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Blood Gas Interpretation
 

Blood Gas Interpretation

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    Blood Gas Interpretation Blood Gas Interpretation Presentation Transcript

    • Blood Gas Interpretation 2005/8/25
    • Before beginning…
      • Allen’s test for radial and ulnar artery
      • Common errors of arterial blood sampling
        • Air in sample: PCO 2 ↓, pH↑, PO 2 ↨
        • Venous mixture: PCO 2 ↑, pH↓, PO 2 ↓
        • Excess anticoagulant (dilution): PCO 2 ↓, pH↑, PO 2 ↨
        • Metabolic effects: PCO 2 ↑, pH↓, PO 2 ↓
      • Simultaneous electrolytes panel
    • Acid Base Physiology
      • The Law of Mass Action
      • [A] + [B]  [C] + [D]
      • K 1 /K 2 = [C][D]/[A][B]
      • Dissociation constant for an acid
      • Ka = [H + ][A - ]/[HA]
      K 1 K 2
    •  
    • Henderson-Hasselbalch Equation
      • CO 2 + H 2 O  H 2 CO 3  H + + HCO3 -
      • [H + ] = K x [CO 2 ]/[HCO 3 - ]
      • = 24 PCO 2 /[HCO 3 - ]
      • pH = 6.1 + log ([HCO3 - ]/0.0301xPCO 2 )
    • Normal Range
      • pH = 7.35-7.45
      • PCO 2 = 35-45 mmHg (40 mmHg)
      • HCO 3 - = 22-26 mEq/L (24 mEq/L)
    • Bicarbonate Buffering System
      • CO 2 + H 2 O  H 2 CO 3  H + + HCO3 -
      Oral intake Kidney Metabolism Oral intake Kidney Stomach Metabolism Lung
    • Acid Production and Elimination
      • Reaction Products Elimination
      • Glucose H + + HCO 3 -
      • Fat H + + HCO 3 -
      • Glucose H + + lactate
      • Cysteine H + + sulfate
      • Phosphoproteins H + + phosphate
      Anaerobic +O2 +O2 +O2 +O2 Lungs 24,000 mEq/day Volatile acid Kidneys 50-100 mEq/day Non-volatile acid
    • Determinants of CO 2 in the alveolus
      • V A = V E – V D = V T x f (1- V D /V T )
      • P A CO 2 = k x (VCO 2 /V A )
      • Physiologic dead space = anatomic dead space + alveolar dead space
    • PaCO 2 PaCO 2 > 40 mmHg, MV = 2x normal PaCO 2 > 80 mmHg  CO2 nacrosis
    • Renal Regulation of Bicarbonate
      • “ Reabsorption“ of filtered HCO 3 - (4000 mmol/day)
      • Formation of titratable acid (4000 mmol/day H + )
      • Excretion of NH4+ in the urine
      • 80-90% of HCO 3 - : reabsorbed in the proximal tubule
      • Distal tubule: reabsorption of remained bicarbonate and secretion of hydrogen ion
    • Proximal Renal Tubule
    • Distal Renal Tubule
    • Distal Tubule – NH 4 + excretion
    • Acid Base Disturbance
      • Metabolic acidosis: HCO 3 - ↓
      • Metabolic alkalosis: HCO 3 - ↑
      • Respiratory acidosis: PCO 2 ↑
      • Respiratory alkalosis: PCO 2 ↓
      • Simple
      • Primary
      • Secondary
      • mixed
    • Metabolic Acidosis
      • Indogenous acid production (lactic acidosis, ketoacidosis)
      • Indogenous acid accumulation (renal failure)
      • Loss of bicarbonate (diarrhea)
      • High anion gap
      • Normal (hyperchloremic )
    • Pathophysiologic Effect of Metabolic Acidosis
      • Kussmaul respiration
      • Intrinsic cardiac contractility ↓, normal inotropic function
      • Peripheral vasodilatation
      • Central vasoconstriction  pulmonary edema
      • Depressed CNS function
      • Glucose intolerance
    • Anion Gap
      • AG = Na + - (Cl - + HCO3 - )
      • Unmeasured anions in plasma (normally 10 to 12 mmol/L)
      • Anionic proteins, phosphate, sulfate, and organic anions
      • Correction: if albumin < 4
