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Zhao Mingyao BMC.ZZU.

Disorder of potassium metabolism. Zhao Mingyao BMC.ZZU. Disorder of potassium metabolism [K + ]s mmol/L Status 3.5 ~ 5.5 Normal level < 3.5 Hypokalemia > 5.5 Hyperkalemia. ?.

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Zhao Mingyao BMC.ZZU.

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  1. Disorder of potassium metabolism Zhao Mingyao BMC.ZZU.

  2. Disorder of potassium metabolism [K+]s mmol/L Status 3.5 ~ 5.5 Normal level < 3.5 Hypokalemia > 5.5 Hyperkalemia ?

  3. Function of K+ enzyme activity cellular electricity cellular osmolality acid-base balance . H+ K+ Na+

  4. Part 1 General introduction 1.Potassium content and distribution Source: fruit, vegetable, coffee

  5. 50~55mmol/Kg×BW K+ K+ 3.5~5.5 mmol/L 140~160mmol/L ECF ICF 1.4% 90% Potassium content and distribution

  6. 2.Maintenance of K+ balance

  7. intake ICF ECF K+ K+ pump 3.5~5.5 mmol/L channel 140~160mmol/L Direction of K+ shifting kidney GI tract 90% Skin? 10% Maintenance of K+ balance

  8. (1) The control of K+ transfer between intra- & extracellular compartments The Na+/K+ATPase (membrane pump ) Permeability of ion channels

  9. ICF ECF K+ pump channel Insulin, β-adrenergic agonist, ADS, [K+]s↓, exercise, pH ↓, ECFosmolanity ↑ K+ shifts between ICF and ECF

  10. (2) Regulation of renal K+ excretion ?

  11. tubular lumen tubular cell ICF K+ K+ Na+-K+ ATPase Na+ Na+ - - - - K+ ADS, guanylin, [K+]s, urinary flow rate, pH, distal delivery of sodium, impermeable anion kidney 90% Regulation of renal K+ excretion

  12. Part 2 Hypokalemia Defined as [k+]s < 3.5 mmol/L may or may not be associated with K deficit?

  13. Causes (1)K+ Intake↓ (2)K+ redistribution pH↑, some drugs, Familial Hypokalemic Periodic Paralysis (3)K+ loss infant －by gastrointestinal tract adult － by kidney: diuretics, renal tubular acidosis, ADS ↑, Mg2+ ↓

  14. 2.Effect on body Neuromuscular irritability ↓ hyperpolarization impeding

  15. ~ Effects on Neuromuscular Excitability +35 0 Millivolts -60 Threshold -90 Milliseconds Nernst equation：Em∝ -60lg[K+]icf / [K+]ecf (mv)

  16. 30 Action potential (AP) 0 -30 -60 TMP RMP -90 -120 Normal Low [K+] High [K+] mv The effects of [K+]s concentration on cellular membrane excitability

  17. RMP more negative than normal [K+]i / [K+]e ↑ Acute Hypokalemia ( Em - Et ↑) hyperdepolarization block, excitability↓ muscle weakness, flaccid paralysis, smooth muscle symptoms

  18. (2) Effect on heart Excitability ↑ ---- Et-Em ↓ Conductivity ↓ ---- Em ↓, phase 0, rapid Na+ inward flow ↓ Automaticity ↑ ---- slow K+ outward flow ↓ Contractility ↑ ---- Ca2+ inward flow ↑

  19. normal low [K+]e a v Threshold potential repolarization normal prolonged Effects of low [K+]s on the AP of the myocardial cell

  20. Typical feature of ECG during hypokalemia < 2.5 mmol/L + U wave(ECG) aura sign of cardiac asystole

  21. due to increased excitability shortened ERP (effective refractory period ) prolonged SNP (supranormal period) increased automaticity decreased conductivity Cardiac arrhythmias

  22. The conducting system of the heart

  23. (3) Miscellaneous effect Metabolic alkalosis Paradoxical acidic urine

  24. 3. Principle of prevention & treatment oral slow: ≤10mmol of K/h low concentration: KCl≤40mmol/L limited total amount/d: 40~120mmol K+/day urine existence (iv instillation: Never inject !)

  25. Part 3 Hyperkalemia Defined as [k+]s >5.5 mmol/L Except false phenomena?

  26. 1.Causes (1)K+ Intake ↑ (2)K+ shift into ECF ↑ pH ↓, some drugs (β-R antagonist), cell injury, familial hyperkalemic periodic paralysis (3)Renal K+ excretion ↓ GFR ↓ ↓, ADS ↓(Addison`s disease), diuretics with blocking ADS

  27. 2. Effect on body Neuromuscular irritability ↑, then↓ ( Partial depolarization? Excitation ↑) Depolarization impeding

  28. (2) Effect on heart Excitability ↑, then↓ ---- Et-Em ↓, closing Conductivity ↓---- Em, phase 0, rapid Na+ inward flow ↓ Automaticity ↓---- slow K+ outward flow↑ Contractility ↓---- Ca2+ inward flow ↓

  29. Typical feature of ECG during hyperkalemia > 7.5mmol/L + tent-like T wave aura sign of cardiac asystole

  30.  absent "P ", tall tented "T" and widening of QRS ECG K+ 7.8 mmol/L

  31. （3）Effect on acid and base Metabolic acidosis Paradoxical alkaline urine ( due to K+↑or ? )

  32. 3. Principle of prevention and treatment ①Limit origination: intake ↓ ② Sodium and calcium salt opposite the toxicity of hyperkalemia ③ Shifted into cell (transient, such as GI fluid, pH ↑) ④ Remove K+ out of body Na+-K+ cation exchange resin enema hemodialysis

  33. THANKS!

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