3. ABG – Procedure and Precautions
Site- (Ideally) Radial Artery
Femoral Artery
Ideally - Pre-heparinised ABG syringes
- Syringe should be FLUSHED with 0.5ml
of 1:1000 Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE
SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
Only small 0.5ml Heparin for flushing and discard it
Syringes must have > 50% blood. Use only 2ml or less syringe.
4. Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
– Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN
5. Patients Body Temperature affects the values of
PCO2 and HCO3.
ABG Analyser is controlled for Normal Body
temperatures
Any change in body temp at the time of sampling
leads to alteration in values detected by the
electrodes
Cell count PO2
ABG Sample should always be sent with relevant information regarding
O2, FiO2 status and Temp.
7. Acid Base Balance
o H+ ion concentration in the body is precisely
regulated
o The body understands the importance of H+
and hence devised DEFENCES against any
change in its concentration
BICARBONATE
BUFFER SYSTEM
Acts in few seconds
RESPIRATORY
REGULATION
Acts in few minutes
RENAL
REGULATION
Acts in hours to days
A
C
I
D
B
A
S
E
8. Regulation of Acid Base
1. Bicarbonate Buffer System
CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3
-
In Acidosis - Acid = H+
H+ + HCO3 H2CO3 CO2 + H2O
In Alkalosis - Alkali + Weak Acid = H2CO3
CO2 + H20 H2CO3 HCO3
- + H+
+
ALKALI
9. 2. Respiratory Regulation of Acid Base
Balance:
H+ PaCO2
H+ PaCO2
ALVEOLAR
VENTILATION
ALVEOLAR
VENTILATION
10. 3. Renal Regulation of Acid Base Balance:
Kidneys control the acid-base balance by excreting
either an acidic or a basic urine.
This is achieved in the following ways:
Reabsorption Secretion of H+
of HCO3 ions in tubules
in blood and excretion
• Proximal Convulated Tubules (85%)
• Thick Ascending Limb of Loop of Henle (10%)
• Distal Convulated Tubule
• Collecting Tubules(5%)
11. Another mechanism by which the kidney
controls the acid base balance is by the
Combination of excess H+ ions in urine with
AMMONIA and other buffers- A mechanism
for generating NEW Bicarbonate ions
In CKD, the dominant mechanism by which acid is
eliminated by the Kidneys is excretion of NH4+
GLUTAMINE
2HCO3
- 2NH4
+REABSORBED EXCRETED
+
H+, Cl-
13. ABG ELECTRODES
pH (Sanz Electrode)
Measures H+ ion concentration of sample against a
known pH in a reference electrode, hence potential
difference. Calibration with solutions of known pH (6.384
to 7.384).
P CO2 (Severinghaus Electrode)
CO2 reacts with solution to produce H+ higher CO2-
more H+ higher P CO2 measured.
P O2 (Clark Electrode)
O2 diffuses across membrane producing an electrical
current measured as P O2.
14. Measured Values
Temperature Correction:
Is there any value to it?
Calculated Data:
Which are the useful ones?
Entered Data:
Derived from other sources
The Anatomy of a Blood Gas Report
15. The Anatomy
of a Blood Gas Report
----- XXXX Diagnostics ------
Blood Gas Report
248 05:36 Jul 22 2000
Pt ID 2570 / 00
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
pH 7.439
pCO2 47.6 mm Hg
pO2 123.5 mm Hg
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
ct CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Measured Values
Temperature Correction:
Is there any value to it?
Calculated Data:
Which are the useful ones?
Entered Data:
Derived from other sources
16. Temperature Correction:
“ There is no scientific basis ... for applying
temperature corrections to blood gas
measurements…”
Shapiro BA, OTCC, 1999.
