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Potassium Homeostasis & Its disorders By Dr. Mohammad El-Tahlawi.

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Presentation on theme: "Potassium Homeostasis & Its disorders By Dr. Mohammad El-Tahlawi."— Presentation transcript:

1 Potassium Homeostasis & Its disorders By Dr. Mohammad El-Tahlawi

2 Objectives Potassium homeostasis Hypokalamia Definition Definition Causes Causes Effects Effects Diagnosis Diagnosis Treatment Treatment

3 POTASSIUM Potassium play an important role in: 1-Electerophysiology of cell membrane for all cells in which polarization- for all cells in which polarization- depolaization cycles are functionally depolaization cycles are functionally relevant(cardiac and neuromuscular cells). relevant(cardiac and neuromuscular cells). 2-Carbohydrates and protien synthesis

4 POTASIUM DISTRIBUTION In 70 kg Intracellular 98% 3430 meq K content = 50 meq/kg Total body K = 3500 meq Extracellular 2% 70 meq Plasma 20% 15 meq Na-K ATPase

5 Intracellular K=140 meq/L Extra cellular K=4 meq/L ( meq) K level in meq / L

6 intracellular K deficit BY meq Decrease in plasma K from meq/L

7 intracellular K deficit BY meq Decrease in plasma K from meq/L

8 Plasma K concentration Correlates poorly with the total body k deficit poorly with the total body k deficit

9 Plasma potassium concentration Potassium Intake Intercompartmental distribution Potassium Excretion

10 Dietary K intake = 80 meq/day Excretion = 70 meq/day (urine). Excretion = 70 meq/day (urine). = 10 meq/day (GIT). = 10 meq/day (GIT).

11 Regulation of K excretion The major determinant of urinary K excretion Extra cellular K Aldesterone level Tubular flow rate

12 Intercompartmental shift of Potassium 1- Extracellular pH. 2- Circulating insulin level. 3- Circulating catecholamine activity. 4- Plasma osmolality. 5- Hypothermia. 6- Exercise.

13 pH K 0.6 meq/L every.01 Change in pH Acidosis Alkalosis Insulin Na-K ATPase Sympathetic activity (Na-K ATPase) B2-agonist B2-blokade CELL Plasma osmolality increase K 0.6meq/L per increase10mosm/L Hypothermia Rewarming

14 HYPOKALEMIA

15 HYPOKALAEMIA (K ion less than 3.5 meq/L) Causes : 1-Intercompartmental shift of K. 1-Intercompartmental shift of K. 2-Increase k loss. 2-Increase k loss. 3-Inadequate k intake. 3-Inadequate k intake.

16 Causes of hypokalamia Intercompartmental shift of K: Alkalosis Alkalosis Insulin administration Insulin administration B2 adrenergic agonist B2 adrenergic agonist Hypothermia Hypothermia Treatment of megaloplastic anaemia Treatment of megaloplastic anaemia Periodic paralasis Periodic paralasis Transfusion of frozen blood Transfusion of frozen blood

17 Causes of hypokalamia Increase K losses (Renal or extrarenal) Renal : Diuretics Increase mineralocorticiod activity Renal tubular acidosis KetoacidosisHypomagesaemia Urinary diversion with long ileal loop Carbinecillin and Amphotericin B

18 Causes of hypokalamia Extrarenal : GIT : Diarrhea,Vomiting,Fistula, GIT : Diarrhea,Vomiting,Fistula, Laxative abuse,Urinary diversion. Laxative abuse,Urinary diversion. Sweet Sweet Dialysis Dialysis Decrease K intake

19 Effects of hypokalemia Most of the patients are asymptomatic until Most of the patients are asymptomatic until K level below 3 meq/L. K level below 3 meq/L. Cariovascular effects are most prominent Cariovascular effects are most prominent

20 Effects of hypokalamia Cardiovascular ECG changes ECG changes Dysrhythmia Dysrhythmia Myocardial dysfunction Myocardial dysfunction Myocardial fibrosis Myocardial fibrosis Orthostatic hypotension Orthostatic hypotension Increase digitalis toxicity Increase digitalis toxicity

