2. Contents
Uses
Contraindications
ABG procedure and precautions
Normal values
Interpretation
-Oxygenation
-Acid base balance
Definitions and terminologies
Regulation of acid base balance
Step wise interpretation ofABG
Causes
3. Why it is important to know about
ARTERIAL BLOOD GASES?
Blood pH <6.8 or >7.8 not compatible with
life and indicates irreversible cell damage or
death.
Aids in establishing a diagnosis and severity of
respiratory failure.
Assess adequacy of ventilation and oxygenation
Adequacy of CO2 excretion
Assess changes in acid- base homeostasis
Helps to guide treatment plan.
Helps in management of ICU patients.
4. Contraindication
▶ Cellulitis or other infections over puncture site.
▶ Absence of palpable arterial pulse.
▶ Negative result of anAllen test/modifiedAllen test
▶ Coagulopathies / anticoagulant therapy.
▶ History of arterial spasm following previous puncture.
▶ Severe PVD
▶ Arterial grafts.
▶ Dialysis shunt – choose another site.
6. ABG – Procedure and Precautions
Pre-heparinisedABG syringes
Syringe should be FLUSHED with 0.05ml to 0.1ml of 1:1000 Heparin
solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE
HEPARIN DILUTIONAL
EFFECT
HCO3
PCO2
Use only 2ml or less syringe.
7. Ensure NoAir Bubbles. Syringe must be sealed immediately after
withdrawing sample.
▶ Contact withAIR 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
8.
9. ABGAnalyser is controlled for Normal Body temperatures
Sample of hyperthermic patient >37°C, Measured values of PaO2
and PaCO2 are less than actual.
Hypothermic patient < 37°C measured values of PaO2 and PaCO2
are more than the actual values.
Every 1◦C ↓in temperature PCO2↓
pH ↑
PCO2 ↑
pH ↓
Every1◦C ↑in temperature
Body temperature
10. ABG Sample should always be sent with relevant
information regarding O2, FiO2 status and Temp .
Before you withdraw a sample forABG
After any change in FiO2 wait for 20min
And wait for 30 min after any change in ventilatory
parameters to ensure steady state.
11. Complications:
▶ Pain
▶ Bruising and haematoma
▶ Nerve damage
▶ Aneurysm
▶ Spasm
▶ A
V fistula
▶ Infection
▶ Air or thromboembolism
▶ Anaphylaxis from local anaesthetic
12. Normal Values
ANALYTE Normal Value Units
pH 7.35 - 7.45
PCO2 35 - 45 mm Hg
PO2 72 – 104 mm Hg`
[HCO3] 22 – 30 meq/L
SaO2 95-100 %
Anion Gap 12 + 4 meq/L
∆HCO3 +2 to -2 meq/L
13. Blood Gas Norms
pH pCO2 pO2 HCO3 BE
Arterial 7.35-7.45 35-45 80-100 22-26 -2 to +2
Venous 7.30-7.40 43-50 ~45 22-26 -2 to +2
14. Determination of PaO2
2
PaO is dependent upon Age, FiO , P
2 atm
As Age the expected PaO2
• PaO2 = 109 - 0.4 (Age)
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
A 2 B
P O = partial pressure of oxygen in alveolar gas, P = barometric pressure
(760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
inspired oxygen, PCO2 = partial pressure of CO2 in theABG, R = respiratory
quotient (0.8)
15. Determination of the PaO2 / FiO2 ratio
InspiredAir FiO2 = 21%
PiO2 = 150 mmHg
PalvO2 = 100 mmHg
PaO2 = 90 mmHg
O2
CO2
(along with other criteria)
P/Fratio
16. 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
PaO2 60 90
FiO2 21% (0.21) 50% (0.50)
P:F
Ratio
285 180
21. ROLE OF KIDNEY
It retains and regenerate HCO3- thereby regenerating the body
buffer with the net effect of eliminating the non-volatile acid
load
a. H+ secretion
1. Free urinary H+ - minimal contribution
2. Ammonia
3. Phosphorus
b. HCO3- reabsorption
1. Proximal tubule – 90%
2. Distal tubule -10%
22. Assessment of ACID BASE Balance
▶ 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)
23. 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
MixedAcid Base Disorder – Presence of more than one acid
base disorder simultaneously .
24. BASE EXCESS
▶ Base excess is the amount of acid or base (expressed in mEq/L)
that must be added for blood pH to return to 7.40 and Paco2 to
return to 40 mm Hg at full O2 saturation and 37°C.
▶ The metabolic component of an acid–base disturbance.
▶ Apositive value indicates metabolic alkalosis.
▶ whereas a negative value reveals metabolic acidosis.
26. ▶ STEP 0- IS THISABGAUTHENTIC?
