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Basics in Arterial
Blood Gas
InterpretationCrisbert I. Cualteros, M.D.
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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
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Techniquefor Radial Artery Puncture
Explain process to patient. Examine skin,
palpate radial & ulnar arteries. Performmodified Allen Test.
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The Allen Test
have the patientclench his/her fist
press on both
radial and ulnararteries
have the patientunclench fist
test for goodcollateral flow.
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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 1,000units/ml) & empty. 0.15-0.25 ml of heparin willanticoagulate 2-4 ml of blood.
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Technique for Radial Artery Puncture
Palpate artery with one hand while holdingproperly prepared syringe & needle with other hand. Hold syringe like a pencil & enter skinat 45
o. Advance needle slowly.
Never redirect needle without first withdrawing tosubcutaneous 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.
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Potential Complications
Pain
Hematoma, hemorrhage
Trauma to vessel
Arteriospasm
Air or clotted-blood
emboli
Vasovagal response Arterial occlusion
Infection
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Indications for ABG
Assess ventilation & acid-basebalance
Assess oxygenation status
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Ventilatory/
Acid-Base Status
H d H lb h P t & th i
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Henderson-Hasselbach Parameters & theirnormal laboratory ranges
pH= [HCO3]p
PC02
pH PCO2
(mmHg)
[HCO3]p
(mmol/L)Normal 7.35-7.45 35-45 22-26
Acidotic < 7.35 > 45 < 22
Alkalotic > 7.45 < 35 > 26
T di i l M b li A id B N l
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Traditional Metabolic Acid-Base Nomenclature
Nomenclature pH PCO2
[HCO3]p
BE
Metabolic acidosisUncompensated (acute) q N q q(-)Partly compensated(subacute)
q q q q(-)
Compensated (chronic) N q q q(-)Metabolic alkalosisUncompensated (acute) p N p p(+
)Partly compensated(subacute)
p p p p(+)
Compensated (chronic) N p p p(+)
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Traditional Respiratory Acid-Base Nomenclature
Nomenclature pH PCO2
[HCO3]p
BE
RespiratoryacidosisUncompensated (acute) q p N NPartly compensated(subacute) q p p p
Compensated (chronic) N p p p
Respiratory
alkalosisUncompensated (acute) p q N NPartly compensated(subacute)
p q q q
Compensated (chronic) N q q q
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Base Excess/ Deficit
Blood with large buffering capacity:significant changes in acid content with little change in freeH+concentrations (pH)
Acidemia or alkalemia: i buffering capacity, > potential forpH change from any given change in H+content
Buffering capacity depends on:[HCO3-]
RBC massother factors
Base excess/deficit= (measured pH predicted pH) x 100 x2/3
Normal metabolic acid-base status: + 3 mmol/LRelatively balanced metabolic acid-base status: + 5
mmol/LClinically significant imbalance: + 10
mmol/L
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Nomenclature & Criteria for Clinical Interpretation
Clinical Terminology Criteria
Ventilatory failure(respiratory acidosis) PaCO2> 45mm Hg
Acute ventilatory failure(respiratory acidosis) PaCO2> 45mmHg pH < 7.35
Chronic ventilatory failure(respiratory acidosis) PaCO2 > 45mmHg
pH 7.36- 7.44
Alveolar hyperventilation(respiratory alkalosis) PaCO2< 35mmHg
Acute alveolar hyperventilation(respiratory PaCO2< 35mmHg
alkalosis) pH > 7.45
Chronic alveolar hyperventilation(respiratory PaCO2 < 35mmHg alkalosis) pH 7.36-
7.44
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Nomenclature & Criteria for Clinical Interpretation
Clinical Terminology Criteria
Acidemia pH < 7.35Alkalemia pH > 7.45Acidosis HCO3
- < 22 mmol/L
BD > 5 mmol/LAlkalosis HCO3
-> 26 mmol/LBE > 5 mmol/L
Combined Respiratory Acidosis & Metabolic AcidosisRespiratory Alkalosis & Metabolic Alkalosis
Mixed Respiratory Acidosis & Metabolic AlkalosisRespiratory Alkalosis & Metabolic Acidosis
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Respiratory Acidosis
Acute
r pH = 0.08 x (PCO240)
10
ex. PCO2 = 60
rpH = 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 PCO2increase
Compensation: cellular buffering: HCO3
renal adaptation: H+secretion, Cl- reabsorption,
net acid excretion
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Respiratory acidosis
Chronic
r pH = 0.03 x (PCO240)
10
ex. PCO2= 60r 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
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Respiratory Acidosis
COPD O2excess in COPD
Drugs Barbiturates
Anesthetics Narcotics
Sedatives
Extreme ventilation-perfusion mismatch
Exhaustion
Inadequate MV
Neurologic disorders
Neuromusculardisease Poliomyelitis
ALL
G-B syndrome
Electrolyte deficiencies(K+, PO4
-)
Myasthenia gravis
