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Chapter 4(1) Acid – Base Disorders
§1. Acid- Base balance
1.Concept of acid and base
Acid: Acid is a proton donor. (HCl, NH4+)
HCl → H+ + ClNH4+ → H+ + NH3
Base: Base is a proton acceptor. (OH-, HCO3-, NH3)
OH- + H+ → H2O
HCO3- + H+ → H2CO3
NH3 + H+ → NH4+
2.Origins of acid and base in the body
Source of acid:
1) origins of volatile acid
It results from an end-product of oxidative
metabolism namely CO2.
CO2+H2O = H2CO3
Normally produced CO2 300-400 L/d or H+ 15 mol/d.
2) origins of nonvolatile acid ( fixed acid )
It comes from metabolic processes or incomplete
oxidation of glucose or fats and so on. as: H2SO4,
H3PO4, lactic acid, acetoacetic acid, β-hydroxybutyric
acid.
Sulfuric acid:
Catabolism of sulfur-containing amino acids.
Phosphoric acid;
Catabolism of phosphoesters ,phosphoprotein
,nucleotide.
Lactic acid:
Incomplete oxidation of carbohydrate.
Beta-hydroxybutyric acid, acetoacetic acid:
Incomplete oxidation of fatty acid.
Normally produced H+ 50-100 mmol/d .
3) Exogenous acid intake
Salicin intoxication
Hydrochloric acid
Origin of bases:
1) NH3: It is formed by deamination of
amines, amino acid, purines and so on.
2) Eatting salt of organic acid: Sodium
citratc and sodium lactate come from
vegetable and fruits.
3. Regulation of acid – base balance
1) Chemical buffers:
Buffer system is composed by weak acid and weak acid
salt. It may convert strong acid into weak acid or strong
alkali into weak alkali.
NaHCO3+HCl → NaCl+H2CO3
H2CO3+NaOH → H2O+NaHCO3
Major buffer system in the body
Carbonic acid/Bicarbonate(HCO3-/H2CO3) :
The major extracellular buffer，regulated by lungs
and kidneys，effective，determining the pH of
plasma.
Phosphate (HPO42-/H2PO4- ) : Intracellular
Protein (Pr-/HPr) : Plasma/Intracellular
Hemoglobin (Hb-/HHb and HbO2-/HHbO2 ) : RBC
*A buffer system cannot buffer itself.
 fast / no permanence
2) Respiratory control:
Expelling more CO2 through respiration→to
exclude volatile acid.
H+→chemoreceptor → excite respiratory centre →
hyperventilation → exclude volatile acid
Fast / effectively / only excludes
volatile acid

PaCO2(40-80
mmHg)Blood-brain barrier
permeable to CO2: CO2+H2OH2CO3 H++HCO3-(in
cerebrospinal fluid, CSF) [H+]  Central
chemoreceptor(beneath the ventral surface of the
medulla oblongata) Respiratory center  
Ventilation (Main)
PCO2 80 mmHg, inhibition of respiratory center.
PaO2  (30-60 mmHg) /pH  / PCO2Peripheral
chemoreceptor (Carotid bodies, aortic bodies)
Respiratory center  Ventilation (Minor)
Pa O2  30 mmHg, inhibition of respiratory center
3) Role of kidney (exclusion of acid
with conservation of base)
hydrogen ion secreted
ammonium excreted
bicarbonate reabsorbed
by renal tubular cell
 Effectively ( fixed acid may be
excluded ) / slowly
Role of the kidneys
powerfully, slowly
# Proximal tubule:
H+ secretion coupled with
HCO3- reabsorption
# Collecting tubule
H+ secretion and excretion
coupled with the addition of
new HCO3- to the plasma
Secreted ammonia once the
normal urinary phosphate
buffers are saturated.
NH3 + H+  NH4+
4) Role of tissue and cell
cell: intra and extra ions exchange across the cellular
membrane buffering in the cell or titrating base in ECF
bone:
Ca3(PO4)2+4H+
3Ca2++2H2PO4
Decalcification, osteoporosis.
• Effectively / but need time
Acid-base balance:
Acid and bases are continuously produced
in the body, PH is maintained 7.35-7.45 by
four regulation of the body, This condition is
termed as acid-base balance.
§2. Laboratory parameters
of acid-base balance
1. PH：
pH= log [H+]=log1/ [H+] (The logarithm to the
base 10 of the reciprocal of the [H+])
HCO3-(metabolic factor)
pH= pKa+ log ———————————
H2CO3 (respiratory factor)
= pKa + logHCO3-/α×PCO2＝ 6.1+1.3=7.4
Normal plasma pH 7.35-7.45 ( average 7.4 )
2. PaCO2( respiratory parameter ):
Partial pressure of CO2dissolved in arterial plasma(The
pressure is produced by CO2 dissolved in arterial plasma).
