Are Electrolytes Really Important?

Transcription

1 Are Electrolytes Really Important? Jeff Giullian, MD, MBA Plan of Attack Ions, Ians, Eons & Aeons Sodium: Highs and Lows Potassium: Ups and Downs Magnesium: Increases and Decreases Calcium: Peaks and Valleys Phosphorus: Heights and Depths Other: If we have time Ions, Ians, Eons and Aeons Ions, Ians, Eons and Aeons Name of Gaelic Origin Top 10 name for boys born in England in 1960s o Ranked 80 th in US boys in 2014 Eons and Aeons Indefinite, prolonged period of time o Geologic time divided into eras o Time frame I will be speaking on electrolytes Aeon is also the name of: o A band o A retail store o A game o A science fiction cartoon Back to Ions (and Science) Dissolve in a solution o Has a charge o NaCl Na + Cl - o Total number of electrons protons per atom Electrical current o Can light a bulb o Foundation for batteries Glucose can dissolve in a solution but Cannot light a bulb No electrical current

2 Sodium Hyponatremia: Quiz Which drug class is associated with low sodium A. Diuretics B. SSRI C. Narcotics D. NSAIDs E. All the above Sodium 85% found in extracellular fluid o Plasma o Lymphatic fluid Important for osmotic pressure o Intra/Extracellular water balance o Cellular swelling/shrinkage Sodium/Potassium/ATP pump o Energy dependent o Electrical current, muscle contraction Sodium/Water Imbalance Osmolality Water balance o Dilution o Concentration Solute balance + Solute loss + Solute gain 2 x Na + +Glucose/18 + BUN/2.8 o Normal is around o Because normal sodium is around 140 BUN is an ineffective osmole o Easily crosses cell walls o Does NOT easily cross blood brain barrier EtOH and other alcohols also contribute

3 Changes in Sodium/Water Balance Osmoregulation: ADH Hypernatremia o Stimulates thirst (water intake) o Release of ADH (Vasopressin) Vasopressin o Sensitive to small (1-2%) changes in osmolality o Sensitive to large (10-20%) changes in pressure o Acts on 3 receptors to improve pressure and retain free water Vasopressin Receptors V1-alpha Vasoconstriction V1-beta ACTH release V2 receptor Collecting ducts Reabsorb water Hyponatremia Hypo-osmotic o Salt depletion (Diarrhea, salt wasting, sweat, burns) o Water excess Euvolemic appearance (SIADH) Edematous appearance (CHF, Cirrhosis, Nephrosis) Iso-osmotic o Hyperlipidemia Hyper-osmotic o Hyperglycemia, Mannitol Hyponatremia: Signs & Symptoms Time Dependent o Acute/Chronic o CNS adaptation o Loss of neurotransmitter Non-specific o Nausea o Fatigue o Attention/Executive Modest o Balance o Cramps o Muscle Weakness Severe o Seizures o Resp compromise o Coma o Death

4 SIADH Euvolemic in appearance o Excess ADH (Vasopressin) leads to fluid retention o No edema, rales, JVP elevation Normal amount of sodium in the body Pulmonary & Neuro issues are likely culprit o COPD, Small cell lung cancer, PNA o CNS trauma o Post surgical issues Acute on Chronic sodium drop is common SIADH: Drugs HCTZ 1 in 8 patients on thiazide get low Na + Other diuretics (loop, aldactone) Anti-Seizure Anti-Depressant (SSRI, SNRI) Anti-Psychotic NSAIDs Chemotherapy Osmoregulation: ADH Osmoregulation: SIADH SIADH: Lab Values Low Sodium, low plasma osmolarity High urine sodium (>40) Urine Osmolarity >100 o Not maximally dilute urine o But, does not have to be concentrated urine Low uric acid, low BUN Not responsive to Normal Saline o Pee out all the salt in <1 liter of water To fluid Restrict or Not (Urine Sodium + Urine Potassium) / Serum sodium o If ratio < 0.5 Lots of free water in urine. Free water Restriction will work o If ratio > 1.0 Minimal free water in urine. Free water Restriction will not work o If ratio Grey zone OK to try fluid restriction, but may not work

