ARTERIA

L BLOOD
GASES

Moderator : Dr Puja
Singh
Speaker : Dr Sakshi

Gupta
 DEFINITION
Blood gas analysis, also called arterial blood gas (ABG)


analysis, is a test which measures the amounts of

oxygen and carbon dioxide in the blood, as well as
the acidity (pH) of the blood.


It involves puncturing an artery with a thin needle and

syringe and drawing a small volume of blood.
 Common sites:
 Radial A
 Femoral A
 Brachial A
 Dorsalis Pedis A
 Axillary A
OBJECTIVES & USES
• Understand Ventilation and Perfusion
Mechanics
 Aids in ventilator management
 Improvement in acid/base management allows
for optimal function of medications
 Aids in establishing a diagnosis
 Helps guide treatment plan
 Acid/base status may alter electrolyte
levels critical to patient status/care
• Recognize Signs & Symptoms of Respiratory
Failure
• Analyze and Interpret Acid Base Disturbances



 Before beginning…
 Allen’s test for radial and
ulnar artery
 Common errors of arterial blood
sampling
– Air in sample: PCO2↓, pH↑, PO2↨
– Venous mixture: PCO2↑, pH↓,
PO2↓
– Excess anticoagulant (dilution):
PCO2↓, pH↑, PO2↨
 The plastic, disposable syringe,
prefilledwith a small amount
of an appropriate type of
lyophilized heparin salt is
used.
 Before beginning…
 Collect blood gas specimens in
glass syringes and ice these
samples immediately
Ø Slow down the metabolic rate of
the leukocytes
Ø Minimize the reduction in oxygen
levels


 Arterial line collection requires

that an appropriate volume be
withdrawn initially to assure
that the line contains only
uncontaminated arterial blood
before the actual sample is
collected
 Local anesthesia : to make the
arterial puncture easier to
accomplish
 Heparin is the anticoagulant of
choice for the measurement of
gas analytes .
The Components & desired Ranges
– pH - 7.35 -
7.45
– PaCO2 - 35-45
mmHg
– PaO2 - 80-100
mmHg pH
– HCO3 -24 + 4
mmol/L
– %MetHb < PO2 HCO3
2.0%
– %COHb <
3.0%
– O2sat - 95-
PCO2
100%
– CaO2-16 - 22
ml O2/dl
– Base Excess -
+/-2 mEq/L
Always
 ACID BASE CHEMISTRY

• The Arrhenius Theory

Acid is a substance which is capable of dissociating in water

solution to produce hydrogen ions. A base is defined as a

substance which dissociated in water solution to produce
hydroxide ions
• The Bronsted-Lowry Theory
An acid is defined as a substance which donates a hydrogen

ion to another substance. The substance which accepts the

H+ from the acid is called the ‘conjugate base
• LEWIS THEORY:
Acid Is any compound that is a potential electron pair

acceptor and a base as any compound that was a potential

electron pair donor.
From the medical and biological perspective, the Bronsted-
The hydrogen ion concentration in


extracellular fluid is determined

by (Henderson-Hasselbalch
equation ):


[H+] (nEq/l)= 24 x (pco2/HCO3)



 Pco3=4o mm Hg
 HCO3=24 mEq/l


 [H+]= 40 nEq/l
 pH
• pH is the quantity used to assess the acidity or
alkalinity of a solution. It is measured using an ion-
selective glass electrode


 pH = - log10  [H+ ]
 where [H+ ]is activity of H+


• pH is typically 7.4 in plasma ([H+] about 40 nmol/l) but

lower values of pH are found intracellularly (6.0-7.0)
•
The two reasons why pH is so important for


metabolism :
• Effect on small molecules: Intracellular trapping of
intermediary metabolites (the Davis hypothesis)
• Effect on large molecules (proteins): Maintaining
optimal protein function both intracellularly and
 H ION
CONC . pH
OH ION N . Eq /
L.
158
6 . 80
126
pH stand 6 . 90
100for " power
of 7 . 00
H ION
79 hydrogen"
HO

