Transcript Serum potassium 3.5 mmol/L

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
GI tract: only about 10 %
Major organ of excretion potassium: kidney
Regulative site: renal distal tubule
Hormone of major regulated: ADS
Only the potassium output remains equivalent to
intake every 24 hours, then to ensure
Total body potassium 50-55mmol/kg B.W
Distal and collecting tubule
secretion
(Principal cells)
Regulated by:
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 
Urine flow rate 
 Secretion
Distal delivery of sodium 

 Secretion


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 of 1 ATP→pumping 3 Na+ out off
and 2 K+ into the cell
Total body potassium approximately 98% in ICF
50-55mmol/kg B.W approximately 2% in ECF
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:
Function of the Potassium
The Intracellular and extracellular potassium gradient
is of major importance in maintenance resting cell
membrane potential(Em)
The abundant pool of intracellular potassium is
necessary for maintenance of osmolality and hence the
volume of body cells.
Essential for enzymatic reactions that regulate protein
synthesis,growth,and metabolic processes
The relationship between
serum potassium and total
body potassium
The clinical signs and symptoms are
major depended on concentration of
serum potassium.
Disorders of potassium homeostasis
Serum potassium 3.5 mmol/L
( Potassium depletion: ICF or total potassium  )
Hypokalemia:
Hyperkalemia:
Serum potassium 5.5 mmol/L
Hypokalemia
(1) Concept:
Serum potassium<3.5mmol/L
(2) Causes:
a. Inadequate intake: Inability to eat;
Fast and anorexia;
Administration of K+ -free parenteral solutions
b. 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 syndrome
Treatment with glucocorticoid hormones
c. Intracellular shift:
Alkalosis
Insulin treatment
Familial hypokalemic periodic paralysis
Barium poisoning
(3) Effect on body:
a. Effect on neuromuscular irritability
Acute Hypokalemia:
[K+]I/[K+]e → | Em |↑ (more negative) → ( Em-Er )↑→ Irritability↓→
Hyperpolarized block
Nerve 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 heart
serum [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
Hyperkalemia
Hypokalemia
Shallow T-wave
/Prominent U-wave
(2.5-3.5)
ST depression/
Tall “P” waves
(1.5-2.5)
Ventricular
Tachycardia (1.5)
Tall, peaked Twave(5.5-6.5)
Wide flat Pwave/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)
c. Effects on kidney
Hypokalemia → damage of renal tubules → inability to concentrate
urine
refractoriness to ADH
polyuria, nocturia, low
specific gravity urine ,thirst
prolonged severe hypokalemia: oliguria
d. Effects on acid-base balance
Hypokalemia:
more K+ move out of cells
metabolic alkalasis
more H+ and Na+ of ECF move into cells H+of ECF↓→
with
more H+ are secreted from kidney
abnormal acidic urine
(4) Principle of treatment
a. 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.
Hyperkalemia
(1)Concept :
Hyperkalemia is defined as a serum K+
level greater than 5.5 mmol per liter .
( serum potassium >5.5mmol/L )
(2) Causes:
A. Diminished renal excretion
a. 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. Increased input of potassium
excessive or rapid parenteral infusion of KCl solution
C. Extracellular shifts
a. 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 heart
a. 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.
ECG:
tall peaked and tent-shaped T wave;
disappearance of P wave ;
prolonged P-R interval;
widening of QRS complex
c. effect on acid-base balance
serum 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 treatment
a. 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）