Acid Base Balance

Basic & Clinical Concept

Dr Rudraprasad Chakraborty
2nd yr PG, Deptt. of Oral & Maxillofacial Surgery
Faculty of Dental Sciences
Rama University
Kanpur, UP

19/12/15
 Concept starts with PH
Normal PH : 7.34-7.44
Average : 7.4
H+ ion is the main Contributor

HA H+ + A-

H2CO3 H+ +
HCO3-
 Ions in Body : Cations
Anions
In Blood : Cations = Anions
Cations = Measures Cations +
Unmeasured Cations
Anions = Measured Anions + Unmeasured
Measured Cations+Anions
Unmeasured Cations
= Measured Anions +
Unmeasured Anions
Unmeasured Anions - Unmeasured
Cations
= Measured Cations
 Cations and Anions
Measured Cation Na+
Unmeasured Cation K++, Ca++,
Mg++, Li++,
+ve charged
immunoglobulins
Measured Anion .. Cl-, HCO3-
Unmeasured Anion .. Acetates,
Lactates, Oxalates, Formates, SO4--,
Po4---, Albumin
 U.A U.C = M.C M.A.

Anion Gap
Related to the concept of Metabolic
Acidosis
Normal Anion Gap = + 12
milimol/lit 2
Anion Gap Increases When U.A or
U.C
 A. Causes of Increased
Anion Gap
For Unmeasured Anions :
Acetates
Lactates
Oxalates
Formates
SO4- / PO4-
Albumin ( Found Physiologically )
 Acetate
Acetic Acid Acetate +
H+
Responsible for A.GResponsible for
Acidosis

Lactate
Lactic Acid Lactate + H+
 Toxins
Salicylates ( From Aspirin
Poisoning )

Oxalates ( From Ethylene Glycol

Poisoning )

Formates ( from Methyl Alcohol )

 Renal Failure
Causes Decrease Excretion of SO4- or
PO4-

Unmeasured anion increase in body

Causing Acidosis.
 Acid Base Disorder
Acidosis .. Metabolic / Respiratory
Alkalosis .. Metabolic / Respiratory

Three Compansatory Mechanism

:

1. Immediate System >> Within Minutes

to Hours

2. Acute System >> Works within Hours

 Immediate Systems
1. Chemical Buffer : H2CO3/ HCO3-
Buffer system
Weak H2CO3 HCO3- + Strong
acid acid
H+
In Condn. of Acidosis ( PH /
H+ )
H2CO3 H+ + HCO3-

In Condn. of Alkalosis ( PH /
H+ )
H2CO3 H+ + HCO3-
 Immediate Systems
2. Proteins :
Binds either to H+ or Ca+
normally

In Acidosis : H+ >> Proteins will

bind more to
H+
Proteins will bind
more to
In Alkalosis : >> Leads to
H+Ca+
 Immediate Systems
3. Hemoglobin

HbO2 De Oxy Wants to bind

Hb- with H+

In Acidosis :
More H+ ion
More De Oxy Hb will Bind
to H+
More O2 from Hb to enter
Cell
Increased O2 Dissociation
 Immediate Systems
3. Hemoglobin
HbO2 De Oxy Wants to bind
Hb- with H+

In Alkalosis :
Less H+ ion to take Deoxy
Hb
Less Deoxy Hb Production
More O2 binding with Hb
Less O2 from Hb to enter
Cellular / Tissue
Cell
 Immediate Systems
4. SO4- / H2SO4 System
2H+ + SO4-- Weak
acid
H2SO4
Left Shift occurs in
Alkalosis

Right Shift in
Acidosis
 Immediate Systems
5. PO4--- / H3PO4 system

3H+ + PO4---
H3PO4

It is more effective than Bicarbs, but in

physiological state Bicarb works more
in body
 Acute Systems
Works within Hours
Respiratory System is the only and
The Major system working here

