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Potassium Homeostasis & Its disorders. By. Dr. Mohammad El-Tahlawi. Objectives. Potassium homeostasis Hypokalamia Definition Causes Effects Diagnosis Treatment. POTASSIUM. Potassium play an important role in: 1-Electerophysiology of cell membrane
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Potassium Homeostasis&Its disorders By Dr. Mohammad El-Tahlawi
Objectives Potassium homeostasis Hypokalamia Definition Causes Effects Diagnosis Treatment
POTASSIUM Potassium play an important role in: 1-Electerophysiology of cell membrane for all cells in which polarization- depolaization cycles are functionally relevant(cardiac and neuromuscular cells). 2-Carbohydrates and protien synthesis
POTASIUM DISTRIBUTION Extracellular 2% 70 meq Intracellular98% 3430 meq Plasma 20% 15 meq Na-K ATPase K content = 50 meq/kg In 70 kg Total body K = 3500 meq
K level in meq / L Intracellular K=140 meq/L Extracellular K=4 meq/L (3.5-4.5meq)
Decrease in plasma K from 4 - 3 meq/L intracellular K deficit BY 100 - 200 meq
Decrease in plasma K from 3 - 2 meq/L intracellular K deficit BY 200 - 400 meq
Plasma K concentration Correlates poorly with the total body k deficit
Plasma potassium concentration Potassium Intake Intercompartmental distribution Potassium Excretion
Dietary K intake = 80 meq/day Excretion = 70 meq/day (urine). = 10 meq/day (GIT).
Regulation of K excretion The major determinant of urinary K excretion Extra cellular K Aldesterone level Tubular flow rate
Intercompartmental shift of Potassium 1- Extracellular pH. 2- Circulating insulin level. 3- Circulating catecholamine activity. 4- Plasma osmolality. 5- Hypothermia. 6- Exercise.
pH K 0.6 meq/L every.01 Change in pH Insulin Na-K ATPase Acidosis Alkalosis Hypothermia Rewarming CELL B2-agonist B2-blokade Sympathetic activity (Na-K ATPase) Plasma osmolality increase K 0.6meq/L per increase10mosm/L
HYPOKALAEMIA (K ion less than 3.5 meq/L) Causes: 1-Intercompartmental shift of K. 2-Increase k loss. 3-Inadequate k intake.
Causes of hypokalamia Intercompartmental shift of K: Alkalosis Insulin administration B2 adrenergic agonist Hypothermia Treatment of megaloplastic anaemia Periodic paralasis Transfusion of frozen blood
Causes of hypokalamia Increase K losses (Renal or extrarenal) Renal: Diuretics Increase mineralocorticiod activity Renal tubular acidosis Ketoacidosis Hypomagesaemia Urinary diversion with long ileal loop Carbinecillin and Amphotericin B
Causes of hypokalamia Extrarenal: GIT : Diarrhea,Vomiting,Fistula, Laxative abuse,Urinary diversion. Sweet Dialysis Decrease K intake
Effects of hypokalemia Most of the patients are asymptomatic until K level below 3 meq/L. Cariovascular effects are most prominent
Effects of hypokalamia Cardiovascular ECG changes Dysrhythmia Myocardial dysfunction Myocardial fibrosis Orthostatic hypotension Increase digitalis toxicity
Normal + Flat T - wave Decreasing Serum K Prominent U - wave Depressed ST - segment Effects of hypokalamia Cardiovascular ECG changes T wave flattening Prominent U wave ST segment depresion Increase P wave amplitude Prolongation of PR interval
Effects of hypokalamia Neuromuscular Skletal ms. Weakness up to respiratory failure. Tetany Rhabdomyolysis Ileus , Urine retention Renal Polyuria Increase amonium production Increase HCO3 reabsorption Increase Na retension Increased renin secretion→ increase AngII→ thirst
Effects of hypokalamia Metabolic Decrease insulin secretion Decrease growth hormone secretion Decrease aldesterone secretion Hormonal Negative nitrogen balance Encephalopathy in liver disease
Hypokalemia Urine K Less than 30 meq/L More than 30meq/L Urine Chloride Diarrhea Less than 15meq/L More than 15meq/L NGDrainage Diuretics Alkalosis Mgdepletion
Treatment of hypokalemia The goal of therapy: Is to remove the patient from immediate danger and not necessarily to correct the entire K deficit. Firstly concern : Any condition that promotes transcellular K shift.
Potassium replacement Oral replacement with KcL solution is generally safe(60-80 meq/d) IV replacement :(Remember ) Serious cardiac manifestation. Peripheral line not exceed 8 meq/h. More than 8meq/h, centeral line is indicated. Dextrose containing solution should be avoided. ECG monitoring is mandatory in high rate infusion.
