1. acid-base disturbance

2. What is acid ？
What is base ？

3. The concept of acid and base
H2CO H++HCO3-
NH H++NH3
H2PO H++HPO42-
HPr H++Pr-

4. Regulation of acid-base balance
1.  origin of acid and base in the body
volatile acid: H2CO3 (15mol/day)
sulfuric acid
1) acids phosphoric acid
fixed acid: uric acid
(90mmol/L) mesostate
2) base: salt of organic acid; NH3

5. 2.  regulation of acid-base balance
  1) role of buffer
HCO-3/H2CO %
Hb-/HHb
buffer system HbO-2/HHbO %
Pr-/HPr %
Phosphate %
Henderson-Hasselbalch
pH = pKa + lg [HCO-3]/[H2CO3]
= lg 20/1 = =7.4
buffer of fixed acid: HCO-3/H2CO3
buffer of volatile acid: Hb-/HHb

6. CO2
Cl-
CO2+H2O
C.A.
H2CO3
HCO-3
H+--Hb-
RBC

7. 2) respiratory regulation
alteration of ventilation
alteration of breathe out of CO2
PaCO central
[H+] peripheral respiration
PaO (receptor)
PaCO (＞80mmHg)
inhibition of respiratory center
3) cellular action exchanges of H+ and K+

8. 4) renal regulation ① acidification of proximal renal tubule Blood vessel Renal tubule epithelium Tubule K+
Na+ H+
H2CO3
C.A.
HCO H2O+CO2
Na+ Cl-
HCO-3
H2CO3
H20
泌H+ 与Cl- 重吸收拮抗与泌NH3协同
NH3

9. ② acidification of distal renal tubule
H+-pump
NH+4
Renal tubular epithelial cells
H2CO3 H+
NH3
HCO-3 H2O+CO2 K+

10. Acid Base parameter /Arterial Blood Gases (ABGs)

11. Arterial Blood Gas Sampling

12. 1. pH important and inexact parameter
normal range: 7.35~7.45
2. PaCO2 partial pressure of CO2 of dissolved
in arterial plasma (respiratory parameter)
normal range: 4.4~6.25kPa(33~46mmHg)
primary change:
respiratory acidosis PaCO2
respiratory alkalosis PaCO2
secondary change:
metabolic acidosis PaCO2
metabolic alkalosis PaCO2

13. 3.  standard bicarbonate(SB)
and actual bicarbonate(AB)
SB: [HCO-3] in plasma under standard condition
(38℃; PO2=150mmHg; PCO2=40mmHg)
AB: [HCO-3] in plasma under actual condition
Normal range: 22~27mmol/L ; AB=SB
4. buffer base(BB)
sum of all buffer base in blood
normal range: 45 ~ 55mmol/L
5. base excess(BE)
normal range: ±3mmol/L

14. 6.  anion gap (AG)
Normal range: 12 ± 2 mmol/L
Na+
Cl-
HCO-3 AG

15. acid-base disturbance
Because of the pathological
process of acid-base overload
or regulation disorder lead to
destruction of acid-basestability.

16. [HCO3－] pH=pKa+lg [H2CO3] 20 =pKa+lg 1 = 6.1 +1.3 = 7.4
Henderson-Hasselbalch方程
pH=pKa+lg
[HCO3－]
[H2CO3]
=pKa+lg 20 1
= = 7.4

17. Simple Acid-Base Disorders
Clinical disturbances of acid base metabolism classically are defined in terms of the HCO3¯  /CO2  buffer system.
Acidosis – process that increases [H+] by increasing PCO2 or by reducing [HCO3-] Alkalosis – process that reduces [H+] by reducing PCO2 or by increasing [HCO3-]
Henderson Hasselbalch equation: 
pH = log [HCO3-]/ 0.03 PCO2
Since PCO2 is regulated by respiration, abnormalities that primarily alter the PCO2 are referred to as respiratory acidosis (high PCO2) and respiratory alkalosis (low PCO2).
In contrast, [HCO3¯] is regulated primarily by renal processes. Abnormalities that primarily alter the [HCO3¯] are referred to as metabolic acidosis (low [HCO3¯]) and metabolic alkalosis (high [HCO3¯]).

21. Simple acid-base disturbance
1.  metabolic acidosis
concept: the primary disturbance is a decrease
of [HCO-3] in the arterial plasma
1) cause and pathogenesis
lactic acidosis: hypoxia, diabetes
liver disease
ketoacidosis: diabetes, starvation
① metabolic
acidosis in severe renal failure: fixed acids
increased AG
salicylic acid acid
poisoning: intake food

22. diarrhea;
GI: intestinal suction
(loss of intestinal fistula
HCO-3) biliary fistula
② metabolic
acidosis in early renal failure:
normal AG NH3 secretion
H+ secretion
Renal tubular acidosis:
kidney: depressant of C.A.
(loss of acetazolamide
HCO-3) intake of Cl-
NaCl, NH4Cl
Hyperkalemia

23. 2) compensatory regulation ① buffer: ② respiratory compensation
③ cellular compensation
④ renal compensation
[H+] : C.A H+ secretion
  NH3 secretion
[HCO-3] / [H2CO3] = 20:1 compensation
acidosis
[HCO-3] / [H2CO3] < 20:1 decompensation
(SB AB BB BE PaCO2 AB < SB)

24. 3)  effect on body
① cardiovascular system
hyperkalemia arrhythmia
[H+] : contractility
peripheral resistance
② central nervous system
[H+] ATP , γ-amino butyric acid
(somnolence, coma)
4) principles of treatment

