Basics in

Arterial Blood
CrisbertGas
I. Cualteros, M.D.
Interpretation

Obtaining Blood Gas

Samples
Radial artery- best site

Radial artery- best site

located superficially, easy to palpate
& stabilize
excellent collateral circulation via
ulnar artery
not adjacent to large veins
probing needle relatively pain-free if
periosteum is avoided

Technique for Radial

Artery Puncture

Explain process to patient. Examine skin,

palpate radial & ulnar arteries. Perform
modified Allen Test.

The Allen Test

have the patient

clench his/her fist
press on both
radial and ulnar
arteries
have the patient
unclench fist
test for good
collateral flow.

Technique for Radial

Artery Puncture

Position patient- hyperextend wrist. Clean

site with 70% isopropyl alcohol.
Use latex gloves while doing procedure.
Local anesthesia may be used.
Use G20 or G21 needle. Flush syringe with
sodium heparin (10 mg/ml or 1,000
units/ml) & empty. 0.15-0.25 ml of heparin will
anticoagulate 2-4 ml of blood.

Technique for Radial

Artery Puncture

Palpate artery with one hand while holding

properly prepared syringe & needle with other
hand. Hold syringe like a pencil & enter skin
at 45o. Advance needle slowly.
Never redirect needle without first withdrawing to
subcutaneous tissue.
Obtain 2-4 ml blood. If possible dont aspirate.
Remove air bubbles from syringe. Immediately
seal syringe with cap.
Place sample in ice slush. Analyze blood sample
within 10 minutes.
Apply pressure to site until bleeding has stopped.

Potential Complications

Pain

Hematoma, hemorrhage

Trauma to vessel

Arteriospasm

Air or clotted-blood
emboli

Vasovagal response

Arterial occlusion

Infection

Indications for ABG

Assess ventilation & acid-base

balance
Assess oxygenation status

Ventilatory/
Acid-Base Status

Henderson-Hasselbach Parameters & their

normal laboratory ranges
pH= [HCO3]p
PC02
pH
Normal

PCO2
(mmHg)
7.35-7.45 35-45

[HCO3]p
(mmol/L)
22-26

Acidotic

< 7.35

> 45

< 22

Alkalotic

> 7.45

< 35

> 26

Traditional Metabolic Acid-Base

Nomenclature
Nomenclature
pH
PCO2 [HCO3] BE
p

Metabolic acidosis
Uncompensated (acute)
Partly compensated
(subacute)

Compensated (chronic)

(-)
(-)

(-)

(+)
(+)

(+)

Metabolic alkalosis
Uncompensated (acute)
Partly compensated
(subacute)

Compensated (chronic)

Traditional Respiratory Acid-Base

Nomenclature
Nomenclature
pH PCO [HCO3] BE
p
2
Respiratory
acidosis
Uncompensated (acute)

N
N
Partly compensated

(subacute)

Compensated (chronic)

Respiratory
alkalosis
Uncompensated (acute)
Partly compensated
(subacute)

Compensated (chronic)

Base Excess/ Deficit

Blood with large buffering capacity:

significant changes in acid content with little change in free H +
concentrations (pH)
Acidemia or alkalemia: buffering capacity, > potential for pH
change from any given change in H+ content
Buffering capacity depends on:
[HCO3-]
RBC mass
other factors
Base excess/deficit= (measured pH predicted pH) x 100 x 2/3
Normal metabolic acid-base status:
+ 3 mmol/L
Relatively balanced metabolic acid-base status:
+5
mmol/L
Clinically significant imbalance: + 10 mmol/L

Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology

Criteria

Ventilatory failure (respiratory acidosis)

PaCO2
Acute ventilatory failure (respiratory acidosis)
mmHg
pH < 7.35
Chronic ventilatory failure (respiratory acidosis)
pH 7.36- 7.44
Alveolar hyperventilation (respiratory alkalosis)
mmHg
Acute alveolar hyperventilation (respiratory
mmHg
alkalosis) pH > 7.45
Chronic alveolar hyperventilation (respiratory
alkalosis) pH 7.36-7.44

> 45 mm Hg
PaCO2 > 45
PaCO2 > 45 mmHg
PaCO2 < 35
PaCO2 < 35

PaCO2 < 35 mmHg

Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology
Acidemia
Alkalemia
Acidosis
Alkalosis
Combined
Mixed

