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ABG Interpretation 7

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0% found this document useful (0 votes)
252 views132 pages

ABG Interpretation 7

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sumayya hameed
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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ABG Interpretation

Dr. M. Sreelatha
Prof & Head of Nephrology
Govt Medical College, Calicut
Arterial blood Gases

Arterial blood gas analysis is an


essential part of diagnosing and
managing a patient’s oxygenation status
and acid-base balance. The usefulness
of this diagnostic tool is dependent on
being able to correctly interpret the
results.
Indications
Joseph Priestley
discovered the gas we call oxygen without
understanding its role in
respiration or combustion
Antoine Lavoisier
described the true chemistry of respiration and
combustion.He named the gas oxygen.Probably
France's greatest chemist, but sent to the
guillotine in 1794. 
Lawrence J. Henderson
first to understand and express quantitatively
the buffering effect of carbon dioxide and
bicarbonate interacting with hydrogen ions in
blood.
Acid-base concepts
Acid – A molecule that tends to dissociates releasing
protons or H+ in solution
Base – A molecule that accept protons in solution
Acidemia – H+ conc in plasma is greater than normal
Alkalemia – H + conc in plasma is less than normal
pH = log 1/H+
Pka = pH of solution when acid is 50% dissociated
(dissociation constant)
Henderson-Hasselbach equation

pH = Pka + log base/acid

For BBS : pH = 6.1 + log HCO3/H2CO3


H+ = K x H2CO3/HCO3
= K x PCO2/HCO3 (correction factor 0.03)

H+ = 24 x pCO2/HCO3 – Henderson equation


OH ION14
H + conc(nmol/L) pH

20 7.70
30 7.52
40 7.40
50 7.30
60 7.22

pH stand for "power of hydrogen"


H ION 0
Interconversion of pH & H+
1 nmol/L H+ : changes pH by 0.01 unit
eg: 7.40 = 40 nmol/L H+ 7.41 = 39 nmol 7.39 = 41 nmol

To get H+ ion conc – subtract decimals of pH from 80,


eg : if pH is 7.34, H+ ion conc is 80 – 34 = 46 nmol/L

80% method:-
For an in pH by 0.1 unit multiply H+ by 0.8
eg: 7.00 = 100 nmol
7.10 = 100 x 0.8 = 80
7.20 = 100 x 0.8 x 0.8 = 64 nmol
H+ in the body

Daily consumption – 70,000,000 nmol


Endogenous acid production – 1 mmol/kg/d
Free H+ in the body at any time – 4000 nmol
Conc in ICF : 100 nmol/L
Conc in ECF : 40 nmol/L
Normal acid-base conc in various
body fluids
Art vein CSF ICF

H+ 40 44 48 100

pH 7.40 7.36 7.32 7.0

HCO3 24 28 22 12

PCO240 46 44 50
Buffer systems
Plasma Phosphate
=
Buffer ratio 4:1
(0.8 -1.45 mmol/L)

Plasma Protein
(30 - 55 g/L)

Plasma Bicarbonate Hemoglobin

Buffer ratio 20:1 64% (Male 13.5-18 g/dl)


(Female 11.5-16.5 g/dl)
(24-32 mmol/L)
Buffer systems

EC buffers BBS – immediate buffer

IC buffers Proteins - act in 2- 4 hrs of acid load


Org PO4
Bone buffers (PO4 & CO3) – act after 5 hrs
Buffering of an acid load

(15%) K+ H+
H+ Na+ (36%)
(6%) H+ + A-

H+ + IC proteins
(1%)
EC : BBS (43%)
Handling of an acid or alkali load
1. Buffer systems
2. Lungs – CO2 wash out
3. Kidneys – a) increasing /decreasing HCO3 reabsorption
b) ammoniagenesis
c) distal tubular H+ secretion
d) excretion of titratable acids
Acid (H+) excretion by the kidneys – NH3 + H+  NH4+
HPO4-- + H+ H2PO4 -Titra.acid
NH4+ & H2PO4-  NAE
Role of Kidneys in acid-base
regulation
HCO3 reabsorption

Ammoniagenesis

Distal H+ secretion

Excretion of titratable acids


Ammoniagenesis

Site : S1 & S2 seg of PCT


Substrate : Glutamine
NH3 NH3
Glutamine glutamate alfa ketoglutarate

1 glutamine malate

2 NH3 + 2 HCO3 2 HCO3


Kreb’s cycle
Rate limiting step : Transport of glutamine across the
inner mitochondrial memb
NH3 + H+ NH4+ : excreted in urine
Rate of synthesis : 70 micromole/mt
Ammoniagenesis can be increased by 50% within 24
hrs of an acid load
Distal acidification
H+ secretion
Alfa intercalated cells of CCD & OMCD
H+ ATPase & H+ K+ ATPase on luminal border