21 Effects of hypokalamia Cardiovascular ECG changes ECG changes T wave flattening Prominent U wave ST segment depresion Increase P wave amplitude Prolongation of PR interval Prominent U-wave Flat T-wave Depressed ST-segment Normal Decreasing Serum K +

22 Effects of hypokalamia Neuromuscular Skletal ms. Weakness up to respiratory failure. Skletal ms. Weakness up to respiratory failure. Tetany Tetany Rhabdomyolysis Rhabdomyolysis Ileus, Urine retention Ileus, Urine retentionRenal Polyuria Polyuria Increase amonium production Increase amonium production Increase HCO3 reabsorption Increase HCO3 reabsorption Increase Na retension Increase Na retension Increased renin secretion increase AngII thirst Increased renin secretion increase AngII thirst

23 Effects of hypokalamia Metabolic Decrease insulin secretion Decrease insulin secretion Decrease growth hormone secretion Decrease growth hormone secretion Decrease aldesterone secretion Decrease aldesterone secretionHormonal Negative nitrogen balance Negative nitrogen balance Encephalopathy in liver disease Encephalopathy in liver disease

24 Approach to diagnosis

25 Hypokalemia Urine K Less than 30 meq/L More than 30meq/L Diarrhea Urine Chloride Less than 15meq/LMore than 15meq/L NG Drainage Alkalosis Diuretics Mg depletion

26 Treatment of hypokalemia The goal of therapy: Is to remove the patient from immediate Is to remove the patient from immediate danger and not necessarily to correct the danger and not necessarily to correct the entire K deficit. entire K deficit. Firstly concern : Any condition that promotes transcellular Any condition that promotes transcellular K shift. K shift.

27 Potassium replacement Oral replacement with KcL solution is generally safe(60-80 meq/d) IV replacement :(Remember ) Serious cardiac manifestation. Serious cardiac manifestation. Peripheral line not exceed 8 meq/h. Peripheral line not exceed 8 meq/h. More than 8meq/h, centeral line is indicated. More than 8meq/h, centeral line is indicated. Dextrose containing solution should be avoided. Dextrose containing solution should be avoided. ECG monitoring is mandatory in high rate infusion. ECG monitoring is mandatory in high rate infusion.

28 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. 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)

29 Potassium replacement Deficit =(3.5 - acutal serum K ) x 0.4 BW Maintenence = 1 meq / kg BW / day

30 Potassium replacement Infusion rate (pripheral line) Not exceed 8 meq / h Not exceed 8 meq / h Infusion rate (centeral line) Standard method = 20 meq KcL in 100 ml saline/h Standard method = 20 meq KcL in 100 ml saline/h Maximum rate (serum k less than 1.5 meq/L) Maximum rate (serum k less than 1.5 meq/L) We need peripheral line We need peripheral line = 40 meq kcL / h = 40 meq kcL / h = ( ½ BW meq/h) = ( ½ BW meq/h)

31 Practical approach 1. If K level <2 mEq/L, deficit= 0.4 x wt(normal – measured K) we can give up to 0.5 mEq/kg/hr. 2. If K level reaches 2.5 mEq/L, slowly corrects K by giving 10 mEq/hr. 3. Add the daily intake (1 mEq/kg)

32 It is advisable to give K salts into large but not central vein. It is advisable to give K salts into large but not central vein. Potassium products: Potassium products: 1. IV preparations 2. Oral: 15ml= 40 mEq (if conc. Of KCl in sol. is 10%) 3. Natural sources: -Orange: one orange=300mg K -Orange: one orange=300mg K one litre juice=2.8gm K one litre juice=2.8gm K -Bananas: one piece= 750mg K -Bananas: one piece= 750mg K K therapy in pediatrics: 1-3mEq/kg/every 1mEq decrease in K level with max. 3mEq/kg/day K therapy in pediatrics: 1-3mEq/kg/every 1mEq decrease in K level with max. 3mEq/kg/day

