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POTASSIUM: An Almond Joy a day means an ER stay PowerPoint Presentation
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POTASSIUM: An Almond Joy a day means an ER stay

POTASSIUM: An Almond Joy a day means an ER stay

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POTASSIUM: An Almond Joy a day means an ER stay

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  1. POTASSIUM: An Almond Joy a day means an ER stay DAOUD K. ABU-HAMDAN MD IN MEMORY OF DALE H. SILLIX NEPHROLOGY DIVISION WSU/DMC

  2. Distribution of Body Potassium and External/Internal Balance External Balance Internal Balance Intake 100 mEq ICF 3500 mEq (140-150 mEq/L) (98%) Muscle 2700 mEq Plasma 17 mEq (3.5-5.5 mEq/L) (0.5%) ECF 70 mEq (3.5-5.5 mEq/L) (2%) Stool 10 mEq Liver 250 mEq Bone 300 mEq Erythrocytes 250 mEq Renal Excretion 90 mEq

  3. COMPOSITION OF BODY FLUID COMPARTMENTS COMPOSITION OF ECF AND ICF ECF ICF Na 141 10 K 4.1 120-150 Cl 113 3 HCO3 26 10 PHOSPHATE 2.0 140(ORGANIC) TOTAL BODY POTASSIUM IS 3500-4000mEq/L MOST IN SKELETAL MUSCLE 98% is in ICF volume 40-50 mmol/kg body wt 2% is in ECF volume 1 mmol/kg body wt

  4. MAINTENANCE OF K+ CELLULAR GRADIENT IS DEPENDENT ON Na+K+ATPase K=5mM K=150mM 2K+ ATP ADP 3Na+

  5. GENERATION OF THE RMP NaK ATPase CREATES A K GRADIENT PUMPS A NET 1/3 OF A POSITIVE CHARGE OUT OF CELLS Na CANNOT DIFFUSEINTO CELLS 3 Na+ ATP 2 K+ ADP K+ A- ANIONS CANNOT DIFFUSE OUT OF CELLS K+ Resting Membrane Potential (Em): sets stage for the action potential essential for neural and muscle function.

  6. K+c Em – K+e Action Potential of a myocardial cell and its relation to ion flow Millivolts Overshoot Plateau phase Repolarization + 20 Time 0 20 40 60 Threshold potential 80 Resting potential 90 Na+ K+ Intracellular fluid space K+ K+ Na+K+ ATPase Sarcolemma Na+ Ca++ Extracellular fluid space

  7. K+c Em – K+e Changes in the resting membrane potential during HYPERKALEMIA Millivolts Overshoot Plateau phase Repolarization + 20 Time 0 20 40 60 Threshold potential Resting potential 80 90 Na+ K+ Intracellular fluid space K+ K+ Na+K+ ATPase Sarcolemma Na+ Ca++ Extracellular fluid space

  8. K+c Em – K+e Changes in membrane resting potential in HYPOKALEMIA Millivolts Overshoot Plateau phase Repolarization + 20 Time 0 20 40 60 Threshold potential 80 90 Resting potential Na+ K+ Intracellular fluid space K+ K+ Na+K+ ATPase Sarcolemma Na+ Ca++ Extracellular fluid space

  9. K+ MOVES IN AND OUT OF CELLS IN RESPONSE TO TWO MAJOR STIMULI • CHANGES IN EXTRACELLULAR K • 80% of ingested K moved intracellular • Insulin • -adrenergic agonists • mineralocorticoids • CHANGES IN EXTRACELLULAR pH • Acidemia: organic < mineral acids(K+ out H+ in) • Alkalemia: H+ moves out, K+ in

  10. Factors influencing the distribution of K+ between the cells and the extracellular fluid Physiologic Na+ - K+ - ATPase Insulin Catecholamines Plasma K+ concentration Exercise Pathologic Chronic diseases Arterial pH Rate of cell breakdown Hyperosmolality

  11. PHYSIOLOGIC EFFECTS ON POTASSIUM • Na+ - K+ - ATPase • Insulin • Catecholamines • Plasma K+ concentration • Exercise

  12. EFFECTS OF SOME HORMONES ON DISTRIBUTION OF K+ BETWEEN ICF AND ECF

  13. INSULIN EFFECTS ON POTASSIUM LEVELS • An increase in plasma potassium stimulates insulin release by the pancreatic beta cell. Insulin, in turn, enhances cellular potassium uptake, returning plasma K+ toward normal, thus functioning in a feedback control fashion. • Insulin • May directly stimulate Na+K+ATPase in addition to effect on NHE • Independent of effect on glucose uptake • Insulin deficiency impairs cellular K+ uptake •  K+ stimulates insulin release • Primary physiologic effect is to aid in the disposition of a K+ load, not to regulate the baseline serum K+ concentration.