7 . 10
63
7 . 20
50
7 . 30

Acid Base
The Immediate Response : Buffering

Balance
• Buffering is a rapid physico-chemical phenomenon. The buffering of fixed
acids by bicarbonate changes the [HCO3] numerator in the ratio (in the
Henderson-Hasselbalch equation).
The Respiratory Response : Alteration in Ventilation

• Adjustment of the denominator pCO2 (in the Henderson-Hasselbalch

equation) by alterations in ventilation is relatively rapid (minutes to
hours). An increased CO2 excretion due to hyperventilation will result in
one of three acid-base outcomes:
v correction of a respiratory acidosis
v production of a respiratory alkalosis
v compensation for a metabolic acidosis.
• This respiratory response is particularly useful physiologically because of
its effect on intracellular pH as well as extracellular pH. Carbon dioxide
crosses cell membranes easily so changes in pCO2 affect intracellular
pH rapidly and in a predictable direction.
The Renal Response : Alteration in Bicarbonate Excretion

• This much slower process (several days to reach maximum capacity)

involves adjustment of bicarbonate excretion by the kidney. This
system is responsible for the excretion of the fixed acids and for
compensatory changes in plasma [HCO3] in the presence of respiratory
 Buffer system:
Bicarbonate-carbon dioxide buffer system


•
 CO2 + H2O <--> H2CO3 <--> HCO3- +
H+

 ph = pK` + log ([HCO3] / [0.03 x PCO2])


 ph = 6.10 + log ([HCO3] / [0.03 x
PCO2])

 [H+] (nEq/l)= 24 x (pco2/HCO3)

 BICARB CO 2 CHANGES
pH in opposite direction

compensation HIGH pCO2

pH LOW pH
HIGH HCO3

CO (compensated
)
2

High Primary lesion

CO2 Respiratory acidosis
 Respiratory Acidosis
 Usually because of alveolar
hypoventilation.
 Causes
– CNS depression / neurological injury.
– Pleural disease, pneumonia, pulmonary
edema.
– COPD/ARDS
– Flail chest.
– Musculoskeletal disorders
– Compensation for metabolic alkalosis
– Acute drug intoxication
(narcotics,sedatives)
 Respiratory Acidosis
v Acute vs Chronic
§ Acute- little kidney involvement. Buffering via
titration via Hbor exchange of extracelular
H+ for intracellular Na+ or K+
vpH by 0.08 for 10mmHg  in CO2
.
vHCO3 ↑by 1mEq/l for each 10 mm
Hg↑in PaCO2 above 40 mmHg
§ Chronic - Renal compensation via synthesis
and retention of HCO3 (Cl to balance
charges  hypochloremia)
vpHby 0.03 for 10mmHg in
CO2 .
vHCO3 ↑by 4mEq/l for each 10 mm
 Effects of resp.
CNS effects Acidosis
1.Cerebral VD
2. Incr. ICP
3.Headache
4.In chr. Cases.csf Hco3 rises-restores
&CSF pH
CVS EFFECTS
1.INC. RATE AND FORCE OF CONTRACTION
2.Vd due to direct eff. Of CO2 on
ANS Effect blood vessels.
1.Increased SNS activity. 3.Increased CO.
4.Threashold for ventricular
fibrillation is decreased.
5.Arrhythmias during halothane
RESPIRATORY SYSTEM anesthesia.
1.Stimulates respiratory
centre.
2.Rt. Shift of ODC.
3.
 Treatment
1. Increase alveolar ventilation or reduce CO2
production.
2. Temporizing measures like: bronchodilatation,
reversal of narcosis, respiratory stimulant.
3. pH< 7.20- mechanical ventilation.
4. i/v NaHCO3 is rarely indicated. Use only if
pH<7.10 & HCO3< 15 mEq/l
5. PCO2 should be reduced slowly as rapidly
reduction after long period of hypercapnia
may result in
VI.Sudden hypotension.
VII.Left shift of ODC.
VIII.Rapid rise in CSF ph.- cerebral vasoconstriction and
convulsion.
 CO2
HYPER VENTILATION

compensation
LOW HCO3

pH LOW pH
HCO3 changes
LOW pCO 2 direction
pH in same
(compensated)
HCO3

Low Primary lesion

Alkali
METABOLIC ACIDOSIS
 Metabolic Acidosis: compensation

 12-24 hours for complete activation of

respiratory compensation
 Doesn’t completely normalises pH but
can produce marked hyperventilation
(Kussmaul’s breathing)
 PCO2 by 1.2mmHg for every 1 mEq/L
HCO3
 The degree of compensation is
assessed via the Winter’s Formula
  PCO2 = 1.5(HCO3) +8  2
 Anion Gap
 Anion gap = Na+ – (Cl- + HCO3-)