CO2 is Considered as Acid

CO2 + H2O H2CO3 H+
+ HCO3 -
 Acute Systems
CO2 + H2O H2CO3 H+ +
HCO3 -
In Acidosis :
Decreased PH / Increased H+
Ion
The more CO2 >>> The More
H+Body Needs washing away the
CO2
Hyperventilation
 Acute Systems
CO2 + H2O H2CO3 H+ +
HCO3 -
In Alkalosis :
Increased PH / Decreased H+
Ion
The More H+ is needed by the
body
Hypoventilation
CO2 should be retained in body
 Chronic Systems
Kidney works Mainly
Normally by Three Mechanisms
1. Bicarbonate Reabsorption by PCT
2. H+k+ Antiport system at DCT
3. Ammonia secretion in PTC
 Bicarbonate Reabsorption
By PCT
In Acidosis H+ ion occurs

H2CO3 H+ + HCO3 -

From
PCT
H+k+ Antiport system at
DCT

K
+

H+
 Ammonia secretion in PCT
Normally Ammonia is Secreted
passively at Lumen

NH
3+
H+

NH4 Proton
+ Trapping
 Causes of Acid Base
Disorder
Metabolic Acidosis

Occurs due to H+ in body by metabolic disorder

Biochemically Found : HCO3- Concentration

Primary Cause : Decreased HCO3- in Serum

Compensatory Mechanism : Hyperventilation
Compensatory Response : Decreased PaCO2
Respiratory Acidosis

Occurs due to defect in ventilatory

Process
CO2 retention occurs due to
Hypoventilation
Primary Cause : Increased PaCO2
Compensatory Mechanism : HCO3-
reabsorption
by PCT
Compensatory Response : HCO3-
Concentration
 Metabolic Alkalosis

Due to HCO3- in body by Metabolic

Disorder
Body needs more H+ ion to
Neutralize it
Primary Cause : Increased HCO3- in
Serum
Compensatory Mechanism :
Hypoventilation
Compensatory Response :
Increased PaCO2
Respiratory Alkalosis

Hyperventilation will wash out CO2

from body
No H+ to bind with HCO3-

Primary Cause : Hyperventilation /

PaCO2
Compensatory Mechanism : HCO3-
Reabsorption
Compensatory Response : HCO3-
Primary Disease Primary Cause Compensatory Mechanism
Compensatory response

Metabolic Aciosis HCO3- Hyperventilation

PaCO2

Respiratory Acidosis PaCO2 HCO3- Reabsorption

HCO3- Concentration

Metabolic Alkalosis HCO3- Hypoventilation

PaCO2

Respiratory Alkalosis
PaCO2 HCO3- Reabsorption HCO3-

HCO3- and PaCO2 Both Change in same

direction.

Isolated Values of HCO3- or PaCO2 Has No Value

Analysis and step wise
approach to Acid Base
Disorder
 Step 1 : History
Complaint
Duration
Medical History
Personal History

Step 2 : Ph from ABG strip

Step 3 : Compare Ph with
PaCO2
PaCO2 Normal : 40mm Hg

Ph Decreases = Acidosis
Paco2 changes in same direction .. i.e
Decreases

Cause is Metabolic

Metabolic
Acidosis
Step 3 : Compare Ph with PaCO2

Ph Increases = Alkalosis
Paco2 changes in same direction ..
i.e Increases

Cause is Metabolic

Metabolic
Alkalosis
Step 3 : Compare Ph with PaCO2

Ph Decreases = Acidosis
Paco2 changes in opposite direction ..
i.e Increases

Cause is Respiratory

Respiratory
Acidosis
Step 3 : Compare Ph with PaCO2

Ph Increases = Alkalosis
Paco2 changes in opposite direction ..
i.e Decreases

Cause is Respiratory

Respiratory
Alkalosis
Primary Disease Primary Cause Compensatory Mechanism
Compensatory response

Metabolic Aciosis HCO3- Hyperventilation

PaCO2

Respiratory Acidosis PaCO2 HCO3- Reabsorption

HCO3- Concentration

Metabolic Alkalosis HCO3- Hypoventilation

PaCO2

Respiratory Alkalosis
PaCO2 HCO3- Reabsorption HCO3-

HCO3- and PaCO2 Both Change in same

direction.

Isolated Values of HCO3- or PaCO2 Has No Value

Step 3 : Compare Ph with HCO3-
Normal HCO3- value : 24 mmol/lit.