H+ ATPase
2 major domains : V1 & V0
V1 three A & three B subunits ; 6
B1 & B2 isoforms : B1 specific to kid, placenta & inner
ear
ATP6B1 gene on chr 2p13
H+ ion secreted NH3 + H+ NH4+
HPO4 -- + H+ H2 PO4-
(titratable acidity)

So Net acid exn (NAE) = NH4+ + H2PO4-


Handling of an acid load
Kidneys : max effect in 3-5 days, then bone take over
1. Complete reabn of filtered HCO3 from PCT
• By decreasng the filtered load
• Vol contraction
• activity of Na-H antiporter NAE
2. Augment ammoniagenesis : 50% in 24 hrs
3. Enhances distal acidification
• Enhanced activity of H+ ATPase
• Vol depletion,hyperaldosteronism

NH4 exn by 10 times, Titratable acid exn by 2-3 times


ABG Report & Interpretation
What Is An ABG?
pH [H+]

PCO2 Partial pressure CO2

PO2 Partial pressure O2

SaO2 Oxygen Saturation

HCO3 Bicarbonate
Normal ABG values
pH 7.35 – 7.45

PCO2 35 – 45 mmHg

PO2 80 – 100 mmHg

HCO3 22 – 26 mmol/L
HCO3

BE -2 - +2

SaO2 >95%
Measured values : pH, PCO2, PO2
Calculated values : O2 sat, HCO3, BE
Sampling : percutaneous arterial puncture – radial artery
Alternative to arterial bld : arterialized cap / venous bld
• Ear lobe, dorsum of hand(warm at 45oC x 10 mts), lateral
margin of foot
Collection :
• always glass syringe
• Heparinised, anaerobically, cooled to 4oC
ABG : Errors

Excess heparin : low pH, PCO2 & HCO3

Contamination with room air : PaO2, pH, PaCO2

Delayed analysis : pH, PaCO2, PaO2

• By 10 mts – pH decreases by 0.01


• PCO2 increases by 1 mmHg
• O2 conc decreases by 0.001
Arterial / Venous sample ?

In venous sample:-

 PO2 < 40 mmHg


 pH 0.03 lower
 PCO2 6 mm Hg higher
 [HCO3-] 2 - 4 meq higher
Physiological factors affecting acid-
base status
Body position : sitting / standing PCO2 by 3-4 mm
No diurnal variation
Females : PCO2 2-4 mm lower, pH 0.02 higher
Pregnancy : low PCO2 esp in last TM
Age : children with lower PCO2 ( 33-37 mm)
Diet : Meat decreases HCO3- & PCO2
Altitude : hyperventilaion – lower PCO2
Verify the result for lab error

[H+] = 24 x PCO2
[HCO3]

Calculate [HCO3] by = 24 x PCO2


[H+]
Calculate [H+] from pH
Whether correlating with value of HCO3 in ABG report
The
No click

5
Steps for
Successful
Blood Gas
Analysis
Danish Chemist – Sorrenson 1909
Clinical scenario : Case 1

70 yr old gentleman presented in emergency room


with cardiac arrest

RFT – N, K+ 7.2, ECG sine waves,


ABG : PH 7.24, HCO3 12, PCO2 26,
Na 130, K+ 7.2, Cl 115, HCO3 12
USG : Gr III BHP, B/L HUN

What is the metabolic disorder ?


Is there any acid-base disorder at all ?

Look at HCO3, PCO2

Both normal No acid-base disorder


Case 1

70 yr old gentleman presented in emergency


room with cardiac arrest

• RFT – N, K+ 7.2, ECG sine waves,


• ABG : PH 7.24, HCO3 12, PaCO2 26,
• Na 130, K+ 7.2, Cl 115, HCO3 12
• USG : Gr III BHP, B/L HUN
Step 1:

Normal PH : 7.37 – 7.43

 PH acidosis < 7.35

alkalosis > 7.45


Case 1 ABG : PH 7.24, HCO3 12, PaCO2 26,

PH 7. 24 Acidosis
PaCO2

Normal PaCO2 = 40 mmHg

High PaCO2 > 40 PH low Resp acidosis

Low PaCO2 < 40 PH high Resp alkalosis


Same direction
HCO3 pH META.
Same direction

PaCO2 pH RESP
Opposite direction
No click

PaCO of 10
2
p
Acute change H
.08

Chronic change .03


Case 1
70 yr old gentleman presented in emergency
room with cardiac arrest

RFT – N, K+ 7.2, ECG sine waves,

ABG : PH 7.24, HCO3 12, PaCO2 26

Na 130, K+ 7.2, Cl 115, HCO3 12

USG : Gr III BHP, B/L HUN


Case 1 ABG : PH 7.24, HCO3 12, PaCO2 26

PH low, but PaCO2 also low

Not a Respiratory disorder


HCO3…HCO3…HCO3…
HCO3

Normal HCO3 – 24 meq/L

PH low HCO3 low Met acidosis


PH high HCO3 high Met alk
Same direction
HCO3 pH META.
Same direction

PaCO2 pH RESP
Opposite direction
HCO3

Standard HCO3 : Plasma [HCO3] present in


bld sample that is fully saturated with O2 &
equilibrated at 38o C with PCO2 of 40 mmHg

Usually = actual plasma HCO3


Standard Bicarbonate:
Plasma HCO3 after equilibration
to a PaCO2 of 40 mm Hg
: Reflects non-respiratory acid base change
: No quantification of the extent of the buffer
base abnormality

Base Excess:
D base to normalise HCO3 (to 24)
with PaCO2 at 40 mm Hg
(Sigaard-Andersen)

: Reflects metabolic part of acid base D


: No info. over that derived from pH,
pCO2 and HCO3
: Misinterpreted in chronic or mixed
disorders
BE / Base deficit

Amt of acid or alk that must be added to 1 L of fully


oxygenated bld exposed in vitro to a PCO2 of 40 mmHg at
38oC to achieve a normal pH of 7.40

If initial pH is low – add alk ‘Base deficit’ or ‘neg BE’


Initial pH high – add acid ‘BE’

Normal value : -3 to +3
> -5 Met acidosis, > +5 Met alk
Case 1

70 yr old gentleman presented in emergency


room with cardiac arrest

• RFT – N, K+ 7.2, ECG sine waves,


• ABG : PH 7.24,, HCO3 12 PaCO2 26,
• Na 130, K+ 7.2, Cl 115, HCO3 12
• USG : Gr III BHP, B/L HUN
PH low ; HCO3 low

So a Metabolic disorder Met acidosis


Metabolic Acidosis

pH 7.30

HCO3 15

PaCO2 40
Metabolic Alkalosis

pH 7.50

HCO3 30

PaCO2 40
Four-step ABG Interpretation

Step 4:

Determine if there is a compensatory


mechanism working to try to correct the pH.
four clicks

RESP. ACIDOSIS ALKALOSIS META.

PCO2
+
CO2+H20=H2CO3 = H + HCO3 pH

HIGH
+
H
HIGH
HCO3
HCO3 HCO3
ACUTE RISE : PCO2 10 : pH .08
CHRONIC RISE : PCO2 10 : pH .03
Six clicks

RESP. ALK. ACID. META.

CO2 + H20 = H2CO3 = H + + HCO3

pH
CO2
SERUM
+
LOW H IONS HCO3
Bicarbonate
…LOW HCO3
Is compensation adequate ?
Compensation for MA

For every 1 meq fall in HCO3

PCO2 should fall by 1.2 mmHg

PCO2 = HCO3 x 1.2


Expected compensation

MA – PCO2 fall by 1.2 mm per 1meq fall in HCO3


M alk – PCO2 rise by 0.7 mm per 1meq rise in HCO3
R acidosis: A/c – HCO3 rise by 0.1 meq per 1mm rise in PCO2
C/c- ,, 0.35 ,,
R alk: A/c – HCO3 falls by 0.2 mmeq per 1 mm fall in PCO2
C/c ,, 0.4 ,,
Met alk : PCO2 = HCO3 x 0.7 (increase)

Resp acidosis : HCO3 = PCO2 x 0.1 or 0.3

Resp alk : HCO3 = PCO2 x 0.2 or 0.4


Degree of compensation

eg : for Metabolic acidosis

pH low, PCO2 – N uncompensated

pH low, PCO2 low partially compensated

pH normal, PCO2 low fully compensated


Eg:
pH 7.32, HCO3 6.0 meq/L, PCO2 18

pH 7.32 : acidosis
HCO3 6.0 : Met acidosis
Expected PCO2 : 40 – (18 x 1.2) = 18 mmHg