§ Difference between cations (+) and anions

§ Normal AG = 8-12
§ Normal AG secondary to unmeasured albumin
(anion)
§ Calculation of the anion gap is useful in
determining the cause of the metabolic acidosis
§ Increased AG occurs with decrease in cations
(Na+) or more commonly an increase in anions
(acids, i.e. sulfates, lactate, ketones)
§ Correction: Albumin ↓1  AG ↓ 2.5
 expected AG = observed AG + 2.5 x [4.5 –
measured albumin(g/dl) ]
§
 Normal Anion Gap (8–12 mEq)
 Loss of HCO3–
Diarrhea
Recovery from diabetic ketoacidosis
Pancreatic fluid loss ileostomy
(unadapted)
Carbonic anhydrase inhibitors
Chloride retention
Renal tubular acidosis
Ileal loop bladder
Administration of HCl equivalent or NH4Cl
Arginine and lysine in parenteral nutrition
Causes of High-Anion-Gap Metabolic Acidosis


Increased production of non-volatile acids:



Ø Renal failure
Ø Ketoacidosis
Ø Diabetic
Ø Starvation
Ø Lactic acidosis
Mixed


Ø Non ketotic hyperosmolar coma

Ø Alcoholic
Inborn errors of metabolism


Ingestion of toxin


Ø Salicylate
Ø Methanol
Ø Ethylene glycol
 Treatment of metabolic acidosis
•
• Treatment is directed at the underlying cause.
• NaHCO3 rarely indicated
• Treatment with NaHCO3 is clearly indicated only in certain circumstances . When
metabolic acidosis results from loss of HCO3 − or accumulation of inorganic
acids (ie, normal anion gap acidosis), HCO3 − therapy is generally safe and
appropriate.
• Respiration should be controlled if necessary.
• Hemodialysis is required for renal failure and sometimes for ethylene glycol,
methanol, and salicylate poisoning.
•

• Alternatives to NaHCO3 include

• Tromethamine
THAM----, an amino alcohol that buffers both metabolic (H+) and
respiratory (carbonic acid [H2CO3]) acid
• ︠
Carbicarb, an equimolar mixture of NaHCO3 and Na2CO3
•
 Anaesthetic implications
of Acidosis

Ø Potentiation of most sedative and anesthetic agents on

the CNS
Ø Increased fraction of nonionized form of opioid drugs –
facilitate penetration into brain
Ø Increased risk of aspiration due to increased sedation
and blunted airway reflexes
Ø Exaggerated circulatory depressant responses to volatile
and intravenous anesthetics
Ø Succinlycholine should generally be avoided due to
acidosis induced hyperkalemia
Ø Halothane is generally more arrhythmogenic in acidotic
environments
 BICARB CO 2 CHANGES
pH in opposite direction

compensation
LOW pCO2

pH HIGH pH
LOW HCO3

(compensated
)
CO 2

Low Primary lesion

CO2 Respiratory alkalosis
 Respiratory
alkalosis
• pH, CO2, Ventilation
•  CO2   HCO3 (Cl to balance
charges  hyperchloremia)


• Causes
– Intracerebral hemorrhage
– Salicylate and Progesterone drug
usage
– Anxiety, hypoxemia.
– Cirrhosis of the liver
– Sepsis
– Encephalopathies
 Respiratory
Alkalosis
• Acute vs. Chronic
– Acute - HCO3 by 2 mEq/L for
every 10mmHg  in PCO2
– Chronic - Ratio increases to 4
mEq/L of HCO3 for every
10mmHg  in PCO2
– Decreased bicarb reabsorption and
decreased ammonium excretion
to normalize pH
causes

◆ Excessive mechanical
ventilatory support.
◆ High altitude
◆ Hypoxia
◆ Metabolic acidosis.
◆ Severe head injury.


