Basics in Arterial Blood Gas Interpretation

Crisbert I. Cualteros, M.D.

Obtaining Blood Gas Samples

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 PCO2 (mmHg) 7.35-7.45 35-45 < 7.35 > 7.45 > 45 < 35 [HCO3]p (mmol/L) 22-26 < 22 > 26

Normal
Acidotic Alkalotic

Traditional Metabolic Acid-Base Nomenclature Nomenclature Metabolic acidosis

Uncompensated (acute) Partly compensated
(subacute)

pH

PCO
2

[HCO3] p

BE

q q
N p p N

N q
q N p p

q q
q p p p

q(-) q(-)
q(-) p(+ ) p(+ ) p(+ )

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) q p N N Partly compensated q p p p
(subacute)

Compensated (chronic)

Respiratory alkalosis
Uncompensated (acute) Partly compensated
(subacute)

p p

q q

N q

N q

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: i 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 > 45 mm Hg Acute ventilatory failure (respiratory acidosis) PaCO2 > 45 mmHg pH < 7.35 Chronic ventilatory failure (respiratory acidosis) PaCO2 > 45 mmHg pH 7.36- 7.44 Alveolar hyperventilation (respiratory alkalosis) PaCO2 < 35 mmHg Acute alveolar hyperventilation (respiratory PaCO2 < 35 mmHg alkalosis) pH > 7.45 Chronic alveolar hyperventilation (respiratory PaCO2 < 35 mmHg alkalosis) pH 7.367.44

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 r pH = 0.08 x (PCO2 40) 10 ex. PCO2 = 60 r 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 PCO2 increase
Compensation: cellular buffering: renal adaptation: HCO3 H+ secretion, Cl- reabsorption, net acid excretion

Respiratory acidosis
Chronic r pH = 0.03 x (PCO2 40) 10 ex. PCO2 = 60 r 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

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

Extreme ventilationperfusion mismatch Exhaustion Inadequate MV Neurologic disorders

Excessive CO2 production

TPN Sepsis Severe burns NaHCO3 administration

Respiratory Alkalosis
Acute r pH = 0.08 x (40 PCO2) 10 ex. PCO2 = 20 r 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 PCO2 decrease
Compensation: cellular buffering renal response: retention of endogenous acids, excretion of HCO3

Respiratory Alkalosis
Chronic r pH = 0.03 x (40 PCO2) 10 ex. PCO2 = 20 r 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-

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 pCO2 (hyperventilation) Pathway:
HCO3 pCO2 ratio HCO3 H+ conc pH

Acidification of ECF Stimulation of brainstem Normalization of pH

ECF

RR

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
HCO3 PaCO2 ratio HCO3 H+ conc

Alkalinization of ECF

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
Respiratory Acidosis
Acute Chronic

[HCO3-] meq/L
h0.1- 1/ 10 mmHg PCO2h h1- 3.5/ 10 mmHg PCO2h i0- 2/ 10 mmHg PCO2i i2- 5/ 10 mmHg PCO2i

PCO2 mmHg

Respiratory Alkalosis
Acute Chronic

Metabolic Acidosis
Metabolic Alkalosis

i1- 1.5/ 1 meq/L [HCO3-] i h0.5- 1/ 1 meq/L [HCO3-] h

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?

With O2 supplementation Uncorrected hypoxemia Corrected hypoxemia Overcorrected

PaO2 (mmHg) < 80 80 120 > 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.)

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

Mild hypoxemia Moderate hypoxemia Severe hypoxemia

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 !