Uncorrected pH & pCO2 are reliable reflections
of in-vivo acid base status
Temperature correction of pH & pCO2 do
not affect calculated bicarbonate
pCO2 reference points at 37
o
C are well
established as reliable reflectors of alveolar
ventilation
Reliable data on DO2 and oxygen demand are
unavailable at temperatures other than 37
o
C
----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
pH 7.439
pCO2 47.6 mm Hg
pO2 123.5 mm Hg
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
17. ----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Bicarbonate is calculated on the basis of the
Henderson equation:
[H
+
] = 24 pCO2 / [HCO3
-
]
Bicarbonate:
18. ----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Standard Bicarbonate:
Plasma HCO3 after equilibration
to a PCO2 of 40 mm Hg
: reflects non-respiratory acid base change
: does not quantify the extent of the buffer
base abnormality
: does not consider actual buffering capacity
of blood
Base Excess:
D base to normalise HCO3 (to 24) with PCO2 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
19. ----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Oxygenation
Parameters:
O2 Content of blood:
Hb x O2 Sat x Const. + Dissolved O2
Oxygen Saturation:
Alveolar / arterial gradient:
Arterial / alveolar ratio:
22. PaO2 (Partial pressure of arterial oxygen)
PaO2 is dependant upon Age, FiO2, Patm
As Age the expected PaO2
• PaO2 = 109 - [0.4 (Age)]
• Normal PaO2: 75-100 mmHg
As FiO2 the expected PaO2
• Alveolar Gas Equation:
• PAO2= (PB-P h2o) x FiO2- pCO2/R
O
X
Y
G
E
N
A
T
I
O
N
PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
quotient (0.8)
23. PaO2 / FiO2 ratio:
Inspired Air FiO2 = 21%
PiO2 = 150 mmHg
PalvO2 = 100 mmHg
PaO2 = 90 mmHg
O2CO2
PaO2/FiO2 Ratio Inference
>300 Normal
<300 Acute Lung Injury
<200 ARDS (along with other criteria)
24. PaO2/ FiO2 ratio ( P:F Ratio )
Gives understanding that the patients OXYGENATION
with respect to OXYGEN delivered is more important
than simply the PO2 value.
Example
Patient 1
On Room Air
Patient 2
On MV
PO2 60 90
FiO2 21% (0.21) 50% (0.50)
P:F Ratio 285 180
25. ----- XXXX Diagnostics ------
Blood Gas Report
Measured37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected38.6
o
C
Calculated Data
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
t CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Oxygenation:
O2 Content of blood:
Hb x O2 Sat x 1.34 + Dissolved O2 (given by
Pao2x0.003)
Useful in oxygen transport calculations
Derived from calculated saturation
Oxygen Saturation:
Ideally measured by co-oximetry
Calculated values may be error-prone
Alveolar / arterial gradient:
Hypoxemia causes differentiated by A-a Gradien
Estimate of normal A–a gradient <[age in years/4] + 4
An abnormally increased A–a gradient suggests :
• Defect in diffusion
• V/Q (ventilation/perfusion ratio) mismatch
• right-to-left shunt
Normal A-a Gradient:
• Hypoventilation
Neuromuscular disorders
Central nervous system disorder
• Low inspired FIO2 (e.g. high altitude)
Arterial / alveolar ratio:
Remains stable with change in FIO2
Low a/A (<0.6) = Shunt , V/Q mismatch, diffusion defect
26. Alveolar-arterial Difference
Inspired O2 = 21%= piO2 = (760-45) x .21=150 mmHg ( So at room air PiO2=150 mmHg)
O2
CO2
palvO2 = piO2 - pCO2 / RQ
= 150 - 40/0.8
= 150 – 50 = 100 mm Hg( Calculated)
partO2 = 90 mmHg (Measured)
(palvO2- partO2 )D = 10 mmHg (Normal= =<[age in years/4] + 4)
29. Definitions and Terminology
ACIDOSIS:
Presence of a process which tends to pH by
virtue of gain of H + or loss of HCO3
-
ALKALOSIS:
Presence of a process which tends to pH by
virtue of loss of H+ or gain of HCO3
-
If these changes, change pH, suffix ‘emia’ is added
ACIDEMIA : Reduction in arterial pH (pH<7.35)
ALKALEMIA : Increase in arterial pH (pH>7.45)
30. Simple Acid Base Disorder/ Primary Acid Base
disorder
A single primary process of acidosis or alkalosis due to
an initial change in PCO2 and HCO3
Compensation
The normal response of the respiratory system or
kidneys to change in pH induced by a primary acid-base
disorder
Note: The Compensatory responses to a primary Acid Base disturbance are never
enough to correct the change in pH , they only act to reduce the severity
Mixed Acid Base Disorder
Presence of more than one acid base disorder
simultaneously
32. STEP 0
• Is this ABG Authentic?
