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

Arterial and Venous Blood Gas Analysis in Critical Care

Edward Omron MD, MPH, FCCP

Pulmonary and Critical Care Medicine

Composite Value of ABG and VBG

• Mainstays of diagnosis, therapy in acute illness• VBG historically used as:

– a surrogate measurement of arterial pH, PCO2– ScvO2 or SvO2 measurements– Oxygenation/perfusion abnormalities

• Composite clinical value rarely discussed– Simultaneous initial ABG, VBG

• Powerful initial diagnostic strategy• Clinical decision adjunct in EGDT

Critical Care Medicine Principles

• Fusion of multiple, disparate medical specialties refined by applied bedside physiology

• Goal is to improve morbidity, mortality in acute illness and major surgery

• Outcome from acute illness is a function of time from diagnosis to initiation of EDGT

• All current therapeutic endeavors attempt to contemporaneously improve oxygen delivery and minimize oxygen consumption

INDICATIONS

• ABG– Oxygenation– Ventilation– Acid-Base Status

• VBG– Ventilation and Acid-Base Status– Cardiac Output (venous arterial PCO2 difference)

– Endpoint of resuscitation (ScvO2 and PCO2)

Blood Gas Report(Arterial)

• pH (No Units) 7.35-7.45 • PaCO2 (mm Hg) 35-45

• PaO2 (mm Hg) 110 - 0.5(age)

• HCO3- (mmol/L): calc. 22-26

• B.E. (mmol/L) -2 to 2• O2 saturation: calc. >90%

Blood Gas Report(mixed/central venous)

• pH = 7.32-7.42• PvCO2 = 40 - 50 (mm Hg)

• PvO2 = 36 - 42 (mm Hg)

• Oxygen Saturation > 70%• Base Excess = -2 to +2

ANALYSIS OF VENTILATON

• PaCO2 = VCO2 x K

VA

Hypercapnea > 45 mm Hg (Hypoventilation) Respiratory Acidosis

Hypocapnea < 35 mm Hg (Hyperventilation) Respiratory Alkalosis

Respiratory Acid-Base Status

• Respiratory Disturbances– CO2+H20 H2CO3 H+ + HCO3

– Acute changes:• Delta 10 mm Hg PaCO2, pH changes by 0.08• Chronic change: 40 + B.E

– Alveolar Ventilation• VA CO2 pH

• Respiratory Acidosis PaCO2 > 45• Respiratory Alkalosis PaCO2 < 35

BASE EXCESS(B.E.)

• 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)

Problem Solving 1. LOOK AT THE pH

– Whatever side of pH 7.4 is the primary disorder

2. Look at pH, PCO2 direction– Both decrease or increase, then metabolic– If move in opposite directions, respiratory

3. Respiration: acute or chronic?– Acute: 10 mm Hg / 0.08 change in pH– Chronic: 40+Base Excess

Arterial Draw:• pH = 7.28, PaCO2 = 34, HCO3 = 16

• Na = 153 Cl = 106 Total CO2 = 17

• Alb = 3 g/dL, Saturation = 84%• Primary Acid-Base Disturbance?• Metabolic Acid-Base Status?

74 yo male found unresponsive and pulseless

• Primary Disorder– Acidosis and acidemia (pH < 7.4)

• pH and PCO2 direction– Both down: Metabolic Acidosis

• Base Excess– 16 – 24 = -8 mmols/L

Venous Draw

• pH = 7.08, pCO2 = 75, HCO3 = 21• Na = 145, Cl = 103, Total CO2 =22

• Alb = 3 g/dL, Saturation = 20%• Primary Acid-Base Disorder?• Metabolic Acid-Base Status?