Treatment:
It is directed at treating the

underlying cause.
 EFFECTS
• CNS
1. Cerebral vasoconstriction.
2. Dec. Blood flow, clouding of
consciousness and analgesia.
3. Tetany due to dec. In ionised calcium.

RESP.
1.hypovent.
2. Lt.shift of ODC
CVS EFFECTS
1.PERIPHERAL vc
2. DECR. BP Fetal
3.decr. CO Decresed uteroplacental B.F
Fall in foetal o2 supply and acidosis
4.Coronary VC
 CO2 HYPO VENTILATION

HIGH HCO3
compensation

pH HIGH pH
HIGH pCOdirection
BICARB CHANGES
pH in same 2

HCO3
(compensated )

High Primary lesion

Alkali METABOLIC ALKALOSIS
Metabolic Alkalosis

◆ PCO2 by 0.7 for every

1mEq/L  in HCO3


◆ Causes
– Vomiting
– Diuretics
– Chronic diarrhea
– Hypokalemia
– Renal Failure
 Causes of Metabolic Alkalosis
I. Exogenous HCO3- loads
 A. Acute alkali administration
 B. Milk-alkali syndrome
II. Effective ECFV contraction, K+ deficiency secondary hyperreninemic

hyperaldosteronism
 A. Gastrointestinal origin
 1. Vomiting
 2. Gastric aspiration
 4. Villous adenoma
 B. Renal origin
 1. Diuretics
 2. Edematous states
 3. Posthypercapnic state
 4. Hypercalcemia/hypoparathyroidism
 5. Recovery from lactic acidosis or ketoacidosis
 6. Nonreabsorbable anions including penicillin, carbenicillin
III. ECFV expansion, hypertension, K+ deficiency, and

 mineralocorticoid excess
 A. High renin
 1. Renal artery stenosis
 Treatment of
M.alkalosis
• Treat the cause
• Decreasing M.V to normalize Paco2 (in controlled
ventilation)
• i/v saline(Nacl) & Kcl replacement in chloride
sensitive M.alkalosis.

Cl deficit = 0.2 x wt x (Nr cL – actual Cl)
• Spironolactone in increase in mineralcorticoid
activity.
• I/V Hcl(0.1mol /l),ammonium chloride,arginine
 consideration
s in
alkalemia
• Prolongs opioid induced
respiratory depression.
• Cerebral ischemia can cause
reduced cerebral blood flow
• Precipitation of arrythmias
• Potentiation of NDMR effects.
Mixed Acid - Base Disorders

◆ Patients may have two or more

acid-base disorders at one
time
◆

◆ Delta Gap :

Increase in Anion
Gap

Decrease in
bicarbonate


•
• If one molecule of metabolic acid (HA) is
added to the ECF and dissociates,
the one H+ released will react with one
molecule of HCO3- to produce CO2 and
H2O. This is the process of buffering. The
net effect will be an increase in
unmeasured anions by the one acid anion
A- (ie anion gap increases by one) and a
decrease in the bicarbonate by one.
• Now, if all the acid dissociated in the ECF and
all the buffering was by bicarbonate, then
the increase in the AG should be equal to
the decrease in bicarbonate so the ratio
between these two changes (which we call
the delta ratio) should be equal to one. The
delta ratio quantifies the relationship
between the changes in these two
quantities.
Delta Ratio Assessment Guideline

<0.4 Hyperchloraemic normal anion gap acidosis

0.4-0.8 Consider combined high AG & normal AG acidosis BUT note

that the ratio is often <1 in acidosis associated with
renal failure

1-2 Usual for uncomplicated high-AG acidosis

Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine
ketone loss (esp if patient not dehydrated)

>2 Suggests a pre-existing elevated HCO3 level so consider:

a concurrent metabolic alkalosis, or
a pre-existing compensated respiratory acidosis
COMPENSATION ….
Body’s physiologic response to
Primary disorder
in order to bring pH towards NORMAL
limit
ü
üFull compensation
üPartial compensation
üNo compensation…. (uncompensated)