25. 2. respiratory acidosis
concept: The primary disturbance is an
elevation in plasma [H2CO3]
1) cause and pathogenesis
Barbital
depression of CNS head injury
① CO2 breathe paralysis of respiratory muscles
out disease of airway or lung
chest injury
② inhalation of CO2

26. cells: exchange of H+ and K+ kidney: secretion of H+ and NH3
2) compensation
buffer: Hb-/HHb
cells: exchange of H+ and K+
kidney: secretion of H+ and NH3
(PaCO2 SB AB BB BE AB＞SB)
3) effect on body
① CNS
CO Cerebral vascular dilatation, 
intracranial pressure headache, delirium CO2 narcosis respiration
② cardiovascular system

27. concept: the primary disturbance is
4) principles of treatment
improve ventilation
3. metabolic alkalosis
concept: the primary disturbance is
an increase of [HCO-3] in the
arterial plasma
1) causes and pathogenesis

28. digestive tract
vomiting; gastric suction(loss of HCl)
①loss diuretics distal flow rate
of H (furosemide) blood volume ADS
kidney hyperaldosteronism H+-Na+exchange
H+-K+exchange between
Hypokalemia intra- and extra-cell
renal secretion of H+
hypochloremia

29. NaHCO3
②intake transfusion of banked blood
of base (citrate)
2)   compensation of the body
① respiration compensation are limited
(hypoxia)
② cells compensation hypokalemia
③ kidney pH inhibition of carbonic
anhydrase (C.A.)
secretion of H+
(SB AB BB BE PaCO2 AB＞SB)

30. inhibition of glutamate decarboxylase
3) effects on body
inhibition of glutamate decarboxylase
① CNS γ-amino butyric acid dysphoria
insanity
pH brain-vessel dizziness
contraction brain delirium
O2 dissociation hypoxia Coma
curve shifting to left
② neuromuscle pH free Ca tic
③ hypokalemia arrhythmia

31. 4)  principles of treatment
loss of H+ digestive tract
diuretic ; hypokalemia %NaCl; KCl
hyperaldosteronism
antisterone; diamox( acetazolamide )

32. 4. respiratory alkalosis
concept: the primary disturbance is decrease
of [H2CO3] in plasma
1) cause and pathogenesis
hypotonic hypoxia
pneumonia
hyperventilation hysteria; fever; [NH3]
hyperthyroidism
misoperation of ventilator

33. respiration (slight inhibition)
2) compensation cells (exchange of H+-K+)
kidney secretion of H+
(PaCO2 ; SB AB BB BE ; AB＜SB)
3) effects on body
It is as same as metabolic alkalosis.
dizziness and convulsion are happened easily
4) principles of treatment
inhalation of 5%CO2

34. Increased rate and depth of breathing ("Kussmaul breathing")
Decreased heart rate (bradycardia)

35. Mixed acid-base disturbance
1. dual acid-base disturbance
1) metabolic acidosis plus respiratory acidosis
heart beat [HCO-3]
respiration stop character PaCO pH
2) metabolic alkalosis plus respiratory alkalosis
hepatic NH PaCO2
failure diuretic character [HCO-3] pH
3) respiratory acidosis plus metabolic alkalosis
pulmonary heart disease
diuretic pH ±

36. 5) metabolic acidosis plus metabolic alkalosis ketoacidosis(diabetes)
4) respiratory alkalosis plus metabolic acidosis
infective shock
fever pH ±
5) metabolic acidosis plus metabolic alkalosis
ketoacidosis(diabetes)
vomiting pH ±
2.  triple acid-base disturbance
1) respiratory acidosis; metabolic acidosis
and alkalosis
pulmonary heart disease; vomiting
2) respiratory alkalosis; metabolic acidosis
and metabolic alkalosis
fever; vomiting; diarrhea (food poisoning)

38. Discuss of case method: 1. pH 2. primary factor and parameter
3. secondary factor and compensation
4. expected range of compensation
№1:
patient, female, 46, chronic pyelitis pH
PaCO mmHg
CO2 .CP ml%
SB mmol/L
BE mmol/L

39. The scope of compensatory responses of acid-base disorders
acute respiratory acidosis : △[HCO-3]=0.1×△PaCO2 ±1.5
chronic respiratory acidosis: △[HCO-3]=0.4×△PaCO2 ±3.0
acute respiratory alkalosis : △[HCO-3]=0.2×△PaCO2 ±2.5
chronic respiratory alkalosis:△[HCO-3]=0.5×△PaCO2±2.5
metabolic acidosis: △PaCO2 =1.2×△[HCO-3] ±2.0 
metabolic alkalosis: △PaCO2 =0.7×△[HCO-3] ±5.0

40. №2: patient, male, 45, chronic bronchitis pH 7.26 PaCO2 60mmHg
BB mmol/L
SB mmol/L
BE mmol/L
after treatment pH
PaCO2 70mmHg
BB mmol/L
BE mmol/L

41. №3.
patient, male, 47, purulent appendicitis, he was treated with abdominal suction and persistent gastrointestinal decompression after operation. pH
PaCO mmHg
CO2 .CP. 90ml%
SB mmol/L
BE mmol/L
K mmol/L
Cl mmol/L

42. №4.
A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF.
Lab results
Serum chemistry: Na 132, K 2.7, Cl 79, Glu 815,
Lactate urine ketones 3+
ABG: pH PCO HCO3¯ pO2 82  
 What is the acid base disorder? Why?