Single acid base disorder


Partially compensated Met acidosis
compensation No click

considered
complete
when the pH
returns to
normal range
Clinical blood gases by Malley
When to suspect mixed acid-base disorder ?
pH 7.1, HCO3 6, PCO2 30
pH 7.1 acidosis
HCO3 6.0 Met acidosis
PCO2 30
Expected PCO2 only 18 CO2 retention
Actual PCO2 is 30
Resp acidosis
So Met acidosis + Resp acidosis
pH 7.1, HCO3 6.0, PCO2 10

pH 7.1 acidosis
HCO3 6.0 met acidosis
Expected PCO2 : 18 CO2 washout
Actual PCO2 : 10
Resp alk
So Met acidosis + Resp alk
Case 1 ABG : PH 7.24, HCO3 12, PaCO2 26,

Pt has Met acidosis. What is the expected


PaCO2 ? Is compensation appropriate ?

HCO3 12 meq/L;
Expected PCO2 will be 26
Pt’s PaCO2 is also 26

So only Met Acidosis


Anion gap
Total anions = Total cations
proteins Na Na+K+UC = Cl+HCO3+UA
PO4 K UA – UC = (Na+K)-(Cl+HCO3)
SO4 Ca AGP = Na - (Cl + HCO3)
Cl- Mg = 8 – 12 meq/L
HCO3- UC
UA
“Corrected AGP” – in hypoalb – underestimate AGP – for every 1gm
fall in s. alb below 4.4 gm/L, add 2.5 to AGP
Anion gap

“Foot Print of Met acidosis”

High AGP MA Normal AGP MA


 RTA
• CKD  Ureterosigmoidostomy
• D.ketoacidosis  Biliary fistula
• Lactic acidosis
Case 1 ABG : PH 7.24, HCO3 12, PaCO2 26
Na 130, K+ 7.2, Cl 115

Calculate AGP : (130 + 7) – (115 + 12)


= 10 meq/L - Normal AGP

Diagnosis : BHP – Ob nephropathy – Tubular


dysfunction – Type IV RTA – Normal AGP MA
+ Hyper K
Urinary AGP

Ur. NH4 excretion


Na + K – Cl = 80 meq/L
NH4 excretion high UA - UC( ) = UAG low
NH4 exn reduced UA – UC( ) = UAG high
D – RTA - NH4 exn low. So UAG high
Normal AG MA + UAG low – nonrenal cause
Case 2

18 yr old boy with h/o PUV fulgrated at the age of 3 yrs, now
presented with severe breathlessness following UTI
ABG : PH 7.1, HCO3 10, PCO2 23
Na 130, K 6, Cl 106, HCO3 10
BU 130mg, s.cr 5.8 mg
USG : BUO, B/L HUN

Diagnosis : CKD stage V, CTID.


What is the metabolic disorder ?
PH 7.1 :acidosis, HCO3 10 : Met acid
PCO2 : expected compensation - 23
So pure MA
AGP : (130 + 6) – (106 + 10) = 20
So high AGP MA

AGP (8) < HCO3 (14) = Normal AGP MA +

Final diagnosis : High AGP MA of CKD +


Normal AGP MA of RTA
Hybrid acidosis

AGP ( ) = HCO3( ) pure high AGP MA

AGP = 0 pure Normal AGP MA

AGP < HCO3 high AGP MA + normal AGP MA

‘Hybrid acidosis’
AGP > HCO3 MA + Met alk
A pt with CKD admitted with several days of
vomiting

ABG not available


S.Na 144, K+ 4.2, Cl 95, HCO3 14

What is the acid-base disturbance ?


1. AGP = 144 – (95 + 14) = 35
2. AGP = 35 – 12 = 23
3. HCO3 = 27 – 14 = 13
4. Bicarbonate gap = AGP - HCO3
23 – 13 = 10

So high AGP MA + Met alk


Strong ion difference(SID) –
Stewart approach
Strong ions – Na, K, Ca, Mg, Cl, lactate, protein
SID = Na + K + Ca + Mg - Cl + lactate+ protein
= 40 meq/L – normal, > 40 – MA
Diff from AGP : SID takes into consideration of alb
AGP : For every 1gm fall in s.alb, add 2.5 to AGP

So SID is = alb-corrected AGP


Case 3 :

Intra operative ABG during renal Tx surgery is


like this :