Normal range: 4.39~6.25kPa(33~46mmHg)
Average: 5.32kPa(40mmHg)
PaCO2 ＞ Normal (hypoventilation)
a.primary change: RAC
b.secondary change: MAL with respiratory
compensation
PaCO2 ＜ Normal (hyperventilation)
a.primary change: RAL
b.secondary change: MAC with respiratory
compensation
3. SB AB BB BE (metabolic parameter):
SB: HCO3- in plasma under standard condition
AB: HCO3- in plasma under actual condition
22~27 mmol/L
22~27 mmol/L
Average : 24 m mol/L
BB: BB = HCO3- + Pr - + Hb BE: BE = ΔBB = BB-NBB
MAC: primary decreased
MAL: primary elevated
45~55 mmol/L
-3~+3 mmol/L
Normal condition : PaCO2 ＝ 5.32Kpa( 40mmHg )
AB ＝ SB ＝ 24 mmol/L ( average)
AB ＞ SB → CO2 retention: RAC (primary change)
MAL with respiratory compensation
AB ＜ SB → CO2 expiration:RAL (primary change)
MAC with respiratory compensation
AB↑＝ SB↑→ MAL without respiratory compensation
4. AG( anion gap ):
AG=UA(undetermined anion – UC(undetermined cation )
[HCO3- ]+[Cl- ]+UA= [Na+]+UC
AG=UA-UC=[Na+]-([HCO3-]+[Cl-])=140-(24+104)=12mmol/L±2
§3. Simple acid-base disorder
1. Metabolic acidosis
1) concept:
primary disturbance [HCO3-] ↓ ; PH
.
AB↓ , SB↓ , BB↓ , BE ↓ ; PaCO2 ↓ ; AB＜SB
2) clasification:
Normal AG MAC
High AG MAC
3) pathogenesis and mechnisms:
(1) lose of bases
(2) gaining acids
Metabolic acidosis
Causes:
(1) lose of bases (bicarbonate decreased)
Gastrointestinal losses: diarrhea, fistulae and so on.
Renal losses: proximal renal tubular acidosis and distal
renal tubular acidosis
(2) gaining acids (bicarbonate consumed in buffering)
Lactic acidosis: tissue hypoxia, impaired oxygen utilization,
severe liver dysfunction, and shock
Ketoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning,
or starvation
Renal failure: conservation of acids
Exogenous acid intake: ammonium chloride, salicylate,
ethylene glycol(commonly used in antifreeze), or methanol
intoxication
4) Compensation: all regulation system take part in
5) Effects:
(1) Depression of central neural system
a Elevated activities of glutamate decarboxylase →GABA ↑
b.ATP ↓
(2) Depression of heart and vessel(Ca2+ transport disorder;
hyperkalemia;ATP↓):
cardiac output ↓ ;
cardiac arrhythmias;
peripheral vasodilation.
(3) Skin: warm and flashed
(4) Alteration of skeleton:
decacification, retarding growth and osteodystrophy
6) Treatment: administration of 5%NaHCO3, sodium
lactate, THAM.
Respiratory acidosis
1) Concept:
Primary change : retention of CO2; pH .
PaCO2↑ ; AB↑ SB↑ BB ↑ BE ↑ ; AB ＞ SB
2) Classification:
Acute RAC
Chronic RAC
3) Causes :
Disorder of external respiration Overdosage of sedatives, narcotics,etc.
Cerebrovascular accidents.
Cardiopulmonary arrest
Central nervous system trauma, infections
Poliomyelitis
Inhalation of foreign bodies
Chronic obstructive pulmonary disease
Asthma
Pneumonia
Increased CO2 inhalation –
Misoperation of mechanical ventilator
Inhalation CO2 of high concentration
4) Compensation:
In acute RAC:
ion exchange across the membrane and buffering
in cell
体细胞（somatic cell）
CO2+H2O
H2CO3
HCO3-
+
H+
H++A-
K+
K+
HA
Red blood cell
CO2
CO2+H2O H2CO3
H++Hb -
HHb
+
HCO3-
Cl-
In chronic RAC:
excretion of more H+ and ammonia ion
reabsorption of more HCO3- in kindneys
5) Effects:
(1) Neurological effects:
CO2 narcosis
(2) Cardiovascular effects:
arrhythmias;
pulmonary artery hypertension;
cardiac output decrease.
(3) Mixed acid-base imbalance (RAC+MAC)
(4) Inducting of hyerkalemia and hypochloremia
6) principle of treatment:
improve ventilation
Metabolic alkalosis
1) Concept:
Primary disturbance [HCO3-] ↑ ; PH .