▶ STEP1-ACIDEMIAORALKALEMIA
▶ STEP2-RESPIRATORY OR METABOLIC
▶ STEP3- IF RESPIRATORY-ACUTE OR CHRONIC?
▶ STEP4- IS COMPENSATION ADEQUATE?
▶ STEP5-IF METABOLIC-ANION GAP?
▶ STEP6- IF HIGHANION GAP METABOLIC
ACIDOSIS-ΔGAP?
27. Is this ABG authentic ?
▶ pH = - log [H+]
Henderson-Hasselbalch equation
pH = 6.1 + log HCO3
-
0.03 x PCO2
pHexpected = pHmeasured = ABG is authentic
29. Look at pH
<7.35 - acidemia
>7.45 – alkalemia
STEP1- ACIDEMIA OR ALKALEMIA
30. IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
pH PCO2 or pH PCO2 METABOLIC
pH PCO2 or pH PCO2 RESPIRATORY
In primary respiratory disorders, the pH and PaCO2 change
in opposite directions; in metabolic disorders the pH and
PaCO2 change in the same direction.
STEP2-RESPIRATORY OR METABOLIC
31. STEP3- IS COMPENSATION ADEQUATE?
▶ pH within normal range- No acid base disorder,
Fully compensated
or mixed disorder.
▶ pH out of the range- uncompensated
or partially compensated.
32. Compensation
• PCO2 = (1.5 X [HCO3
-])+8 ±2
• For every 1mmol/l in HCO3 the PCO2 falls
by 1.25 mm Hg
METABOLIC
ACIDOSIS
• PCO2 = (0.7 X [HCO3
-])+ 21± 2
• For every 1mmol/l in HCO3 the PCO2 by
0.75 mm Hg
METABOLIC
ALKALOSIS
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2
34. In Respiratory Disorders
Compensation begins to appear in 6 – 12 hrs and is fully developed
only after a few days.
1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
in PCO2 HCO3 by 0.2
Resp. alkalosis – 1mmHg
meq/l
35. After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
2.CHRONIC (>24 hrs)
37. Mixed Acid-base Disorders are Common
▶ In chronically ill respiratory patients, mixed disorders are probably
more common than single disorders, e.g., RAc + MAlk, RAc + Mac,
Ralk + MAlk.
▶ In renal failure combined MAlk + MAc is also encountered.
Clues to a mixed disorder:
▶ Normal pH with abnormal HCO3 or CO2
▶ PaCO2 and HCO3 move in opposite directions
▶ pH changes in an opposite direction for a known primary disorder
38. Unmask the hidden metabolic
disorders
3 parameters need to be assessed
▶ Anion gap and its change from normalΔAG
▶ Venous CO2 and its change from normalΔCO2
▶ Bicarbonate gap
39. ▶ Anion Gap= measured cations- measured anions
ANION GAP(AG) = Na – (HCO3 + Cl)
Normal Value = 12 + 4 ( 8- 16 meq/l)
▶ ΔAG= MEASUREDAG -12
IFΔAG POSITIVE ORAG>16: METABOLICACIDOSIS
IFΔAG NEGA
TIVE OR LOWAG:
Reduction in unmeasured anions (hypoproteinemia)
Excess of unmeasued cations(lithium toxicity)
Excessively abnormal positively charged
protien(multiple myeloma)
STEP5-IF METABOLIC- ANION GAP?
40. ▶ Albumin is the major unmeasured anion
▶ The anion gap should be corrected if there are gross changes in
serum albumin levels.
AG (CORRECTED) =AG + { (4 – [ALBUMIN]) × 2.5}
If the anion gap is elevated, consider calculating the osmolal gap
in compatible clinical situations:
•Elevation in AG is not explained by an obvious case (DKA,
lactic acidosis, renal failure)
•Toxic ingestion is suspected
41. PLASMA OSMOLAR GAP
Cal. Plasma Osmolarity = 2[Na+] + [Gluc]/18 + [BUN]/2.8
▶ OSM gap = measured Osm – Cal. Plasma Osm
▶ The OSM gap should be < 10 mOsm/kg
Osm gap > 10 mOsm/kg indicates presence of abnormal osmotically
active substance
Ethanol
Methanol
Ethylene glycol
42. STEP6- IF HIGH ANION GAP METABOLIC
ACIDOSIS-DELTA RATIO/ DELTA GAP?
If an increased anion gap is present, assess the relationship between the
increase in the anion gap and the decrease in [HCO3-].