5 SIADH: Treatment Fluid restriction o NOT FREE (Length of Stay) Add Solute o NaCl tabs (+ loop diuretic) o 3% Saline Start at 25ml/hr, measure q4-6hr, increase by 5ml/hr Urine Osm can be predictive of response rate Demeclocycline: Damage to V2 Receptor Vasopressin antagonist Hyponatremia: Overcorrection Acute treatment o Get Na+ up 4-6mEq/L Into temporary safe zone o Can push 3% Saline (100cc at a time) Chronic treatment o Loss of organic osmoles o Replace K+ first (if indicated) o Risk of demyelination (ODS, CPM) o 8-12mEq change in 24 hours (shoot for 4-6mEq) o 6-8mEq next 24 hours o Re-lower with D5W if needed Hyponatremia: Volume Overload Hyponatremia: Heart Failure CHF, Cirrhosis, Nephrosis Dilutional o Sodium Overload o But too much water Low sodium is an independent RF for o Rehospitalization (think 30 day rule!) o Other morbidity o Death Hypernatremia Hyponatremia Think Shrinkage Cellular Shrinkage

6 Hypernatremia Mostly Dehydration (water deficit) Sodium overload o Sea water ingestion o Salt tablet overdose (It actually has happened!) RF: Elderly, Ill, DI, AMS, Heat stroke, Diarrhea Give Free Water o D5W o Dilute IVFs in Abx o NG tube, PO fluids, etc Sodium Points Hyponatremia is imbalance of sodium and water molecules Vasopressin is often elevated Treatment: Add solute or Remove water Do NOT treat too aggressively Potassium Quiz Potassium Medications that affect potassium levels include: A. Loop diuretics B. Aldosterone blocking diuretics C. ACE inhibtitors D. Beta Blockers E. A, B, C but not D Potassium Mostly found intracellular (98%) Chiefly found in muscle, including cardiac Resting membrane potential of cells: o Ratio of intracellular:extracellular potassium o HypoK+ increases this potential in skeletal muscle o HypoK+ lowers this potential in cardiac muscle making cardiac cells more excitable o HyperK+ can also increase cardiac excitability Hypokalemia: Loss vs Movement Losses o Reduced intake (rare) o GI losses (lower GI mostly) o Renal o Sweat Translocation (increased activity of ATP pump) o Insulin (endogenous, exogenous) o Alkalosis (upper GI losses) o B-Adrenergic o Leukocytosis/Leukemia o Hypothermia

7 Urinary Potassium Losses Increased mineralocorticoid activity o Aldosterone (from adrenal gland) o Reabsorb Sodium, Release Potassium o Good for volume depletion as water follows salt High Distal sodium delivery o Diuretics! Non-reabsorbable Anions o Toluene o Penicillin Hypokalemia: Other Causes RTA: Stay tuned Hypomagnesemia o Increases urine K+ losses Ampho B o Increases cell wall permeability Genetic: Bartter s, Gitelman s, Liddle s Hypokalemia: Symptoms Typically only below 3.0 meq/l Weakness (Similar to hyperkalemia) Muscle cramps Rhabdo Cardiac arrhythmias Impaired renal bicarb reabsorption alkalosis Potassium Release Exercise U waves During strenuous activity, potassium is released from muscle cells Dilation of blood vessels, increase in blood flow to muscles Hypokalemia can blunt this response leading to micro-ischemia