Potassium replacement Solutions Potassium chloride and potassium phosphate Kcl: is available in 2meq/mL (5ml) is of choice with metabolic alkalosis as it corrects chloride shifts. Osmolality = 4000 mosm/kgH2O K phosphate: is of choice with coexisting hypophatemia (e.g DKA)
Potassium replacement Deficit =(3.5 - acutal serum K ) x 0.4 BW Maintenence = 1 meq / kg BW / day
Potassium replacement Infusion rate (pripheral line) Not exceed 8 meq / h Infusion rate (centeral line) Standard method = 20 meq KcL in 100 ml saline/h Maximum rate (serum k less than 1.5 meq/L) We need peripheral line = 40 meq kcL / h = ( ½ BW meq/h)
Practical approach • If K level <2 mEq/L, deficit= 0.4 x wt(normal – measured K) we can give up to 0.5 mEq/kg/hr. • If K level reaches 2.5 mEq/L, slowly corrects K by giving 10 mEq/hr. • Add the daily intake (1 mEq/kg)
It is advisable to give K salts into large but not central vein. • Potassium products: • IV preparations • Oral: 15ml= 40 mEq (if conc. Of KCl in sol. is 10%) • Natural sources: -Orange: one orange=300mg K one litre juice=2.8gm K -Bananas: one piece= 750mg K • K therapy in pediatrics: 1-3mEq/kg/every 1mEq decrease in K level with max. 3mEq/kg/day
Response to the treatment At first The serum K may be slow to rise particularly if K losses are ongoing Full replacement usually takes few days. If there is refractory hypokalemia check magnessium level
CONCLUSION Potassium has important role to vital body function . Plasma K concentration is a function of relationship between entry, the intercompartemental distribution and excretion of K. Hypokalemia : serum K less thd 3.5meq/L Cause : Decrease intake, Losses and Intercompartemental shift. Effects : Cardiovascular,Neuromuscular,renal,Hormonal and metabolic. Diagnosis . Treatment :Goals, replacement and response
Hyperkalemia Plasma [K+] > 5.0 Hyperkalemia may be the result of disturbances in external balance (total body K+ excess) or in internal balance (shift of K+ from intracellular to extracellular compartments)
Excessive K+ intake Acute & chronic renal failure Distal tubular flow Mineralocorticoid deficiency Distal tubular dysfunction Hyperkalemia: Disorders of External Balance Pseudo hyperkalemia
Pseudohyperkalemia • Movement of K+ out of cells during or after blood drawing • Hemolysis • Fist clenching (local exercise effect) • Marked leukocytosis
Hyperkalemia: Disorders of External Balance Excessive Potassium Intake • Oral or Parenteral Intake • K pencillin in high doses • Stored blood
Hyperkalemia: Disorders of External Balance Decreased Renal Excretion Acute and Chronic Renal Failure Decreased Distal Tubular Flow • Volume depletion • Decreased effective arterial blood volume (CHF, cirrhosis) • Drugs altering glomerular hemodynamics with a decrease in GFR (NSAIDs, ACE inhibitors, ARBs) Mineralocorticoid Deficiency • Combined glucocorticoid and mineralocorticoid (adrenal insufficiency) • Hyporeninemic hypoaldosteronism (diabetes mellitus) • Drug-induced (ACE inhibitors, ARBs) Distal Tubular Dysfunction • Disorders causing impaired renal tubular function with hyporesponsiveness to aldosterone (interstitial nephritis) • Potassium-sparing diuretics (amiloride, triamterene, spironolactone)
Hyperkalemia: Disorders of Internal Balance • Insulin deficiency • 2-Adrenergic blockade • Hypertonicity • Acidemia • Cell lysis
Clinical Manifestations of Hyperkalemia Clinical manifestations result primarily from the depolarization of resting cell membrane potential in myocytes and neurons Prolonged depolarization decreases membrane Na+ permeability through the inactivation of voltage-sensitive Na+ channels producing a reduction in membrane excitability Cardiac toxicity • EKG changes • Cardiac conduction defects • Arrhythmias Neuromuscular changes • Ascending weakness, ileus
Normal + Peaked T - wave Increasing Serum K Wide QRS Complex Shortened QT Interval Prolonged PR Interval Further Widening of QRS Complex Absent P - Wave Sine - Wave Morphology (e.g. Ventricular Tachycardia) EKG Manifestations of Hyperkalemia
Medical Treatment of Hyperkalemia Membrane Stabilization • IV calcium Internal Redistribution • IV insulin (+ glucose) • -adrenergic agonist (albuterol inhaled) Enhanced Elimination • Kayexalate (sodium polystyrene sulfonate) ion exchange resin • Loop diuretic • Hemodialysis
Practical approach • Mild cases: K<6.5mEq/L→causal management • Moderate cases: K=6.5-8mEq/L: -glucose infusion. -glucose insulin infusion. -NaHCO3 • Severe cases: K>8mEq/L→calcium injection
Emergency measures: -Dextrose 10%: 200-500ml over 30min. 500-1000ml over the next few hours. -Dextrose/insulin infusion Insulin: 0.1U/kg then 1U/kg/hr (add minimum 2-3 glucose/U insulin). Onset of effect is 1-5 min. -NaHCO3: 150mEq over several minutes ?increased pH causes K shift into cells.
Definitive measures: • Key oxalate (Na polysterene) -Oral: 15-30g 2-4 times/day + sorbitol 20-25% (50ml/15gm resin) The resin induces diarrhea and leads to K loss. -Retention enema: 50gm in 200ml sorbitol 25%. Every gm resin combines with 1mEq K in GIT. • Dialysis : in cases of RF.
Potassium Disorders • Normal homeostasis • Hypokalemia • Etiologic factors • Algorithm for diagnosis • Hyperkalemia • Etiologic factors • Algorithm for diagnosis