Respiratory
Respiratory
Respiratory
Respiratory

Criteria
pH < 7.35
pH > 7.45
HCO3- < 22 mmol/L
BD > 5 mmol/L
HCO3- > 26 mmol/L
BE > 5 mmol/L
Acidosis & Metabolic Acidosis
Alkalosis & Metabolic Alkalosis
Acidosis & Metabolic Alkalosis
Alkalosis & Metabolic Acidosis

Respiratory
Acidosis

Acute
pH = 0.08 x (PCO2 40)
10
ex. PCO2 = 60
pH = 0.08 x (60 - 40) = 0.16
10
expected pH = 7.40 0.16 = 7.24
HCO3- increases 0.1 1 meq/L per 10 mmHg PCO 2 increase

Compensation:

cellular buffering:
renal adaptation:

Cl- reabsorption,

HCO3
H+ secretion,

Respiratory acidosis
Chronic
pH = 0.03 x (PCO2 40)
10
ex. PCO2 = 60
pH = 0.03 x (60 40) = 0.06
10
expected pH = 7.40 0.06 = 7.34
HCO3- increases 1-3.5 meq/L per 10 mmHg PCO2
increase

Respiratory
Acidosis

COPD
O2 excess in COPD
Drugs

Barbiturates
Anesthetics
Narcotics
Sedatives

Extreme ventilationperfusion mismatch

Exhaustion
Inadequate MV
Neurologic disorders

Neuromuscular disease

Poliomyelitis
ALL
G-B syndrome
Electrolyte deficiencies
(K+, PO4-)
Myasthenia gravis

Excessive CO2
production

TPN
Sepsis
Severe burns
NaHCO3 administration

Respiratory
Alkalosis
Acute
pH = 0.08 x (40 PCO2)
10
ex. PCO2 = 20
pH = 0.08 x (40 20) = 0.16
10
expected pH = 7.40 + 0.16 = 7.56
HCO3- decreases 0-2 meq/L per 10 mmHg PCO 2
decrease
Compensation:

cellular buffering
renal response: retention of

endogenous acids,

Respiratory Alkalosis
Chronic
pH = 0.03 x (40 PCO2)
10
ex. PCO2 = 20
pH = 0.03 x (40 20) = 0.06
10
expected pH = 7.40 + 0.06 = 7.46

HCO3- decreases 2-5 meq/L per 10 mmHg PCO2

decrease

Respiratory Alkalosis
Primary central
disorders
Hyperventilation
syndrome, anxiety
Cerebrovascular disease
Meningitis, encephalitis
Pulmonary disease
Interstitial fibrosis
Pneumonia
Pulmonary embolism
Pulmonary edema
(some patients)

Hypoxia
Septicemia,
hypotension
Hepatic failure
Drugs
Salicylates
Nicotine
Xanthines
Progestational
hormones
High altitude
Mechanical ventilators

Metabolic Acidosis
Anion Gap
artificial disparity between major plasma cations
& anions that are routinely measured
major plasma cations major plasma anions
[Na+] ([Cl-] + [HCO3-])
12 + 2 (normal)
Minor cations: K+, Ca++
Minor anions: phosphates, sulfates, organic
anions

Metabolic
Acidosis
Anion gap
acidosis
~ process increases minor anions
~ ex. lactatemia, ketonemia, renal failure, excessive
organic salt treatment, dehydration, ingestion
(salicylates, methanol, ethylene glycol,
paraldehyde)
~ process which decreases minor cations rare!
Non-anion gap acidosis
~ associated with increased plasma Cl - that has replaced
HCO3~ ex. GI loss of HCO3- (diarrhea), renal wasting of HCO 3(RTA), ingestion of acids, parenteral
hyperalimentation, carbonic anhydrase inhibitors

Metabolic
Acidosis
Abnormalities:
Overproduction of acids
Loss of buffer stores
Underexcretion of acids

Metabolic Acidosis
Expected PCO2 = ( [HCO3-] x 1.5) + 8 + 2
ex. [HCO3-] = 11
expected PCO2 = (11 x 1.5) + 8 + 2 = 22.526.5
PCO2 decreases 1- 1.5 mmHg per 1 meq/L HCO3decrease