Excessive CO2
production TPN Sepsis
Severe burns
NaHCO3administration
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Respiratory Alkalosis
Acute
r pH = 0.08 x (40 PCO2)
10
ex. PCO2= 20
rpH = 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 PCO2decrease
Compensation: cellular buffering
renal response: retention of endogenous acids,
excretion of HCO3
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Respiratory Alkalosis
Chronic
r pH = 0.03 x (40 PCO2)
10
ex. PCO2= 20r 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
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Respiratory Alkalosis
Primary centraldisorders
Hyperventilationsyndrome, anxiety
Cerebrovascular disease Meningitis, encephalitis
Pulmonary disease
Interstitial fibrosis
Pneumonia Pulmonary embolism
Pulmonary edema(some patients)
HypoxiaSepticemia,
hypotension
Hepatic failure
Drugs Salicylates
Nicotine
Xanthines
Progestationalhormones
High altitude
Mechanical ventilators
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Metabolic Acidosis
Anion Gap
artificial disparity between major plasma cations& anions that are routinely measured
major plasma cationsmajor plasma anions [Na+]([Cl-] + [HCO3-])
12 + 2 (normal)
Minor cations: K+, Ca++
Minor anions: phosphates, sulfates, organicanions
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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 hasreplaced
HCO3-
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Metabolic Acidosis
Abnormalities:
Overproduction of acids
Loss of buffer stores
Underexcretion of acids
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Metabolic Acidosis
Expected PCO2= ( [HCO3-] x 1.5) + 8 + 2
ex. [HCO3-
] = 11expected PCO2= (11 x 1.5) + 8 + 2 = 22.5-
26.5
PCO2decreases 1- 1.5 mmHg per 1 meq/L HCO3-decrease
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Metabolic Acidosis
Compensation
pCO2(hyperventilation)
Pathway:
pCO2
HCO3ratio H
+conc
Acidification of ECF ECF pH
Stimulation of brainstem RR pCO2
Normalization of pH
HCO3
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Metabolic Acidosis
Compensation
Ionic shift
K+moves extracellularly for H+
HCO3-generation, H+excretion
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Corrected [HCO3-] for Anion Gap
Metabolic Acidosis
Measured serum [HCO3-] + (anion gap12)
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Metabolic Alkalosis
Expected PCO2= ( [HCO3-] x 0.75 ) + 20 + 5
ex. [HCO3-
] = 34expected PCO2 = (34 x 0.75) + 20 + 5 = 40.5-
50.5
PCO2increases 0.5- 1 mmHg per 1 meq/L HCO3-increase
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Metabolic Alkalosis
Pathway
HCO3 PaCO2HCO3
ratio H+conc
Alkalinization of ECF PaCO2with mild hypoxemia
Normalization of pH
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Causes of Metabolic lkalosisHypokalemia*
Ingestion of large amounts of alkali or licoriceGastric fluid loss: Vomiting, NG suctioning*
Hyperaldosteronism 20to 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
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Limits of Compensation
Imbalance [HCO3-] meq/L PCO2mmHg
Respiratory Acidosis
Acute h0.1- 1/ 10 mmHg
PCO2h
Chronic h1- 3.5/ 10 mmHg
PCO2
h
Respiratory Alkalosis
Acute i0- 2/ 10 mmHg PCO2i
Chronic i2- 5/ 10 mmHg PCO2i
Metabolic Acidosis i1- 1.5/ 1 meq/L
[HCO3-] i
Metabolic Alkalosis h0.5- 1/ 1 meq/L
[HCO3-] h
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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 orabnormal?
If disturbance metabolic, is the respiratorysystem compensating adequately?
If disturbance is anion gap metabolic acidosis,are there any other metabolic disturbancespresent?
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Oxygenation Status
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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)
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Steps for Analyzing
Oxygenation Status
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1. Is the patient hypoxemic or normoxemic?
Indices of Oxygenation:
a. AaDO2= PAO2PaO2PAO2= FiO2(713) PaCO2
0.8PaO2= obtained from blood gas determination
b. aAO2= PaO2PAO2c. P/F ratio = PO2
FiO2Normal 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
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2. If hypoxemic, is it uncorrected,
corrected, or overcorrected?
With O2 supplementationPaO2 (mmHg)
Uncorrected hypoxemia < 80Corrected hypoxemia 80 120
Overcorrected > 120
FiO2to PaO2Relationship in Normal LungsFiO2 PaO2(mmHg)0.30 > 1500.40 > 2000.50 > 2500.80 > 4001.00 > 500
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Room Air (patient < 60 y. o.)
PaO2(mmHg)
Mild hypoxemia 60 to < 80
Moderate hypoxemia 40 to < 60
Severe hypoxemia < 40
For each year > 60 subtract 1 mmHg for limits ofmild &
moderate hypoxemia.At any age, PaO2 < 40 mmHg indicates severe
hypoxemia.
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3. If normoxemic, is oxygenation
adequate or more than
adequate?
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Thank you !