Basics In Arterial Blood Gas Interpretation

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    Basics In Arterial Blood Gas Interpretation - Presentation Transcript

    1. Basics in Arterial Blood Gas Interpretation Crisbert I. Cualteros, M.D.
    2. 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
    3. Technique for Radial Artery Puncture
      • Explain process to patient. Examine skin, palpate radial & ulnar arteries. Perform modified Allen Test.
    4. 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.
    5. 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.
    6. 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 45 o . Advance needle slowly.
      • Never redirect needle without first withdrawing to subcutaneous tissue.
      • Obtain 2-4 ml blood. If possible don’t 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.
    7. Potential Complications
      • Pain
      • Hematoma, hemorrhage
      • Trauma to vessel
      • Arteriospasm
      • Air or clotted-blood emboli
      • Vasovagal response
      • Arterial occlusion
      • Infection
    8. Indications for ABG
      • Assess ventilation & acid-base balance
      • Assess oxygenation status
    9. Ventilatory/ Acid-Base Status
    10. Henderson-Hasselbach Parameters & their normal laboratory ranges pH= [HCO 3 ]p P C02 > 26 < 35 > 7.45 Alkalotic < 22 > 45 < 7.35 Acidotic 22-26 35-45 7.35-7.45 Normal [HCO3]p (mmol/L) PCO2 (mmHg) pH
    11. Traditional Metabolic Acid-Base Nomenclature  (+)   N Compensated (chronic)  (+)    Partly compensated (subacute)  (+)  N  Uncompensated (acute) Metabolic alkalosis  (-)   N Compensated (chronic)  (-)     Partly compensated (subacute)  (-)   N  Uncompensated (acute) Metabolic acidosis BE [HCO3]p PCO 2 pH Nomenclature
    12. Traditional Respiratory Acid-Base Nomenclature    N Compensated (chronic)     Partly compensated (subacute) N N   Uncompensated (acute) Respiratory alkalosis    N Compensated (chronic)     Partly compensated (subacute) N N   Uncompensated (acute) Respiratory acidosis BE [HCO3]p PCO2 pH Nomenclature
    13. 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:
      • [HCO 3 - ]
      • 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
    14. Nomenclature & Criteria for Clinical Interpretation
      • Clinical Terminology Criteria
      • Ventilatory failure (respiratory acidosis) P a CO 2 > 45 mm Hg
      • Acute ventilatory failure (respiratory acidosis) P a CO 2 > 45 mmHg pH < 7.35
      • Chronic ventilatory failure (respiratory acidosis) P a CO 2 > 45 mmHg
      • pH 7.36- 7.44
      • Alveolar hyperventilation (respiratory alkalosis) P a CO 2 < 35 mmHg
      • Acute alveolar hyperventilation (respiratory P a CO 2 < 35 mmHg
      • alkalosis) pH > 7.45
      • Chronic alveolar hyperventilation (respiratory P a CO 2 < 35 mmHg alkalosis) pH 7.36-7.44
    15. Nomenclature & Criteria for Clinical Interpretation
      • Clinical Terminology Criteria
      • Acidemia pH < 7.35
      • Alkalemia pH > 7.45
      • Acidosis HCO 3 - < 22 mmol/L BD > 5 mmol/L
      • Alkalosis HCO 3 - > 26 mmol/L
      • BE > 5 mmol/L
      • Combined Respiratory Acidosis & Metabolic Acidosis
      • Respiratory Alkalosis & Metabolic Alkalosis
      • Mixed Respiratory Acidosis & Metabolic Alkalosis
      • Respiratory Alkalosis & Metabolic Acidosis
    16. Respiratory Acidosis
      • Acute
      •  pH = 0.08 x (PCO 2 – 40)
      • 10
      • ex. PCO 2 = 60
      •  pH = 0.08 x (60 - 40) = 0.16
      • 10
      • expected pH = 7.40 – 0.16 = 7.24
      • HCO 3 - increases 0.1 – 1 meq/L per 10 mmHg PCO 2 increase
      Compensation: cellular buffering: HCO 3 renal adaptation: H + secretion, Cl - reabsorption, net acid excretion
    17. Respiratory acidosis
      • Chronic
      •  pH = 0.03 x (PCO 2 – 40)
      • 10
      • ex. PCO 2 = 60
      •  pH = 0.03 x (60 – 40) = 0.06
      • 10
      • expected pH = 7.40 – 0.06 = 7.34
      • HCO 3 - increases 1-3.5 meq/L per 10 mmHg PCO 2 increase
    18. Respiratory Acidosis
      • COPD
      • O 2 excess in COPD
      • Drugs
        • Barbiturates
        • Anesthetics
        • Narcotics
        • Sedatives
      • Extreme ventilation-perfusion mismatch
      • Exhaustion
      • Inadequate MV
      • Neurologic disorders
      • Neuromuscular disease
        • Poliomyelitis
        • ALL
        • G-B syndrome
        • Electrolyte deficiencies (K + , PO 4 - )
        • Myasthenia gravis
      • Excessive CO 2 production
        • TPN
        • Sepsis
