(4) Respiratory alkalosis

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(4) Respiratory alkalosis

• 1) Concept
• Respiratory alkalosis is defined as a
  primary decrease in H2CO3 (CO2, PaCO2) in
  plasma
• Hypocapnia
• The secondary change is the decrease of
  HCO3 in plasma due to the renal compensation.

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2) Causes and Pathogenesis

• Increased alveolar ventilation
• Hypoxia due to high altitude
• Hysteria
• Fever
• Central nervous diseases
• Gram-negative septicemia
• Salicylate intoxication
• The basic reason of hyperventilation is the
  stimulation of respiratory center.
• Mis-operation of mechanical ventilator

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3) Compensation

• The compensation of respiratory
  alkalosis is in the opposite direction of the
  compensation of respiratory acidosis.
• The main mechanisms are cellular
  and renal compensation
• (How about buffering system, respiration?)

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Cellular compensation for acute typea) H-K
exchange
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b)CO2 moves out of the cells
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(b)The renal compensation for chronic type

• The renal compensation in respiratory
  alkalosis is the same as the renal compensation
  in metabolic alkalosis.
• It may take 35 days to reach the maximal
  renal compensation.

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Changes of laboratory parameters

• Primary decrease of H2CO3
• PaCO2 ?
• Secondary compensation
• AB,SB,BB ???
• AB ?? SB
• BE ?
• pH ?

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Changes of laboratory parameters

• Primary decrease of H2CO3
• PaCO2 decrease
• Secondary compensation
• AB,SB,BB decrease
• AB lt SB
• BE negative value increases
• pH tends to increase.

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Predicted compensatory formula for acute
respiratory alkalosis

• ?HCO3- 0.2x ?PaCO2 2.5
• HCO3- 240.2x (PaCO2 -40)
  2.5
• Secondary compensation primary change
• Value measured gt value predicted with
  metabolic alkalosis
• Value measured lt value predicted with
  metabolic acidosis.
• Maximal compensatory value up to18 mmol/L

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Predicted compensatory formula for chronic
respiratory alkalosis

• ?HCO3- 0.5x ?PaCO2 2.5
• HCO3- 240.5x (PaCO2
  -40)2.5
• Secondary compensation primary change
• Value measured gt value predicted with
  metabolic alkalosis
• Value measured lt value predicted with
  metabolic acidosis.
• Maximal compensatory value up to12 mmol/L

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(3) Effects on the body

•  1) Effects on the central nervous system.
• 2) Effects on metabolism
•  (hypophosphatemia)

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1) Effects on the central nervous system

• (a) Excitability is increased.
• Manifestations are more severe than those
  of metabolic alkalosis.

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The reasons

• (a) Hyperventilation leads to low CO2 in
  plasma and cerebral vasoconstriction, the oxygen
  supply to the brain is decreased.
• (b) The left-shift of oxygen-hemoglobin
  dissociation curve leads to brain hypoxia.

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• Glutamic acid

Glutamate decarboxylase
r-GABA, r-aminobutyric acid
r-GABA transminase
Succinic acid
Krebs cycle
(c) 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.
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2) ???? hypophosphatemia

• ?????????????,?????????????6-???????????,?
  ????, ??????????

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Treatment principle

• For respiratory alkalosis
• Let the patient inhale the air that
  is exhaled by himself (herself) with a mask.

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Thinking method of diagnosis

• (1) via pH acidosis or alkalosis ?
• compensatory or decompensatory ?
• (2) via history primary change
• metabolic or respiratory ?
• (3) via predicted compensatory value
• simple or mixed ?

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Case discussion

• A 32-year-old male presented with vomiting
  of one weeks duration. On examination, he
  appeared dysphoria and had a supine blood
  pressure of 90/60 mmHg and a pulse of 116/min.
• The laboratory results were
• Arterial blood pH7.55 PaCO246 mmHg
• PaO290mmHg
• HCO3-38 mmol/L.

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• See pH
• See primary history
• ?PaCO20.7x?HCO3- 5
• 0.7x 14 5
• 10 5 (515)mmHg
• Predicted 40 5154555,
• measure 46,
• Decompensatory metabolic alkalosis.

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Case discussion

• A 58-year-old man with pulmonary heart
  disease had 3 days of diarrhea.
• pH7.12, PaCO2 85 mmHg,HCO3 - 26 mmol/L
• Na137 mmol/L, Cl- 85 mmol/L
• ?HCO3 - 0.4 x?PaCO2 3 18 3
• Predicted 2418 3 3945

(1) via pH decompensatory acidosis (2) via
history primary change respiratory (3) via
predicted compensatory value mixed Respiratory
acidosis metabolic acidosis (AG??)
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A patient with diabetes

• Measured
• pH 7.32
• PaCO2 30mmHg
• Checked
• Chronic metabolic acidosis
• HCO3- 16 mmol/L
• BE -9 mmil/L

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A patient with CHD

• Measured
• pH7.22
• PaCO2 50mmHg
• Checked
• Respiratory acidosismetabolic acidosis

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Section 3. Mixed types of acid-base disturbances

• (1) Double??? acid-base disorders
• 1)?????????
• ????
• ????
• ????
• ????
• 2)?????
• ????
• ?AG???Cl??
• 3) ???????

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Case discussion

• A 45-year-old man had chronic cough for
  20 years. He had a shortness of breath, orthopnea
  with edematous ankles for 1 month. The
  laboratory findings were
• pH 7.26 PaO255 mmHg
• PaCO260 mmHg AB 22 mmol/L
• See pH Decompensated acidosis
• See history Respiratory disorder
• Calculate

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• Predicted ?HCO3- 0.4x ?PaCO2 3
• HCO3- 240.4x 20 32935
• Measured 22

Respiratory acidosis metabolic
acidosis pH?? HCO3- ??
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Respiratory alkalosis metabolic acidosis

• A patient with salicylic acid poisoning
• (stimulating respiratory center)
• pH 7.45
• PaCO220mmHg
• HCO3-13 mmol/L
• ?HCO3- 0.2x ?PaCO2 2.5
• Predicted HCO3- 24 - 4 20 2.5

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• In metabolic acidosis metabolic alkalosis
• pH is in normal range,
• HCO3- is in normal range.

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(2) Triple??? acid-base disorders

• A 62-year-old woman with chronic
  bronchitis and emphysema for more than 15 years.
  was admitted to the hospital in a confused
  state. Her temperature was 38.5?.
• The laboratory data
• pH 7.27 PaCO265 mmHg
• AB28mmol/L

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Respiratory acidosis metabolic acidosis

• Predicted ?HCO3- 0.4x ?PaCO2 3
• HCO3- 240.4x 25 33137
• Measured28

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• The next day she presented with severe
  vomiting . The laboratory finding
• In venous blood
• K 3.3 mmol/L Cl- 54 mmol/L
• pH 7.4 AB52 mmol/L

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• Respiratory acidosis metabolic acidosis
• metabolic alkalosis
• (causes?)

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• A patient with pulmonary heart disease
  treated by diuretics.
• pH 7.43, PaCO261mmHg, HCO3-38 mmol/L
• Na140mmol/L, Cl- 74 mmol/L,
• K 3.5mmol/L
• PredictedHCO3-32.4
• AG140-(7438)28
• Respiratory acidosismetabolic alkalosismetabolic
  acidosis with increased AG