– PH 7.2, HCO3 20, PaCO2 55 mmHg


• pH 7.2 : acidosis
• PaCO2 : Resp acidosis
• Expected HCO3 : 24 + (15 x 0.1) = 25.5
• Actual HCO3 : 20

– So Resp acidosis + Met acidosis


Most common mixed acid-base disoder MA + RA
Tripple acid-base disorder
– MA + Met alk + RA COPD - RA
diuretics or vomiting - Met alk
sepsis, BP,
PO2 - MA

– MA + Met alk + Resp alk Alcoholic - MA


vomiting - Met alk
PaO2
Indicate arterial oxygenation
Normal : Neonates – 40-70 mmHg
Adult – 80-100
>60 yrs – 80

Hypoxemia – PaO2 < 80 mmHg


mild - 60-80
moderate - 40-60
severe - < 40
O2 saturation (SaO2)
Saturation of Hb with O2
At PaO2 97mmHg - SaO2 is 97% 80
’’ - 95%
60 ’’ - 90%
40 ’’ - 75%
27 ’’ - 57%
O2 content : amt of O2 in 100 ml bld
• 1 gm Hb contain 1.34 ml O2 when fully oxygenated
• Each 100 ml plasma dissolve 0.003 ml per mmHg PaO2
• Hg 15gm, SaO2 100%, PaO2 100 mmHg O2 content =
20.13 ml in 100 ml bld(15 x 1.34 + 0.003 x 100)
A(alv) – a(art) PO2 –used to clsssify resp
failure

Hypoxia defect in ventilation – (A-a PO2 normal)


intrinsic lung disease
PO2 of atmospheric air = 150 mmHg
0.21(760 – 47) barometric Pr & water vapour Pr

Alv PO2 = inspired air PO2 – PCO2 / 0.8


= 150 – 40/0.8 = 100 mmHg

Calculate A – a PO2 = 100 – PO2 in ABG


Eg: pH 7.2, PCO2 64, PO2 66

Alv PO2 = 150 – 64/0.8 = 70 mmHg

A - a PO2 = 70 – 66 = 4 mmHg - normal

So hypoxia is due to hypoventilation, no intrinsic lung


disease
Alveolar-arterial Difference
Inspired O2 = 21 %
piO2 = (760-45) x . 21 = 150 mmHg

palvO2 = piO2 – pCO2 / RQ


O2 = 150 – 40 / 0.8
CO2 = 150 – 50 = 100 mm Hg

PaO2 = 90 mmHg

One click and wait


palvO2 – partO2 = 10 mmHg
No click

Alveolar- arterial Difference


Oxygenation Failure Ventilation Failure
WIDE GAP NORMAL GAP
piO2 = 150 piO2 = 150
pCO2 = 40
pCO2 = 80
palvO2= 150 – 40/.8
=150-50 palvO2= 150-80/.8
=100 O2 =150-100
PaO2 = 45 = 50
CO2
PaO2 = 45
D = 100 - 45 = 55 D = 50 - 45 = 5

PAO2 (partial pres. of O2. in the alveolus.)


760 – 45 = 715 : 21 % of 715 = 150 = 150 - ( PaCO2 / .8 )
Expected PaO2 =
Normal situation

FiO2 × 5 = PaO2

20 × 5 = 100
No click

5
th step

Clinical correlation
Case 8,,,,,,,,,,,,,,,,,,

What is the
Diagnosis ?
pH 7.583
PCO2 19.8
Click for answer
HCO3 18.7 Respiratory
Alkalosis
Is it acute ?
One click for answer

Case 1
Blood Gas Report
o 16 year old female with
Measured 37.0 C
pH 7.523 sudden onset of dyspnea.
PaCO2 30.1 mm Hg
PaO2 105.3 mm Hg No Cough or Chest Pain
Calculated Data
HCO3 act 22 mmol / L Vitals normal but RR 56,
O2 Sat 98.3% anxious.
PO2 (A - a) 8 mm Hg D
PO2 (a / A) 0.93

Entered Data Acute respiratory alkalosis


FiO2 21.0% And why acute ?
Five clicks
Case 2 6 year old male with progressive respiratory distress
Muscular dystrophy . pH <7.35 :acidemia
Blood Gas Report
o Res. Acidemia : High PaCO2 and low pH
Measured 37.0 C
pH 7.301 D CO2 =76-40=36
PaCO2 76.2 mm Hg Expected D pH for (chronic) = .03 for 10
PaO2 45.5mm Hg Expected pH = 7.40 – (3.6 x .03)
Calculated Data = 7.40 – 0.108 = 7.29
HCO3 act 35.1 mmol / L Chronic resp. acidosis