AB↑, SB↑, BB↑, BE↑; PaCO2 ↑ ; AB＞SB
2) Classification:
Chloride – responsive MAL
Chloride – resistant MAL
3) Causes and mechanism:
Mechanism:
a. Excessive gain of alkali (bicarbonate)
b. Excessive loss of hydrogen ions, chloride or
potassium ions
Causes:
a.Excessive gain of alkali (bicarbonate)
Bicarbonate intake:treatment of MAC
citrate-containing blood transfusions
Parenteral solution containing lactate
b.Excessive loss of hydrogen ions, chloride or potassium
ions
Gastrointestinal H+ loss:vomiting,gastric suction
Renal H+ loss:Aldosteronism,cushing’s syndrome
thiazide and loop diuretic
potassium deficit
c.Volume contraction
Dehydration
Diuretic therapy
4) Compensation:
Blood buffer role
limitation
Respiratory regulation
Ion exchange and H+ out cell to titrate bicarbonate
Renal role: excluding bicarbonate and conserving H+
5) Effects:
(1) Hypoventilation→ PaCO2 ↑, PaO2 ↓
(2) Agitation of central neural system: GABA↓ → seizures
(3) Increase excitability of the neuromuscle: free [Ca2+] decrease →
muscle tremors
(4) Mental dysfunction: O2 dissociated curve leftshift → impairing O2
release → ATP ↓. At 6-8 hs, 2,3-DPG and curve shifts back towards the
right.
(5) Hypokalemia → reduced fibrillation threshold
6) Principle of treatment:
a. Etiology treatment
b. Replacing N.S or NH4Cl solution.
c. Administration of KCl. or spironolactone if K+
and Cl- deficits are present
d. Carbonic anhydrase inhibitor: acetazolamide
Respiratory alkalosis
1) Concept:
Primary change : H2CO3 ↓ or PaCO2 ↓ ; pH
PaCO2↓ ; AB↓ SB↓ BB↓ BE↓ ; AB<SB
2) Classification:
a. Acute RAL
b. Chronic RAL
.
3) Causes and mechanisms:
Mechanisms: Hyperventilation
Causes:
a. Psychogenic hyperventilation:Hysteria
b. Stimulation of respiratory center:
High altitude hypooxia
Salicylate toxication
Blood ammonia↑(Hepatic encephalopathy)
Encephalitis
Brain injury
Fever
c. Inappropriately high ventilator settings
4) Compensation:
In acute RAC:
Ion exchange, H+ out of cell to titrate base in ECF
In chronic RAC:
Decreased excretion of H+ and NH4+
Decreased reabeorption of HCO3-
5) Effects:
(1) Increased excitability of the nerve and muscle
(2) Mental dysfunction
(3) Hypokalemia,hypochloridemia
6) Principle of treatment:
a. Decreased ventilation by administration of sedative.
b. Application of a plastic bag to inspire more amount of
CO2 gas
Parameter changes of simple types
Disorder
Primary Change
Second Response pH
Metabolic acidosis
HCO3- 
PaCO2 
pH
Respiratory acidosis
PaCO2 
HCO3- 
pH
Metabolic alkalosis
HCO3- 
PaCO2 
pH
HCO3- 
pH
Respiratory alkalosis PaCO2 
Compensated X：after compensation, pH still in normal.
Uncompensated X： after compensation, pH still abnormal.
§4. Mixed acid –base disturbance
Definition : more than one primary acid-base disorde
coexist in a patient.
Double disorders
1) MAC+RAC: diabetic ketosis with pulmonary disease
2) MAL+RAL: vomiting with hyperventilation
3) MAC+RAL: uremia with high fever
4) MAL+RAC: diuretics with respiratory failure
5) MAC+MAL: heart failure with hypokalemia
Triple disorders :
respiratory acidosis
+ MAC + MAL
respiratory alkalosis
§5. Diagnosis
1. According to pathogensis establishing primary change
2. Manifestation: excitation — alkalosis
inhibition — acidosis
3. According to PH
PH<7.35 —acidemia — acidosis
PH>7.45 — alkalemia — alkalosis
PH=7.35~7.45: normal condition
complete compensation
mixed acid-base disturbance
4. Condition of compensation:direction；predicted compensative
value；compensative limit
5. Estabolilshed triple disorders: utilized AG
The patient was suffered from salicylate intoxication. His bloodgas parameters (lab. Value): PH = 7.45 PaCO2 = 2.6 kpa (20mmHg)
HCO3- =13mmol/L .what acid-base disorders presented in
this patient ?
Causes: salicylate intoxication. Primary change is HCO3- decreased.
HCO3- =13mmol/L<24mmol/L
MAC
pH: pH=7.45=N
compensated MAC
mixed acid-base imbalance (MAC+RAL)
Compensatory condition:
PaCO2 =2.6kpa(20mmHg)<5.32kpa(40mmHg)
Calculate: 1.2×ΔHCO3±2=1.2 ×(24-13) ±2=13.2 ±2=11.2-15.2
Predicted PaCO2 value =40 - (11.2or15.2)=24.8-28.8mmHg
Actual PaCO2=20mmHg < predicted PaCO2=24.8 –28.8mmHg
diagnosis: MAC+RAL