      • Albumin ↓ 1  AG ↓ 2.5
    • Anion Gap
      • Increase
        • Increased unmeasured anions
        • Decreased unmeasured cations (Ca ++ , K + , Mg ++ )
        • Increase in anionic albumin
      • Decrease
        • Increase in unmeasured cations
        • Addition of abnormal cations
        • Reduction in albumin concentration
        • Decrease in the effective anionic charge on albumin by acidosis
        • Hyperviscosity and severe hyperlipidemia ( underestimation of sodium and chloride concentration)
    •  
    •   Renal failure (acute and chronic) Starvation   Salicylates Alcoholic   Methanol Diabetic   Ethylene glycol Ketoacidosis   Toxins Lactic acidosis Causes of High-Anion-Gap Metabolic Acidosis
    • Metabolic Alkalosis
      • Net gain of [HCO 3 - ]
      • Loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid
      • Kidneys fail to compensate by excreting HCO 3 - (volume contraction, a low GFR, or depletion of Cl - or K + )
    • Respiratory Acidosis
      • Severe pulmonary disease
      • Respiratory muscle fatigue
      • Abnormal ventilatory control
      • Acute vs. Chronic (> 24 hrs)
    • Respiratory Acidosis
      • Acute: anxiety, dyspnea, confusion, psychosis, and hallucinations and coma
      • Chronic: sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis
      • Headache: vasocontriction
    •  
    • Respiratory Alkalosis
      • Strong ventilatory stimulus with alveolar hyperventilation
      • Consuming HCO 3 -
      • > 2-6 hrs: renal compensation (decrease NH4+/acid excretion and bicarbonate re-absorption)
    • Respiratory Alkalosis
      • Reduced cerebral blood flow
        • dizziness, mental confusion, and seizures
      • Minimal cardiovascular effect in normal health
      • Cardiac output and blood pressure may fall in mechanically ventilated patients
      • Bohr effect: left shift of hemoglobin-O 2 dissociation curve  tissue hypoxia (arrhythmia)
      • intracellular shifts of Na + , K + , and PO 4 - and reduces free [Ca 2+ ]
    • Stepwise Approach
      • Do comprehensive history taking and physical examination
      • Order simultaneous arterial blood gas measurement and chemistry profiles
      • Assess accuracy of data
      • Direction of pH: always indicates the primary disturbance
      • Calculate the expected compensation
      • Second or third disorders
    • N Respiratory alkalosis Metabolic alkalsosis Metabolic acidosis Respiratory acidosis 7.4 7.6 7.2 pH 30 40 50 PCO 2 (mmHg) Determination of primary acid-base disorders
    •  
    • Compensatory Mechanisms
      • Respiratory compensation
        • Complete within 24 hrs
      • Metabolic compensation
        • Complete within several days
      • Both the respiratory or renal compensation almost never over-compensates
    •   [HCO3-] will ↑ 4 mmol/L per 10-mmHg ↑ in PaCO2 Chronic   [HCO3-] will ↑ 1 mmol/L per 10-mmHg ↑ in PaCO2 Acute   Respiratory acidosis   [HCO3-] will ↓ 4 mmol/L per 10-mmHg ↓ in PaCO2 Chronic   [HCO3-] will ↓ 2 mmol/L per 10-mmHg ↓ in PaCO2 Acute   Respiratory alkalosis   PaCO2 = [HCO3-] + 15   PaCO2 will ↑ 6 mmHg per 10-mmol/L ↑ in [HCO3-] or   PaCO2 will ↑ 0.75 mmHg per mmol/L ↑ in [HCO3-] or Metabolic alkalosis   PaCO2 = [HCO3-] + 15   PaCO2 will ↓ 1.25 mmHg per mmol/L ↓ in [HCO3-] or   PaCO2 = (1.5x HCO3-) + 8 or Metabolic acidosis   Prediction of Compensation Disorder Prediction of Compensatory Responses on Simple Acid-Base Disturbances
