitHow do we determine a patient's water deficit so that we can then treat their Hypernatremia with Hypotonic fluid?The water deficit is found by subtracting the present total body water from a normal total body waterWhat kind of fluid would we use to treat Hypernatremia?Hypotonic fluidWhat are the TWO general steps in Hypernatremia Treatment?1. Calculate the water deficit 2. Replace the water deficit over 48hrs with a hypotonic IV fluid****100% Test Question**** What are the THREE steps in calculating a patient's water deficit?1. Calculate normal TBW by using the following equation: -(patient's weight in kg)(percentage of body weight that is water) 2. Calculate present TBW by using the following equation: -(Normal TBW)(Normal [Na+]) = (Present [Na+])(Present TBW) -(Normal TBW)(Normal [Na+]) = (Present [Na+])(x) -Then: Solve for x 3. Subtract present TBW from normal TBW****100% Calculation question on TBW with hypernatremia treatment****What is the end goal of treatment, in regards to Na+ [ ]?Goal is to get to normal [Na+] = 140****Clinical Scenario**** -70kg male -Na+ = 160mEq/L -Desired Na+ = 140mEq/L Given this information, answer the following: 1. What is the water deficit? 2. How many mL/hr hypotonic solution should be administered (over 48hrs)?1. (Normal TBW)(Normal Na+) = (Present TBW)(Present Na+) Step 1: Solve for present TBW Step 2: Subtract from TBW -Normal TBW = 42L -Present TBW = 36.7L -Answer: Water deficit = 5.3L 2. Answer = 110mL/hrWhat is the inherent cause of Central Diabetes Insipidus?Insufficient secretion of ADH by the Posterior PituitaryWhat is the Etiology of Central DI? What effect does this have on the body's tonicity?1. There are multiple etiologies (head trauma, pituitary tumor, recent craniotomy, etc) 2. The excess water loss leads to hypernatremia (hypovolemic = hypernatremic = water deficit = hypotonic fluid)What are the THREE treatment options for Central Diabetes Insipidus?1. Hypotonic Fluids 2. DDAVP (only for Central) 3. Thiazide Diuretic****Don't need to know the thiazide diuretic mechanism for treating central DI (it's in red), but the mechanism is on the other side****1. Thiazides decrease sodium reabsorption in the DISTAL tubule 2. Diuresis occurs 2a. Plasma volume decreases 2b. GFR decreases 2c. Sodium & water reabsorption in the proximal tubule INCREASES 3. Less fluid reaches the distal nephron 4. Overall fluid conservationWhat is the essential cause of Nephrogenic Diabetes Insipidus?The kidney's do not respond adequately to ADHWhat is the key difference between Central and Nephrogenic DI?Central DI is caused by an insufficiency of ADH production, while Nephrogenic DI is caused NOT by lack of ADH, but by an inadequate response by the kidney's to the ADH itselfWhat is the Etiology of Nephrogenic DI? What effect does this have on the body's tonicity?1. There are multiple etiologies (genetics, sickle cell disease, polycystic kidney disease, electrolyte abnormalities, etc) 2. The excess water loss leads to hypernatremiaWhat are the TWO treatment options for Nephrogenic DI?1. Hypotonic fluids 2. Thiazide diureticWhat treatment can you use for Central DI that you can't for Nephrogenic DI, and explain why?1. DDAVP 2. Can use DDAVP for Central and not Nephrogenic DI because in Central DI the issue is the lack of ADH production, which can be treated with DDAVP since it is essentially a synthetic form of ADH. For Nephrogenic DI, the issue is the insufficient response of the kidney's to ADH, not a lack of ADH, so DDAVP would provide no therapeutic benefitWhat is the most common Electrolyte Abnormality in Hospitalized Patients?HyponatremiaWhat Na+ concentration would indicate Hyponatremia?Hyponatremia = Na+ < 135mEq/L****this is in red so don't need to know it, but hyponatremia classification on other side****Classification -Mild hyponatremia (130-135mEq/L) -Moderate hyponatremia (125-130mEq/L) -Severe hyponatremia (<120mEq/L)What are the TWO possible causes of Hyponatremia?1. Water retention -Excessive ADH secretion 2. Sodium loss -Diuretic therapy, GI losses, adrenal insufficiency, renal disease, trauma (i.e., burns), etcWhat are the FOUR possible Physical (not electrolyte