(2) Respiratory acidosis

• 1) Concept
• 2) Causes and Pathogenesis
• 3) Compensation
• 4) Effects on the body
• 5) Principle of treatment
 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.
•
•
•
 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
 (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脊髓灰白质炎, Guillain-Barre syndrome
脊神经根炎),
• 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.
 (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)
 3) Compensation against respiratory
acidosis

• (a) Non- [HCO3¯ ]/[H CO ] buffering systems

2 3

• (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? )
(a) Non- NaHCO3/H2CO3 buffering
systems
Hb-/HHb
HbO-2/HHbO2
Pr-/HPr
Phosphate
(b) H+ moves into the cell
 (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
 Predicted compensatory formula of acute
respiratory acidosis

ΔHCO3 - = 0.1x ΔPaCO2 ± 1.5

HCO3- = 24+ 0.1x ΔPaCO2 ± 1.5
Secondary compensation , primary change
The maximal increased value up to
30 mmol/L
Decompensation
 (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 )
Predicted compensatory formula of chronic
respiratory acidosis

ΔHCO3- = 0.4x ΔPaCO2 ± 3

HCO3- = 24+0.4x ΔPaCO2 ± 3
Secondary compensation primary change
Value measured > value predicted: with
metabolic alkalosis
Value measured < value predicted: with
metabolic acidosis.
Maximal compensatory value up to:45mmol/L
 Changes of laboratory parameters

• Primary increase of [H2CO3]:

• PaCO2 ?
• Secondary compensation:
• AB,SB,BB ???
• AB ?? SB
• BE ?
• pH ?
 Changes of laboratory parameters

• Primary increase of [H2CO3]:

• PaCO2 increases
• Secondary compensation:
• AB,SB,BB increases
• AB > SB
• BE positive value increases
• pH tends to decrease.
 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
 (A) Depression of mental activity
• (a) Manifestations
• Obtundation (thinking slowly) , headache,
somnolence嗜睡, 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 肺性脑病 in
l
respiratory failure.
(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.
 Glutamic acid
Glutamate decarboxylase

r-GABA, r- gama aminobutyric acid

r-GABA transaminase
Succinic acid

Kreb’s 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).
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 α-receptor in cerebral
vessels, so vasodilation in brain.
(B) Effects on the cardiovascular system

• (a) Impairment of myocardial contraction

• (b) The hemodynamic effect
• (c) Arrhthmias due to hyperkalemia

(C) hyperkalemia
 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.
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
Before:Decompensatory respiratory
• acidosis
• After: Decompensatory metabolic alkalosis.

• Reasons: too fast elimination of CO2

• slow renal elimination of HCO3-
• (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.
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: pH=7.34 PaCO2=60 mmHg
• PaO2=50 mmHg
• [HCO3-]=31mmol/L.
•
• ΔHCO3-= 0.4x ΔPaCO2 ± 3=??