Chapter4(2) Potassium Disorders 1.Normal potassium metabolism: (1) Balance of potassium intake and excretion : K + intake : 50-200mmol/day from vegetable and fruit K + excretion : kidney:approximately 90% of dietary potassium
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Chapter4(2) Potassium Disorders
1.Normal potassium metabolism: (1) Balance of potassium intake and excretion:K+intake : 50-200mmol/day from vegetable and fruit
kidney:approximately 90% of dietary potassium
GI tract: only about 10 %
Major organ of excretion potassium: kidney Regulative site: renal distal tubuleHormone of major regulated: ADS
Only the potassium output remains equivalent to intake every 24 hours, then to ensureTotal body potassium 50-55mmol/kg B.W
Distal and collecting tubule secretion
1 Na+-K+ ATPase
2 Electrochemical gradient of across the apical membrane
3 permeability of the apical membrane
Factors of affecting renal handling potassium
Aldosterone Activates Na+-K+ ATPase Sodium channels in the luminal membrane Na+reabsorption
Potassium channels in the luminal membrane
Intracellular potassium content Secretion
Urine flow rate Secretion
Distal delivery of sodium Secretion
Acid-base balance: Acute acidosis Secretion
(2) Balance of potassium distribution:
It is depended Na+—K+—ATPase on the cellular membrane(pump leak).
consumption of1 ATP→pumping3 Na+ out offand2 K+ intothe cell
Total body potassium approximately 98% in ICF50-55mmol/kg B.W approximately 2% inECF
ICF (3500mmol ): 150-160mmol/L
ECF (70 mmol ): serum potassium 3.5-5.5mmol/L
Influence factor of potassium distribution between ICF and ECF(1)Function of the Na+-K+ pump: anoxia → Na+-K+ ATPase ↓[K+]e: Na+-K+ ATPase ↑
(2)Influence of acid-base balance: H+-K+ exchanges across the cellular menbrane Acidosis company with hyperkalemia Alkalosis company with hypokalemia
(3) Influence of hormone: Insulin----K+ into cell Aldosterone----increases excretion of K+Catecholamines : -R net influx into the cells
-R plasma K+
(4) Rate of cell breakdown: crush syndrome
(5) Plasma osmolality:
The relationship between serum potassium and total body potassium
The clinical signs and symptoms are major depended on concentration ofserum potassium.
(2)Causes:a. Inadequate intake: Inability to eat; Fast and anorexia; Administration of K+ -free parenteral solutionsb. Excessive losses:Gastrointestinal losses – Vomiting; Diarrhea; suction; Fistula.Renal losses – Polyurine phase of acute renal failure,Diuretic therapy (except triamterene and spironolactone).Increased mineralocorticoid levels – primary and second aldosteronism Cushing’s syndromeTreatment with glucocorticoid hormonesc. Intracellular shift:AlkalosisInsulin treatmentFamilial hypokalemic periodic paralysis Barium poisoning
(3)Effect on body:a. Effect on neuromuscular irritabilityAcute Hypokalemia:[K+]I/[K+]e → | Em |↑(more negative) → ( Em-Er )↑→ Irritability↓→ Hyperpolarized blockNerve system manifestation: Depression, apathy, coma .Muscle system manifestation: striated muscle----Fatigue ,weakness, flaccid paralysis smooth muscle----vessel dilation; decreased intestinal motion, abnormal distension,constipation and paralytic ileus.
Chronic hypokalemia: The intracellular K+ moves into ECF to maintain nearly normal RMP. So it has no above mentioned manifestation.