imbalances) symptoms of Hyponatremia?1. Cerebral edema 2. Altered mental status 3. Muscle weakness 4. No effect on the ECG -"Hypernatremia does not cause any significant changes on the ECG"True or False: Hyponatremia often causes potentially dangerous arrhythmias?False -"Hyponatremia does not cause any significant changes on the ECG"What are TWO possible causes of Hyponatremia due to Water Retention? Explain both?1. SIADH (Syndrome of Inappropriate ADH) -This causes an excessive ADH release -More water retention = hyponatremia 2. AIDS -Adrenal infection leads to excessive ADH releaseIf a patient is Hyponatremic, what can we assume about their volume status (normally)?That they are Hypervolemic, because their Na+ [ ] is dilutedHow does the body try to compensate for the loss of sodium in the plasma, or if there is too much water in body?Whenever the plasma loses sodium (or has too much water), the body attempts to compensate by suppressing ADH releaseHow does the body's suppression of ADH production help treat Hyponatremia?The decrease in ADH production promotes diuresis, decreasing the blood volume, and increasing the plasma sodium concentrationHow does the body try to compensate if the patient is BOTH Hyponatremic AND Hypovolemic? Explain why, and what this response tells us about the difference in priory for regulating plasma volume and plasma osmolarity?1. If a patient is both hyponatremic AND hypovolemic, the body will not suppress ADH release 2. This is because the body doesn't want to decrease blood volume in a hypovolemic patient 3. This tells us that plasma volume takes precedence over plasma osmolarityWhat are the THREE steps to treatment of Hyponatremia? Provide some examples?1. Find out how many mEq/L the patient is deficient in sodium -For example if the current [Na+] is 120mEq/L, and the target [Na+] is 135mEq/L, the patient has a 15mEq/L [Na+] deficit 2. Find out how many total mEq the patient is deficient in sodium -This is easy if you just know the total body water -For example, if the above patient has a total body water of 40L, they are deficient of 600mEq total sodium -(40L)(15mEq/L) = 600mEq 3. Replace deficit with a sodium containing fluid****Clinical Scenario**** -80kg female -Current [Na+] = 118mEq/L -Target [Na+] = 130mEq/L Given this information: 1. How many mL 0.9% N/S (154mEq/L Na+) will it take to replace the Na+ deficit? -Provide each step and calculation for solving thisStep 1: Determine what the mEq/L Na+ deficit is. -Target [Na+] - Current [Na+] = Na+ Deficit -130mEq/L- 118mEq/L = 12mEq/L deficit Step 2: Calculate the patient's total body water. -TBW = 50% (female) x 80kg = 40L TBW Step 3: Calculate the total body sodium deficit. -(Current Na+ deficit) x (TBW) = 480mEq Total Body Na+ Deficit Step 4: Calculate how many liters of 0.9% N/S (154mEq/L Na+) the patient should receive to correct the imbalance. -Total Na+ deficit / mEq per L of 0.9% N/S = (480mEq/L)/(154mEq/L) = 3.12LWhat are some complications and points of caution for Treatment of Hyponatremia?Rapid hyponatremia correction can cause any of the following: -Central pontine myelinolysis (caused by cell shrinkage) -pulmonary edema (caused by fluid overload) -hypokalemia (caused by increased sodium reabsorption) -hyperchloremic acidosis****don't need to know this because it's in red, but the other guidelines for how fast to treat hyponatremia with fluids is on the other side****Below are the guidelines to the speed in which hyponatremia can be corrected -Mild symptoms (0.5mEq/L/hr) -moderate symptoms (1mEq/L/hr) -severe symptoms (1.5mEq/L/hr) -Max daily rate (10-12mEq/L)What does the Term TURP stand for?TURP = Transurethral Resection of the ProstateWhat is required for visualization during a TURP procedure?An irrigation solution is required to allow visualizationWhat are the general Pros and Cons of performing TURP with Cautery?This method is faster, but the surgeon can't use normal saline as an irrigation solution because saline disperses the electrocautery current****Probable Test Question**** What TWO complications can occur with the use of hypotonic N/S as an irrigation solution for TURP with Cautery, and the name of this condition? Explain why/how this happens?