(g) Exercise

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(g) Exercise

• Exercise can promote K shift out of cells
  through
• opening of ATP-dependent K channels
• (2) decrease Na -K ATPase activity due to ATP
  depletion.

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• ???huweicheng_at_sdu.edu.cn
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• ????Sun, 16 Mar 2008 004438 0800 (CST)
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• Work hard
• Ability to analyse and solve problems
• Ability to study independently

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• Exercise can promote K shift out of cells
  through
• (1) opening of ATP-dependent K channels
• ?????
• ???????????
• ???????????
• KATP??
• ???????ATP??????????????ATP????3-4
  mmol.L-1, KATP?????????????ATP?KATP??????????????,
  ?????????????,????,??ATP????0.2
  mmol.L-1?????,K??,
• ?????? (1)????,???????????????KATP??,K??,??
  ?????,?????????,Ca2????,?????
• (2)Ca2????,????????,????????? ?

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Hyperkalemia

• (1) Concept
• Serum Kgt5.5mmol/L is defined as
  hyperkalemia.
• If the increase of serum K is
  caused by the movement of potassium from ICF to
  ECF, the hyperkalemia does not mean potassium
  excess.

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(2) Causes and mechanism

• 1) Increased potassium intake
• 2) Decrease of renal excretion potassium
• 3) Increased movement of potassium from
• cells to ECF
• 4) Blood concentration
• 5) Pseudohyperkalemia

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1) Increased potassium intake

• Before the intravenous administration of
  KCl , we must make sure that the renal function
  is good enough to eliminate potassium.(????)
• Too rapid intravenous administration of
  KCl leads to a severe incident, which is fatal.
• It takes time (gt 15 hours, longer in
  diseases) to get the balance of Ke and Ki.

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Accidents

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  ???????????????.??????NaHCO3??,?KCl??.????NaHCO3?
  ?,?KCl??,?????
• ???????,?????????????

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• Transfusion of blood in stock
• --------------------------------------------------
  ---------
• period of stock increase of plasma K
• --------------------------------------------------
  ----------
• 2 weeks 45 times
• 3 weeks 10 times
• --------------------------------------------------
  ----------
• (2)Infusion of Penicillin Potassium

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• Oral administration of potassium can
  rarely cause fatal hyperkalemia.
• Less absorption in gut.
• Vomiting diarrhea

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2) Decrease of renal excretion potassium

• (a) Normally 90 of potassium is excreted
  from kidneys. In renal failure (GFRlt15ml/min) ,
  the renal K excretion will decrease.
• In acute RF oliguria
• In chronic RF less functional
  nephrons
• (compensation)

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anuria

• The serum K increases 0.7 mmol/L
  per day with anuria, and 10 days later, the
  patient with anuria will die from hyperkalemia.
• No K intake ??

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• (b) Decreased secretion of aldosterone
  leads to reduced excretion of potassium.
• Usually hyponatremia occurs first.
• If there is increased Na intake, more
  Na-K exchange will be in distal tubules. (no
  hyperkalemia)
• If there is no increased Na intake,
  less Na-K exchange will be in distal tubules. (
  hyperkalemia)

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(d) Over-dose of digitalis(???) suppresses the
Na - K ATPase, the excretion of K reduce.

• (c) Some diuretics (e.g. spironolactone???, an
  antagonist of aldosterone) inhibit the sodium
  reabsorption and the secretion of K is reduced.

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3) Increased movement of potassium from cells to
ECF

• (a) Acidosis results in the shift of
  potassium out of the cells.
• (b) Cell destruction often occurs with
  tissue trauma, burn, rhabdomyolysis, lysis of
  tumor cells by cytotoxic agents and hemolysis.
• (c) Insulin deficiency ,hyperglycemia and
  acidosis results in the decreased entry of K
  into the cells by inhibiting Na - K ATPase.
• (d) Low ATP production caused by hypoxia

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(e) Medicines

• ß receptor blokages (e.g. ???) blocks the inward
  movement of K by inhabiting Na-K ATPase,
• Muscle relaxants increase the K permeability of
  skeletal muscular cell membrane.

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• 4) Familiar hyperkalemic periodic paralysis
  is a rare genetic disease, in which the serum
  K is suddenly increased, so the paralysis
  occurs.
• 5) Blood concentration
• 6)Pseudohyperkalemia may occur if the RBC
  destruction happens during draw of blood for lab
  investigation.

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For example traffic accident.

• (1) Increased potassium production by more
  endogenous K.
• (2) Decrease of renal excretion potassium
• Bleeding leads to renal ischemia and then
  oliguria.
• (3) Increased movement of potassium from cells to
  ECF
• 1) Tissue injury
• 2) Tissue hypoxia, less ATP production
  , pump
• dysfunction.
• 3) metabolic acidosis

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(3) Effect on the body

• 1) Effect on the neuromuscular irritability
• 2) Effect on the heart
• 3) Effect on acid-base balance

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• 1) Effect on the neuromuscular irritability
  (Biphasic)
• In mild hyperkalemia (lt7mmol/L),
• In hyperkalemia, the difference between
  Ki and Ke is decreased, the resting
  membrane potential (RMP) is less negative
  (partial depolarization), which means that a
  smaller stimulus will evoke an action potential
  (AP).

