Arterial  and Venous Blood Gas Analysis in Critical Care<br />Edward Omron MD, MPH, FCCP<br />Pulmonary and Critical Care ...
Composite Value of ABG and VBG<br />Mainstays of diagnosis, therapy in acute illness<br />VBG historically used as: <br />...
Critical Care Medicine Principles<br />Fusion of multiple, disparate medical specialties refined by applied bedside physio...
INDICATIONS<br />ABG<br />Oxygenation<br />Ventilation<br />Acid-Base Status<br />VBG<br />Ventilation and Acid-Base Statu...
Blood Gas  Report(Arterial)<br />pH (No Units)                 7.35-7.45   <br />PaCO2  (mm Hg)            35-45<br />PaO2...
Blood Gas  Report(mixed/central venous)<br />pH = 7.32-7.42<br />PvCO2 = 40 - 50 (mm Hg)<br />PvO2 = 36 - 42 (mm Hg)<br />...
ANALYSIS OF VENTILATON<br />PaCO2 = VCO2 x K<br /><ul><li>                   VA
Hypercapnea  > 45 mm Hg (Hypoventilation)
Respiratory Acidosis
Hypocapnea  < 35 mm Hg (Hyperventilation)
Respiratory Alkalosis</li></li></ul><li>Respiratory Acid-Base Status<br />Respiratory Disturbances<br />CO2+H20       H2CO...
BASE EXCESS(B.E.)<br /><ul><li>Positive value, excess base, metabolic alkalosis
Negative value, excess acid, metabolic acidosis
Metabolic component of acid-base status
PCO2 independent
Estimated by BE = (Total CO2 – 25)</li></li></ul><li><ul><li>Problem Solving
1. LOOK AT THE pH</li></ul>Whatever side of pH 7.4 is the primary disorder<br /><ul><li>2. Look at pH, PCO2 direction</li>...
74 yo male found unresponsive and pulseless<br /><ul><li>Arterial Draw:</li></ul>pH = 7.28,  PaCO2 = 34,  HCO3 = 16<br />N...
Primary Disorder<br />Acidosis  and acidemia (pH < 7.4)<br />pH and PCO2 direction<br />Both down:  Metabolic Acidosis<br ...
<ul><li>Venous Draw</li></ul>pH = 7.08, pCO2 = 75, HCO3 = 21<br />Na = 145,  Cl = 103, Total CO2 =22  <br />Alb = 3 g/dL, ...
Primary Disorder<br />pH < 7.4, acidosis and acidemia<br />pH and PCO2 direction<br />Opposite therefore RESPIRATORY acido...
74 yo male found unresponsive and pulseless<br />Why a metabolic acidosis in arterial bed and respiratory acidosis in veno...
PaO2 vs PvO2  in Cardiogenic Shock<br />Arterial Venous Saturation Difference<br />SHOCK<br />
Paradoxical Respiratory Acidosis of Cardiopulmonary Arrest<br />Venous Arterial CO2 Difference<br />
Fick Equation for oxygen consumption (VO2)<br />VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)<br />VO2 = 1.34*Hgn*10*    C.O.*   (Sa...
Fick Equation for CO2 production<br />VCO2 =Carbon dioxide production (200 mL/min)<br />VCO2 = 10*C.O.*(PvCO2 – PaCO2)<br ...
Conclusion: Venoarterial PCO2 differences… from pulmonary artery <br />and central venouscirculations inversely correlate ...
Mixed Venous Arterial PCO2 Gradient<br />
Central Venous-Arterial PCO2 Gradient<br />
In a mathematical model of tissue CO2 exchange, the venous and tissue CO2 increase during IH but not during HH. These resu...
Conclusion: In ICU- resuscitated patients, targeting only ScvO2 may not be sufficient to guide therapy. When the 70% ScvO2...
Venous Arterial CO2 Difference<br />Circulatory Failure<br />Associated with Tissue Hypercarbic Acidosis<br />Hypovolemia,...
74 yo male found unresponsive and pulseless<br />Why a metabolic acidosis in arterial bed and respiratory acidosis in veno...
PaO2 vs PvO2  in Cardiogenic Shock<br />Arterial Venous Saturation Difference<br />SHOCK<br />
VO2 or Oxygen Consumption<br />VO2 = Arterial O2 delivery – Venous O2 delivery<br />The difference represents the amount o...