Same as PaCO2.

If the direction of changes of Ph &

HCO3- are in same direction.
Metabolic Cause

If the directions are opposite.

Respiratory cause
 ABG : The Blood Gas
Measurement
Blood Drawn from Artery ( Usually Radial or
Femoral )
Sent to Lab in Ice with patients Body
Temperature
Current O2 supplementation is also
Recorded
 Normal ABG values
Ph : 7.35 7.45
PCO2 : 34 45 mm Hg
HCO3- : 20 28 mmol/lit
PO2 : 80 95 mm Hg
%SaO2 : should be greater than 95%
Step 4 : Calculating Compansatory
Response
If primary disorder is METABOLIC
Calculate the EXPECTED
PaCO2 Value

In case of both Metabolic Acidosis &

Alkalosis
EXPECTED PaCO2 = 15 + HCO3- Value.
Eg : PH = 7.2 i.e Acidosis
HCO3- = 20mmol/lit ( decreased
than normal )
= Metabolic

Expected PaCO2 = 15 + 20 = 35mm Hg

Eg : PH = 7.5 i.e Alkalosis

HCO3- = 30mmol/lit ( Increased
than normal )
= Metabolic

Expected PaCO2 = 15 + 30 = 45mm Hg

 If primary disorder is RESPIRATORY
Calculate the EXPECTED
BiCarb Value

In case of Respiratory Acidosis

Value Differs in Acute & Chronic
 Acute Respiratory Acidosis
For every 1 increase in PaCO2 from
40mmHg
HCO3- Increases by 0.1 from
24mmol/lit.
Eg : PaCO2 = 70mmHg, Ph : 7.3
Expected BiCarb = (70-40) = 30 unit
30 X 0.1 = 3
Expected BiCarb Value increase = 24 + 3
= 27 mmol/ lit
Chronic Respiratory Acidosis
For every 1 increase in PaCO2 from
40mmhg
BiCarb Value increases by 0.4 from
24mmlo/lit
Eg : PaCO2 = 70mm Hg, Ph =7.3
Expected Bicarb = for 30 unit increase
PaCo2
30 X 0.4 = 12
= 12 + 24 = 36
mmol/lit
 Respiratory Alkalosis
Acute : For every 1 decrease in PaCO2 from 40mmHg
HCO3-
decreases by 0.2 from 24 mmol/lit

Eg : PaCO2 = 20mm Hg
Ph = 7.5
Expected HCO3- will be..
40-20 = 20unit
20 X 0.2 = 4
24 4 = 20 mmol/lit
 Respiratory Alkalosis
Chronic : For every 1 decrease in PaCO2 from
40mm Hg, HCO3-
decreases by 0.4 from 24mmol/lit

Eg : PaCO2 = 20 mm Hg
Ph = 7.5
Expected HCO3- value = 40 20 = 20 unit
20 X 0.4 = 8
24 8 =
16mmol/lit
It is found that in chronic condition
the compensation is more.
 Step 5
Compare the expected compansatory
value with the value seen in the pts
ABG report

If Given value expected value

calculated
Diagnosis is a Mixed Disorder
 If the main disorder is
Metabolic
(From Step
3)
Calculate expected PaCO2 in
Step 4
Two Probabilities
Given PaCO2 is Given PaCO2 is less
more than than
expected/calculate expected/calculate
d value d value
Metabolic Metabolic
Disorder Disorder
+ +
Respiratory Respiratory
Acidosis Acidosis
 Metabolic Metabolic
Disorder Disorder
+ +
Respiratory Respiratory
Acidosis Ph : Acidosis
7.5
Ph : 7.5 HCO3- = 30 mmol/lit
HCO3- = 30 mmol/lit PaCO2 = 35 mm Hg
PaCO2 = 60 mm Hg

Primary Dx :
Primary Dx : Metabolic
Metabolic Alkalosis
Alkalosis
Expected
Expected
PaCO2 = 30 +
PaCO2 = 30 +
15 = 45mm Hg
15 = 45mm Hg
Given Value is More than Given Value is less than
Expected Expected