BUT never overshoots,

If a overshoot pH is there,
Take it granted it is a MIXED
disorder
PRIMARY DISORDER EXPECTED RESULTS

M. ACIDOSIS PaCO2 = (1.5 x HCO3) + (8±2)

M. ALKALOSIS PaCO2 = (0.7 x HCO3) + (21±2)

ACUTE R. ACIDOSIS pH = 7.4 – [0.008 x (PaCO2 –

40)]
ACUTE R. ALKALOSIS pH = 7.4 + [0.008 x (40 –
PaCO2)]
CHRONIC R. ACIDOSIS pH = 7.4 – [0.003 x ( PaCO2 –
40)]
CHRONIC R. ALKALOSIS pH = 7.4 + [0.003 x (40 –
PaCO2)]
 PAO 2
PaO 2
O2 SaO 2
CaO 2
DO 2
To calculate A-a gradient….
Is the pt. hypoxic?
Type and severity of Hypoxia.

Relationship of PaO2 and FiO2?

FiO2 X 5 = Expected PaO

Whether PaO2 is appropriate for the given FiO2

Is the O2 content (CaO2) enough to prevent hypo

 Alveolar - arterial
Difference
Oxygenation Ventilation
Failure Failure
Normal Gap

Wide Gap PCO2 = 80

PCO2 = 40 PaO2 = 45
PaO2 = 45 O2 PAO2 = 150-1.2(80)
PAO2 = 150 – 1.2 CO 2 =
(40) 150-100
= 150 - = 50
50 Alveolar arterial G.
Alveolar – arterial G.
= 100
100 - 45 = 55 50 – 45 = 5
……………….Wide A-a …………….Normal A-a
Expected PaO2 =
Normal
20 × 5 = 100

We always correlate PaO2 with FiO2

FiO2 × 5 = PaO2
BUT………………………….
never forget to correlate with PaCO2
328 03:44
nov. 22, 2010
Pt ID 3245 / 00

Measured
37 . 0 0C
pH 7 . 452
pCO2 45 . 1
mm Hg
pO2 112 . 3
mm Hg

Corrected
38 . 6 0C

The Anatomy
pH 7.436
pCO2 47.6
mm Hg
pO2 122.4

of a Blood Gas
mm Hg

Calculated Data
HCO3
HCO3
Report
act
std
31 . 2
mmol / L
30 . 5
mmol / L
B E 6.6
mmol / L
O2 ct 15 . 8
mL / dl
O2 Sat 98 . 4
%
ct CO2 32 . 5
mmol / L
pO2 ( A - a ) 30 . 2
mm Hg 
pO2 ( a / A ) 0 . 78

Entered Data
Temp 38 . 6
328 03:44
Feb 5 2006
Pt ID 3245 / 00

Measured
37 . 0 0C
Standard Bicarbonate:
pH 7 . 452 Plasma HCO3 after equilibration
pCO2 45 . 1
to a PCO2 of 40 mm Hg
mm Hg
pO2 112 . 3 : reflects non-respiratory acid base
mm Hg
change
Corrected : does not quantify the extent of the
38 . 6 0C
buffer base abnormality
pH 7.436
pCO2 47.6 : does not consider actual buffering
pO2
mm Hg
122.4
capacity of blood
mm Hg

Calculated Data
HCO3 act 31.2
Base Excess:
mmol / L D base to normalise HCO3 (to 24) with PCO2 at
HCO3 std 30 . 5 40 mm Hg (Sigaard -Andersen )
mmol / L
B E 6.6 : reflects metabolic part of acid base
mmol / L D
O2 ct 15 . 8
mL / dl : no info. over that derived from pH,
O2 Sat 98 . 4
% pCO2 and HCO3
ct CO2
mmol / L
32 . 5 : Misinterpreted in chronic or mixed
pO2 ( A - a ) 30 . 2 disorders
mm Hg 
pO2 ( a / A ) 0 . 78