O2 Sat 78 %
PO2 (A - a) 9.5 mm Hg D
PO2 (a / A) 0.83

Entered Data
FiO2 21 %
Chronic respiratory acidosis
Hypoxemia
Normal A-a gradient With hypoxia due to hypoventilation
Hypoventilation
8-year-old male asthmatic with resp. distress
Six clicks

Blood Gas Report


Case 3
pH <7.35 ; acidemia

Measured 37.0 C
o PaCO8-year-old male
2 >45; respiratory asthmatic;
acidemia
pH 7. 32 D CO2 = 349days
- 40 = 9of cough, dyspnea
PaCO2 49.1 mm Hg
Expectedand
D pHorthopnea
( Acute ) = 9/10not
x 0.08 = 0.072
PaO2 66.3mm Hg
Expectedresponding to usual
pH ( Acute ) = 7.40 - 0.072 = 7.328
Calculated Data Acute resp. acidosis
bronchodilators.
HCO3 act 18.0 mmol / L
WITH INCREASE IN CO2 BICARB MUST RISE ?
BicarbonateO/E: Respiratory distress;
O2 Sat 92 %
153-66= 87 D is low………
PO2 (A - a) mm Hg
suprasternal
Metabolic acidosis + respiratoryand
acidosis
PO2 (a / A)
intercostal retraction;
Entered Data tired looking; on 4 L NC.
FiO2 30 %
Hypoxia
piO2 = 715x.3=214.5 / palvO2 = 214-49/.8=153 Wide A / a gradient
Case 4 8 year old diabetic with resp. distress, fatigue and loss of appetite.
Three clicks

pH <7.35 ; acidemia
Blood Gas Report

Measured 37.0 C
o
Last two digits of pH
pH 7.23 Correspond with co2
PaCO2 23 mm Hg
PaO2 110.5 mm Hg
Calculated Data
HCO3 act 14 mmol / L
HCO3 <22; metabolic acidemia
O2 Sat %
PO2 (A - a) mm Hg D
PO2 (a / A)
If Na = 130,
Entered Data Cl = 90
FiO2 21.0%
Anion Gap = 130 - (90 + 14)
= 130 – 104 = 26
Case 5 : 10 year old child with encephalitis
Four clicks

Blood Gas Report

Measured 37.0 C
o
pH almost within normal range
pH 7.46 Mild alkalosis
PaCO2 28.1 mm Hg
PaO2 55.3mm Hg PaCO2 is low , respiratory
Calculated Data low by around 10
HCO3 act 19.2 mmol / L ( Acute ) by .08
(Chronic ) by .03
O2 Sat %
PO2 (A - a) mm Hg D Bicarb looks low ?
PO2 (a / A) Is it expected ?
Entered Data
FiO2 24.0%

BICARBINATURIA
Treatment of MA

Rx only if pH < 7.2 or HCO3 < 12 meq/L


HCO3 deficit = HCO3 distribution space x deficit
40% of BW (normal person with HCO3 24)

Target of therapy pH 7.2 - 7.25


HCO3 15 meq/L

Amt of HCO3 (in meq) to be given


= 0.7 x BW x (15 – pt’s HCO3) to be given in 12 – 24
hrs
NaHCO3

Mol wt 84
1 gm NaHCO3 contain 12 mmol of NaHCO3
1 ml 8.4% NaHCO3 contain 1 meq of NaHCO3
25 ml 7.5% NaHCO3 contain 22 mEq NaHCO3
Oral preparation - 600 mg / tablet
Rx of Metabolic alkalosis

Rx of underlying cause

Adequate correction of vol with isotonic saline


+/- correction of hypokalemia
It’s not magic understanding ABG’s, it just
takes a little practice!!
Case 6…………. One click

pH 7.39
PCO2 l5mmHg
HCO3 8mmol/L
PaO2 90 mmHg

These findings are most consistent with….


a) Metabolic acidosis with compensatory Hypocapnia.
b) Primary metabolic acidosis with
respiratory alkalosis.
c) Acute respiratory alkalosis fully compensated.
d) Chronic respiratory alkalosis fully compensated.

