Hypokalemia and Potassium Deficit

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Hypokalemia and Potassium Deficit

• (1) Concept
• (2) Causes and mechanism
• (3) Effect on the body
• (4) Principle of treatment

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(1) Concept

• Hypokalemia indicates the K
  in plasma is lt 3.5 mmol/L.
• If the hypokalemia is caused by the
  movement of K from ECF to ICF,
• reduced K ? K deficiency in the body.

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(2) Causes and mechanism

• 1) Decreased intake
• 2) Excessive loss of K
• 3) More moving of K into cells
• 4) Blood dilution

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1)Decreased intake

• Since food is the main source of
  potassium in the body, fast, anorexia or
  inability to eat may cause hypokalemia.
• At the same time, there is still loss
  of potassium from kidneys (510 mmol/ day at
  least).

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• Renal excretion of potassium continuously
• --------------------------------------------------
  ---
• amount of K excretion
• --------------------------------------------------
  ---
• Normal 38150 mmol/day
• No K intake
• 13 day 50 mmol/ day
• 47 day 20 mmol/ day
• 10 day 510 mml/ day
• --------------------------------------------------
  ----

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2) Excessive loss of K

• (a) From gastrointestinal tract
• (b) Excessive renal loss

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(a) From gastrointestinal tract

• The gastric and intestinal juices are
  rich in potassium.
• -----------------------------------------
• position K (mmol/L)
• ------------------------------------------------
• Gastric juice
• high acidity 10
• low acidity 25
• Bile 10
• Juice in small intestine 20
• Watery stool 40
• -----------------------------------------------

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Persistent vomiting, diarrhea, gastric
suction and fistula are the common ways to lose
potassium directly.
At the same time hypovolemia may lead
to increased secretion of aldosterone. Increased
aldosterone (caused by hypovolemia) will enhance
the loss of potassium from gastrointestinal tract
like the renal tubules.
At the same time, loss of gastric juice
may lead to metabolic alkalosis.
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(b) Excessive renal loss

• Renal loss is the main way to lose
  potassium.
• ? Hyperaldosteronism
• Primary hyperaldosteronism is caused by
  adrenal tumors.
• Secondary hyperaldosteronism is caused by
  markedly reduced effective arterial volume in
  congestive heart failure, liver cirrhosis and
  nephritic syndrome.

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• Increased aldosterone secretion will
  increase the potassium loss from kidneys.
• Administration of large amount of
  glucocorticoids can also produce hypokalemia.

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• ? Diuretics
• The most common diuretics losing
  potassium are thiazines???, furosemide ?? and
  ethacrynic acid???, which block the reabsorption
  of Na and Cl- in proximal tubule and Henles
  loop, then deliver more Na and Cl- to the distal
  tubules.
• More K are exchanged with Na
  and the loss of potassium will increase.

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• Acetazolamide ???? inhabits the activaty of
  CA in proximal tubule, H-Na exchange decreases,
  More Na arrive at distal tubules, K-Na
  exchange increases, K excretion increases.
• All diuretics including increase osmotic
  diuretics mannitol???,can increase the urine
  volume.

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? Type I of Renal Tubular Acidosis

• There are two kinds of ion exchanges in
  tubular cells
• Na- K
• Na-H
• Failure of hydrogen excretion is the
  character of this disease, so more K is excreted
  to exchange for Na.

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? Increased negative charges in distal tubular
fluid

• More ß-hydroxybutyric acid and
  acetoacetic acid (ketone bodies) in distal
  tubular fluid of patients with ketosis
  (diabetes).

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3) More K moves into cell

• (a) In alkalosis, H moves out of the cells,
  at the same time, K moves into the cells.
• For each 0.1 unit increase of pH in
  ECF, the K of serum decreases 0.7 mmol/L.
• (b) Insulin stimulates glycogen synthesis in
  the liver and skeletal muscle cells, at the same
  time, K moves into cells.
• Insulin stimulates Na-K ATPase.
  

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• (c) Familiar hypokalemia periodic
  paralysis is a rare disease, there is a acute
  shift of K from ECF to ICF, the Ke will
  reduce, which causes paralysis of the limb and
  trunk.
• (d) Hyperthyroidism ?? Over-dose
  thyroxin stimulates Na-K ATPase.
• (e) Barium poisoning ??? Brium ion is
  a K channel block in cell membrane.