    •  
    •  
    • Mixed Acid Base Disorders Metabolic alkalosis Metabolic acidosis Respiratory alkalosis Respiratory acidosis    Metabolic alkalosis    Metabolic acidosis   Respiratory alkalosis   Respiratory acidosis Secondary Primary
    • Oxygenation
      • Poor diffusion across alveolar membrane
      • Small pressure gradient between P A O 2 and PaO 2
      • Large alveolar area is required for gas transfer
      • Hemoglobin carries the majority of oxygen in the blood
    •  
    • Oxygenation
      • Ventilation and alveolar disease
      • Ventilation ↓  P A O2 ↓  PaO2 ↓, combined PCO 2 ↑
      • Alveolar disease
        • Reduced alveolar area
        • Thickened alveolar membrane
        • V/Q mismatch
        • Shunt
    • Alveolar-arterial Oxygen Gradient
      • P A O 2 = F iO2 (P B -P H2O ) – PCO 2 /R
      • = 0.21(760-47) – 40/0.8
      • = 100
      • R: respiratory quotient
      • P(A-a)O 2 = P A O 2 – PaO 2
      • (= Age x 0.4)
    •  
    • Oxygen Content and Saturation
      • O 2 content = 1.34 x Hb x Saturation + 0.0031xPO 2
    • Pulse Oximeters
      • Percentage of oxygenated hemoglobin in blood
      • Absorption of light in the red and infra-red spectra
      • Continuous monitor
      • Accurate (  3%) at high saturation, less below 80%
      • Insensitive around the normal PO 2
      • COHb and MetHb
    • Clinical Example 1
      • 72 y/o male, COPD with acute exacerbation
      • Under O 2 2L/min
      • pH 7.44, PCO 2 54, PO 2 60, HCO 3 36
      • Metabolic alkalosis with respiratory compensation
      • Mixed respiratory acidosis
    • Clinical Example 2
      • 30 y/o male, sudden onset dyspnea
      • Room air
      • 7.33/24/111/12
      • Metabolic acidosis
      • Respiratory compensation
      • Normal A-a O2 gradient
      • O2 ↑: hyperventilation
    • Clinical Example 3
      • 70 y/o male, acute hemoptysis and dyspnea
      • Room air
      • 7.50/31/88/24
      • Respiratory alkalosis
      • Not been renal compensated yet
      • Normal PO2, but A-a O2 gradient ↑
    • Clinical Example 4
      • 18 y/o female, chest tightness and dyspnea for 4 hrs
      • RR 28/min, distressed, widespread wheezing
      • O2 mask 6L/min
      • 7.31/49/115/26
      • Respiratory acidosis
      • Normal bicarbonate  acute
      • May have problems with oxygenation
    • Clinical Example 5
      • 37 y/o female, mild asthma history
      • Wheezes for 3 weeks, increasing chest tightness and dyspnea for 24 hrs, call for ambulance with Oxygen use
      • RR 18/min, anxious and distressed
      • Room air
      • 7.37/43/97/27
      • Normal?
      • r/o CO 2 retention
      • Low A-a O 2 : Oxygen use in the ambulance
    • Clinical Example 6
      • 19 y/o male, Duchenne muscular dystrophy on wheelchair for 7 yrs
      • No previous respiratory problems but frequent UTI
      • Room air
      • 7.21/81/44/36
      • Respiratory acidosis
      • Metabolic compensation
      • Normal A-a O2  pure ventilatory failure
    • Clinical Example 7
      • 57 y/o male, smoker, one week URI then 36 hrs productive cough, fever and dyspnea
      • RR 36/min, distressed, CXR: RLL pneumonia
      • 7.33/27/51/22, 2L/min
      • 7.34/32/58/24, 10L/min mask
      • Early metabolic acidosis
      • Severe hypoxemic respiratory failure
      • Intra-pulmonary shunting
    • Thank you for your attention