(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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(a) Cellular compensation for acute
type
a) 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 3~5 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 < SB
BE negative value increases
pH tends to increase.
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Predicted compensatory formula for
acute respiratory alkalosis
ΔHCO3HCO3-
= 0.2x ΔPaCO2 ± 2.5
= 24+0.2x (PaCO2 -40)± 2.5
Secondary compensation
primary change
Value measured > value predicted: with
metabolic alkalosis
Value measured < value predicted: with
metabolic acidosis.
Maximal compensatory value up to:18 mmol/L
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Predicted compensatory formula for
chronic respiratory alkalosis
ΔHCO3HCO3-
= 0.5x ΔPaCO2 ± 2.5
= 24+0.5x (PaCO2 -40)±2.5
Secondary compensation
primary change
Value measured > value predicted: with
metabolic alkalosis
Value measured < value predicted: with
metabolic acidosis.
Maximal compensatory value up to:12 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
Kreb’s 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) 低磷血症 hypophosphatemia
细胞内碱中毒使糖元分解增多,在磷酸
化酶作用下形成葡萄糖6-磷酸盐等磷酸化合
物增多,需用磷增多, 细胞外磷进入细胞内。
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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 week’s 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: pH=7.55
PaCO2=46 mmHg
PaO2=90mmHg
[HCO3-]=38 mmol/L.
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See pH
See primary history
ΔPaCO2=0.7xΔHCO3- ± 5
= 0.7x 14 ± 5
= 10 ± 5 (5~15)mmHg
Predicted 40+ 5~15=45~55,
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.
pH=7.12, PaCO2= 85 mmHg,HCO3 - =26 mmol/L
Na+=137 mmol/L, Cl- =85 mmol/L
ΔHCO3 - =0.4 xΔPaCO2 ± 3 = 18 ± 3
Predicted 24+18 ± 3 = 39~45
(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:
pH=7.22
PaCO2 = 50mmHg
Checked:
Respiratory
acidosis+metabolic
acidosis
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Section 3. Mixed types of acid-base
disturbances
（1） Double双重性 acid-base disorders
1）呼吸性+代谢性混合型
呼酸+代酸
呼酸+代碱
呼碱+代酸
呼碱+代碱
2）代谢混合型
代酸+代碱
高AG代酸+高Cl代酸
3) 呼吸混合型？？
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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
PaO2=55 mmHg
PaCO2=60 mmHg
AB = 22 mmol/L
See pH: Decompensated acidosis
See history: Respiratory disorder
Calculate:
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Predicted: ΔHCO3- = 0.4x ΔPaCO2 ± 3
HCO3- = 24+0.4x 20 ± 3=29~35
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
PaCO2=20mmHg
HCO3-=13 mmol/L
ΔHCO3- = 0.2x ΔPaCO2 ± 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三重性 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
PaCO2=65 mmHg
AB=28mmol/L
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Respiratory acidosis + metabolic acidosis
Predicted: ΔHCO3- = 0.4x ΔPaCO2 ± 3
HCO3- = 24+0.4x 25 ± 3=31~37
Measured:28
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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
AB=52 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, PaCO2=61mmHg, HCO3-=38 mmol/L
Na+=140mmol/L, Cl- = 74 mmol/L,
K+ = 3.5mmol/L
Predicted[HCO3-]=32.4
AG=140-(74+38)=28
Respiratory acidosis+metabolic
alkalosis+metabolic acidosis with increased AG
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