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(e) Barium poisoning ??? Brium ion is a K
channel block in cell membrane.

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4) Blood dilution

• The concentration of potassium in plasma
  will reduce in dilute blood.
• Multiple factors in diabetes with ketosis and
  coma.

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(3) Effect on the body

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

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1) Effect on neuromuscular irritability

• Neuromuscular
• irritability (excitability)
• indicates the degree of
• difficulty or easy to start AP.
• High excitability means
• easy to start AP.
• Excitability is determined by the
  distance between the RMP and TMP. The less
  distance (difference) , the higher of
  excitability.

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(a) Decrease the neuromuscular irritability in
acute hypokalemia.

• The negative value of RMP is
  increased (cell membrane is hyperpolarization,
  hyperpolarizative block).
• The difference between resting and
  threshold potential is increased.
• A greater stimulus is needed to
  produce an action potential (AP).

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(b) manifestations

• ? Effect on skeletal muscles
• The effects of hypokalemia depend on
  partly the decrease speed of serum k.
• The rapidly decreased serum k leads to
  skeletal muscle weakness, flabbiness (soft), and
  flaccid (soft) paralysis.
• The most severe problem of muscular
  paralysis is ??

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•   In chronic potassium depletion, the k
  in ICF moves to ECF, both intracellular and
  extracellular k are decreased, the ratio of
  ki to ke is not obviously changed, the
  resting potential is not changed.
• Chronic potassium depletion may lead to
  the muscle atrophy (thin and weakness of the
  muscle) , which is mainly caused by disturbance
  of protein metabolism. Chronic K deficiency
  decreases the ATP production and ATPase
  activity.

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• In severe K deficiency (lt2.5mmol/L),
• during strenuous exercises the cells cannot
  release enough K to dilate the vessels, which can
  lead to ischemia and necrosis of muscle cells
  with energy metabolism disturbance (exertional
  rhabdomyolysis).

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? Effect on SMC gastrointestinal tract,

• Decreased neuromuscular irritability
  causes
• decreased intestinal motility,
• abdominal distension,
• anorexia,
• nausea
• constipation.
• bowel sound???disappear,
• paralytic ileus ??????.

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? Effect on vascular SMC

• Decreased muscular excitability leads to
  postural hypotension.

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• ? If there are some other electrolytes
  disturbances at the same time, the manifestations
  will change.
• Low k leads to more negative of RMP
• High Ca2 leads to the elevation of
  TMP.
• (Ca2 inhabits the Na into the cells)
• Low k High Ca2 will increase the
  distance between the RMP and TMP and cause very
  low neuromuscular excitability.

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• Low k leads to more negative of RMP
• Low Ca2 leads to the decrease of TMP.

• Low k low Ca2 will restore the
  normal distance between the RMP and TMP and
  cause the normal neuromuscular excitability.

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• Ca2 ?? combining calcium
• H OH-

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2) Effect on heart (a)Effects on myocardiac
cells
a) Arrhythmia b) Abnormal contractibility c)
Abnormal electrocardiogram (ECG)
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? The excitability of myocardiac cell is
increased.

• The potassium permeability of myocardiac
  cell is reduced in hypokalemia.
• Less K moves outside the cell, the RMP
  is less negative.
• The difference between RMP and TMP is
  reduced. Smaller stimulus may produce the AP.

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• Prolonged exaltation phase??? caused by
  decreased K permeability and rate of phase 3
  (repolarization)
• Short absolute refractory period caused by
  short phase 2.

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?The conductivity of myocardiac cell is
reduced.

• The rate of depolarization and
  repolarization is reduced in hypokalemia, because
  the RMP is near the TMP.

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? The autorhythmicity is increased.

• In phase 4, the potassium permeability
  in hypokalemia is reduced, the outward potassium
  current is decreased and inward sodium current is
  relatively increased.The speed of spontaneous
  depolarization is increased. (Slope rise steeply)

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Summary of the effect of hypokalemia on the
myocardiac cells

• The excitability is increased.
• Prolonged exaltation phase?????
• Short absolute refractory period??????
• The conductivity is reduced.
• The autorhythmcity is increased.