: unmask the co-existence of two metabolic disorders
∆Anion Gap = MeasuredAG – NormalAG
MeasuredAG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase inAG, HCO3 will fall by 1 meq/L
43. DELTA GAP
▶ DELTAGAP =ΔAG-ΔHCO3
▶ DELTAGAP = (MEASUREDAG-12) – (24-MEASURED HCO3)
▶ DELTAGAP = Na-Cl-36
▶ POSITIVE OR DELTAGAP > +6
METABOLICALKALOSIS
BICARBONATE RETENTION FOR RESPIRATORYACIDOSIS
▶ NEGA
TIVE OR DELTAGAP < -6meq/l
NORMALANION GAP METABOLICACIDOSIS
45. HighAnion Gap MetabolicAcidosis
M METHANOL
U UREMIA - ARF/CRF
D DIABETIC KETOACIDOSIS & other KETOSIS
P PARALDEHYDE, PROPYLENE GLYCOL
I ISONIAZIDE, IRON
L LACTICACIDOSIS
E ETHANOL, ETHYLENE GLYCOL
S SALICYLATE
Metabolic Acidosis
46. 1. Hypokalemic
a. GI losses of HCO3 –
i. Ureterosigmoidostomy
ii. Diarrhea, ingestion of CaCl2
iii. Ileostomy
2. Normokalemic or hyperkalemic
a. Renal tubular disease
i. Acute tubular necrosis
ii. Chronic tubulointerstitial disease
iii. Distal RTA(type I and IV)
iv. Hypoaldesteronism
NORMALANION GAP METABOLIC ACIDOSIS
(hyperchloremic)
b. Renal losses of HCO3 –
i. proximal RTA
ii. carbonicAnhydrase
inhibitors
b. Pharmacological
i. Ammonium chloride
ii. Hyperalimentation
iii. Dilutional acidosis.
48. 1. Loss of H+ ions (e.g. vomiting, diuretics)
2. Increased reabsorption of bicarbonate – Low intravascular volume
– Hypokalemia
– High pCO2
– Increased mineralocorticoids
(aldosterone).
3. Administration of alkali (in setting of renal impairment) e.g. Ringer’s
lactate where lactate gets metabolised to bicarbonates in liver adding to
alkali pool.
METABOLIC ALKALOSIS
49. RESPIRATORYACIDOSIS
1. Airway/pulmonary parenchymal disease
a. Upper airway obstruction
b. Lower airway obstruction
c. Pulmonary -
i. Cardiogenic pulmonary edema
ii. Pneumonia iii.ARDS
iv. Pulmonary perfusion defect—PE—air/fat/tumor
2. CNS depression -head injury ,medications such as narcotics, sedatives, or anesthesia
3. Neuromuscular disease and impairment
4. Ventilatory restriction—due to pain, chest wall injury/ deformity, or abdominal
distension.
50. ▶ Increased CO 2 production
Large caloric loads
Malignant hyperthermia
Intensive shivering
Prolonged seizure activity
Thyroid storm
Extensive thermal injury (burns)
52. URINARYANION GAP
▶ Urinary NH4
+ levels can be estimated by calculating the urine
anion gap (UAG)
▶ UAG = [Na+ + K+]u – [Cl–]u
▶ [Cl–]u > [Na+ + K+], the urine gap is negative by definition
▶ Helps to distinguish GI from renal causes of loss of HCO3 by
estimating Urinary NH4+ (elevated in GI HCO3 loss but low in
distal RTA).
▶ Hence a -ve UAG (av -20 meq/L) seen in former while +ve value
(av +23 meq/L) seen in latter.
53. Urine PH
▶ NonAG metabolic acidosis:
▶ If urine pH > 5.5 : Type 1 RTA
▶ If urine pH < 5.5 : Type 2 or Type 4 RTA
▶ Type 2 or Type 4 RTAcan be later differentiated using serum
K+ level
54.
55. References
1. Paul L.Marino – The ICU Book.
2. Millers anaesthesia- eighth edition.
3. Morgan and Mikhails’s – Clinical anaesthesiology 5th
edition
4. Prof.A. K. Sethi EORCAPS 2013
5. Davenport – TheABC ofAcid Base Chemistry, 6th edition
6. Handbook of blood gas /Acid base interpretation-Ashfaq
Ahmed
57. STEWART APPROACH
Its variables are pCO2 , strong ion difference (SID) andAtot (Total weak acids)
– Respiratory disorders are due to alterations in pCO2 similar to the traditional
approach
– Metabolic disorders are due to primary alterations in strong ion difference
(SID) and Strong ion gap (SIG) orAtot
– The cations are Na+, K+, Ca++ and Mg++
– The anions are Cl– , Lactates and other strong ions
– SID apparent SIDa= (Na+k+Ca+Mg)–(Cl) –Lactate-other strong ions
– (Na + k + Ca + Mg) – (Cl)
Normal strong ion difference is about 40 mEq/L
– SID effective SIDe = (HCO3 ) + (A– ) whereA– is the total concentration of
dissociated weak noncarbonic acids, mainly albumin and PO4 –
– Strong ion gap (SIG) orAtot = SIDa- SIDe.
Normal Strong ion gap is zero.