Final Dx = Metabolic Final Dx = Metabolic

Alkalosis Alkalosis
+ +
 If the main disorder is
Respiratory
(From Step
3)
Calculate expected HCO3-
value in Step 4
Two Probabilities
Given HCO3- value Given HCO3- value
is more than is less than
expected/calculate expected/calculate
d value d value
Respiratory Respiratory
Disorder Disorder
+ +
Metabolic Metabolic
Alkaosis Acidosis
 But.
For Respiratory Disorder
Evaluate Both Acute or Chronic
State
Ph : 7.31
HCO3- = 32 mmol/lit
PaCO2 = 60 mm Hg Acute
H/O : Acute Bronchial
Asthema
Step 1 : H/O Acute state
Step 2 : Ph 7.3 < 7.4 .. Acidosis
Step 3 : Compare with PaCO2 .. Change is opposite
direction Respiratory
Step 4 : Expected Compansatory value of HCO3- in
Acute Stage
24mmol/L + (20X 0.1) = 24 + 2 = 26mmol/L

Step 5Dx
Final : given HCO3- = 32mmol/L
: Respiratory which is more
Acidosis withthan
expected value
Metabolic Alkalosis
Chronic
Ph : 7.31
HCO3- = 30 mmol/lit
PaCO2 = 60 mm Hg
H/O : Chronic Bronchial
Asthema
Step 1 : H/O Chronic state
Step 2 : Ph 7.3 < 7.4 .. Acidosis
Step 3 : Compare with PaCO2 .. Change is opposite
direction Respiratory
Step 4 : Expected Compansatory value of HCO3- in
Chronic Stage
24mmol/L + (20X 0.4) = 24 + 8 = 32mmol/L

Step 5 : given HCO3- = 30mmol/L which is less than

expected
Final Dxvalue
: Respiratory Acidosis with
Metabolic Acidosis
 No H/O Acute or Chronic
Ph : 7.31, HCO3- : 32mmol/L, PaCO2 : 70mmHg
Step 1 : H/O Step 2 : Ph is Acidic =
???? Acidosis
Step 3 : Direction of Ph and Paco2/HCO3- changes are
opposite Respiratory
Respiratory
Acidosis
If Chronic :
If Acute :
Expected Comp HCO3- Expected Comp HCO3-
Value.. Value..
70-40mm hg = (30 X 0.1 ) 70-40mm hg = (30 X 0.4 ) +
+ 24mmol 24mmol
= 27 = 36 mmol/L
mmol/LMetabolic ( Given
Metabolic value is
Acidosis
( Given value less )
Alkalosis +
is more )
+ Respiratory
Respiratory Acidosis
 ???........ Step 6
History is Diagnosed !!
Acute Condition :
For every 10 changes of PaCO2 from 40mmHg,
Ph Changes by 0.08 from 7.4
2 70mmHg, 30 increased from 40mmHg, i.e , 3 times 10 unit chan

So 3 X 0.08 = 0.24. + / - ??
Primary Dx was Acidosis Ph has to be decreased
So deduct from 7.4
7.4 0.24 = 7.16 NOT MATCHING
with given Ph
Ph : 7.31, HCO3- : 32mmol/L, PaCO2 70mmHg
 Step 6
Chronic Condition :
For every 10 changes of PaCO2 from 40mmHg,
Ph Changes by 0.03 from 7.4
2 70mmHg, 30 increased from 40mmHg, i.e , 3 times 10 unit chan

So 3 X 0.03 = 0.09

Ph should be 7.4 0.09 = 7.31

MATCHING !!
Final Dx : Respiratory Acidosis +
Metabolic Acidosis
Ph : 7.31, HCO3- : 32mmol/L, PaCO2 70mmHg
 Should I
Continue ?
 Clinical Manifestation &
Management
Metabolic Acidosis
1.High Anion Gap Acidosis
2.Non Anion Gap Acidosis

