Acid-base disturbance

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Acid-base disturbance
Zhao Mingyao BMC.ZZU
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• Acid? ------- Base?
• pH in arterial blood 7.357.45

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H concentration in body fluid

• ECF H
  mol/L pH
• Arterial blood 4.0 10-8 7.40
  0.05
• Venous blood 4.5 10-8 7.35
• Interstitial fluid 4.5 10-8
  7.35
• Intracellular fluid 1.0 10-6 6.0
• to 4.0 10-8
  7.4
• Gastric fluid
  0.91.8 (3.0)
• Pancrea fluid
  7.8 8.4

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Metabolic processes generate acids
Cells
H 100 nmol/L (pH 7)
H
H
Artery
H 36 nmol/L pH7.4
H
H
H 44 nmol/L pH7.36
Capillary
Vein
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• Section 1 Acid-base biochemistry

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1. Generation of Acid-Base

• (1) Sources of acid
• 1)volatile acid
• CO2 H2O ? H2CO3 ? H HCO3-
• ( H
  15 mol /d)
• 2)fixed acid (non-volatile acid)
• phosphoric, sulfuric, lactic, ketone
  bodies etc.
• H 0.05 0.10 mol /d

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Sources of acid in body
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(2) Sources of bases 1)products of
metabolism (small amounts)Such as ammonia (NH3)
2)dietary intake(vegetables and fruits)
sodium citrate
acids production gtgtbases, in commen
renal reabsorption

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renal reabsorption

pH 7.357.45 in Arterial blood
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2. Henderson-Hasselbalch Equation
HCO3-
pHpKalg
H2CO3
6.1 lg HCO3- / 0.03 PCO2 6.1 lg 24 /
1.2 7.4
6.1 1.3 7.4
pH 7.357.45
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HCO3-
pH ?
H2CO3
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Strong acid pulse
pH
?
Strong base pulse
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( eg . 24/1.2 or 40/2 or 10/0.5)
1
20
?
( lt20/1 or gt20/1 )
1
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Henderson-Hasselbalch Equation

• Compensatory pH normal, but ? change
• Decompensatory pH, HCO3 -, H2CO3 change
• 
  

HCO3-
?
pH
H2CO3
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fulcrum
Relationship between Henderson-Hasselbalch
Equation and pH
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• Section 2 Regulation of acid-base
• in body fluid

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What happens in its body
H
iv lactic acid
iv bicarbonate
?
?
?
?
acidosis
alkalosis
death
death
?H?
7.8
7.35 7.45
6.8
pH
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Why does body keep acid-base balance of body
fluid ?
H
Cellular signal
? Enzyme ATP
cell
Ion distribution? electrical action
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• body maintain humoral acid-base balance by
• 1. blood buffer system
• 2. lung
• 3. kidney
• 4. cell

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1. Blood buffer system

HCO3- / H2CO3 Hb- / HHb Pro- / HPro HPO42-
/ H2PO4-
A-/HA
Buffer system can bind and release H
Dissociated buffer H H undissociated
buffer
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HCO3- / H2CO3 determines the pH of blood

• pH pK lg HCO3- / H2CO3
• HCO3- / H2CO3 is the major extracellular
• buffer 53
• H2CO3 regulated by lung
• HCO3- regulated by kidney
  
  
• 
  
  
  
  

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2. Pulmonary regulation
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Pulmonary regulation
Central control
PaCO2
CNS
chemoreceptor

Peripheral chemoreceptor
respiration
PaO2?pH?PaCO2
in the carotid and aortic bodies
peripheral regulation
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3. Renal regulation
excreting H keeping base
(1) bicarbonate reabsorption (NaHCO3)
(2) phosphate acidification
(3) ammonia excretion
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(1)Reabsorption of HCO3- in different segments of
renal tubule
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Bicarbonate reabsorption in proximal tubules
Na
CA
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(2) Phosphate acidification in distal tubules
ATP
Cl-
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(3) Ammonia excretion in proximal tubular cells