Entered Data
 Feb 5 2006
Pt ID 3245 / 00

Measured
37 . 0 0C
Oxygenation
pH
pCO2
mm Hg
45 . 1
7 . 452
Parameters :
pO2
mm Hg
112 . 3
/limitations
Corrected
38 . 6 0C O 2 Content of blood :
pH 7.436
pCO2 47.6 (Hb x1.34x O2Sat + 0.003x Dissolved O2 )
mm Hg
pO2 122.4 Remember Hemoglobin
mm Hg
Oxygen Saturation:
Calculated Data ( remember this is calculated …error
HCO3 act 31 . 2
prone)
mmol / L
HCO3 std 30 . 5 Alveolar / arterial gradient :
mmol / L
B E 6.6 ( classify respiratory failure)
mmol / L
O2 ct 15 . 8
mL / dl Arterial / alveolar ratio :
O2 Sat 98 . 4 Proposed to be less variable
%
ct CO2 32 . 5 Same limitations as A-a gradient
mmol / L
pO2 ( A - a ) 30 . 2
mm Hg 
pO2 ( a / A ) 0 . 78

Entered Data
Temp 38 . 6
 7
Systematic and Pointed
………. approach
Steps for
Successful
Blood Gas
Analysis
 1.
2. Look at pH?
Consider the clinical settings!
3Anticipate
. Who is the
the disorder
culprit ?...Metabolic /
Respiratory
4. If respiratory…… acute
and /or chronic
5. If metabolic acidosis,
Anion gap ↑ed and/or normal
or both?
pet s 7

6.Is more than one disorder

present?
Step 2
Look at the pH
Is the patient acidemic
pH < 7.35
or alkalemic pH > 7.45

If pH = 7.4 …… Normal

Mixed or Fully compensated

Step 3 …….
CULPRIT?
üHCO3…… METABOLIC HCO3 =
Base
Normal…22-
> 26 ….. Met. Alkalosis 26

< 22 ……Met. Acidosis

ü CO2 =
üPCO2 ……RESPIRATORY ACID
Normal…35-
45
> 45 …… Resp. Acidosis
Step 4 …
If there is a primary Respiratory
disturbance,
is it acute ?

10 mm
Change .=08 change in pH ( Acute )
PaCO2 .03 change in pH (Chronic)

Remember………… relation of CO2 and pH

 ep 4 continued …
tep
pH 80 – PaCO2
Last two digits

PaCO 2 pH
70 7.10
60 7.20
50 7.30
40 7.40
30 7.50
20 7.60
Acute respiratory change
tep 4 continued …

PIRATORY disorders…
ected HCO3 for a Change in CO2 ......... 1 2 3 4

Acidosis…. (expected) HCO3

cute respiratory
= 0.1 x ∆ CO2
Alkalosis…. (expected) HCO3
= 0.2 x ∆ CO2
hronic respiratory
Acidosis…. (expected) HCO3
= 0.35 x ∆ CO2
Alkaosis…. (expected) HCO3
Step 5
If it is a primary Metabolic
disturbance,
whether respiratory compensation
Remember If :
appropriate?
For metabolic acidosis:
Suspect .............
Expected PCO 1 5 x HCO 8 2
CO2 isadditional
2
equal
= ( . [
to3
actual PaCO is more than expected
(Winter’s equation)
2
]) +
...respiratory
+

Last
For metabolic
actualPCO2
Expected
two
PaCO=is(0less
digits
acidosis
alkalosis :
than) expected
.7 x HCO3
2 + 21 ±
2 of
………UNCERTAIN alkalosis
pH
additional ...respiratory
COMPENSATION
Step 5 cont .

If metabolic acidosis is there

How is anion gap ? Is it wide ...

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

- -

If >12, Anion Gap Acidosis :

M ethanol
U remia
Common pediatric causes D iabetic Ketoacidosis
P araldehyde
üLactic acidosis I nfection (lactic acid)
üMetabolic disorders E thylene Glycol
üRenal failure S alicylate
 Mixed Acid-Base
Disorders : Clues
-- Clinical history


-- pH normal, abnormal PCO2 n HCO3



-- PCO2 n HCO3 moving opposite

directions
-- Degree of compensation for primary

 disorder is inappropriate
-- Find Delta Gap
 7
th step

Clinical correlation
Thank you