Fick Equation for Oxygen Consumption<br />VO2= Oxygen Consumption (250 mL/min)<br />VO2 = 10*C.O.*(CaO2 –CvO2)<br />VO2 = ...
Four Determinants of Mixed Venous Oximetry<br /> SvO2 = SaO2  - (VO2 / C.O. x Hgn x 1.34)<br />SvO2= Mixed venous saturati...
Mixed Venous Saturation<br />Percentage of hemoglobin saturated with oxygen in mixed venous blood<br />Flow weight average...
Why measure SvO2?<br />A decrease in SvO2 is an early indicator of a threat to tissue oxygenation<br />Earlier information...
Master EquationScvO2 SvO2 = SaO2  - (VO2 / C.O. x Hgn x 1.34)<br />Acute Illness or Post-op Surgery<br />SaO2, VO2, Cardi...
Central Venous Oxygen Saturation ScvO2<br />Allows separation of early and late shock<br />Easily measured with venous blo...
In-hospital mortality was 30.5 percent in the early goal-directed therapy group, compared with 46.5 percent in the standar...
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Arterial and Venous Blood Gas Analysis in Critical Care Edward Omron MD, MPH

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The focus of this presentation is to discuss the composite clinical value of combined and simultaneous arterial and venous blood gas analysis as an initial diagnostic strategy; and, as a powerful clinical decision making adjunct during early, goal directed resuscitation in critical illness.
Edward Omron MD, MPH, FCCP
Pulmonary, Critical Care Medicine
Morgan Hill, CA 95037

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Arterial and Venous Blood Gas Analysis in Critical Care Edward Omron MD, MPH

  1. 1. Arterial and Venous Blood Gas Analysis in Critical Care<br />Edward Omron MD, MPH, FCCP<br />Pulmonary and Critical Care Medicine<br />
  2. 2. Composite Value of ABG and VBG<br />Mainstays of diagnosis, therapy in acute illness<br />VBG historically used as: <br />a surrogate measurement of arterial pH, PCO2<br />ScvO2 or SvO2 measurements<br />Oxygenation/perfusion abnormalities<br />Composite clinical value rarely discussed<br />Simultaneous initial ABG, VBG<br />Powerful initial diagnostic strategy<br />Clinical decision adjunct in EGDT<br />
  3. 3. Critical Care Medicine Principles<br />Fusion of multiple, disparate medical specialties refined by applied bedside physiology<br />Goal is to improve morbidity, mortality in acute illness and major surgery<br />Outcome from acute illness is a function of time from diagnosis to initiation of EDGT<br />All current therapeutic endeavors attempt to contemporaneously improve oxygen delivery and minimize oxygen consumption<br />
  4. 4. INDICATIONS<br />ABG<br />Oxygenation<br />Ventilation<br />Acid-Base Status<br />VBG<br />Ventilation and Acid-Base Status<br />Cardiac Output (venous arterial PCO2 difference)<br />Endpoint of resuscitation (ScvO2 and PCO2)<br />
  5. 5. Blood Gas Report(Arterial)<br />pH (No Units) 7.35-7.45 <br />PaCO2 (mm Hg) 35-45<br />PaO2 (mm Hg) 110 - 0.5(age) <br />HCO3- (mmol/L): calc. 22-26 <br />B.E. (mmol/L) -2 to 2<br />O2 saturation: calc. >90%<br />
  6. 6. Blood Gas Report(mixed/central venous)<br />pH = 7.32-7.42<br />PvCO2 = 40 - 50 (mm Hg)<br />PvO2 = 36 - 42 (mm Hg)<br />Oxygen Saturation > 70%<br />Base Excess = -2 to +2<br />
  7. 7. ANALYSIS OF VENTILATON<br />PaCO2 = VCO2 x K<br /><ul><li> VA
  8. 8. Hypercapnea > 45 mm Hg (Hypoventilation)
  9. 9. Respiratory Acidosis
  10. 10. Hypocapnea < 35 mm Hg (Hyperventilation)
