Download (3) Metabolic alkalosis

(3) Metabolic alkalosis
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1) Concept
2) Classification and Pathogenesis
3) Compensation
4) Effects on the body
5) Principle of treatment
• 1)Concept
• Metabolic alkalosis is defined as a primary
increase of [HCO3¯ ] in plasma, the pH has a
tendency to increase. (means ?)
2) Classification and Pathogenesis
• According to the therapeutic effect of 0.9% NaCl,
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(a) chloride-sensitive type
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(b) chloride-resistant type.
(a) Chloride-sensitive type
Pathogenesis
a) Increased loss of H+ from stomach
• b) Increased loss of H+ from kidney
• c) H+ enters into cells
• d) Overload of HCO3¯
a) Increased loss of H+ from stomach
There is a lot of H+ in the gastric juice.
Vomiting and gastric suction will lose gastric
fluid .
HCO3- is absorbed into blood, then to
intestinal juice to neutralize H+.
b) Increased loss H+ from kidneys:
Some diuretics (e.g.
furosemide速尿) can inhibit
the reabsorption of Cl¯ and
Na+ in loop, urine volume is
increased (50~60L/24hs).
Increased loss H+ from
kidneys
Concentrated [HCO3¯]
c) H+ enters into cells
• Hypokalemia
• Unusual aciduria
d) Overload of HCO3¯
Patients with gastric ulcer may be orally
given excessive NaHCO3 to neutralize gastric
juice .
Sharp correction of acidosis by excessive
alkali administration can lead to metabolic
alkalosis.
Lactate and citrate can be catalyzed into
HCO3¯ .
Transfusion of anticoagulant blood with
sodium citrate.
(b) Chloride-resistant type
a) Primary
hyperaldosteronism
Secondary
hyperaldosteronism
caused by hypovolemia
Effect:
Stimulate H+-ATPase.
b)Severe hypokalemia(??)
K+-Na+ exchange
H+ -Na+ exchange
c)Cushing Syndrome:
more glucocorticoids.
3) Compensation of metabolic alkalosis
The secondary change is the increased
[H2CO3] in plasma.
The compensation of metabolic
alkalosis is the opposite direction of the
compensation in metabolic acidosis.
(a) Buffering system in ECF
(b) Pulmonary compensation
(c) Cellular buffering
(d) Renal compensation
(a) Buffering system in ECF
After the addition of alkali, the buffering
system initiates immediately.
NaHCO3 Na2HPO4
------------- -------------H2CO3
NaH2PO4
Hb------HHb
H2CO3 combines the excessive OH¯ (strong)
to form HCO3¯ (weak alkaline).
increased pH
Via
central
chemoreceptors
(b) Respiratory
compensation
inhibit the respiratory center
slow shallow respiration
more carbon dioxide can be
accumulated in blood
decrease of pH
Limitation:
High PaCO2 and
low PaO2 stimulate
the respiratory
center.
(c) Cellular buffering
+ moves out of cells into ECF, at the
The
H
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same time K+ moves into the cells.
(d) Renal compensation
The reabsorption of [HCO3¯ ] is decreased.
The acids excretion is decreased.
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In metabolic
alkalosis, the activity of
carbonic anhydrase (CA)
decreases, the H+
production is decreased,
the H+-Na+ exchange is
decreased, the
reabsorption of HCO3¯ is
decreased.
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In metabolic alkalosis,
the activity of glutaminase is
decreased, less glutamine
will be decomposed into
HCO3¯ and NH3. Thus less
HCO3¯ will be reabsorpted
to the blood, more HCO3¯
will be eliminated.
Decreased net acid excretion with urine
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Less H2PO4 ¯
and NH4+ are in the
end urine.
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The pH of urine
will elevate due to the
decreased net acid
excretion with urine .
Changes of laboratory parameters
• Primary increase of [HCO3¯]:
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AB,SB,BB ???
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AB ?? SB
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BE ?
• Secondary compensation:
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PaCO2 ?
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pH ?