• Primary Disorder– pH < 7.4, acidosis and acidemia

• pH and PCO2 direction– Opposite therefore RESPIRATORY

acidosis• Base Excess

–22 – 24 = -2 mmol/L

74 yo male found unresponsive and pulseless

• Why a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?– Venous arterial PCO2 difference?– PvCO2 (75) - PaCO2 (34) = 41– PvCO2 – PaCO2 1 / cardiac index– Normal ≤ 6 mm Hg

• Venous vs Arterial saturation difference?– PaO2 = 50 mm Hg, saturation = 84%– PvO2 =18, Venous Saturation = 20%– Increased oxygen extraction from circulatory

failure

PaO2 vs PvO2 in Cardiogenic Shock

Arterial Venous Saturation Difference

SHOCK

Paradoxical Respiratory Acidosis of Cardiopulmonary Arrest

Venous Arterial CO2 Difference

Fick Equation for oxygen consumption (VO2)

• VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)

• VO2 = 1.34*Hgn*10* C.O.* (SaO2 –SvO2)

– A decrement in C.O. must be accompanied by an increase in the arteriovenous difference at constant oxygen consumption

Fick Equation for CO2 production

• VCO2 =Carbon dioxide production (200 mL/min)

• VCO2 = 10*C.O.*(PvCO2 – PaCO2)

• If cardiac output decreases and VCO2 remains constant, what must happen to venous-arterial CO2 difference?

• VCO2 = 10* C.O.* (PvCO2 – PaCO2)– A decrement in C.O. must accompany an increase

in venous-arterial CO2 difference at a constant VCO2.

Conclusion: Venoarterial PCO2 differences… from pulmonary artery and central venous circulations inversely correlate with cardiac index. Substitution of a central for a mixed venous PCO2 difference provides an accurate and alternative method for calculation of cardiac output

Mixed Venous Arterial PCO2 Gradient

Central Venous-Arterial PCO2 Gradient

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.

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.

Venous Arterial CO2 Difference

• Circulatory Failure– Associated with Tissue Hypercarbic

Acidosis– Hypovolemia, sepsis, shock …

• Cardiac Index = e (1.787 – 0.151(v-a CO2))

– Endpoint of Resuscitation

74 yo male found unresponsive and pulseless

• Why a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?– Venous arterial PCO2 difference?– PvCO2 (75) - PaCO2 (34) = 41– PvCO2 – PaCO2 1 / cardiac index– Normal ≤ 6 mm Hg

• Venous vs Arterial saturation difference?– PaO2 = 50 mm Hg, saturation = 84%– PvO2 =18, Venous Saturation = 20%– Increased oxygen extraction from circulatory

failure

PaO2 vs PvO2 in Cardiogenic Shock

Arterial Venous Saturation Difference

SHOCK

VO2 or Oxygen Consumption

• VO2 = Arterial O2 delivery – Venous O2 delivery

• The difference represents the amount of oxygen consumed by the tissues

• Normal = 250 mL/min or 5 mL/100 mL blood

• Oxygen Utilization Coefficient = 0.25 – SaO2 – SvO2 25%

Fick Equation for Oxygen Consumption

• VO2= Oxygen Consumption (250 mL/min)

• VO2 = 10*C.O.*(CaO2 –CvO2)

• VO2 = 10 * C.O. * (1.34*Hgn*SaO2 -1.34*Hgn*SvO2)

• VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)

• Solve for SvO2? Or the mixed venous saturation?

Four Determinants of Mixed Venous Oximetry

SvO2 = SaO2 - (VO2 / C.O. x Hgn x 1.34)

SvO2 = Mixed venous saturation (%)

SaO2 = Arterial oxygen saturation (%)

VO2 = Oxygen consumption mL (O2/min)

Hgn = Hemoglobin concentration (g/dL)Cardiac Output (C.O.) = dL/min

Mixed Venous Saturation

• Percentage of hemoglobin saturated with oxygen in mixed venous blood

• Flow weight average of the venous saturations from all perfused vascular beds

• Four Determinants:– SaO2, VO2, Cardiac Output, and Hgn

• Physiologic oxygen reserve in times of stress

Why measure SvO2?