b. Effect on heartserum [K+]↓→ reducing potassium conductance↓→ |Em|↓→ (Em-Er)↓→ irritability↑ serum [K+]↓→ reducing potassium conductance↓→ decrease K+ outward and accelerating Na+ inward in 4 phase → automaticity↑ serum [K+]↓→ |Em|↓→ inward of Na+ in phase 0 ↓ → conductivity↓ early stage or mild serum [K+]↓→ accelerating of Ca2+ inward in phase2 → contractivity↑ severe serum [K+]↓→ Ca2+ transport disorder ; ATP decreased; myocardium degeneration → contractivity↓ ECG: low T wave ; high U wave ; prolonged Q-T interval ; fallen S-T segment
Tall, peaked T-wave(5.5-6.5)
Wide flat P-wave/Prolonged PR interval/Widened QRS complex /Deep S-wave (6.5-8.0)
Ventricular fibrillation. Sine-wav: proceed to asystole (absence of heartbeat)(8.0)
Shallow T-wave /Prominent U-wave (2.5-3.5)
Tall “P” waves
Ventricular Tachycardia (1.5)
c. Effects on kidneyHypokalemia → damage of renal tubules → inability to concentrate urine refractoriness to ADHpolyuria, nocturia, low specific gravity urine ,thirst
prolonged severe hypokalemia: oliguria
d. Effects on acid-base balance
Hypokalemia:more K+ move out of cells metabolic alkalasismore H+ and Na+ of ECF move into cells H+of ECF↓→ with more H+ are secreted from kidney abnormal acidic urine
(4) Principle of treatmenta. In mild hypokalemia:
replenishment of KCl by the oral route is preferable because it is safer than I.V. administration.b. In severe hypokalemia:
adding KCl to glucose water intravenously at a final concentration of 40 mmol/L, and infusing KCl at a rate of 10-20 mmol/h, since KCl is an irritating substance. Usually the repair of hypokalemia needs several days. Never give KCl solution by direct intravenous injection to patients.
(2)Causes:A. Diminished renal excretiona. reduced GFR: oliguria phase of acute renal failure terminal phase of chronic renal failure b. reduced tubular secretion of K+ addison’s disease; hypoaldosteronism application of potassium sparing diuretic(spironolactone ,triamterene). B. Increasedinput of potassiumexcessive or rapid parenteral infusion of KCl solutionC. Extracellularshiftsa. acidosis b. cell destruction(trauma, burns, hemolysis, tumor lysis, rhabdomyolysis c. Familial hyperkalemic periodic paralysis
(3)Effects on body :A. Effects on neuromuscular irritability
a. mild serum [K+] ↑→ [K+]I/[K+]e↓→ |Em|↓( as partial depolarization)→ (Em- Er)↓→ irritability↑→ Excitation（ Diarrhea,intestinal colic,paresthesia)
b. severe serum [K+]↑→ [K+]I/[K+]e↓↓→ |Em|↓↓→|Em|≤ |Et| → Na+channel inactive → irritability↓→ Depolarized block（weakness, paralysis, mental confusion and coma。）
b. Effect on hearta. Mild serum [K+] ↑→ [K+]I/[K+]e↓→ |Em|↓( as partial depolarization)→ (Em- Er)↓→ irritability↑b. Severe serum [K+]↑→ [K+]I/[K+]e↓↓→ |Em|↓↓→|Em|≤ |Et| → Na+channel inactive → irritability↓Serum [K+] ↑ →increased potassium conductance → accelerating K+ outward and decreased Na+ inward in 4 phase → autodepolarization ↓ → automaticity↓ Serum [K+] ↑ → [K+]I/[K+]e↓→ |Em|↓ → inward of Na+ in 0 phase ↓ → decreased velocity and extent of depolarization → conductivity↓ Serum [K+] ↑ → depression Ca2+ inward in 2 phase → contractivity↓clinic signs and symptom :sinus bradycardia, heart block, asystole and heart arrest.
tall peaked and tent-shaped T wave; disappearance of P wave ; prolonged P-R interval; widening of QRS complex
c. effect on acid-base balanceserum K+↑→K+ of ECF move into cells and H+of ICF move out of cell; decreased secretion of H+ due to intensive exchange between Na+ and K+ by distal tubules → metabolic acidosis with abnormal alkali urine
(4) Principles of treatmenta. Treating primary disease b. Restriction of potassium intake c. Shift of K+ from ECF into cell (insulin+glucose) d. Increased in K+ excretion from body (furosemide, ethacrynic acid) e. Antagonizing the effects of hyperkalemia on heart (Ca2+ or NaHCO3）