Changes of laboratory parameters
• Primary increase of [HCO3¯]:
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AB,SB,BB increase
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AB > SB
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BE positive increase
• Secondary compensation:
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PaCO2 increase
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pH tends to increase.
Predicted compensatory
formula
ΔPaCO2(mmHg)
Secondary compensation
= 0.7 x ΔHCO3- ±5
primary change
Or:
PaCO2=40+0.7xHCO3-±5
PaCO2 can increase maximal to 55 mmHg.
Value measured > value predicted: with respiratory
acidosis
Value measured < value predicted: with respiratory
alkalosis
4) Effects on the body
(a) The left-shift of oxygen-hemoglobin
dissociation curve
(b) Effects on the central nervous system.
(c) Decrease of ionized calcium (Ca2+) in
plasma
(d) Hypokalemia
(a)The left-shift of oxygenhemoglobin dissociation
curve leads to hypoxia.
This “left –shift” means
the Hb combines more
oxygen under the same
PaO2 and the O2 is more
difficult to dissociate from
Hb. (hypoxia)
(b) Effects on the central nervous
system
• a) Manifestations:
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Excitability is increased.
dysphoria (agitation),
malaise (discomfort),
delirium ( mental disturbance with wild talk
and wild excitement),
• confusion,
b)The reasons :
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The left-shift of oxygen-hemoglobin
dissociation curve leads to brain hypoxia.
Glutamic acid
Glutamate decarboxylase
r-GABA, r-aminobutyric acid
r-GABA transaminase
Succinic acid
Kreb’s cycle
The production of GABA (gama
aminobutyric acid, a inhibitory transmitter) is
decreased due to the activity of enzyme for
the production is reduced in alkalosis.
(c) Decrease of Ca2+ in plasma
More calcium combines to the plasma
proteins in alkalosis.
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OH• Ca2+
protein-bound calcium
• Ca2+
protein-bound calcium
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H+
Manifestation:
• The main character is the increased
neuromuscular excitability.
• The symptoms include :
• a) twitching 颤搐(quick uncontrollable muscle
movement)
• b) tetany手足搐搦
• c) cramping (convulsions)
(d) Hypokalemia
• Causes:
• a)H+ shifts out of the cells as the
compensation of alkalosis.
Therefore the K+ moves into the
cells as an exchange for electroequilibrium.
b) Less H+ -Na+ exchange and more K+-Na+
exchange leads more K+ excretion with urine.
Manifestations: arrhythmias
(4) Principle of treatment.
• 1) For chloride-sensitive type
• (A) Replenish 0.9% NaCl
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[Na+]
[Cl-]( mmol/L)
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--------------------------------------------------------0.9%NaCl 154
154
Plasma
140
104
--------------------------------------------------------A) Dilute the [HCO3-]
B) Increase the blood volume, reduce the reabsorption of HCO3-.
• C) Increased Cl- in distal tubule leads to increased excretion of
HCO3- in collecting duct.
• (B) Replenish KCl for the patients with
potassium deficiency.
2) For chloride-resistant type
Treating of underlying disorders
Antagonists of aldosterone
Replenish KCl
Acetazolamide乙酰唑胺( inhabit the CA
activity) for the patients with edema with
alkalosis.
• A 25-year-old woman was brought to the
emergency room by her husband. The
patient had one-week history of weakness.
She denied vomiting, diarrhea, or diuretic
use (but a urine test for diuretics is
positive). There was no history of fever or
chills.
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Physical examination:
BP=110/80 mmHg,
Pulse=84/min,
Temperature=37.C.
The neurological examination found weakness
in both lower extremities.
Laboratory results:
[Na+] = 138 mmol/L,
[K+] = 2.1 mmol/L,
[Cl-] = 85 mmol/L,
[HCO3-] = 41 mmol/L,
pH = 7.45,
PaCO2=50 mmHg,
EKG: Sinus rhythm, flattened T-wave
• Hypokalemia,
• metabolic alkalosis.
ΔPaCO2(mmHg)
Secondary compensation
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(12)
• 40+12=52 ±5
= 0.7 x ΔHCO3- ±5
primary change
(41-24)