  14. CATECHOLAMINE EFFECT ON POTASSIUM LEVELS • adrenergic system;Increases cellular K+ uptake • 2 receptors • Promote K+ uptake by liver and muscle • Nonselective B blockers impair K+ uptake • Catecholamines as well as adrenergic nerve stimulation effect K+ • No regular role when K+ is in normal physiologic range • 2 agonists lower serum K+

  15. CATECHOLAMINE EFFECT ON POTASSIUM LEVELS • Alpha adrenergic system • Increase serum K+ by promoting hepatic release • May also modify muscle uptake • Alpha agonists --increase serum K+

  16. TOTAL K EFFECTS ON POTASSIUM LEVELS • Direct effect of intra/extracellular K+ levels on Na+K+ATPase • Increased serum K+ with exercise (opens ADP dependent K+ channels) • Usually modest and proportionate to the intensity of the exercise EXERCISE EFFECTS ON POTASSIUM LEVELS

  17. MUSCLE CELLS KIDNEY

  18. PATHOLOGICAL EFFECTS ON POTASSIUM • Arterial pH • Hyperosmolality • Rate of cell breakdown • Chronic diseases

  19. ACID BASE EFFECTS ON POTASSIUM LEVELS • Largest changes occur in acute metabolic acidosis induced by mineral acid. • Little with organic acid because anion is capable entering cell and K+ doesn't shift out. • Respiratory acidosis is associated with smaller changes as is respiratory alkalosis • Serum HC03- • Increases pH resulting in intracellular shift of K+ • Can modify K+ independent of pH

  20. BUFFERING OF H+ AND THE K+ SHIFT H+ HYPOXIA, NO INSULIN HCl or H2SO4 Cl- L-LACTATE -, -HB - H+ L-LACTATE -, -HB - H+ H-BUFFER+ H-BUFFER+ BUFFER BUFFER K SHIFTS OUT OF CELL IN MINERAL ACIDOSIS -NOT ORGANIC ACIDOSIS (WHICH ALSO STIMULATES INSULIN) K+ KIDNEY K EXCRETION ALTERED BY ALDOSTERONE, RENAL STATUS

  21. ACID BASE EFFECTS ON POTASSIUM LEVELS • Acute acidosis inhibits K+ secretion • Chronic acidosis can tubular flow rates and increase K+ urinary losses • Acute alkalosis stimulates K+ secretion • Ammoniagenesis • K+ depletion results in increased ammonia production. •  K+ inhibits renal ammoniagenesis •  ammonia production and ammonia excretion decrease K+ excretion

  22. POSM EFFECTS ON POTASSIUM LEVELS • K+ shift from intracellular to extracellular fluid • Solvent drag responsible for this shift

  23. ALDOSTERONE EFFECTS ON POTASSIUM LEVELS • Production and release stimulated by  K+ • Cause a shift of extracellular K+ to intracellular compartment • ALDOSTERONE AND SERUM POTASSIUM CONCENTRATION IN CONCERT ARE THE MAJOR PHYSIOLOGIC REGULATORS OF RENAL POTASSIUM SECRETION

  24. ALDOSTERONE EFFECTS ON POTASSIUM LEVELS • Major role in K+ homeostasis • High levels stimulate secretion • Low levels inhibit secretion • Receptors in cortical and medullary collecting tubule • Cortical collecting tubule is the primary target • Effect on principal cells • Stimulates each of the major transport steps in principal cells • Increases the # of open Na+ and K+ channels in the luminal membrane • Enhances Na+-K+ ATPase activity at the basolateral pump resulting in increased K+ movement into the cell raising intracellular K+ concentration and increasing the transport pool.