• Glutamine
  Tubular
• 
  lumen
• glutaminase
  
• 
  NH3 NH3
• ?-ketoglutaric acid
• 
  NH4 NH4
• H2CO3
  Na
• Na
• HCO3- H
  H

ATP
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4. cellular buffer

• H-K exchange between intra- and extra- cell
• Cl--HCO-3 exchange between intra- and extra-RBC
  or/ gastric cell

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Section 3 Laboratory tests

• Parameters of acid-base representing
• pH
• PaCO2
• HCO3- ( SB, BE, BB )
• Annion gap

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1. pH in normal level
(1) true normal (2) compensatory (3) mixed
with opposite effect
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Weak tolerance to alkalosis
7.35 7.45
6.8
pH
7.8
acidosis
alkalosis
death
death
16 nmol/L
40
160
?H?
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2. Partial pressure of CO2, PaCO2
tension produced by CO2 dissolved physically in
plasma
Normal 40mmHg (3545) H2CO3 40
0.03 1.2mmol/L
PaCO2? Res Acidosis or ?PaCO2 ?Res alkalosis
or ?
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3. HCO3-
normal 24 mmol/L (2227)
SB and AB
BB
BE
Primary and secondary change ?
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4. Anion gap (AG)
AG UA UC UA Undetermined anion UC
Undetermined cation
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AG UA - UC


Cl- (104)
Na (140)
Na UC Cl- HCO3- UA
AG Na - Cl- - HCO3- 140-104-24
12 (mmol/L)
HCO3- (24)
AG
UA (23)
UC (11)
Normal 1014mmol/L
Distinguishing metabolic acidosis
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An elevated Anion Gap always strongly suggests a
Metabolic Acidosis

• If AG is 20-30 then high chance (67) of
  metabolic acidosis
• If AG is gt 30 then a metabolic acidosis is
  definitely present

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Summary of indexes
1. pH 2. Metabolic factor HCO3- SB, BB,
BE, AG 3. Respiratory factorPaCO2

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Section 4 Simple acid-base disorders

• Concept
• Compensation

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Classification of
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Analysis of simple acid-base disorder
7.4?
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• Part 1 Metabolic acidosis
• Concept HCO3-p ? primarily

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Changes of laboratory test
Primary pH ? HCO3- ? Secondary
PaCO2 ? Kb?
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Classification

• Met acidosis with High AG
• Met acidosis with Normal AG

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Met acidosis with normal AG
Comparison between Met acidosis with High AG and
normal AG
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1. Cause and mechanisms

• (1) fixed acid production? lactic acidosis,
  ketoacidosis, excess acetylsalicylic acid , drugs
  yielding hydrochloride acid
• (2) fixed acid removing? RTA, RF
• (3) HCO3- loss? diarrhea , intestinal suction
• (4) hyperkalemia
• (5) hyperchloremia

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2. Compensation of body
(1) Blood buffer system (2) lung (3) kidney (4)
cell
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3.Effects on the body
(1) Cardiovascular system

• Inhibiting myocardial contraction

• Arrythmia

• Responsibility?of vessel to
• catecholamine

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(2) Central nervous system

• Cerebral energy production?

• GABA ?

decarboxylase ()
Glutamate
GABA?
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(3) Hyperkalemia
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4. Principle of prevention treatment
1.Treatment of primary disease
2.Supplement of base NaHCO3 THAM( Tris,
Trishydroxymethyl amino methane, C4H11NO3 )
lactic sodium
3.Correcting and preventing water, electrolytes
disorders
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• Part 2 Respiratory acidosis

Concept H2CO3 p?primarily
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Changes of laboratory test
Primary pH ? PaCO2
? Secondary HCO3- ? Kp ?

