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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 )
Causing Acidosis.
Acid Base Disorder
Acidosis .. Metabolic / Respiratory
Alkalosis .. Metabolic / Respiratory
In Condn. of Alkalosis ( PH /
H+ )
H2CO3 H+ + HCO3-
Immediate Systems
2. Proteins :
Binds either to H+ or Ca+
normally
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
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
Respiratory Alkalosis
PaCO2 HCO3- Reabsorption HCO3-
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
Respiratory Alkalosis
PaCO2 HCO3- Reabsorption HCO3-
Same as PaCO2.
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
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
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
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
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
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)
Thiamine
Pyrophosphate
Alcohol
E1 Enzyme Complex
Pyruvate Lactic
Acid
Rx : Inj Vit
B1
Lab Work For ketoacidosis
Single most important : Blood
Glucose level
Frequent
Vomitting
Increased HCl
Loss
Metabolic
Alkalosis H+ Loss
Salicylate Poisoning :
While in Blood :
Respiratory
Alkalosis
Mixed Acid Base Disorder
Rx of Salicylate Poisoning
For Stomach : NG Tube + Lavage
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
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 :
Metabolic
Alkalosis
Misc.
Pt ingested Exogenous Alkali + Milk ( Ca++)
Hyperventilation
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
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