For metabolic acidosis: FULL COMPENSATION


Expected PaCO2 = (1.5 x [HCO3]) + 8 ) + 2
(Winter’s equation)
PCO 2 ……SHOULD BE 20
Case 7……….
Adolescent boy with appendicitis , posted for surgery , he is a known
case of SLE.
His pre-op ABG shows
: Room air No click
pH 7.39
pCO2 l5mmHg
paO2 90 mmHg
HCO3 8mmol/L

These findings are most consistent with….


a) Metabolic acidosis with compensatory Hypocapnia.
b) Primary metabolic acidosis with respiratory alkalosis.
c) Acute respiratory alkalosis fully compensated.
d) Chronic respiratory alkalosis fully compensated.

What is the probable cause for the above findings ? Are they OK
as far as oxygenation is concerned ?
No click
Patient was hypo volumic , received Normal Saline bolus...
Corrected acidosis
He was operated ….but post-op became drowsy
His ABG……..
FiO2….30%

pH 7.38
PaCO2 38
PaO2 60

1) Why hypoxemia ?
2) Were the lungs bad to begin with ? ( Pre OP PaO2 90 mmHg )
3) Micro atelectesis during surgery ? Anesthetist goofed up the case
4) Pure and simple hypoventilation …..Sedation ?
Case study No. 4

27 yo retarded  with insulin-dependent DM arrived at ER


from the institution where he lived. On room air ABG & VS:

pH 7.15 BP 180/110 mmHg


PCO2 22 mmHg Pulse 130/min
PO2 92 mmHg RR 40/min
HCO3 9 mmol/L VT 800ml
BE -30 mmol/L MV 32L

Interpretation: Partly compensated metabolic acidosis.


Case No: 5
74 yo  with hx chronic renal failure and chronic diuretic therapy
was admitted to ICU comatose and severely dehydrated. On
40% oxygen her ABG & VS:

pH 7.52 BP 130/90 mmHg


PCO2 55 mmHg Pulse 120/min
PO2 92 mmHg RR 25/min
HCO3 42 mmol/L VT 150ml
BE 17 mmol/L MV 3.75L

Interpretation: Partly compensated metabolic alkalosis with


corrected hypoxemia.
Case No:
43 yo  arrives in ER 20 minutes after a MVA in which he
injured his face on the dashboard. He is agitated, has mottled,
cold and clammy skin and has obvious partial airway obstruction.
An oxygen mask at 10 L is placed on his face. ABG & VS:

pH 7.10 BP 150/110 mmHg


PCO2 60 mmHg Pulse 150/min
PO2 125 mmHg RR 45/min
HCO3 18 mmol/L VT ? ml
BE -15 mmol/L MV ? L

Interpretation: Acute ventilatory failure (resp. acidosis) and


Case No:
17 yo, 48 kg  with known insulin-dependent DM came to ER
with Kussmaul breathing and irregular pulse. Room air
ABG & VS:

pH 7.05 BP 140/90 mmHg


PCO2 12 mmHg Pulse 118/min
PO2 108 mmHg RR 40/min
HCO3 5 mmol/L VT 1200ml
BE -30 mmol/L MV 48L

Interpretation: Severe partly compensated metabolic


acidosis without hypoxemia
Case contd..
This patient is in diabetic ketoacidosis.
IV glucose and insulin were immediately administered. A
judgement was made that severe acidemia was adversely
affecting CV function and bicarb was elected to restore pH to
 7.20.
Bicarb administration calculation:
Base deficit X weight (kg)
4

30 X 48 = 360 mmol/L Admin 1/2 over 15 min &


4 repeat ABG
Case No contd..
ABG result after bicarb:

pH 7.27 BP 130/80 mmHg


PCO2 25 mmHg Pulse 100/min
PO2 92 mmHg RR 22/min
HCO3 11 mmol/L VT 600ml
BE -14 mmol/L MV 13.2L
One click
Why hypoxemia ?
Lungs were bad to begin with ?
Micro atelectesis during surgery
Pure and simple hypoventilation ? sedation

PRE OP ….ABG on room air


pH 7.39
PaCO2 l5mmHg
PaO2 90 mmHg Oxygenation status good …..?
HCO3 8mmol/L

Pre OP .....A/a gradient


palvO2 = PiO2 – PaCO2 / RQ
= 150 – 15 / 0.8
= 150 – 18 = 132 mm Hg
132 – 90= 42 WIDE A / a gradient
No click

Apparently the lungs looked good with PaO2 of 90…….


But have a good look at the ABG again
With wash out of CO 2 ……….
The expected PaO2 should have been more than 90 .