STEP 1
• ACIDEMIA or ALKALEMIA?
STEP 2
• RESPIRATORY or METABOLIC?
STEP 3
• If Respiratory – ACUTE or CHRONIC?
STEP 4
• Is COMPENSATION adequate?
STEP 5
• If METABOLIC – ANION GAP?
STEP 6
• If High gap Metabolic Acidosis–
GAP GAP?
33. If the pH and the [H+] are inconsistent, the ABG is probably not valid.
[H+] = 24(PaCO2)
[HCO3-]
H+ ion (mmol/L) pH
100 7.00
79 7.10
63 7.20
50 7.30
45 7.35
40 7.40
35 7.45
32 7.50
25 7.60
STEP0: Is this ABG Authentic?
34. Look at pH
<7.35 : acidemia
>7.45 : alkalemia
NOTE – An acid base abnormality is present even if either
the pH or PCO2 are Normal.
ACIDEMIA OR ALKALEMIA?STEP 1
35. PRIMARY
DISORDER
PRIMARY RESPONSES COMPENSATORY
RESPONSESH+ ion pH Primary
Conc. Defect
Metabolic
Acidosis H+ pH HCO3
PCO2
Alveolar
Hyperventilation
Metabolic
Alkalosis H+ pH HCO3
PCO2
Alveolar
Hypoventilation
Respiratory
Acidosis H+ pH PCO2 HCO3
Respiratory
Alkalosis H+ pH PCO2 HCO3
RESPIRATORY or METABOLIC?STEP 2
RULE- If either the pH or PCO2 is Normal, there is a
mixed metabolic and respiratory acid base disorder.
37. ----- XXXX Diagnostics ------
Blood Gas Report
Measured 37.0
o
C
pH 7.301
pCO2 76.2 mm Hg
pO2 45.5 mm Hg
Calculated Data
HCO3 act 36.1 mmol / L
O2 Sat 78 %
pO2 (A - a) 9.5 mm Hg D
pO2 (a / A) 0.83
Entered Data
FiO2 21 %
Case 1
60 year old male smoker
with progressive
respiratory distress
and somnolence.
D CO2 =76-40=36
Ac D pH = 36/10 x0.08=0.29
Exp Acute pH = 7.40-0.29=7.11
Chronic D pH= 36/10 x0.03=0.10
Exp Chr pH = 7.40-0.10=7.30
Chronic resp. acidosis
pH <7.35 ; acidemia
pCO2 >45; respiratory acidemia
Hypoxia
Normal A-a gradient
Due to hypoventilation
38. ----- XXXX Diagnostics ------
Blood Gas Report
Measured 37.0
o
C
pH 7. 232
pCO2 60.1 mm Hg
pO2 66.3 mm Hg
Calculated Data
HCO3 act 24.5 mmol / L
O2 Sat 92 %
pO2 (A - a) mm Hg D
pO2 (a / A)
Entered Data
FiO2 30 %
Case 2
18-year-old male asthmatic;
3 days of cough, dyspnea
and orthopnea not
responding to usual
bronchodilators.
O/E: Respiratory distress;
suprasternal and
intercostal retraction;
tired looking; on 4 L NC.