All the alters make it easy to
produce arrhythmia (increased heart rate, ectopic
beats from Purkinje fiber and ventricular
muscle). (Ectopic pacemaker) (nodus
sinuatrialis)
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b) Abnormal contractibility,

• The contractibility of myocardiac cell is
  increased first, then reduced. K in ECF can
  inhibit the inward flow of calcium ions, this
  inhibiting effect is reduced in hypokalemia.
• More Ca 2 within myocardiac cell will
  increase the contractibility.

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• In severe hypokalemia , ATP production
  and ATPase activity are reduced which causes low
  myocardial contractibility.

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Electrocardiogram (ECG)

• The P wave reflects depolarization of atrial
  muscle and represents the original impulse passes
  through the atrium.

• The QRS complex represents
  depolarization of the ventricular muscle mass,
  and reflects the speed of conduction throughout
  the ventricle.

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• The S-T segment represents the period
  between the end of depolarization of ventricular
  muscle and the beginning of repolarization of
  ventricle. The S-T segment corresponds to the
  plateau (phase 2) of AP.
• The T wave represents the major
  portion of repolarizatione after ventricular
  contraction. T wave corresponds to the phase 3 of
  AP.

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C) Abnormal ECG
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• Broad and flat T wave appears because the
  potassium permeability in hypokalemia is reduced,
  the rate of repolarization is reduced. The phase
  3 is prolonged.

Prolonged QRS complex are caused by
reduced conductivity.
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• Suppressive S-T segment is related to
  the short phase 2 due to accelerated inward flow
  of calcium.
• Prominent U wave can be often seen in
  hypokalemia, but it is hard to explain the
  mechanism.

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3) Effect on the acid-base balance

•   Hypokalemia leads to metabolic
  alkalosis.
• When Ke of ECF reduce, the K of
  ICF moves out of the cells, at the same time, H
  moves into the cells for electric neutrality.

• Then the H in ECF will be reduced,
  which is called metabolic alkalosis.
• (Depending on the primary disease)

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• There are two kinds of ion exchange in
  renal tubules
• K -- Na
• H -- Na ,.
• In hypokalemia, the K-Na exchange is
  reduced, the H--Na exchange will increase, so
  the excretion of H from kidneys is increased,
  which leads to acidic urine.

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• Usually in alkalosis, the elimination of H
  is reduced from kidneys, and the urine should be
  alkaline.
• But in the alkalosis caused by
  hypokalemia, the urine is acidic, it is unusual,
  so it is called unusual aciduria.

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4) Effect on the kidney

• Pathologic study found the swelling,
  proliferation, vacuolation in proximal tubular
  cells, the renal tubular cells can not produce
  sufficient cAMP, which is necessary for ADH to
  work, so the tubules lose the concentrating
  ability to urine.
• The volume of urine is increased and the
  specific gravity will reduce.
• Thirst may occur in patients with
  hypokalemia.

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4. Principle of treatment

•   1) Etiological treatment is to correct the
  underlying diseases.
• 2) The major problem of replacement of
  potassium is to produce the hyperkalemia
• Replacement of potassium salts
  slowly after urination (no oliguria).????
• Oral potassium chloride is better
  than intravenous administration.
• We must pay attention to the rate of
  intravenous administration and the potassium
  concentration of potassium chloride solution.

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• (a) When K deficiency and oliguria, the Ke may
  not be severely reduced because of dehydration
  and acidosis at the same time.
• (b) It will take 12 days to get the balance of
  KI and Ke. (1015 days)

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• Replenish KCl may correct both
  hypokalemia and metabolic alkalosis.
• Replenish KHCO3 may correct both
  hypokalemia and metabolic acidosis. .

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Case Discussion No.1

• 1. A 36-year-old man was hospitalized with
  a 3-day history of fever and watery diarrhea. His
  blood pressure was 90/60 mmHg, the pulse was
  112/min, temperature is 38.0?. The abdomen was
  distended with low skin elasticity.
• The laboratory results were
• Arterial blood
• pH7.21, PaCO226 mmHg
• PaO2 108 mmHg. Na135 mmol/L
• K 3.0 mmol/L HCO3- 16 mmol/L
• Urine pH5.0, Specific gravity 1.028
•  

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• The patients problems were
• (1)isotonic dehydration
• (2)metabolic acidosis
• (3)hypokalemia.

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