(2) Respiratory acidosis

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(2) Respiratory acidosis

• 1) Concept
• 2) Causes and Pathogenesis
• 3) Compensation
• 4) Effects on the body
• 5) Principle of treatment

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1) Concept

• Respiratory acidosis refers to the primary
  increase of H2CO3, which is initiated by an
  elevation of carbon dioxide tension (increased
  PaCO2).
• The increase of H2CO3 is also called
  hypercapnia.
•  

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2) Causes and Pathogenesis

• The basic reasons
• (a) decreased ventilation, which leads to the
  decreased elimination of CO2 from lung
• (b) increased inhalation of CO2.
• Acute
• Chronic

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(a) Acute respiratory acidosis

• a) depression of respiratory center by cerebral
  diseases (trauma, infections) and drugs
  (over-dosage of anesthetics, sedatives),
• b) neuromuscular disorders (acute hypokalemia,
  poliomyelitis??????, Guillain-Barre
  syndrome?????),
• c) cardiopulmonary arrest.
• d) obstruction of respiratory tract.
• e) Chest wall diseases (fracture of rib),
• f)mis-operating of respirator.
• (b) increased inhalation of CO2.

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(b) Chronic respiratory acidosis

• Chronic obstructive pulmonary diseases
  (emphysema, chronic bronchitis with
  hypoventilation) cause the chronic respiratory
  acidosis.
• Brain tumors (affecting the respiratory center in
  which the ventilation is decreased)

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3) Compensation against respiratory acidosis

• (a) Non- HCO3 /H2CO3 buffering systems
• (b) Cellular compensation
• H moves into the cell
• CO2 moves into the cells
• (c)The renal compensation for chronic
  resppiratory acidosis.
• ( How about buffer pair HCO3 /H2CO3 and
  respiratory compensation? )

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(a) Non- NaHCO3/H2CO3 buffering systems

• Hb-/HHb
• HbO-2/HHbO2
• Pr-/HPr
• Phosphate

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(b) H moves into the cell
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(c) CO2 moves into the cells

• When CO2 in ECF(serum) is increased, CO2 will
  move into the cells, CO2 combines H2O to form
  carbonic acid, then H2CO3 dissociates to form H
  and HCO3 .
• The HCO3 moves out of the cells as a exchange
  for electric neutrality, at the same time Cl
  moves into the cells for electrical balance.
• HCO3 and Cl exchange

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Predicted compensatory formula of acute
respiratory acidosis

• ?HCO3- 0.1x ?PaCO2 1.5
• HCO3- 24 0.1x ?PaCO2 1.5
• Secondary compensation , primary change
• The maximal increased value up to 30
  mmol/L
• Decompensation

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(c) The renal compensation

• The renal compensation in respiratory acidosis is
  the same as the renal compensation in metabolic
  acidosis.
• a) The activity of carbonic anhydrase (CA)
  increases,
• b) The activity of glutaminase is increased, more
  NH4 is excreted into tubular lumen.
• c) The end urine is more acidic. (NaH2PO4 )
•  

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Predicted compensatory formula of chronic
respiratory acidosis

• ?HCO3- 0.4x ?PaCO2 3
• HCO3- 240.4x ?PaCO2 3
• Secondary compensation primary change
• Value measured gt value predicted with
  metabolic alkalosis
• Value measured lt value predicted with
  metabolic acidosis.
• Maximal compensatory value up to45mmol/L

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Changes of laboratory parameters

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

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Changes of laboratory parameters

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

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4)Effects on the body

• In metabolic acidosis the H in plasma is
  increased.
• In respiratory acidosis both H and CO2
  concentration are increased.
• The main manifestations are
• (A) depression of mental activity
• (B) effects on the cardiovascular system.
• (C) hyperkalemia

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(A) Depression of mental activity

• (a) Manifestations
• Obtundation (thinking slowly) , headache,
  somnolence??, confuse, coma and asterixis
  (fluttering-like tremor ) may be noted.
• These effects on CNS caused mainly by elevated
  CO2 have been termed CO2 narcosis.
• Pulmonary encephalopathy ???? in respiratory
  failure.

l
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(b) Mechanisms

• a) Increased H cause cerebral vasodilatation,
  then cause brain edema. Increased blood volume
  will cause high intracranial pressure.
• b) High H increases the permeability of
  cerebral blood vessels. Decreased plasma COP and
  increased interstitial COP can lead to brain
  edema.

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• Glutamic acid

Glutamate decarboxylase
r-GABA, r- gama aminobutyric acid
r-GABA transaminase
Succinic acid
Krebs cycle
C) The production of GABA (gama
aminobutyric acid, a inhibitory transmitter) is
increased due to the activity of enzyme for the
production is increased, and the activity of
enzyme for the decomposition is decreased in low
pH (acidosis).
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d) Increased CO2 leads to ( brain ) vasodilation
directly. (higher intracranial pressure)

• Increased CO2 stimulates via
  chemoreceptor sympathetic activity, then leads
  indirectly to stronger vasoconstriction than
  vasodilation.
• There is no a-receptor in cerebral
  vessels, so vasodilation in brain.

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(B) Effects on the cardiovascular system

• (a) Impairment of myocardial contraction
• (b) The hemodynamic effect
• (c) Arrhthmias due to hyperkalemia
• (C) hyperkalemia  

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5) Principle of treatment

• (a) Treat the primary diseases which cause
  respiratory acidosis. (antibiotic, antispastic
  drugs)
• (b) Improve properly the ventilation.
• (c) Prevent from (respiratory alkalosis)
  over-ventilation during artificial respiration.

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Case Discussion No.3

• Female, 11 years old. Guillain-Barre syndrome
• before respirator
  after respirator
• pH 7.29
  7.56
• PaCO2(mmHg) 85
  45
• BE(mmol/L) 9.9
  16
• BB(mmol/L) 56
  61
• SB(mmol/L) 32.8
  39
• AB(mmol/L) 39.5
  39

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• BeforeDecompensatory respiratory
• acidosis
• After Decompensatory metabolic alkalosis.
• Reasons too fast elimination of CO2
  
• slow renal elimination of HCO3-

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• (c) Can we replenish alkaline (HCO3, sodium
  lactate ) to the patients with respiratory
  acidosis?
• (d) pay attention to K in serum during the
  treatment of acidosis.

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Case Discussion

• A 52-year-old man with chronic obstructive lung
  disease was admitted to the hospital with
  worsening dyspnea. He appeared cyanotic and in
  respiratory distress.
• The laboratory data
• Arterial blood pH7.34 PaCO260 mmHg
• PaO250 mmHg
• HCO3-31mmol/L.
•  
• ?HCO3- 0.4x ?PaCO2 3??