  11. 11. Respiratory Alkalosis</li></li></ul><li>Respiratory Acid-Base Status<br />Respiratory Disturbances<br />CO2+H20 H2CO3 H+ + HCO3<br />Acute changes:<br />Delta 10 mm Hg PaCO2, pH changes by 0.08<br />Chronic change: 40 + B.E<br />Alveolar Ventilation<br /> VA CO2 pH<br />Respiratory Acidosis PaCO2> 45<br />Respiratory Alkalosis PaCO2< 35<br />
  12. 12. BASE EXCESS(B.E.)<br /><ul><li>Positive value, excess base, metabolic alkalosis
  13. 13. Negative value, excess acid, metabolic acidosis
  14. 14. Metabolic component of acid-base status
  15. 15. PCO2 independent
  16. 16. Estimated by BE = (Total CO2 – 25)</li></li></ul><li><ul><li>Problem Solving
  17. 17. 1. LOOK AT THE pH</li></ul>Whatever side of pH 7.4 is the primary disorder<br /><ul><li>2. Look at pH, PCO2 direction</li></ul>Both decrease or increase, then metabolic<br />If move in opposite directions, respiratory<br /><ul><li>3. Respiration: acute or chronic?</li></ul>Acute: 10 mm Hg / 0.08 change in pH<br />Chronic: 40+Base Excess<br />
  18. 18. 74 yo male found unresponsive and pulseless<br /><ul><li>Arterial Draw:</li></ul>pH = 7.28, PaCO2 = 34, HCO3 = 16<br />Na = 153 Cl = 106 Total CO2 = 17<br />Alb = 3 g/dL, Saturation = 84%<br />Primary Acid-Base Disturbance?<br />Metabolic Acid-Base Status?<br />
  19. 19. Primary Disorder<br />Acidosis and acidemia (pH < 7.4)<br />pH and PCO2 direction<br />Both down: Metabolic Acidosis<br />Base Excess<br />16 – 24 = -8 mmols/L<br />
  20. 20. <ul><li>Venous Draw</li></ul>pH = 7.08, pCO2 = 75, HCO3 = 21<br />Na = 145, Cl = 103, Total CO2 =22 <br />Alb = 3 g/dL, Saturation = 20%<br />Primary Acid-Base Disorder?<br />Metabolic Acid-Base Status? <br />
  21. 21. Primary Disorder<br />pH < 7.4, acidosis and acidemia<br />pH and PCO2 direction<br />Opposite therefore RESPIRATORY acidosis<br />Base Excess<br />22 – 24 = -2 mmol/L<br />
  22. 22. 74 yo male found unresponsive and pulseless<br />Why a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?<br />Venous arterial PCO2 difference?<br />PvCO2 (75) - PaCO2 (34) = 41<br />PvCO2 – PaCO2  1 / cardiac index<br />Normal ≤ 6 mm Hg<br />Venous vs Arterial saturation difference?<br />PaO2 = 50 mm Hg, saturation = 84%<br />PvO2 =18, Venous Saturation = 20%<br />Increased oxygen extraction from circulatory failure<br />
  23. 23. PaO2 vs PvO2 in Cardiogenic Shock<br />Arterial Venous Saturation Difference<br />SHOCK<br />
  24. 24. Paradoxical Respiratory Acidosis of Cardiopulmonary Arrest<br />Venous Arterial CO2 Difference<br />
  25. 25. Fick Equation for oxygen consumption (VO2)<br />VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)<br />VO2 = 1.34*Hgn*10* C.O.* (SaO2 –SvO2)<br />A decrement in C.O. must be accompanied by an increase in the arteriovenous difference at constant oxygen consumption<br />
  26. 26. Fick Equation for CO2 production<br />VCO2 =Carbon dioxide production (200 mL/min)<br />VCO2 = 10*C.O.*(PvCO2 – PaCO2)<br />If cardiac output decreases and VCO2 remains constant, what must happen to venous-arterial CO2 difference?<br />VCO2 = 10* C.O.* (PvCO2 – PaCO2)<br />A decrement in C.O. must accompany an increase in venous-arterial CO2 difference at a constant VCO2.<br />
  27. 27.
  28. 28.
  29. 29.
  30. 30. Conclusion: Venoarterial PCO2 differences… from pulmonary artery <br />and central venouscirculations inversely correlate with cardiac index. <br />Substitution of a central for a mixed venous PCO2 difference provides an <br />accurate and alternative method for calculation of cardiac output<br />
  31. 31.