  25. MUSCLE CELLS KIDNEY

  26. Collecting tubules have selective Na channels in luminal surface (favored movement by Na levels low in cells and intracellular negativity). Pumped out of tubular cells by NaK-ATPase. Tubular lumen negatively charged and favors K movement into lumen by K channels. Aldo when combined with its receptor enhances Na reabsorption & K secretion via  # Na channels & # NaK-ATPase pumps. Amiloride & Triamterene close Na channels directly Spironolactone competes w/ aldosterone ANP inhibits Na reabsorption by closing Na channels

  27. ADDISON’S DISEASE A LACK OF ALDOSTERONE LEADS TO: INCREASED URINARY SODIUM LOSSES HYPERKALEMIA METABOLIC ACIDOSIS

  28. DISORDERS OF POTASSIUM LEVELS ARE LIKE A DRIVE-BY ATTACK. FINDING OUT WHAT STARTED IT IS AS/OR MORE IMPORTANT THAN PATCHING THE HOLES! CAUSE K DISORDER

  29. CAUSES OF HYPERKALEMIA • Pseudohyperkalemia • Redistribution • Increased input • Decreased excretion

  30. Pseudohyperkalemia • Mechanical trauma • Extracorporialpotssium shifts when WBC count is over 50.000, or platelets count over 1.000.000/mm3 • Plasma K+ normal vs.Serum K+ level high

  31. REDISTRIBUTION insulin deficiency  blockade acidosis(mineral acids, especially) hyperkalemic periodic paralysis digitalis intoxication (ATPase) hypertonicity( effective Posm) cell necrosis/exercise membrane depolarizing anesthetics (Succinylcholine)

  32. INCREASED INPUT endogenous hemolysis rhabdomyolysis exogenous salt substitutes (50-65mEq/tsp) urinary alkalinizing agent (Shohl’s, Polycitra) potassium penicillin

  33. DECREASED EXCRETION renal failure(acute or chronic) decreased circulating volume potassium sparing diuretics angiotensin converting enzyme inhibitors heparin(aldosterone syntetase) deficiency of adrenal steroids Addison’s disease Type 4 RTA (hyporeninemic hypoaldosteronism) tubular unresponsiveness to aldosterone sickle cell anemia systemic lupus erythematosus renal allograft obstructive uropathy

  34. SIGNS & SYMPTOMS OF HYPERKALEMIA • NEUROMUSCULAR • Weakness, ascending paralysis, flaccid paralysis, respiratory arrest • Dysphagia, ileus • CARDIOVASCULAR • Hypotension, syncope, cardiac arrest • ARRYTHMIAS • Bradycardia,heartblocks,asystole,ventricularfibrillation

  35. HYPERKALEMIA: MILD

  36. HYPERKALEMIA: MODERATE

  37. HYPERKALEMIA: SEVERE

  38. FACTORS THAT DECREASE URINARY POTASSIUM EXCRETION 1. LOW URINE FLOW RATES 2. DECREASED Na+ DELIVERY TO DISTAL TUBULE 3. DECREASED K+ STORES 4. DECREASED MINERALOCORTICOID ACTIVITY

  39. TREATMENT OF HYPERKALEMIA 1. CALCIUM 10mL OF 10%Ca GLUCONATE OVER 10 MINUTES 2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE 3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV 4.KAYEXALATE 30-60 G PO OR 60 G AS ENEMA 5.HEMODIALYSIS

  40. RESPONSE TO HYPERKALEMIA HYPERKALEMIA PANCREAS ADRENAL GLAND KIDNEY GLUCAGON EPINEPHRINE  Na-K ATPase  ALDOSTERONE INSULIN  CELLULAR K UPTAKEURINARY K EXCRETION

  41. TREATMENT OF HYPERKALEMIA 1. CALCIUM 10mL OF 10%Ca GLUCONATE OVER 10 MINUTES 2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE 3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV 4.KAYEXALATE 30-60 G PO OR 60 G AS ENEMA 5.HEMODIALYSIS

  42. TREATMENT OF HYPERKALEMIA 1. CALCIUM 10mL OF 10%Ca GLUCONATE OVER 10 MINUTES 2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE 3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV 4.KAYEXALATE 30-60 G PO OR 60 G AS ENEMA 5.HEMODIALYSIS

  43. HORMONES THAT SHIFT K+ INTO CELLS ACTIVATED BY 2ADRENERGICS 3 Na+ 2 K+ ELECTROGENIC ATP ADP Na+ K+ GLUCOSE ATP H+ ACTIVATED BY INSULIN ADP ACTIVATED BY INSULIN ELECTRONEUTRAL SYNTHESIS OF NEW NaK ATPase G6P2- (CREATES NEW ANIONS)