??? ? ?(hypoxia)

1
Disorder of potassium metabolism
Zhao Mingyao BMC.ZZU.
2

• Disorder of potassium metabolism
• Ks mmol/L Status
• 3.5 5.5 Normal level
• lt 3.5 Hypokalemia
• gt 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
5055mmol/KgBW
K
K
3.5 5.5 mmol/L
140160mmol/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
140160mmol/L
Direction of K shifting
kidney
GI tract
Skin?
90
10
Maintenance of K balance
8
(1) The control of K transfer between intra-
extracellular compartments

• The Na/KATPase (membrane pump )
• Permeability of ion channels

9
ICF
ECF
K
pump
channel
Insulin, ß-adrenergic agonist, ADS, Ks?,
exercise, pH ?, ECF osmolanity ?

K shifts between ICF and ECF
10
(2) Regulation of renal K excretion

• ?

11
tubular cell
tubular lumen
ICF
K
K
Na-K ATPase
Na
Na
-
-
-
-
K
ADS, guanylin, Ks, urinary flow rate, pH,
distal delivery of sodium, impermeable anion
kidney
90
Regulation of renal K excretion
12
Part 2 Hypokalemia

• Defined as ks lt 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
Nernst equationEm? -60lgKicf / Kecf (mv)
16
mv
The effects of Ks concentration on cellular
membrane excitability
17
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
Effects of low Ks on the AP of the myocardial
cell
20

• Typical feature of ECG during hypokalemia
• lt 2.5 mmol/L U wave(ECG)
• aura sign of cardiac asystole

21
Cardiac arrhythmias

• due to
• increased excitability
• shortened ERP (effective refractory period )
• prolonged SNP (supranormal period)
• increased automaticity
• decreased conductivity

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 KCl40mmol/L
• limited total amount/d 40120mmol K/day
• urine existence
• (iv instillation Never inject ! )

25
Part 3 Hyperkalemia

• Defined as ks gt5.5 mmol/L
• Except false phenomena?

26

• 1.Causes
• (1)K Intake ?
• (2)K shift into ECF ?
• pH ?, some drugs (ß-R antagonist), cell
  injury, familial hyperkalemic periodic paralysis
• (3)Renal K excretion ?
• GFR ? ?, ADS ?(Addisons 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
• gt 7.5mmol/L tent-like T wave
• aura sign of cardiac asystole

30
ECG
K 7.8 mmol/L

•  absent "P ", tall tented "T" and widening of QRS

31
(3)Effect on acid and base

• Metabolic acidosis
• Paradoxical alkaline urine ( due to K? or ? )

32
3. Principle of prevention and treatment

• ?Limit origination intake ?
• ? Sodium and calcium salt opposite the
  toxicity
• of hyperkalemia
• ? Shifted into cell (transient, such as GI
  fluid, pH ?)
• ? Remove K out of body
• Na-K cation exchange resin enema
  hemodialysis

33
THANKS!