8 Hypokalemia: Replacement Pain and phlebitis if IV >10mEq/hour Can be faster if central line Typically requires 10-50mEq per 0.1 Oral preparations: KCl is best absorbed K+ sparing diuretics Hyperkalemia: Etiology Reduced excretion Hypoaldosteronism Potassium loads (or K+ sparing diuretics) Metabolic Acidosis Medications o ACEi, ARB, B-Blockers, Spironolactone, Amiloride Pseudo-hyperkalemia (blood draws) Blood Draw Induced HyperK+ Cell lysis from small needle/shear stress K+ movement out of cell from fist pumping + tourniquet Thrombocytosis: K+ moves out of platelets after clotting Hereditary due to passive movement out of certain RBCs HyperK+ in CKD/ESRD Reduced renal excretion Metabolic Acidosis Meds (ACEi, ARB, B-Blocker, Aldactone) Reduced distal sodium delivery in patients with CHF, volume depletion Insulin deficiency Hyperkalemia: Cardiac Risk Hyperkalemia: Treatment Move K+ into cells (temporary) o Insulin (give with glucose) o B-agonists (It takes A LOT of albuterol) o Bicarbonate (Only works if acidotic) Stabilize the myocardium o Calcium gluconate, Calcium Chloride o (Requires central line but 3x more potent) o Antagonizes membrane action

9 Hyperkalemia: Treatment Diuretics: Minimally effective acutely Kayexelate: Sodium Polystyrene o Exchanges Na+ for K+ o Oral or rectal o Avoid in patients with ileus, GI surgery Zirconium (ZS-9): Not yet FDA approved o Exchanges Na+ and H+ for K+ Patiromer: Not yet FDA approved o Exchanges Ca++ for K+ Hyperkalemia Dialysis is ultimate treatment if needed Post-dialysis rebound o 0.5mEq/L min post HD o Greater in patients that received pre-hd Rx Small molecule Acid removal (bicarb bath) helps as well Renal Tubular Acidosis Type I is DISTAL Type II is Proximal Type III is non-existant Type IV is due to low mineralocorticoid Renal Acid Handling Acid comes from food, changes in respiration Kidney excretes excess hydrogen load daily Filtered bicarb is reclaimed by proximal tubule Ammonium (NH3 + H + NH4 + Distal RTA (Type I) Defect in Hydrogen ion excretion Impairs distal acidification Plasma bicarb usually quite low (10 meq/l) Typically leads to hypokalemia Improves with bicarb therapy Distal RTA (Type I) Familial Autoimmune disorders (Sjogrens, SLE, RA) Ampho B, Lithium Hypercalcemia (Sarcoid, Vit D, HyperPTH) Obstruction

10 Proximal RTA (Type I) Inability to reclaim filtered bicarbonate Carbonic anhydrase inhibitors Rarely causes much acidosis as Ammonium can be generated distally Serum bicarb modestly depressed Aminoglycosides, Heavy metals, Fanconi s Type 4 RTA Hyperkalemia Mineralocorticoid deficiency o Potassium and Hydrogen reabsorption o Sodium losses NSAIDs, CNI, Heparin, Bactrim Sickle Cell Anemia Occasionally DM Electrolytes and Blood Pressure HTN Quiz Which of the following is correct A. Low sodium diet always lowers blood pressure B. Low sodium diet when coupled with low chloride and high potassium lowers blood pressure more than low sodium alone C. Low potassium diet lowers blood pressure D. Sodium in the diet only affects Caucasians Salt Sensitivity HTN is rare in societies with low dietary sodium Low salt diet takes 4-5 weeks to work Modest effect overall o Greater effect in salt sensitive individuals Sodium leads to water retention Increases with Age AA > Caucasion Salt Sensitivity Sodium may inhibit vasodilation HCTZ certainly works initially to lower salt/water Longer term effects on vasoconstriction High sodium diet may limit effectiveness of ACEi, ARB and CCB Possible direct role in LVH