• A decrease in SvO2 is an early indicator of a threat to tissue oxygenation

• Earlier information results in earlier diagnosis with interventions

• Normal range of SvO2 = 60-80%

Master Equation

ScvO2 SvO2 = SaO2 - (VO2 / C.O. x Hgn x 1.34)

• Acute Illness or Post-op Surgery– SaO2, VO2, Cardiac Output, and Hgn are

dynamically changing concurrently– Optimize each parameter then recheck ScvO2

to assess response to intervention

Effect of changes in PaO2 on SvO2

600200

10080

60

40

0

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0 100 200 300 400 500 600 700

PaO2 (mm Hg)

SvO

2

SvO2

Effect of changes in Hgn on SvO2

13

10

7.5

5

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Hemoglobin (g/dL)

Sv

O2

SvO2

The Effects of Cardiac Output on SvO2

0.870.83

0.73

0.66

0.55

0.31

0

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Cardiac Output (L/min)

Sv

O2

SvO2

Effect of Oxygen Consumption (VO2) on SvO2

0.850.79

0.74

0.68

0.57

0.46

0

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0.2

0.3

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0 100 200 300 400 500 600

Oxygen Consumption (VO2)

Sv

O2

SvO2

Central Venous Oxygen Saturation ScvO2

• Allows separation of early and late shock• Easily measured with venous blood gas• Surrogate measurement of mixed venous

oxygen sat.– 5-18% higher– A low ScvO2 always means a low SvO2!

• Normal ScvO2 68-76%

– 25% extraction coefficient of normal physiology

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).

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).

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)

SEPTIC SHOCK PRESENTSBP ≤ 90 mmHg or MAP ≤ 65 mmHg

ORLactate ≥ 4 mmol/L

PLUSClinical Picture c/w Infection

Fluid bolus 20 ml/kg(.9 NaCl or LR)

PLUSVasopressors if MAP is

judged to be critically low

SBP < 90 mmHg, orMAP < 65 mmHg, orLactate > 4 mmol/L

CVP < 8 mmHg

Insert CVP

Catheter

Boluses crystalloid or colloid equivalent

until CVP > 8 mmHg

CheckMAP

Assess

ScvO2

Achieve ALL

Goals?

< 70%

Dobutamine or RBCs depending

on HCT

MAP ≥ 65

Resuscitation complete. Establish re-

evaluation intervals.

YES

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)

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.

Summary

• Simultaneous ABG and VBG– Initial O2 delivery and consumption state

– Serial measurements adequacy of interventions

• ABG– Oxygenation via Alveolar Gas Equation– Ventilation by PaCO2

– Acid Base Status by pH, PCO2, HCO3, SBE

• VBG (mixed or central)– Oxygen extraction ratio– ScvO2 or SvO2

– Veno-arterial CO2 difference for cardiac output

• 65 year old man presents to the ER in Shock

– BP 60/30, HR 150 bpm– Paleness– Cool Skin– Dilated Pupils– Semi comatose state– Low Urine Output

Two Possible Causes of the Low Blood Pressure were Considered

• Cardiogenic Shock• Hemorrhagic Shock

Match the ABG VBG with the Associated Condition

(a) pH = 7.25, PCO2 = 30, PaO2 = 75, saturation = 97%, BE = -15, LA = -15(v) pH = 7.20, PCO2 = 36, PvO2 = 25, venous saturation = 45%

(a) pH = 7.30, PCO2 = 25, PaO2 50, BE = -10, saturation = 85% LA = -10(v) pH = 7.20, PCO2 = 50, PvO2 = 25, venous saturation = 45%

Hemorrhagic Shock

Cardiogenic Shock

Additional References

• http://www.slideshare.net/edofiron• Chest 2005;128:554s-560s• Intensive Care Medicine 2004; 30:2170-2179• Crit Care Med 2003; 31:S658-S667• Current Opinion Critical Care 2001; 7: 204-211• Critical Care Medicine 2002; 30: 1686-1692• Circulation 1969; 40: 165• Thorax 2002; 57: 170-177• Academic Emer Med 1999; 6: 421