        • Severe burns
        • NaHCO 3 administration
    19. Respiratory Alkalosis
      • Acute
      •  pH = 0.08 x (40 – PCO 2 )
      • 10
      • ex. PCO 2 = 20
      •  pH = 0.08 x (40 – 20) = 0.16
      • 10
      • expected pH = 7.40 + 0.16 = 7.56
      • HCO 3 - decreases 0-2 meq/L per 10 mmHg PCO 2 decrease
      Compensation: cellular buffering renal response: retention of endogenous acids, excretion of HCO 3
    20. Respiratory Alkalosis
      • Chronic
      •  pH = 0.03 x (40 – PCO 2 )
      • 10
      • ex. PCO 2 = 20
      •  pH = 0.03 x (40 – 20) = 0.06
      • 10
      • expected pH = 7.40 + 0.06 = 7.46
      • HCO 3 - decreases 2-5 meq/L per 10 mmHg PCO 2 decrease
    21. 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
    22. 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
    23. 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
      • HCO 3 -
      • ~ ex. GI loss of HCO 3 - (diarrhea), renal wasting of HCO 3 -
      • (RTA), ingestion of acids, parenteral hyperalimentation, carbonic anhydrase inhibitors
    24. Metabolic Acidosis
      • Abnormalities:
      • Overproduction of acids
      • Loss of buffer stores
      • Underexcretion of acids
    25. Metabolic Acidosis
      • Expected PCO 2 = ( [HCO 3 - ] x 1.5) + 8 + 2
      • ex. [HCO 3 - ] = 11
      • expected PCO 2 = (11 x 1.5) + 8 + 2 = 22.5- 26.5
      • PCO 2 decreases 1- 1.5 mmHg per 1 meq/L HCO 3 - decrease
    26. Metabolic Acidosis
      • Compensation
      •  pCO 2 (hyperventilation)
      • Pathway:
       pCO 2 HCO 3 ratio  H + conc Acidification of ECF  ECF  pH Stimulation of brainstem  RR  pCO 2 Normalization of pH  HCO 3
    27. Metabolic Acidosis
      • Compensation
      • Ionic shift
        • K + moves extracellularly for H +
        • HCO 3 - generation, H + excretion
    28. Corrected [HCO 3 - ] for Anion Gap Metabolic Acidosis
      • Measured serum [HCO 3 - ] + (anion gap – 12)
    29. Metabolic Alkalosis
      • Expected PCO 2 = ( [HCO 3 - ] x 0.75 ) + 20 + 5
      • ex. [HCO 3 - ] = 34
      • expected PCO 2 = (34 x 0.75) + 20 + 5 = 40.5- 50.5
      • PCO 2 increases 0.5- 1 mmHg per 1 meq/L HCO 3 - increase
    30. Metabolic Alkalosis
      • Pathway
      HCO 3  PaCO 2 HCO 3 ratio  H + conc Alkalinization of ECF  PaCO 2 with mild hypoxemia Normalization of pH
    31. Causes of Metabolic Alkalosis Hypokalemia* Ingestion of large amounts of alkali or licorice Gastric fluid loss: Vomiting, NG suctioning* Hyperaldosteronism 2 0 to nonadrenal factors Bartter’s 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
    32. Limits of Compensation  0.5- 1/ 1 meq/L [HCO 3 - ]  Metabolic Alkalosis  1- 1.5/ 1 meq/L [HCO 3 - ]  Metabolic Acidosis  2- 5/ 10 mmHg PCO 2  Chronic  0- 2/ 10 mmHg PCO 2  Acute Respiratory Alkalosis  1- 3.5/ 10 mmHg PCO 2  Chronic  0.1- 1/ 10 mmHg PCO 2  Acute Respiratory Acidosis PCO 2 mmHg [HCO 3 - ] meq/L Imbalance
    33. Steps for Analyzing Acid- Base Disturbances
      • Is patient acidemic or alkalotic? pH
      • Is disturbance primarily respiratory or metabolic?
      • PCO 2 , [HCO 3 - ]
      • 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?
    34. Oxygenation Status
    35. 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)
    36. Steps for Analyzing Oxygenation Status
    37. 1. Is the patient hypoxemic or normoxemic?
      • Indices of Oxygenation:
      • a. AaDO 2 = PAO 2 – PaO 2
      • PAO 2 = FiO 2 (713) – PaCO 2
      • 0.8
      • PaO 2 = obtained from blood gas determination
      • b. aAO 2 = PaO 2
      • PAO 2
      • c. P/F ratio = PO 2
      • FiO 2
      • 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
    38. 2. If hypoxemic, is it uncorrected, corrected, or overcorrected?
      • With O 2 supplementation
      • PaO 2 (mmHg)
      • Uncorrected hypoxemia < 80
      • Corrected hypoxemia 80 – 120
      • Overcorrected > 120
      • FiO 2 to PaO 2 Relationship in Normal Lungs
      • FiO 2 PaO 2 (mmHg)
      • 0.30 > 150
      • 0.40 > 200
      • 0.50 > 250
      • 0.80 > 400
      • 1.00 > 500
    39. Room Air (patient < 60 y. o.)
      • PaO 2 (mmHg)
      • Mild hypoxemia 60 to < 80
      • Moderate hypoxemia 40 to < 60
      • Severe hypoxemia < 40
      • For each year > 60 subtract 1 mmHg for limits of mild &
      • moderate hypoxemia.
      • At any age, PaO 2 < 40 mmHg indicates severe hypoxemia.
    40. 3. If normoxemic, is oxygenation adequate or more than adequate?
    41. Thank you !

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