-This can cause TURP syndrome -TURP syndrome develops because N/S is hypotonic and readily absorbed into the body, and there is a large amount of the fluid used for this procedure, leading to: 1. Volume overload (Hypervolemia) 2. HyponatremiaWhat is the defining electrolyte abnormality of TURP syndrome?Hyponatremia****Probable Test Question**** What are THREE Advantages to performing a TURP with Laser versus a TURP with cautery? What is the ONE real Disadvantage to TURP with Laser?-TURP with laser does not require cautery resection and offers the following advantages 1. Normal saline can be used as an irrigation solution, and thus no risk of TURP syndrome (Hyponatremia) 2. Less blood loss (safer for patients on anticoagulants) 3. Shorter hospital stay -Disadvantage: 1. Despite these advantages, operating times are longer, and there are still questions as to whether or not it effectively removes most or all of the BPH tissueWhat are the THREE Possible Irrigation Solutions used for TURPs? Provide a few details about each?1. Distilled water -This is rare nowadays because it is extremely hypotonic, leading to possible hemolysis, shock, and renal failure 2. 0.9% Normal Saline -NOT used with cautery -ONLY used if TURP is done with a laser 3. Glycine -This is currently the most popular irrigation solution used with cautery resected TURP -Can lead to possible transient visual impairmentFor Elective Surgery, what [K+] would be the: 1. Highest Allowable K+ concentration 2. Lowest Allowable K+ Concentration1. The highest potassium concentration that should be allowed before cancelling an elective surgery is 5.5mEq/L 2. The lowest potassium concentration that should be allowed before cancelling an elective surgery is 2.8mEq/LWhat effect does Insulin have on the K+ Concentration, and explain how?1. Insulin drives potassium intracellularly and DECREASES plasma potassium concentration 2. Anything that increases insulin concentration should cause a decrease in potassium concentrationWhat effect do Beta Agonists have on the K+ Concentration, and explain how?Beta receptor activation has the same effect as insulin and decreases plasma potassium concentrationWhat are some examples of Beta Agonists, and what affect they would have on K+ levels?1. Examples would include any sympathetic response or any beta agonist (i.e. albuterol)What effect does a Beta Blocker like Labetalol have on K+ levels?Beta blockade (i.e. labetalol) increases plasma potassium concentrationWhat does the term Hydrogen Potassium Shift refer to?refers to the relationship between the movement of H+ and K+ into and out of cells countercurrent to each other, and their relationship to alkalosis and acidosis****100% Test Question**** In regards to the Hydrogen Potassium Shift, describe the movement of H+ and K+: 1. In Acidosis 2. In Alkalosis 3. In a Hypokalemic state1. In acidosis (↑H+): -H+ enters cells; K+ exits cells. -Therefore: -Acidosis = possible hyperkalemia 2. In alkalosis (↓H+): -H+ exits cells; K+ enters cells. -Therefore: -Alkalosis = possible hypokalemia 3. In hypokalemia: -K+ exits cells; H+ enters cells -Therefore, hypokalemia = possible alkalosisWhat would be the Fastest way to immediately treat Hyperkalemia if you needed to perform emergency surgery on a patient?Start an Insulin and Glucose infusionWhat are the SEVEN possible Etiologies of Hyperkalemia?1. Acidosis & beta blockers 2. Succinylcholine -An intubation dose raises serum [K+] by 0.5mEq/L 3. RBC transfusions -Extracellular K+ in stored blood increases over time 4. Cell lysis -Tumor lysis syndrome, rhabdomyolysis, etc 5. Both renal and adrenal insufficiency -This is due to low aldosterone production, which causes sodium/H2O excretion and potassium reabsorption 6. ACE inhibitors -DECREASE aldosterone levels, which leads to decreased K+ excretion 7. Rewarming following hypothermia -Hypothermia lowers plasma potassium concentration, because it causes sympathetic stimulation (which causes K+ to shift intracellularly) -During rewarming, the sympathetic stimulation goes away, and this K+ comes back out of cells (which means rewarming can increase plasma K+ concentration)What are the THREE Temporary Treatments of Hyperkalemia?1. Methods to shift potassium intracellularly 2. 