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• The excitability ( irritability) of skeletal
  muscles is increased at first.
• The manifestation of skeletal muscle at first ,
  is stabbing pain
• abnormal sensation ( too sensitive for pain)
• mild tremor

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In severe stage (gt78mmol/L), RMPltTMP
depolarizative block Na channel will
not open. The excitability is decreased to
disappear. The excitability (
irritability) of skeletal muscles is then
decreased at last. (Biphasic)
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• Manifestation
• muscle weakness
• weak tendon reflex even disappear
• flaccid paralysis?????.
• from limbs to trunk (respiratory muscle)

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• The excitability ( irritability) of smooth
  muscles of GI tract is increased at first, then
  decreased at last. (Biphasic)
• It may be manifested by diarrhea,
  intestinal colic ( abdominal pain) and abnormal
  sensitivity (paresthesia) at first, then
  abdominal distension.

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2) Effect on the heart

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• ??????,
• ???????,
• ??KCl.

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(a) A gradual increase of serum K
produces biphasic sequences of excitability of
myocardiac cells.

• An initial increase of excitability is
  followed by a decrease. Cardiac arrest occurs in
  diastolid state.

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• (b) Potassium permeability (K conductance
  ???) of membrane of myocardiac cells is
  increased, which accelerates the repolarization.
• Shortening of refractory period

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?The conductivity of myocardiac cell is
reduced.

• The rate and range of depolarization is
  reduced in hyperkalemia, because the RMP is
  near the TMP.
• The most dangerous to the body is
  severe heart blocking and cardiac arrest.

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• (c) The autorhythmicity is decreased,
  because the membrane permeability to potassium is
  increased, the outward potassium current is
  increased and the inward sodium current is
  relatively decreased.
• The autorhythmicity of sinoatrial node
  in reduced, there will be progressive sinus
  bradycardia even cardiac arrest may occur.
•  

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Summary of the effect on the myocardiac cells

• The excitability is increased.
• Shortening of refractory period
• The conductivity is reduced.
• The autorhythmcity is reduced, sinus
  bradycardia
• All make it easy to form reciprocal excitation
  (????) and ventricular fibrillation (????).

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(No Transcript)
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• (d) The contractivity is reduced due to
  decreased intracellular calcium.
• The high Ke inhibits the inward flow
  of calcium.

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(e) Changes of ECG
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• T wave is peaked and tent-shaped
  because phase 3 is accelerated due to rapid
  outward of potassium (K67mmol/L).
• P wave is prolonged and eventual
  disappear due to the decreased conductivity and
  excitability in atrium (K8mmol/L).
• QRS complex is widened due to the
  decreased conductivity in ventricle
  (K10mmol/L).

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• Prolonged P-Q (P-R) interval ??
• Short Q-T interval

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ECG in ?
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• Multiple factors can alter the effect of
  hyperkalemia on the heart.
• If the hyperkalemia develops slowly, the
  cardiac manifestation is minimal.
• If there are some other electrolytes
  disturbances at the same time, the cardiac
  manifestation will change.

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• 3) Effect on acid-base balance
• (a) extracellular acidosis and (b) unusual
  alkalinuria.

(a) When K of ECF is increased in
hyperkalemia, the K of ECF moves into the
cells, at the same time the H in IEF moves into
the ECF for electric neutrality. Then the H in
ECF will be increased.
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Mechanism

• (b) unusual alkalinuria.
• There are two kinds of ion exchange,
  K-Na and H-Na , in renal tubules.
• In hyperkalemia, the K--Na exchange is
  increased, the H--Na exchange will decrease, so
  the excretion of H from kidneys is reduced,
  which leads to and basic (alkaline) urine.

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• Usually in acidosis, the elimination of
  H is increased from kidneys, and the urine
  should be acidic.
• But in the acidosis caused by
  hyperkalemia, the urine is alkaline, it is
  unusual, so it is called unusual alkalinuria.

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(4) Principle of treatment

• 1) Complete restriction of exogenous
• potassium intake.
• 2) Control of the underlying disease
• (etiologic treatment)
• 3) Transport of the serum K into cells
  (a) Administration of insulin and glucose
  to transport the potassium from ECF into the
  cells.
• (b) Bicarbonate infusion (alkaline
  solution) can drive the potassium into the cells.

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4) Increase the elimination of potassium

• (a) A sodium polystyrene sulfonate resin
  ????????? is used to remove potassium from
  colon. (Na-K exchange)
• (b) Peritoneal dialysis
• (c) Hemodialysis

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Peritoneal Dialysis
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Hemodialysis

• Blood is circulated through artificial cellophane
  membrane that permits a similar passage of water
  and solutes

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(5)Protection of cardiac cells

• A increased Ca2 may raise the
  threshold potential, which may reestablish the
  difference between the resting and threshold
  potential and restores the excitability.
• (10 calcium gluconate?????)

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• A increased Na will increase the inward sodium
  current in phase 0 (depolarization) to increase
  the excitability of heart muscle.
• 11.2 sodium lactate ???