Unmeasured Anions - Unmeasured Cations

= Measured Cations -
Measured Anions
Acetates, Lactates, Oxalates, Formates, SO4- /
PO4-, Albumin
High Anion Gap Acidosis
A.Ketoacidosis
i. Diabetic Ketoacidosis
ii. Starvation
iii. Alcoholic Ketoacidosis
 Diabetic Ketoacidosis
Pt with T1DM, with Non Compliance
to Insulin
Mechanism Lack
: of Insulin

No Prevention of
Lipolysis

More/ Increased
Lipolysis

Fatty Acid
 Diabetic Ketoacidosis
H/O : Early onset T1DM, Noncompliance to insulin
C/F : Altered Consciousness, Gasping, ketotic smell

Rx :
1. IVF >>> 0.9% Nacl / Isotonic Saline
No RL or Exogenous
Bicarbs
2. IV Insulin ( Avoid Subcut )
3. K+ Supplement
 Starvation
H/O : Prolonged Fasting
Mechanism :
Prolonged Fasting

Glycogenolysis
Gluconeogenesis (Within 8 to 12
hrs) (After 12 hrs)

Rx : IV 5% or 10% Adipocyte Breakdown

Dextrose
Fatty Acid & Glycerol
To Prevent
Gluconeogenesis
Glucose + Ketoacid Production
 Alcoholic Ketoacidosis
Alcohol prevents normal breakdown of Fatty
Acid
Fatty Acid >>> Ketoacid Blood
Alcohol prevents Glycogenolysis Glucos
Gluconeogenesis e Level

Rx : IV 5% Dextrose >>> Inhibition of Fatty

Acid to
produce Ketoacid

Volume of IVF will flush out alcohol in urine

 Alcoholic Ketoacidosis
Glycolysis >>> TCA Cycle
Pyruvate Acetyl Co.A

Thiamine
Pyrophosphate
Alcohol
E1 Enzyme Complex

Pyruvate Lactic
Acid
Rx : Inj Vit
B1
 Lab Work For ketoacidosis
Single most important : Blood
Glucose level

1. Increased BS (more than 250mg/dl)

>>> DKA
2. Normal BS >>> starvation
3. Decreased BS ( less than 40mg/dl)
>>> AK
High Anion Gap Acidosis
B. Lactic Acidosis
Type A : Due to Increased Synthesis
Two
Type B : Due to Decreased
Types
Catabolism of L.A
Type A : In anaerobic condition
Causes :
Hypovolemic
1.Hypoperfusion of O2 to Shock
cell
2.Severe Anaemia Cardiogenic
Shock
3.CO poisoning
4.Cyanide Poisoning
B. Lactic Acidosis

Type B. When catabolism of lactic

acid in liver
and kidney is disturbed
Causes :
Liver and Renal Failure >> Treat
Acordingly
Drugs :
Biguanides >>> Metformin
(OHA)
Isoniazide >>> Direct
hepatotoxic Drugs
 Rx of Lactic Acidosis
Hypovolemic Shock >> IVF 0.9% NS ( Not
RL)
Target Ph in Acute Phase >> 7.20 (To
avoid Alkalosis)
Cardiogenic Shock >> Digoxin or Digitalis
Fluid should be Judicial to avoid
Pulmonary Oedema
Severe Anaemia >> BT

CO Poisoning >> 100% O2, Hyperbaric

Therapy
C. Toxins
1. Salicylate Poisoning :
Occurs due to excess overdose of
Aspirin
While inorally
Stomach : Severe Gastritis

Frequent
Vomitting

Increased HCl
Loss
Metabolic
Alkalosis H+ Loss
 Salicylate Poisoning :
While in Blood :

Salicylic acid H+ + Salicylate

H+ causes Acidosis
Salicylate leads to Increased Anion
Gap
U.A U.C = M.C M.A

High Anion Gap Metabolic

Acidosis
 Salicylate Poisoning :

Salicylic acid H+ + Salicylate

Salicylate can cross BBB

>> Reach Respiratory
Centre
>>
Stimulates it Hyper Ventilation

Respiratory
Alkalosis
Mixed Acid Base Disorder
 Rx of Salicylate Poisoning
For Stomach : NG Tube + Lavage