2. Stabilize myocytes with calcium 3. Avoid Lactated Ringers for maintenance fluidsWhat are the THREE methods to shift K+ intracellularly for treatment of Hyperkalemia?1. Give Insulin 2. Induce Alkalosis -give bicarb and/or hyperventilate the patient 3. Give Beta agonists -like albuterol, or epinephrine -"...epinephrine induces hypokalemia." -However, because of its hemodynamic effects, epinephrine probably shouldn't be used in the routine treatment of hyperkalemiaAt what rate should Insulin be infused for the treatment of hyperkalemia? What else needs to be giving concurrently with the insulin to avoid Hypoglycemia?1. Insulin should be infused with glucose in order to prevent hypoglycemia 2. The rate should be approximately 5g dextrose per 1 unit of insulin (1 amp of dextrose per 5 units insulin)Explain how/why Calcium can be used to temporarily treat Hyperkalemia? How long does its effects last for?1. Calcium antagonizes K+ in cardiac muscle 2. The effects dissipate after 15-30 minutes (may have to redose)What are the THREE Permanent Treatments of Hyperkalemia?-all three treatments are aimed at the excretion of K+ 1. Kaexylate 2. Diuretics = Lasix 3. DialysisExplain how/why Kaexylate can be used to Permanently treat Hyperkalemia? What is the primary consideration to be aware of when administering this drug?1. This drug binds potassium in the intestine 2. "Kaexylate has been shown to cause intestinal obstruction and potential rupture...diarrhea needs to be simultaneously induced with treatment." -Essentially, the patient diarrheas themselves to get rid of the extra K+****Know**** What is the Pneumonic for Hyperkalemia Treatment?Hyperkalemia Treatment Pneumonic: CBIGKD Calcium Bicarb Insulin + Glucose Kaexylate Diuretic/Dialysis)What are the FIVE ECG features of Hyperkalemia?1. Peaked T waves 2. Smaller P amplitude 3. Increased PR interval 4. Widened QRS 5. Eventual sine wave ECG and possible Vfib/asystole****ECG strip on other side**** HyperkalemiaWhat electrolyte abnormality does this patient have?****ECG strip on other side**** 1. Hyperkalemia 2. Could hyperventilate them, give insulin, or beta agonist 3. Could still do surgery, but need to get the K+ down to an acceptable level firstA patient arrives in the ER for an emergency appendectomy. During preop, you see this ECG rhythm strip. Based on this, what is: 1. The cause of this abnormal ECG strip 2. Your treatment options for this condition 3. Can you still go forward with the surgery?****No question, just a few more notes on Hyperkalemia on the other side****In addition to the ECG changes, hyperkalemia may result in muscular weakness and impair the ability of the kidneys to correct metabolic acidosis Critical Care Medicine: Principles of Diagnosis and Management in the Adult, 4th edition, page 1004 "In contrast to sodium, the neurological manifestations of potassium imbalance...rarely involve the CNS."What are the NINE possible Etiologies of Hypokalemia?1. Insulin 2. Catecholamines -Head trauma (increased ICP) 3. Alkalosis 4. RBC transfusions -This is a result of potassium depleted RBCs "taking up" K+ ions following infusion 5. Diuresis 6. Dialysis 7. GI loss (N/V, diarrhea, NG suction) -This is due to metabolic alkalosis (loss of acidic gastric fluid) 8. Small bowel obstruction (N/V) -Also causes metabolic alkalosis (loss of acidic gastric fluid) 9. Hypothermia -Via sympathetic stimulationWhat is the Usual treatment for Hypokalemia?Usually, a 100mL N/S bag with 20mEq potassium is infused into the patient through an infusion pumpA patient comes in for elective surgery, and after runnings labs the [K+] is low (hypokalemia). How/at what rate would you treat this condition so that the patient can have surgery, if the patient has a: 1. Peripheral IV only 2. Central Line1. Up to 8-10mEq/hr if the patient only has peripheral IV access 2. Up to 20mEq/hr if the patient has a central lineHow much should 20mEq of K+ increase plasma K+ levels?20mEq of potassium should increase the plasma level by ≈ 0.25mEq/LIf you are treating a