D CO2 = 60 - 40 = 20
Expect Acute D pH = 20/10x0.08= 0.16
Expect Ac pH = 7.40 - 0.16 = 7.24
Acute resp. acidosis
pH <7.35 ; acidemia
pCO2 >45; respiratory acidemia
Hypoxemia
piO2 = (760-45)x.3=214.5 / palvO2 = 214-60/.8=129
129-66= 63
Oxygenation failure
39. ADEQUATE COMPENSATION?STEP 4
IS THE COMPENSATORY RESPONSE ADEQUATE OR NOT?
METABOLIC DISORDER PCO2 expected
Metabolic acidosis: PaCO2(e)= (1.5 x [HCO3-]) +8± 2
Metabolic alkalosis:PaCO2(e)= (0.7 x [HCO3-])+ 21 + 2
PCO2measured ≠ PCO2expected MIXED DISORDER
RESPIRATORY DISORDER pHexpected (acute-chronic)
pHm ≠ pHe range MIXED DISORDER
40. CASE 1
Mr. Shamshuddin, 62/M,
Nagina
k/c/o COPD
Breathlessness,
progressively increased,
aggravated on exertion, 2
days
Chronic smoker
O/E
RS- B/L expiratory rhonchi
22/7/11 7:30 am
pH 7.20
PCO2 92 mmHg
PO2 76 mmHg
Actual
HCO3
21.00 mmol/l
SO2 89
FiO2 37%
42. METABOLIC ACIDOSIS-
ANION GAP?
STEP 5
IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP?
ANION GAP(AG) = Na – (HCO3 + Cl)
Normal Value = 12 + 4 ( 8- 16 Meq/l)
Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)
50% in S. Albumin 75% in Anion Gap !!!
Metabolic Acidosis
High Anion Gap Metabolic Acidosis
Normal Anion Gap Acidosis
43. Anion Gap
AG based on principle of electroneutrality:
Total Serum Cations = Total Serum Anions
M cations + U cations = M anions + U anions
Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
Na + UC = HCO3 + Cl + UA
But in Blood there is a relative abundance of Anions, hence
Anions > Cations
Na – (HCO3 + Cl) = UA – UC
Na – (HCO3 + Cl) = Anion Gap
44. CASE 3
Mr.Dharam Dutt, 63/M,
Bijnor
k/c/o CRF(conservativeRx)
Breathlessness
Decreased Urine Otpt. 2days
Vomiting 10-15
O/E
No pedal edema, dehydration +
RS – B/L A/E Normal
31/7/11 11:30pm
pH 7.18
PCO2 21.00
PO2 90
Actual
HCO3
7.80
Base Excess -18.80
SO2 95
Na 140.6
Chloride 102
T.Protein 6
Albumin 2.4
45. STEP 1 – ACIDEMIA
STEP 2 – pH PCO2
METABOLIC
STEP 4 – PCO2expected
PCO2exp = (1.5 x HCO3)+8+2
(1.5X7.80)+8+2
19.7+2= 17.7 – 21.7
STEP5 – ANION GAP
= Na – (HCO3 +Cl)
= 140.6-(7.80+102)
= 30.8
AG corrected for albumin = 30.8+5.25
AG = 36.05
HIGH AG Met. Acidosis
46. High Anion Gap Metabolic Acidosis
M
U
D
P
I
L
E
S
METHANOL
UREMIA - ARF/CRF
DIABETIC KETOACIDOSIS & other KETOSIS
PARALDEHYDE, PROPYLENE GLYCOL
ISONIAZIDE, IRON
LACTIC ACIDOSIS
ETHANOL, ETHYLENE GLYCOL
SALICYLATE
47. Non Anion Gap Metabolic Acidosis
U
S
E
D
C
R
A
P
URETEROENTEROSTOMIES
SMALL BOWEL FISTULA
EXCESS CHLORIDE
DIARRHOEA
CARBONIC ANHYDRASE INHIBITOR
RTA
ADDISSION’S DISEASE
PANCREATOENTEROSTOMIES
48. CO EXISTANT METABOLIC
DISORDER – “Gap Gap”?
