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    Arterial Blood Gas Interpretation: Joseph Brian L. Costiniano, MD, DPCP

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    Gio Tamaño Balisi
    The document provides guidelines for interpreting arterial blood gas (ABG) results using a 6-step approach: 1. Check for internal consistency of values using Henderson-Hasselbach equation. 2. Identify if there is alkalemia or acidemia present based on pH value. 3. Determine if the disturbance is respiratory or metabolic based on relationship between pH and PaCO2 changes. 4. Assess if there is appropriate compensation for the primary disturbance. 5. Calculate anion gap if metabolic acidosis is present. 6. Assess relationship between change in anion gap and change in bicarbonate if anion gap is increased.

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    Arterial Blood Gas Interpretation: Joseph Brian L. Costiniano, MD, DPCP

    Uploaded by

    Gio Tamaño Balisi
    51 views39 pages
    The document provides guidelines for interpreting arterial blood gas (ABG) results using a 6-step approach: 1. Check for internal consistency of values using Henderson-Hasselbach equation. 2. Identify if there is alkalemia or acidemia present based on pH value. 3. Determine if the disturbance is respiratory or metabolic based on relationship between pH and PaCO2 changes. 4. Assess if there is appropriate compensation for the primary disturbance. 5. Calculate anion gap if metabolic acidosis is present. 6. Assess relationship between change in anion gap and change in bicarbonate if anion gap is increased.

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    ABG-Notes

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    The document provides guidelines for interpreting arterial blood gas (ABG) results using a 6-step approach: 1. Check for internal consistency of values using Henderson-Hasselbach equation. 2. Identify if there is alkalemia or acidemia present based on pH value. 3. Determine if the disturbance is respiratory or metabolic based on relationship between pH and PaCO2 changes. 4. Assess if there is appropriate compensation for the primary disturbance. 5. Calculate anion gap if metabolic acidosis is present. 6. Assess relationship between change in anion gap and change in bicarbonate if anion gap is increased.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    51 views39 pages

    Arterial Blood Gas Interpretation: Joseph Brian L. Costiniano, MD, DPCP

    Uploaded by

    Gio Tamaño Balisi
    The document provides guidelines for interpreting arterial blood gas (ABG) results using a 6-step approach: 1. Check for internal consistency of values using Henderson-Hasselbach equation. 2. Identify if there is alkalemia or acidemia present based on pH value. 3. Determine if the disturbance is respiratory or metabolic based on relationship between pH and PaCO2 changes. 4. Assess if there is appropriate compensation for the primary disturbance. 5. Calculate anion gap if metabolic acidosis is present. 6. Assess relationship between change in anion gap and change in bicarbonate if anion gap is increased.

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    Arterial Blood Gas

    Interpretation
    Joseph Brian L. Costiniano, MD, DPCP
    American Thoracic Society
    ABG Reading Guidelines
    • https://www.thoracic.org/professionals/clinical-
    resources/critical-care/clinical-education/abgs.php
    Components of ABG

    Blood Gas

    Oxygenation Ventilation Acid-Base

    PaO2, SaO2 PCO2 pH, HCO3, BE


    Critical Care Medicine
    ABG Interpretation
    6-stepwise approach
    Step 1: Assess the internal consistency of the values using
    the Henderson-Hasselbach equation:

    [H+] = 24(PaCO2)
    [HCO3-]

    Kaufman, D., American Thoracic Society


    • If the pH and the [H+] are inconsistent, the ABG is
    probably not valid.
    pH Approximate [H+]
    (mmol/L)
    7.00 100
    7.05 89
    7.10 79
    7.15 71
    7.20 63
    7.25 56
    7.30 50
    7.35 45
    7.40 40
    7.45 35
    7.50 32
    7.55 28
    7.60 25
    7.65 22
    Kaufman, D., American Thoracic Society
    Step 2: Is there alkalemia or acidemia present?

    pH < 7.35 acidemia


    pH > 7.45 alkalemia

    •This is usually the primary disorder


    •Remember: an acidosis or alkalosis may be
    present even if the pH is in the normal range
    (7.35 – 7.45)
    •You will need to check the PaCO2, HCO3- and
    anion gap

    Kaufman, D., American Thoracic Society


    Step 3:
    - Is the disturbance respiratory or metabolic?
    - What is the relationship between the direction of
    change in the pH and the direction of change in the
    PaCO2?
    - In primary respiratory disorders, the pH and PaCO2
    change in opposite directions; in metabolic disorders
    the pH and PaCO2 change in the same direction.
    Acidosis Respiratory pH ↓ PaCO2 ↑
    Acidosis Metabolic& pH ↓ PaCO2 ↓
    Alkalosis Respiratory pH ↑ PaCO2 ↓
    Alkalosis Metabolic pH ↑ PaCO2 ↑