patient for hypokalemia, how long should it take to raise the plasma level by 1.0mEq/L?should take 4 hours to accomplish this, since 20mEq of potassium should increase the plasma level by ≈ 0.25mEq/LWhat are the TWO points of Caution with Treatment of Hypokalemia? Explain both?1. Avoid dextrose replacement solutions -Causes insulin secretion, which further decreases potassium 2. Avoid aggressive treatment in: 2a. Hypothermia -Because of possible hyperkalemia upon rewarming 2b. Head trauma -Because of possible hyperkalemia upon relief of increased ICPWhat are the TWO ECG features of Hypokalemia?1. T waves flatten or become inverted 2. U waves appearBesides ECG changes and cardiac arrhythmias, what other effects can Hypokalemia have on the body?In addition to ECG changes and cardiac arrhythmias, hypokalemia can lead to muscular weakness, potentiation of muscle relaxants, and eventual respiratory distress/arrestWhat effect does Parathyroid Hormone (PTH) have on the body?Parathyroid hormone decreases bone calcium and increases plasma calcium concentrationWhat effect does Calcitonin have on the body?Calcitonin decreases plasma calcium concentration and increases bone calciumWhat is the stimulus for the secretion of: 1. Parathyroid hormone 2. Calcitonin1. Low Ca2+ levels 2. High Ca2+ levelsWhat is the relationship between pH and Calcium levels in the body?1. As pH goes down (acidosis), serum calcium goes up 2. As pH goes up (alkalosis), serum calcium goes down****no question, but mechanism of how acidosis can lead to hypercalcemia on other side****"Acidosis can also lead to hypercalcemia via the following mechanisms. First, acidosis will cause...displacement of calcium by hydrogen ions from binding sites on albumin. Secondly, with time, hydroxyapatite in the bones will be used to buffer the hydrogen ions. The hydroxyapatite releases calcium and phosphate into the blood as it releases the hydroxyl group to neutralize the acid. If this process continues for a protracted period of time, the bone will become demineralized and will be easily fractured."What is the easy way to remember the relationship between Ca2+ and pH?-Direct correlation -An easy way to remember it is if H+ goes up, Ca+2 also goes up, and if H+ goes down, Ca+2 also goes downWhat are the FOUR clinical manifestations of Hypercalcemia?1. A shortened QT interval on the ECG 2. Muscular weakness 3. Potentiation of muscle relaxants 4. CNS symptoms such as drowsiness, confusion, coma, etcWhat are the FIVE Clinical Management points for Hypercalcemia?1. Rehydrate with saline 2. Give a loop diuretic (must be after the rehydration) 3. Give calcitonin 4. Consider dialysis 5. Avoid acidosisWhat are the FOUR clinical manifestations of Hypocalcemia?1. A prolonged QT interval on the ECG 2. Hyperreflexia and muscular tetany, including laryngeal stridor, masseter spasm, and laryngospasm -Severe hypocalcemia can lead to respiratory arrest 3. Muscle weakness and potentiation of muscle relaxants 4. CNS symptoms such as confusion and seizuresHow is Hypocalcemia treated?It is simply treated with intravenous calcium chloride or gluconateWhat are the FIVE clinical manifestations of Hypermagnesemia?1. The ECG resembles hyperkalemia -shortened QT interval, prolonged PR interval, T wave abnormalities 2. Muscular hyporeflexia and weakness, leading to potential respiratory arrest 3. Potentiation of nondepolarizing muscle relaxants 4. Hypocalcemia -due to suppression of PTH 5. CNS symptoms -such as sedation, confusion, or comaWhat are the THREE treatment options for Hypermagnesemia?1. Saline hydration and a loop diuretic (i.e. Lasix) 2. Intravenous calcium chloride -Temporarily antagonizes the effects of hypermagnesemia 3. Potential dialysisWhat are the THREE clinical manifestations of Hypomagnesemia?1. ECG findings -"It is generally acknowledged that hypomagnesemia is not detected on the ECG" -Prolongation of the QT and PR intervals, widened QRS complex, and ventricular arrhythmias 2. Muscular weakness and potentiation of muscle relaxants 3. CNS symptoms -such as confusion, seizures, or a comaWhat is the Treatment for Hypomagnesemia?1-2 grams of magnesium chloride over 10 minutes