STEP 6
If an increased anion gap is present:
Assess the ratio of the change in the anion gap (∆AG ) to the
change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
∆AG/D HCO3
- = 1 Pure High AG Met Acidosis
D AG/D HCO3
- > 1 Assoc Metabolic Alkalosis
D AG/D HCO3
- < 1 Assoc Non AG Met Acidosis
49. CASE 4
Mr.Dharam Dutt, 63/M,
Bijnor
k/c/o CRF(conservativeRx)
Breathlessness
Decreased Urine Otpt. 2days
Vomiting 10-15
O/E
No pedal edema, dehydration +
RS – B/L A/E Normal
31/7/11 11:30pm
pH 7.18
PCO2 21.00
PO2 90
Actual
HCO3
7.80
Base Excess -18.80
SO2 95
Na 140.6
Chloride 102
T.Protein 6
Albumin 2.4
50. STEP 1 – ACIDEMIA
STEP 2 – pH PCO2
METABOLIC
STEP 4 – PCO2expected
PCO2exp = (1.5 x HCO3)+8+2
(1.5X7.80)+8+2
19.7+2= 17.7 – 21.7
COMPENSATED
STEP5 – ANION GAP
= Na – (HCO3 +Cl)
= 140.6-(7.80+102)
= 30.8
AG corrected for albumin = 30.8+5.25
AG = 36.05
HIGH AG Met. Acidosis
52. Normal AG= 12; D Gap = 16 - 12 = 4
Normal HCO3=24;DHCO3 = 24 -14 = 10
D AG/D HCO3
- < 1(4/10)
Indicates additional non-gap Met.acidosis
----- XXXX Diagnostics ------
Blood Gas Report
Measured 37.0
o
C
pH 7.236
pCO2 34 mm Hg
pO2 110.5 mm Hg
Calculated Data
HCO3 act 14 mmol / L
O2 Sat %
pO2 (A - a) mm Hg D
pO2 (a / A)
Entered Data
FiO2 21.0 %
Case 5
28 year old diabetic with
respiratory distress
fatigue and
loss of appetite.
pH <7.35 ; acidemia
HCO3 <22; metabolic acidemia
Limits:
Expected pCO2 = (1.5 x HCO3)+8 + 2
= (1.5 x 14)+ 8 + 2
= 29 + 2 = 27 to 31
Met. Acidosis + Resp. acidosis
If Na = 130,
Cl = 100
Anion Gap = 130 - (100 + 14)
= 130 - 114= 16
53.
54. Question1.
A 45 year-old woman with a history of inhalant abuse presents to the
emergency room complaining of dyspnea. She has an SpO2 of 99% on room air
and is obviously tachypneic on exam with what appears to be Kussmaul’s
respirations. A room air arterial blood gas is performed and reveals: pH 6.95,
PCO2 9, PO2 128, HC3- 2. A chemistry panel revealed sodium of 130, chloride 98,
HCO3- 2.
Answer1.
The patient has a very low pH (acidemia)
The low pH in conjunction with the low bicarbonate tells us that the metabolic
acidosis is the primary process
The anion gap is elevated at 30[130-(98+2)]. This tells us that the patient has a
primary elevated anion gap metabolic acidosis.
Compensated as PaCO2 (e)=9-13(1.5x2+8+-2)
delta AG is 30-12 = 18
Delta AG/D HCO3
- < 1( 18/22) ,So there is an additional non-gap metabolic
acidosis as well.
Combined elevated anion gap and non-gap metabolic acidoses with
compensatory respiratory alkalosis.
55. Question2.
A 45 year-old man with a history of very severe COPD (FEV1~ 1.0L, < 25%
predicted) and chronic carbon dioxide retention (Baseline PCO2 58) presents to
the emergency room complaining of worsening dyspnea and an increase in the
frequency and purulence of his sputum production over the past 2 days. His
oxygen saturation is 78% on room air. Before he is placed on supplemental
oxygen, a room air arterial blood gas is drawn and reveals: pH 7.25, PCO2 68,
PO2 48, HCO3-31.