Metabolic
Acidosis
Compensation
pCO (hyperventilation)
2

Pathway:
HCO3

pCO2 ratio
HCO3

Acidification of ECF
Stimulation of brainstem
Normalization of pH

H+ conc

ECF
RR

pH
pCO2

Metabolic
Acidosis
Compensation
Ionic shift
K+ moves extracellularly for H+
HCO3- generation, H+ excretion

Corrected [HCO3-] for Anion

Gap Metabolic Acidosis
Measured serum [HCO3-] + (anion gap
12)

Metabolic Alkalosis
Expected PCO2 = ( [HCO3-] x 0.75 ) + 20 + 5
ex. [HCO3-] = 34
expected PCO2 = (34 x 0.75) + 20 + 5 = 40.550.5
PCO2 increases 0.5- 1 mmHg per 1 meq/L HCO3increase

Metabolic
Alkalosis

Pathway
PaCO2
ratio
HCO3

HCO3

Alkalinization of ECF

H+ conc

PaCO2 with mild hypoxemia

Normalization of pH

Causes of Metabolic Alkalosis

Hypokalemia*
Ingestion of large amounts of alkali or licorice
Gastric fluid loss: Vomiting, NG suctioning*
Hyperaldosteronism 20 to nonadrenal factors
Bartters syndrome
Inadequate renal perfusion
diuretics (inhibiting NaCl reabsorption)*
Bicarbonate administration
Sodium bicarbonate overcorrection
Blood transfusion
Adrenocortical hypersecretion (e.g tumor)
Steroids*
Eucapnic ventilation posthypercapnia
* Common in the ICU

Limits of Compensation
Imbalance

[HCO3-] meq/L

PCO2 mmHg

Respiratory Acidosis
Acute
Chronic

0.1- 1/ 10 mmHg
PCO2
1- 3.5/ 10 mmHg
PCO2

Respiratory Alkalosis
Acute

0- 2/ 10 mmHg PCO2

Chronic

2- 5/ 10 mmHg PCO2

Metabolic Acidosis
Metabolic Alkalosis

1- 1.5/ 1 meq/L
[HCO3-]
0.5- 1/ 1 meq/L
[HCO3-]

Steps for Analyzing Acid- Base

Disturbances

Is patient acidemic or alkalotic? pH

Is disturbance primarily respiratory or metabolic?
PCO2, [HCO3-]
If disturbance respiratory, is it acute or chronic?
If disturbance metabolic, is anion gap normal or
abnormal?
If disturbance metabolic, is the respiratory
system compensating adequately?
If disturbance is anion gap metabolic acidosis, are
there any other metabolic disturbances present?

Oxygenation Status

Normal Values

Seated PO2 = 104.2 0.27 (age in years)

Supine PO2 = 103.5 0.42 (age in years)
Patients < 60 y. o.
PO2 = 100 + 20
Patients > 60 y. o.
PO2 = 80 (# years > 60)

Steps for Analyzing

Oxygenation Status

1. Is the patient hypoxemic or normoxemic?

Indices of Oxygenation:

a. AaDO2 = PAO2 PaO2

PAO2 = FiO2 (713) PaCO2
0.8
PaO2 = obtained from blood gas determination
b. aAO2 = PaO2
PAO2
c. P/F ratio = PO2
FiO2
Normal Value: patients < 60 y. o. > 400
patients > 60 y. o. expected P/F = 400
[(age in years 60) x 5]
Actual P/F Ratio < expected = hypoxemic
Actual P/F Ratio > expected = normoxemic

2. If hypoxemic, is it
uncorrected,
corrected, or overcorrected?
supplementation

With O2 supplementation
PaO2 (mmHg)
Uncorrected hypoxemia
< 80
Corrected hypoxemia 80 120
Overcorrected > 120

FiO2 to PaO2 Relationship in Normal Lungs

FiO2
PaO2 (mmHg)
0.30
> 150
0.40
> 200
0.50
> 250
0.80
> 400
1.00
> 500

Room Air (patient < 60 y. o.)

Mild hypoxemia
Moderate hypoxemia
Severe hypoxemia

PaO2 (mmHg)
60 to < 80
40 to < 60
< 40

For each year > 60 subtract 1 mmHg for limits of

mild &
moderate hypoxemia.
At any age, PaO2 < 40 mmHg indicates severe
hypoxemia.

3. If normoxemic, is oxygenation
adequate or more than
adequate?

Thank you !