This coupled with correction of acidosis


( normalizing PaCO2 )
Lowered the PaO2 …post operatively.
Conclusion ……..
Lungs were not normal to begin with ( SLE )……..
Step 1
Look at the pH
Is the patient acidemic pH < 7.35
or alkalemic pH > 7.45

Step 2
Who is responsible for this change in pH ( culprit )?
 CO2 will change pH in opposite direction
 Bicarb. will change pH in same direction
Acidemia: With HCO3 < 20 mmol/L = metabolic
With PCO2 >45 mm hg = respiratory

Alkalemia: With HCO3 >28 mmol/L = metabolic


With PCO2 <35 mm Hg = respiratory
No click

Step 3
If there is a primary respiratory disturbance, is it
acute ?

10 mm
Change = .08 change in pH ( Acute )
.03 change in pH ( Chronic )
PaCO2
Step 4 No click
If the disturbance is metabolic is the respiratory
compensation appropriate?
For metabolic acidosis:
Expected PaCO2 = (1.5 x [HCO3]) + 8 ) + 2
or simply…
expected PaCO2 = last two digits of pH

For metabolic alkalosis:


Expected PaCO2 = 6 mm for 10 mEq. rise in
Bicarb.

Suspect if .............
actual PaCO2 is more than expected : additional
…respiratory acidosis
actual PaCO2 is less than expected : additional …
No click

Step 4 cont.
If there is metabolic acidosis, is there a wide anion gap ?

Na - (Cl-+ HCO3-) = Anion Gap usually <12

If >12, Anion Gap Acidosis : M ethanol


U remia
Common pediatric causes
D iabetic Ketoacidosis
1) Lactic acidosis
P araldehyde
2) Metabolic disorders
I nfection (lactic acid)
3) Renal failure
E thylene Glycol
S alicylate
Bicarbonate buffer

Immediate buffer for an acid load


Virtually the only buffer in ECF
ECF BBS – 86%, non-HCO3 – 14%
ICF BBS – 36%, non-HCO3 – 64%
Via BBS – 600 nmol [H+] can be buffered (2.3 slykes)
350 by BBS in ECF, 250 by BBS in ICF
Amt of HCO3 in ECF : 15L (ECF vol) x 25 (HCO3 conc)
PO4 buffer

pH = pK + log HPO4-- / H2PO4- major anion in ICF

pH HPO4-- / H2PO4- HPO4-- filtered by glo


ECF 7.4 4/1
ICF 7.1 2/1 bind with H+

Urine 5.8 1/10 form H2PO4-

excreted as Titrable acidity


IC protein buffering

Major buffer in ICF


Mainly Histidines of proteins & dipeptides
Total Histidine content of a 70 kg adult – 2400mmol
About 400 mmol of H+ can be buffered by Histidine
Bone buffering

Alkali reserve - 35,000meq


Can contribute upto 40% of buffering of an acid load
Become significant by 5 hrs of acid load
H+ uptake & titration associated with loss of bone
cation Ca++
Hence ROD in CKD & rickets in RTA
NHE3
• 5 isoforms
• 800 aminoacids
• NHE1 & NHE3 principal isoforms
• NHE1 ubiquitous, localized on B/L memb
• NHE3 kidney specific, apical memb of PCT
& TAL
• Gene(NHE3) : SLC9A3 – on chr 5p15.3
Carbonic enhydrase (CA)
Zn metalloenz, 15 isoforms
H2CO3 H2O + CO2 (reversible hydration of CO2)
CA I, II, III, VII – cytoplasmic CA IV – apical memb PCT
IV, VI, IX, XII, XIV – extracellular CA12 – TALHL & DCT

CA V – mitochondrial CA15 – PCT, Thin asc limb

In kidney 95% of total CA activity – CA II, 5% IV


CAII – 29 kDa, 259 a.acids
CAIX : asso with clear cell ca kidney
Primarily found in PCT cells & intercalated cells of CCD & OMCD
Gene : CA II – 8q22, CA IV - 17q23
Bicarbonate gap
In simple MA, in AGP = HCO3;
– So bicarbonate gap = 0

+ve bicarbonate gap (if > 6meq/L)


– a) asso met alk +
– b) HCO3 retention as compensation for resp acidosis

Neg bicarbonate gap (< -6) - HCO3 is high


– actual HCO3 is less than needed
– So MA + asso normal AGP MA or Resp alk
Osmolar gap
Used to reveal alcohol in bld

Measured osmolality – calculated osmolality

Calculated osmolality = 2 x Na + RBS/18 + BU/6

High osmolality (>15mOsm/L) – presence of


unmeasured uncharged particle - ? alcohol

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