11 NaCl and Hypertension Sodium and Hypertension Primary hypertension (Essential hypertension Primarily in societies with average sodium intakes above 2.3 g/day Rare with average sodium less than 1.2 g/day Chloride appears to be a major component Hypertension Low sodium diet (<2 grams) help in salt sensitive individuals o African Americans > Whites o Na-K-2Cl in Loop Low renin HTN Higher potassium diet increases vasodilation Sodium-to-Potassium ratio assoc with HTN Chloride may increase HTN, so NaCl and KCl not optimal. Dietary Potassium is different Magnesium Quiz Magnesium Low Magnesium is often associated with: A. Hyperkalemia B. Changes in parathyroid hormone C. Hyponatremia D. Hypokalemia

12 Magnesium Thick Ascending Limb of LOH Both GI absorption and excretion Bulk of renal reabsorption is in the loop of Henle Paracellular route as opposed to directly through the TAL cells Unlike all other ion, no hormonal regulation Hypomagnesemia Torsade de Pointes Exacerbated by alkalosis, hypokalemia Neuromuscular complications o Hyperexcitability o Tetany o??migraines Cardiovascular complications o Widening of QRS, AV arrhythmias o Torsades de Pointes (Polymorphic VT) Hypomag: Etiology Renal or GI losses o Loop diuretics > Thiazides PPI: Omeprazole is biggest culprit Alcohol abuse o Very common, 30% o Defect in urinary excretion Abx: Aminoglycosides, Ampho B, Pentamadine Hypomag: Treatment Check K+ and Ca++ levels o Often associated with either hypok+ or hypoca++ o If HypoCa++, check PTH Oral replacement OK, but can cause diarrhea o Milk of Magnesia! (MgOH) o Mag Citrate o Slo Mag: Mag Chloride IV Mag Sulfate 2-4 grams is usually sufficient

13 Hypermagnesemia Rarely an issue other than OB patients Iatrogenic or other excess dosing o Decrease neuromuscular excitability o Used to reduce preterm labor Magnesium Enemas o Large amount of absorption in GI tract Disorders of Calcium & Phos Not going to address this issue in terms of advanced CKD and ESRD This is a HUGE topic covered elsewhere Inextricably linked in CKD but not necessarily linked in normal renal function Hormonal Involvement PTH and Vitamin D help control Calcium Levels Low PTH leads to low bone turnover Vitamin D (sun liver kidney) leads to increased GI calcium absorption Sarcoid, TB and Small Cell lung cancer o Ectopic Vitamin D o PTH related protein Calcium Hypocalcemia Calcium is bound to proteins o Hypoalbuminemia leads to low Calcium lab test o Correct Calcium for albumin or check ionized Ca++ Leads to Hypotension in ICU patients Parasthesias Leads to tetany at very low levels o Trousseau s sign: Hand contracture with BP cuff x 3 min o Chvostek s sign: Hyperexcitability of facial nerve

14 Hypocalcemia: Cardiac Effects Bradycardia Impaired contractility Narrowing of QRS and Prolongation of QT Hypocalcemia Effect on PTH Vitamin D Supplements Nutritional Vitamin D o 25-OH Vitamin D2: Ergocalciferol o 25-OH Vitmain D3: Cholecalciferol o Increase Calcium and Phos levels, Decrease PTH Activated Vitamin D o 1, 25-OH Vitamin D: Calcitriol (Rocaltrol) o Increase Calcium and Decrease PTH, may increase Phos Vitamin D Analogs Paracalcitol (Zemplar) Doxercalciferol (Hecterol) May improve PTH without causing as much hyperphosphatemia

15 Hypercalcemia: CHIMPANZEES Calcium Intake Hyperparathyroid Immobility (Iatrogenic) Milk Alkali Paget s Dz of Bone Acromegaly Neoplasia Zollinger-Ellison Excess Vitamin D Excess Vitamin A Sarcoidosis Hungry Bone Syndrome Post parathyroidectomy Bones avidly take up calcium Recalcitrant hypocalcemia Hypophosphatemia and Hypomagnesemia Hyperkalemia: Common but unclear etiology May need oral calcium, IV calcium, nutritional Vitamin D, activated Vitamin D