IVF : To Maintain Fluid Loss

5% Dextrose
To Neutrilize Acidosis
Salicylates cause Liver
damage which leads to
decreased
If all fails >> Hemodialysis Glycogenolysis,
Gluconeogenesis
 C.
Toxins
2. Methanol Poisoning
Alcohol
Dehydrogenese
CH3OH H-CHO

Toxic product of the Methanoic

reaction Acid
Causes Optic Neuritis

H+ leads to HCOO-
( Formate )
Acidosis
Causes high
Anion gap
High Anion Gap metabolic
Acidosis
 Rx of Methanol Poisoning
Goal is to inhibit the enzyme Alcohol
Dehydrogenase
Drugs : Fomepezole
Alternative : Divert the route of enzyme
IV Ethanol

Depression of CNS

Supressed Resp. centre

Respiratory
CO2 Retention
Acidosis
C.
Toxins
3. Ethylene Glycol : Anti freeze in Car

Ethylene Oxalic Acid

glycol

Acute Renal Tubular Oxalate + H+

Necrosis

High Anion Gap Metabolic

Acidosis
Rx : Same as Methanol poisoning
Normal / Non Anion Gap M.
A.
U.A U.C = M.C M.A.
Anion Gap = Na+ - ( Cl- +
HCO3- )
Main mechanism of Non Anion Gap M. A is
HCO3- Loss
Compansatory same unit of Cl- Gain

Cl- Concentration

Hyperchloremic Metabolic
Alkalosis
 U.A U.C = M.C M.A.
Anion Gap = Na+ - ( Cl- +
HCO3- )
Remains
Same
Measured Anion charge remains
same
Etiology of HCO3- Loss :

1. GIT Loss >> HCO3 Loosing Diarrhoea

2. Renal Loss >> Any tubular disfunction
3. Drugs
 Drugs causing Normal Anion Gap
M.A
Drugs : Increasing K+ Concentration
Body Pumps it back in cells
To balance +ve ions H+ ion
exchanges out.
H+ ion binds with HCO3-
Less HCO3- concentration
Leading to Metabolic
Acidosis
Exmpl : K+ Sparing Diuretics .
Spironolactone
Trimethoprim
 Respiratory Acidosis
Known as Type II Respiratory failure
Main Mechanism : Hypoventilation /
PaCO2
Causes :
Depression of Respiratory centre
Spinal Cord Lesion above C3,4,5
Phrenic Nerve Lesion
Neuromuscular Jn. Disorders
Muscles
Chest wall
Chronic Small airway Damage Rx :
All underlying
Causes
 Metabolic Alkalosis
HCO3- in Blood
Two types : Chloride responsive
Chloride
unresponsive
Chloride Responsive : Cl- loss
leading to
Causes :
compansatory HCO3-
GIT Loss >> Cl- Loosing Diarrhoea
Renal Loss >> Diuretics ( Loop /
Thiazide )
Skin >> Cystic Fibrosis >> Cl-
 Metabolic Alkalosis
Chloride Unresponsive :
Depends upon
Fx of Aldosterone
In Hyper Aldosteronism : Na+ Reabsorption, K+ &
H+ excretion

Metabolic
Alkalosis
 Misc.
Pt ingested Exogenous Alkali + Milk ( Ca++)

Serum Ca++ Level

Extra load of Serum Ca++ level will cause Renal

Tubular Necrosis

Leads to renal Failure

Metabolic Alkalosis due to H+ ion Reabsorption

 Misc.
-Ve Charged Drugs .. Eg : Penecillin
Overdose

Causes -Ve Condition in Renal Tubule

Attracts and Excretes H+ & K+

Metabolic Alkalosis + HypoKalemia

 Respiratory Alkalosis
Primary cause is Hyperventilation

Any stimulus to Respiratory Centre

Hyperventilation

CO2 wash out

Alkalosis
 Respiratory Alkalosis
Stimulus can be of two different
origin
1. Central
i. Drugs
ii. Infection
iii. Anxiety Neurosis
2. Peripheral
Lungs or Other Cytokine
Alveolar Hypoxia Systemicrelease
Diseases
Alveolar Oedema Resp Centre
ARDS stimulation
Hyperventilation
 Thanks

Lets Practice