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Potassium Homeostasis & Its disorders

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Presentation on theme: "Potassium Homeostasis & Its disorders"— Presentation transcript:

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

2 Objectives Potassium homeostasis Hypokalamia Definition Causes Effects
Diagnosis Treatment

3 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

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

5 K level in meq / L K=140 meq/L Extra cellular K=4 meq/L (3.5-4.5meq)
Intracellular K=140 meq/L Extra cellular K=4 meq/L ( meq)

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

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

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

9 Plasma potassium concentration
Intake Intercompartmental distribution Potassium Excretion

10 Dietary K intake = 80 meq/day Excretion = 70 meq/day (urine).
= 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 Insulin Hypothermia Rewarming Sympathetic activity
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


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

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

17 Increase K losses (Renal or extrarenal) Renal:
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 Prim and Sec hyper alderostenism

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

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

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

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

22 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

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

24 Approach to diagnosis

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

26 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.

27 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.

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. 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 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)

31 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)

32 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

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

34 ?

35 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

36 Hyperkalemia

37 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 Acute & chronic renal failure Pseudo hyperkalemia  Distal tubular flow Distal tubular dysfunction Mineralocorticoid deficiency

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

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

41 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)

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 QRS Complex Shortened QT Interval Prolonged PR Interval Further Widening of QRS 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
Moderate cases: K=6.5-8mEq/L: -glucose infusion. -glucose insulin infusion. -NaHCO3 Severe cases: K>8mEq/L→calcium injection

47 Emergency measures: -Dextrose 10%: ml over 30min. 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: 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.

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

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