  32. 32. Mixed Venous Arterial PCO2 Gradient<br />
  33. 33. Central Venous-Arterial PCO2 Gradient<br />
  34. 34. In a mathematical model of tissue CO2 exchange, the venous and tissue CO2 increase during IH but not during HH. These results support the hypothesis that increases in tissue CO2 and the arteriovenous PCO2 gradient reflect only microcirculatory stagnation, not tissue dysoxia. Thus, … increases in tissue and venous PCO2 are insensitive markers of tissue dysoxia and merely reflect vascular hypoperfusion.<br />
  35. 35. Conclusion: In ICU- resuscitated patients, targeting only ScvO2 may not be sufficient to guide therapy. When the 70% ScvO2 goal- value is reached, the presence of a P(cv-a)CO2 larger than 6 mmHg might be a useful tool to identify patients who still remain inadequately resuscitated.<br />
  36. 36. Venous Arterial CO2 Difference<br />Circulatory Failure<br />Associated with Tissue Hypercarbic Acidosis<br />Hypovolemia, sepsis, shock …<br />Cardiac Index = e (1.787 – 0.151(v-a CO2))<br />Endpoint of Resuscitation<br />
  37. 37. 74 yo male found unresponsive and pulseless<br />Why a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?<br />Venous arterial PCO2 difference?<br />PvCO2 (75) - PaCO2 (34) = 41<br />PvCO2 – PaCO2  1 / cardiac index<br />Normal ≤ 6 mm Hg<br />Venous vs Arterial saturation difference?<br />PaO2 = 50 mm Hg, saturation = 84%<br />PvO2 =18, Venous Saturation = 20%<br />Increased oxygen extraction from circulatory failure<br />
  38. 38. PaO2 vs PvO2 in Cardiogenic Shock<br />Arterial Venous Saturation Difference<br />SHOCK<br />
  39. 39. VO2 or Oxygen Consumption<br />VO2 = Arterial O2 delivery – Venous O2 delivery<br />The difference represents the amount of oxygen consumed by the tissues<br />Normal = 250 mL/min or 5 mL/100 mL blood<br /> Oxygen Utilization Coefficient = 0.25 <br />SaO2 – SvO2  25%<br />
  40. 40.
  41. 41. Fick Equation for Oxygen Consumption<br />VO2= Oxygen Consumption (250 mL/min)<br />VO2 = 10*C.O.*(CaO2 –CvO2)<br />VO2 = 10 * C.O. * (1.34*Hgn*SaO2 -1.34*Hgn*SvO2)<br />VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)<br />Solve for SvO2? Or the mixed venous saturation?<br />
  42. 42. Four Determinants of Mixed Venous Oximetry<br /> SvO2 = SaO2 - (VO2 / C.O. x Hgn x 1.34)<br />SvO2= Mixed venous saturation (%)<br />SaO2 = Arterial oxygen saturation (%)<br />VO2= Oxygen consumption mL (O2/min)<br />Hgn= Hemoglobin concentration (g/dL)<br />Cardiac Output (C.O.) = dL/min<br />
  43. 43. Mixed Venous Saturation<br />Percentage of hemoglobin saturated with oxygen in mixed venous blood<br />Flow weight average of the venous saturations from all perfused vascular beds<br />Four Determinants:<br />SaO2, VO2, Cardiac Output, and Hgn<br />Physiologic oxygen reserve in times of stress<br />
  44. 44.
  45. 45.
  46. 46. Why measure SvO2?<br />A decrease in SvO2 is an early indicator of a threat to tissue oxygenation<br />Earlier information results in earlier diagnosis with interventions<br />Normal range of SvO2 = 60-80%<br />
  47. 47.
  48. 48.
  49. 49.
  50. 50. Master EquationScvO2 SvO2 = SaO2 - (VO2 / C.O. x Hgn x 1.34)<br />Acute Illness or Post-op Surgery<br />SaO2, VO2, Cardiac Output, and Hgn are dynamically changing concurrently<br />Optimize each parameter then recheck ScvO2 to assess response to intervention<br />
  51. 51.
  52. 52.
  53. 53.
  54. 54.
  55. 55. Central Venous Oxygen Saturation ScvO2<br />Allows separation of early and late shock<br />Easily measured with venous blood gas<br />Surrogate measurement of mixed venous oxygen sat.<br />5-18% higher<br />A low ScvO2 always means a low SvO2!<br />Normal ScvO2 68-76%<br />25% extraction coefficient of normal physiology<br />
  56. 56.