    Kaufman, D., American Thoracic Society


    Step 4: Is there appropriate compensation for the primary
    disturbance? Usually, compensation does not return the pH
    to normal (7.35 – 7.45).
    Disorder Expected compensation Correction factor
    Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ±2
    Acute respiratory acidosis Increase in [HCO3-]= ∆ ±3
    PaCO2/10
    Chronic respiratory Increase in [HCO3-]= 3.5(∆
    acidosis (3-5 days) PaCO2/10)
    Metabolic alkalosis Increase in PaCO2 = 40 +
    0.6(∆HCO3-)
    Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆
    PaCO2/10)
    Chronic respiratory Decrease in [HCO3-] = 5(∆
    alkalosis PaCO2/10) to 7(∆ PaCO2/10)

    If the observed compensation is not the expected compensation, it is likely that more
    than one acid-base disorder is present.
    Kaufman, D., American Thoracic Society
    Step 5: Calculate the anion gap (if a metabolic acidosis
    exists): AG= [Na+]-( [Cl-] + [HCO3-] )-12 ± 2
    • A normal anion gap is approximately 12 meq/L.
    • In patients with hypoalbuminemia, the normal anion gap is lower
    than 12 meq/L; the “normal” anion gap in patients with
    hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL
    decrease in the plasma albumin concentration
    • 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

    Kaufman, D., American Thoracic Society


    Step 6: If an increased anion gap is present, assess the
    relationship between the increase in the anion gap and the
    decrease in [HCO3-].
    • Assess the ratio of the change in the anion gap (∆AG ) to
    the change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
    • This ratio should be between 1.0 and 2.0 if an
    uncomplicated anion gap metabolic acidosis is present.
    • If this ratio falls outside of this range, then another
    metabolic disorder is present:
    - If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion
    gap metabolic acidosis is likely to be present.
    - If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic
    alkalosis is likely to be present.

    Kaufman, D., American Thoracic Society


    Selected etiologies of respiratory acidosis

    o Airway obstruction
    - Upper
    - Lower
    o COPD
    o asthma
    o other obstructive lung disease
    o CNS depression
    o Sleep disordered breathing (OSA or OHS)
    o Neuromuscular impairment
    o Ventilatory restriction
    o Increased CO2 production: shivering, rigors, seizures, malignant
    hyperthermia, hypermetabolism, increased intake of carbohydrates
    o Incorrect mechanical ventilation settings

    Kaufman, D., American Thoracic Society


    Selected etiologies of respiratory alkalosis

    o CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain
    trauma, brain tumor, CNS infection
    o Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2
    o Stimulation of chest receptors: pulmonary edema, pleural effusion,
    pneumonia, pneumothorax, pulmonary embolus
    o Drugs, hormones: salicylates, catecholamines, medroxyprogesterone,
    progestins
    o Pregnancy, liver disease, sepsis, hyperthyroidism
    o Incorrect mechanical ventilation settings

    Kaufman, D., American Thoracic Society


    Selected causes of metabolic alkalosis

    o Hypovolemia with Cl- depletion


    o GI loss of H+
    o Vomiting, gastric suction, villous adenoma, diarrhea with
    chloride-rich fluid
    o Renal loss H+
    o Loop and thiazide diuretics, post-hypercapnia (especially
    after institution of mechanical ventilation)
    o Hypervolemia, Cl- expansion
    o Renal loss of H+: edematous states (heart failure, cirrhosis,
    nephrotic syndrome), hyperaldosteronism, hypercortisolism,
    excess ACTH, exogenous steroids, hyperreninemia, severe
    hypokalemia, renal artery stenosis, bicarbonate
    administration

    Kaufman, D., American Thoracic Society


    Selected etiologies of metabolic acidosis

    oElevated anion gap: oNormal anion gap: will have increase in [Cl-]GI
    o Methanol intoxication loss of HCO3-
    o Uremia o proximal RTA
    o Diabetic ketoacidosisa, alcoholic o Diarrhea, ileostomy, proximal colostomy,
    ketoacidosis, starvation ketoacidosis ureteral diversion
    o Paraldehyde toxicity oRenal loss of HCO3-
    o Isoniazid o carbonic anhydrase inhibitor
    o Lactic acidosisa (acetazolamide)
    o Type A: tissue ischemia oRenal tubular disease
    o Type B: Altered cellular metabolism o ATN
    o Ethanolb or ethylene glycolb intoxication o Chronic renal disease
    o Salicylate intoxication o Distal RTA
    o Aldosterone inhibitors or absence
    o NaCl infusion, TPN, NH4+ administration

    Kaufman, D., American Thoracic Society


    Selected mixed and complex acid-base disturbances
    Disorder Characteristics Selected situations Disorder
    Respiratory acidosis with ↓in pH •Cardiac arrest Respiratory acidosis with
    metabolic acidosis ↓ in HCO3 •Intoxications metabolic acidosis
    ↑ in PaCO2 •Multi-organ failure