33 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

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35 CONCLUSION Potassium has important role to vital body function. Plasma K concentration is a function of relationship between entry, the in tercompartemental distribution and excretion of K. Hypokalemia : serum K less thd 3.5meq/L Hypokalemia : serum K less thd 3.5meq/L Cause : Decrease intake, Losses and Intercompartemental Cause : Decrease intake, Losses and Intercompartemental shift. shift. Effects : Cardiovascular,Neuromuscular,renal,Hormonal Effects : Cardiovascular,Neuromuscular,renal,Hormonal and metabolic. and metabolic. Diagnosis. Diagnosis. Treatment :Goals, replacement and response Treatment :Goals, replacement and response

36 Hyperkalemia

37 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) 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)

38 Hyperkalemia: Disorders of External Balance Excessive K + intake Distal tubular flow Mineralocorticoid deficiency Acute & chronic renal failure Distal tubular dysfunction Pseudo hyperkalemia

39 Pseudohyperkalemia Pseudohyperkalemia Movement of K+ out of cells during or after blood drawing Movement of K+ out of cells during or after blood drawing Hemolysis Hemolysis Fist clenching (local exercise effect) Fist clenching (local exercise effect) Marked leukocytosis Marked leukocytosis

40 Hyperkalemia: Disorders of External Balance Excessive Potassium Intake Oral or Parenteral Intake Oral or Parenteral Intake K pencillin in high doses K pencillin in high doses Stored blood Stored blood

41 Hyperkalemia: Disorders of External Balance Decreased Renal Excretion Acute and Chronic Renal Failure Decreased Distal Tubular Flow Volume depletion Volume depletion Decreased effective arterial blood volume (CHF, cirrhosis) Decreased effective arterial blood volume (CHF, cirrhosis) Drugs altering glomerular hemodynamics with a decrease in GFR (NSAIDs, ACE inhibitors, ARBs) Drugs altering glomerular hemodynamics with a decrease in GFR (NSAIDs, ACE inhibitors, ARBs) Mineralocorticoid Deficiency Combined glucocorticoid and mineralocorticoid (adrenal insufficiency) Combined glucocorticoid and mineralocorticoid (adrenal insufficiency) Hyporeninemic hypoaldosteronism (diabetes mellitus) Hyporeninemic hypoaldosteronism (diabetes mellitus) Drug-induced (ACE inhibitors, ARBs) Drug-induced (ACE inhibitors, ARBs) Distal Tubular Dysfunction Disorders causing impaired renal tubular function with hyporesponsiveness to aldosterone (interstitial nephritis) Disorders causing impaired renal tubular function with hyporesponsiveness to aldosterone (interstitial nephritis) Potassium-sparing diuretics (amiloride, triamterene, spironolactone) Potassium-sparing diuretics (amiloride, triamterene, spironolactone)

42 Hyperkalemia: Disorders of Internal Balance –Insulin deficiency – 2 -Adrenergic blockade –Hypertonicity –Acidemia –Cell lysis

43 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

44 EKG Manifestations of Hyperkalemia Wide QRSComplex Shortened QT Interval Prolonged PR Interval Further Widening ofQRS Complex Absent P-Wave Sine-Wave Morphology (e.g. Ventricular Tachycardia) Peaked T-wave Normal Increasing Serum K +

45 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

46 Practical approach Mild cases: K<6.5mEq/L causal management Mild cases: K<6.5mEq/L causal management Moderate cases: K=6.5-8mEq/L: Moderate cases: K=6.5-8mEq/L: -glucose infusion. -glucose infusion. -glucose insulin infusion. -glucose insulin infusion. -NaHCO3 -NaHCO3 Severe cases: K>8mEq/Lcalcium injection Severe cases: K>8mEq/Lcalcium injection

47 Emergency measures: Emergency measures: -Dextrose 10%: ml over 30min ml over 30min ml over the next few hours ml 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.

48 Definitive measures: Definitive measures: Key oxalate (Na polysterene) 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. Every gm resin combines with 1mEq K in GIT. Dialysis : in cases of RF. Dialysis : in cases of RF.

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50 Potassium Disorders Normal homeostasis Normal homeostasis Hypokalemia Hypokalemia –Etiologic factors –Algorithm for diagnosis Hyperkalemia Hyperkalemia –Etiologic factors –Algorithm for diagnosis


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