  57. 57. In-hospital mortality was 30.5 percent in the early goal-directed therapy group, compared with 46.5 percent in the standard therapy group (P=0.009).<br />From 7 to 72 hours, in the early goal- directed therapy group: higher mean central venous oxygen saturation (70.4±10.7 percent vs. 65.3±11.4 percent), lower lactate concentration (3.0±4.4 vs. 3.9±4.4 mmol per liter), lower base deficit (2.0±6.6 vs. 5.1±6.7 mmol per liter), and higher pH (7.40±0.12 vs. 7.36±0.12) than the standard therapy group (P«0.02). <br />Early goal-directed therapy provides significant benefits with respect to outcome in patients with severe sepsis and septic shock. (N Engl J Med 2001;345:1368-77)<br />
  58. 58. SEPTIC SHOCK PRESENT<br />SBP ≤ 90 mmHg or MAP ≤ 65 mmHg<br />OR<br />Lactate ≥ 4 mmol/L<br />PLUS<br />Clinical Picture c/w Infection<br />Fluid bolus 20 ml/kg<br />(.9 NaCl or LR)<br />PLUS<br />Vasopressors if MAP is<br />judged to be critically low<br />SBP < 90 mmHg, or<br />MAP < 65 mmHg, or<br />Lactate > 4 mmol/L<br />YES<br />Assess ScvO2<br />Boluses crystalloid or colloid equivalent until <br />CVP > 8 mmHg<br />CVP < 8 mmHg<br />Insert CVP Catheter<br />< 70%<br />MAP ≥ 65<br />Achieve ALL Goals?<br />Check<br />MAP<br />Dobutamine or RBCs depending on HCT<br />Resuscitation complete. Establish re-evaluation intervals.<br />
  59. 59. Studies of acute myocardial infarction, trauma, and stroke have been translated into improved outcomes by earlier diagnosis and application of therapy at the most proximal stage of hospital presentation. <br />The end points used in the EGDT protocol, the outcome results, and the cost-effectiveness have subsequently been externally validated, revealing similar or even better findings than those from the original trial. (CHEST 2006; 130:1579–1595)<br />
  60. 60. Summary<br />Simultaneous ABG and VBG<br />Initial O2 delivery and consumption state<br />Serial measurements adequacy of interventions<br />ABG<br />Oxygenation via Alveolar Gas Equation<br />Ventilation by PaCO2<br />Acid Base Status by pH, PCO2, HCO3, SBE<br />VBG (mixed or central)<br />Oxygen extraction ratio<br />ScvO2 or SvO2<br />Veno-arterial CO2 difference for cardiac output<br />
  61. 61. 65 year old man presents to the ER in Shock<br />BP 60/30, HR 150 bpm<br />Paleness<br />Cool Skin<br />Dilated Pupils<br />Semi comatose state<br />Low Urine Output<br />
  62. 62. Two Possible Causes of the Low Blood Pressure were Considered<br />Cardiogenic Shock<br />Hemorrhagic Shock<br />
  63. 63. Match the ABG VBG with the Associated Condition<br />(a) pH = 7.25, PCO2 = 30, PaO2 = 75, saturation = 97%,<br /> BE = -15, LA = -15<br />(v) pH = 7.20, PCO2 = 36, PvO2 = 25, venous saturation = 45%<br />Hemorrhagic Shock<br />(a) pH = 7.30, PCO2 = 25, PaO2 50, <br /> BE = -10, saturation = 85% LA = -10<br />(v) pH = 7.20, PCO2 = 50, PvO2 = 25, venous saturation = 45%<br />Cardiogenic Shock<br />
  64. 64. Additional References<br />http://www.slideshare.net/edofiron<br />Chest 2005;128:554s-560s<br />Intensive Care Medicine 2004; 30:2170-2179<br />Crit Care Med 2003; 31:S658-S667<br />Current Opinion Critical Care 2001; 7: 204-211<br />Critical Care Medicine 2002; 30: 1686-1692<br />Circulation 1969; 40: 165<br />Thorax 2002; 57: 170-177<br />Academic Emer Med 1999; 6: 421<br />

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