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1. Causes and mechanisms

• Excreting CO2 ?
• Inhaling excessive CO2

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2. Compensation of respiratory acidosis
Blood Lung Kidney cell
H2CO3 p?
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Changes of laboratory test
Acute pH PaCO2 HCO3-
PaCO2 10mmHg
HCO3- compensatory ? 1 mmol/L
Chronic pH PaCO2 HCO3-
PaCO2 10mmHg
HCO3- compensatory? 3.5 mmol/L
Cl- ?
K ?
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3. Effect of
Similar to Met Acidosis, but obvious sign of CNS

• CNS Acidosis

• Cerebral blood flow?

• With hypoxia in same time

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4. Principle of prevention treatment
(1)improving alveolar ventilation
(2)supplement of base
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• Part 3 Metabolic alkalosis

Concept HCO3-p ?primarily
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Changes of laboratory test
Primary pH ? HCO3- ? Secondary PaCO2
? Kb ?
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• 1.Causes and mechanisms
• Base intake ?
• H loss ?
• Hypokalemia
• hypochloremia
• Volume contraction

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Classification saline-responsive alkalosis
---- induced by hypochloremia
saline-resistant alkalosis ---- induced by
nonhypochloremia
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2. Compensation
(1) Blood buffer system ( limited ) (2) lung (3)
kidney (4) cell
HCO3-
pH?
H2CO3
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3. Effects
(1) CNS ?

• GABA?

decarboxylae (-)
Glutamate
GABA ?
Hypoxia
GABA transaminase ()
succinate semialdehyde
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(2)Neuromuscular excitability

• mechanism
• pH?,Free Ca2b?
• CNS

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(3) left-shift of oxyhemeglobin
dissociation curve
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(4) Hypokalemia
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4. Principle of prevention treatment

• (1)Treatment of primary disease
• (2)Normal saline
• ? saline-responsive alkalosis
• saline-resistant alkalosis
• CA inhibitor
• ADS inhibitor
• (3)Acid-containing drug

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• Part 4 Rrespiratory alkalosis

H2CO3p ?primarily
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Changes of laboratory test
Primary pH ? PaCO2 ? Secondary
HCO3- ? Kp ?
Cl-p ?
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1. Causes and mechanisms
Excreting excessive CO2
(1) Hypotonic hypoxia (2) Disease of CNS
(3) Psychological factors (4) Hypermetabolism
(5) Drugs
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2. Compensation of respiratory alkalosis
Blood Lung Kidney cell
?
H2CO3 p?
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Compensatory changes
Acute PaCO2 ? 10 mmHg HCO3-
compensatory ? 2 mmol/L
Chronic PaCO2 ? 10 mmHg HCO3-
compensatory ? 4 mmol/L
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3. Effect of

• Similar to Met Alkalosis

Rapid and obvious
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4.Principle of prevention treatment
1.treatment of primary disease
2. inhaling CO2 (Paper mask or 5 CO2 )
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Section 5 Mixed acid-base disorders
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Mixed acid-base disorders

• Double acid base disorders
• Metabolic Metabolic
• acidosis
  alkalosis
• Respiratory Respiratory
• acidosis
  alkalosis

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Double acid-base disorders and pH change
Type HCO3- / H2CO3 20/1 pH
Met acid Res acid ?/? ? ?
Met acid Res alko ?/ ? ? ? ?
Met acid Met alko ?/ ? ? ? ?
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? R acidosis M acidosis M alkalosis
? R alkalosis M acidosis M alkalosis
Triple Acid-base disturbances
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Summery

• Metabolic acidosis is induced by primary decrease
  of HCO-3 owing to increased production or
  retention of fixed acides or HCO-3 loss.
• Metabolic alkalosis is induced by primary
  increase of HCO-3 due to H loss.
• Respiratory acidosis or alkalosis is induced by
  primary increase or decrease of CO2 caused by
  hypoventilation or hyperventilation.

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• Acidosis depresses activity of CNS and myocardial
  contractility, and induces cardiac arrhythmia
  and vasodilation.
• Alkalosis results in dysfunction of CNS and
  cramping.
• Different kinds of acid-base disorders may
  coexist in patients.

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Scientific poem
H ion in body life
H ion You, we love You, we also hate So a little
change You let life lost forever
___ ?
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End
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