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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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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 ?
Function of K+ enzyme activity cellular electricity cellular osmolality acid-base balance . H+ K+ Na+
Part 1 General introduction 1.Potassium content and distribution Source: fruit, vegetable, coffee
50~55mmol/Kg×BW K+ K+ 3.5~5.5 mmol/L 140~160mmol/L ECF ICF 1.4% 90% Potassium content and distribution
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
(1) The control of K+ transfer between intra- & extracellular compartments The Na+/K+ATPase (membrane pump ) Permeability of ion channels
ICF ECF K+ pump channel Insulin, β-adrenergic agonist, ADS, [K+]s↓, exercise, pH ↓, ECFosmolanity ↑ K+ shifts between ICF and ECF
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
Part 2 Hypokalemia Defined as [k+]s < 3.5 mmol/L may or may not be associated with K deficit?
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+ ↓
2.Effect on body Neuromuscular irritability ↓ hyperpolarization impeding
~ Effects on Neuromuscular Excitability +35 0 Millivolts -60 Threshold -90 Milliseconds Nernst equation:Em∝ -60lg[K+]icf / [K+]ecf (mv)
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
RMP more negative than normal [K+]i / [K+]e ↑ Acute Hypokalemia ( Em - Et ↑) hyperdepolarization block, excitability↓ muscle weakness, flaccid paralysis, smooth muscle symptoms
(2) Effect on heart Excitability ↑ ---- Et-Em ↓ Conductivity ↓ ---- Em ↓, phase 0, rapid Na+ inward flow ↓ Automaticity ↑ ---- slow K+ outward flow ↓ Contractility ↑ ---- Ca2+ inward flow ↑
normal low [K+]e a v Threshold potential repolarization normal prolonged Effects of low [K+]s on the AP of the myocardial cell
Typical feature of ECG during hypokalemia < 2.5 mmol/L + U wave(ECG) aura sign of cardiac asystole
due to increased excitability shortened ERP (effective refractory period ) prolonged SNP (supranormal period) increased automaticity decreased conductivity Cardiac arrhythmias
(3) Miscellaneous effect Metabolic alkalosis Paradoxical acidic urine
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 !)
Part 3 Hyperkalemia Defined as [k+]s >5.5 mmol/L Except false phenomena?
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
2. Effect on body Neuromuscular irritability ↑, then↓ ( Partial depolarization? Excitation ↑) Depolarization impeding
(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 ↓
Typical feature of ECG during hyperkalemia > 7.5mmol/L + tent-like T wave aura sign of cardiac asystole
absent "P ", tall tented "T" and widening of QRS ECG K+ 7.8 mmol/L
(3)Effect on acid and base Metabolic acidosis Paradoxical alkaline urine ( due to K+↑or ? )
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