Answer2.
The patient has a low pH (acidemia)
The combination of the low pH and the high PCO2 tells us that the respiratory
acidosis is the primary process.
pH(e-acute)=7.2 and pH(e-chronic)=7.3 (If pH(m) = between pH(e- acute) & pH(e-
chronic) - partially compensated metabolic alkalosis.
The alveolar-arterial oxygen difference is 17 mmHg(As ABG is taken before
placing him on supplemental oxygen, So PiO2 will be 150 and RQ will be 0.8).
palvO2= piO2 - pCO2 / RQ= 150-68/0.8=65 , And A-a gradient= palvO2 –PaO2=65-48=17
This value is elevated, suggesting that the hypoxemia is due to either shunt or
areas of low V/Q (the more likely explanation in a patient with COPD) and
cannot be explained by hypoventilation alone.
Primary respiratory acidosis with partially compensated metabolic
alkalosis with hypoxemia due to either shunt or V/Q mismatch.
I would like to thank my mentor of this seminar dr. sushil pathak sir for providing insight and for inspiring and helping us to dig dipper into abg interpretation
Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg.
A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.
actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.
A typical reference range for base excess is −2 to +2 mEq/L
More negative values of base excess may indicate:
Lactic acidosis
Ketoacidosis
Ingestion of acids
Cardiopulmonary collapse
Shock
More positive values of base excess may indicate:
Loss of buffer base
Hemorrhage
Diarrhea
Ingestion of alkali
PO2 (partial pressure of oxygen) reflects the amount of oxygen gas dissolved in the blood. It primarily measures the effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere.
Elevated pO2 levels are associated with:
Increased oxygen levels in the inhaled air
Polycythemia
Decreased PO2 levels are associated with:
Decreased oxygen levels in the inhaled air
Anemia
Heart decompensation
Chronic obstructive pulmonary disease
Restrictive pulmonary disease
Hypoventilation
ARDS:acute, meaning onset over 1 week or less, bilateral opacities consistent with pulmonary edema, PF ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP) .“must not be fully explained by cardiac failure or fluid overload.
ARDS Severity PaO2/FiO2* Mild 200 – 300 Moderate 100 – 200 Severe < 100
Interpretation: Hypoxemia causes differentiated by A-a Gradient
Increased A-a Gradient
Right to Left Intrapulmonary Shunt (due to fluid filled alveoli)
Congestive Heart Failure
Adult Respiratory Distress Syndrome (ARDS)
Lobar Pneumonia
V/Q Mismatch (due to lung dead space)
Pulmonary Embolism
Atelectasis
Pneumonia
Obstructive Lung Disease (e.g. Asthma, COPD)
Pneumothorax
Alveolar hypoventilation
Interstitial Lung Disease
Normal A-a Gradient
Hypoventilation
Neuromuscular disorders
Central nervous system disorder
Low inspired FIO2 (e.g. high altitude)
Type 1 respiratory failure is defined as a low level of oxygen in the blood (hypoxemia) without an increased level of carbon dioxide in the blood (hypercapnia)
PaO2 decreased (< 60 mmHg (8.0 kPa)) PaCO2 normal or decreased (<50 mmHg (6.7 kPa)) PA-aO2 increased
Type 2 respiratory failure is defined as Hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa)
PaO2 decreased (< 60 mmHg (8.0 kPa)) PaCO2 increased (> 50 mmHg (6.7 kPa)) PA-aO2 normal pH decreased
Causes:Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation)
Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
Neuromuscular problems (Guillain–Barré syndrome,[2] motor neuron disease)
Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.[2]
Respiratory acidosis:
Acute-Increase in [HCO3-]= ∆ PaCO2/10 +-3
Chronic-Increase in [HCO3-]=3.5(∆PaCO2/10)
Respiratory alkalosis:
Acute-Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic-Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)