    Respiratory alkalosis with↑in pH •Cirrhosis with diuretics Respiratory alkalosis with


    metabolic alkalosis ↑ in HCO3- •Pregnancy with metabolic alkalosis
    ↓ in PaCO2 vomiting
    •Over ventilation of
    COPD
    Respiratory acidosis with pH in normal range •COPD with diuretics, Respiratory acidosis with
    metabolic alkalosis ↑ in PaCO2, vomiting, NG suction metabolic alkalosis
    ↑ in HCO3- •Severe hypokalemia

    Respiratory alkalosis withpH in normal range •Sepsis Respiratory alkalosis with


    metabolic acidosis ↓ in PaCO2 •Salicylate toxicity metabolic acidosis
    ↓ in HCO3 •Renal failure with CHF
    or pneumonia
    •Advanced liver disease
    Metabolic acidosis with pH in normal range •Uremia or ketoacidosis Metabolic acidosis with
    metabolic alkalosis HCO3- normal with vomiting, NG metabolic alkalosis
    suction, diuretics, etc.
    Kaufman, D., American Thoracic Society
    SAMPLE PROBLEMS
    CASE: The patient is a 35 year -old female with AIDS brought to the emergency room
    with a fever of 39oC and a three month history of copious diarrhea.

    On physical exam the patient is a well-developed, thin female in moderate distress.


    Vital signs-(supine) blood pressure 100/60, pulse 100 and (standing) blood pressure
    80/40, pulse 125, respirations 18 and she was afebrile. HEENT exam was normal.
    Cardiac exam demonstrated an S1 and S2 without S3, S4 or murmur. Lungs were
    clear to auscultation and percussion. The abdomen was supple and minimally tender
    to palpation. Bowel sounds were hyperactive.

    pH 7.35
    PCO2 32 mmHg
    PO2 90 mmHg
    HCO3 14 mmol/L
    With O2 via NC @4LPM
    • Primary Disorder?
    • Compensated? Mixed or Pure?
    • FiO2?
    • Expected PO2 for Age?
    • Oxygenation? Corrected or Uncorrected?
    • Primary Disorder? METABOLIC ACIDOSIS
    HCO3 14
    MEAN HCO3 24
    DIFFERENCE OF 10

    PCO2 32
    MEAN 40
    DIFFERENCE OF 8
    • Primary Disorder? METABOLIC ACIDOSIS
    • Compensated? Mixed or Pure?
    PaCO2 = (1.5 X HCO3) + 8
    = (1.5 X 14) + 8
    = 29 +-2
    PaCO2 OF PATIENT: 32 → RESPIRATORY ACIDOSIS
    • FiO2?
    FiO2 = 20 +(4 x LPM)
    FiO2 = 36
    • DESIRED PO2 for Age?
    104 – (0.43 X AGE)
    104 – (0.43 X 35)
    = 88.95
    • Expected PO2 = FiO2 x 5
    = 36 x 5
    = 180
    • Oxygenation? Corrected or Uncorrected?
    PO2 = 90 < Expected PO2 180
    UNCORRECTED HYPOXEMIA AT AN FIO2 OF 36

    MIXED METABOLIC ACIDOSIS WITH RESPIRATORY ACIDOSIS with


    UNCORRECTED HYPOXEMIA AT AN FIO2 OF 36%
    IV DRIPS COMPUTATION
    • Norepinephrine
    • potent vasoconstrictor and inotropic stimulant
    • Usually started at 2 to 4 mcg/min
    • Ceiling: 15 mcg/min
    • Usual prep: 8mg in 100cc D5W or 16mg in 250 D5W
    IV DRIPS COMPUTATION
    • Dopamine
    • Augments BP and cardiac output in cardiogenic shock
    • May be used to increase HR in patients with blocks
    • Usual prep: 200mg in 250 cc D5W → single strength
    • 400 mg in 250 cc D5W → double strength
    • Dose: <2 mcg/kg/min – RENAL
    • 2-10 – inotrope. Norepinephrine release. Increased CO
    • >10 – Increased vascular resistance
    IV DRIPS COMPUTATION
    • Dobutamine
    • DOC for myocardial dysfunction
    • Positive inotropic action
    • As dose increased → may cause HYPOTENSION by VASODILATION
    • Usual prep: 500mg in 250cc D5W
    IV DRIPS COMPUTATION

    • Concentration Factor = (Prep) mg/mL x 1000


    60

    • Actual dose = CF x rate


    wt (kg)
    SAMPLE
    • Calculate the actual dose of the following Norepinephrine drip:

    Levophed 16 mg in 100cc D5W @ 30cc/hr in a 60kg female patient.

    • Actual dose = CF x rate CF = 16/100 x 1000 CF = 2.67


    wt (kg) 60

    AD = 2.67 x 30 AD = 1.33
    60

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