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Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA [email protected] September 17, 2009

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Page 1: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Lawrence Martin, M.D.Clinical Professor of Medicine

Case Western Reserve University School of Medicine

Cleveland, OHIO [email protected]

September 17, 2009

Page 2: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Because your understanding the PaCO2 equation will:Save lives!Improve patient care!Help wean patients off the ventilator!Shorten length of stay!

Page 3: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO2 2 Equation: PaCOEquation: PaCO22 reflects ratio of reflects ratio of metabolic COmetabolic CO22 production (VCO2) to production (VCO2) to alveolar ventilation (VA)alveolar ventilation (VA)

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation = f (tidal volume)VD = dead space ventilation = f (dead space

volume)0.863 converts VCO2 and VA units to mm Hg

Condition State of

PaCO2 in blood alveolar ventilation

> 45 mm Hg Hypercapnia Hypoventilation

35 - 45 mm Hg Eucapnia Normal ventilation

< 35 mm Hg Hypocapnia Hyperventilation

Page 4: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO2 2 Equation: PaCOEquation: PaCO22 reflects ratio of metabolic reflects ratio of metabolic COCO22 production (VCO2) to alveolar ventilation (VA) production (VCO2) to alveolar ventilation (VA)

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation = f (tidal volume)VD = dead space ventilation = f (dead space

volume)0.863 converts VCO2 and VA units to mm Hg

Normal Resting

VCO2 = 200 ml/minute

f(tidal volume) = 12 (500 ml) = 6 l/min

f(dead space vol.) = 12 (150 ml) = 1.80 l/min

VA = 6 – 1.80 = 4.2 l/min

200 x 0.863

PaCO2 = ----------------- = 41 mm Hg

4.2

Page 5: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO2 2 Equation: PaCOEquation: PaCO22 reflects ratio of metabolic reflects ratio of metabolic COCO22 production (VCO2) to alveolar ventilation (VA) production (VCO2) to alveolar ventilation (VA)

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation = f (tidal volume)VD = dead space ventilation = f (dead space

volume)0.863 converts VCO2 and VA units to mm Hg

Rapid Breathing, normal tidal volume

VCO2 = 200 ml/minute

f(tidal volume) = 24 (500 ml) = 12 l/min

f(dead space vol.) = 24 (150 ml) = 3.60 l/min

VA = 12 – 3.60 = 8.4 l/min

200 x 0.863

PaCO2 = ----------------- = 20.5 mm Hg

8.4

Page 6: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO2 2 Equation: PaCOEquation: PaCO22 reflects ratio of metabolic reflects ratio of metabolic COCO22 production (VOC2) to alveolar ventilation (VA) production (VOC2) to alveolar ventilation (VA)

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation = f (tidal volume)VD = dead space ventilation = f (dead space

volume)0.863 converts VCO2 and VA units to mm Hg

Rapid Breathing, Shallow Tidal Volume

VCO2 = 200 ml/minute

f(tidal volume) = 20 (300 ml) = 6 l/min

f(dead space vol.) = 20 (150 ml) = 3.00 l/min

VA = 6 – 3 = 3 l/min

200 x 0.863

PaCO2 = ----------------- = 57.5 mm Hg

3

Page 7: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO2 2 Equation: PaCOEquation: PaCO22 reflects ratio of metabolic reflects ratio of metabolic COCO22 production (VCO2) to alveolar ventilation (VA) production (VCO2) to alveolar ventilation (VA)

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation = f (tidal volume)VD = dead space ventilation = f (dead space

volume)0.863 converts VCO2 and VA units to mm Hg

Rapid breathing, increased dead space (severe COPD)

VCO2 = 200 ml/minute

f(tidal volume) = 16 (500 ml) = 8 l/min

f(dead space vol.) = 16 (300 ml) = 4.80 l/min

VA = 8 – 4.8 = 3.2 l/min

200 x 0.863

PaCO2 = ----------------- = 54 mm Hg

3.2

Page 8: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Oxygenation Acid-Base

PAO2 = FIO2 (BP-47) – 1.2 (PCO2) HCO3 pH ~ ------------ PaCO2

PaO2

VCO2 x .863 PaCO2 = -------------------- VA where VA = VE -

VD

Note: PaCO2 is from ABGs. HCO3 is calculated from ABG measurement of pH and PaCO2 or measured in venous blood as part of electrolytes. When measured in venous blood it is variously labeled ‘bicarbonate’, ‘HCO3’ or ‘CO2’ (the latter NOT to be confused with PaCO2).

PaCO2 is the center of the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base balance.

Page 9: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Arterial blood – blood gases

Venous blood - BMP

Page 10: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCO2PaCO2

PaO2PaO2pHpH

HCO3HCO3SaO2SaO2

PaCO2 is the center of the blood gas universe. .

Page 11: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

You can’t learn this material from a lecture!!Review:www.lakesidepress.com/pulmonary/index-phys.html

index to web sites on pulmonary physiologywww.lakesidepress.com/ABGQuiz2009-Questions.htm

multiple-choice blood gas quizwww.lakesidepress.com/pulmonary/papers/eq/tablecontents.html

4 Most Important Equations in Clinical Practice

www.lakesidepress.com/pulmonary/ABG/MixedAB.htm

Diagnosing mixed acid-base disorderswww.lakesidepress.com/pulmonary/ABG/PO2.htm

PaO2, SaO2 & CaO2 – What’s the Difference?

Page 12: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Hypercapnia – PaCO2 > 45 mm HgHypercapnia – PaCO2 > 45 mm Hg

VCO2 x 0.863PaCO2 = ------------------

VA where VA = VE – VD

Hypercapnia is a serious respiratory problem. The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of metabolic CO2 production (VCO2).

Since alveolar ventilation (VA) equals minute ventilation (VE) minus dead space ventilation (VD), hypercapnia can arise from insufficient VE, increased VD, or a combination of both.

Page 13: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

VCO2 x 0.863

PaCO2 = ------------------ VA where VA =

VE – VD VA = f(tidal vol.)

– f(dead

space vol.)

Examples of inadequate VE leading to decreased VA and hypercapnia: sedative drug overdose; respiratory muscle paralysis; central hypoventilation

Examples of increased VD leading to decreased VA and hypercapnia: chronic obstructive pulmonary disease; severe restrictive lung disease (with shallow, rapid breathing)

HypercapniaHypercapnia (cont)

Page 14: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Dangers of HypercapniaDangers of Hypercapnia

Besides indicating a serious derangement in the respiratory system, elevated PaCO2 poses a threat for three reasons:

1) An elevated PaCO2 will lower the PAO2 (see Alveolar gas equation) and as a result will lower the PaO2.

2) An elevated PaCO2 will lower the pH (see Henderson-Hasselbalch equation) and as result lead to acidosis.

3) The higher the baseline PaCO2, the more it will rise for a given fall in alveolar ventilation, e.g., a given decrease in VA will raise the PaCO2 more when PaCO2 is 50 mm Hg than when it is 40 mm Hg.

Page 15: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Dangers of Hypercapnia – lowers PAO2 & PaO2Dangers of Hypercapnia – lowers PAO2 & PaO2

An elevated PaCO2 will lower the PAO2 and as a result will lower the PaO2

Alveolar Gas Equation determines the alveolar PO2 (PAO2). PAO2 is one of two main factors that determine PaO2. (The other is ventilation-perfusion relationships within in the lungs.)

PAO2 = FIO2 (BP-47) – 1.2 (PaCO2)

PaO2

Page 16: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Dangers of Hypercapnia – lowers PAO2 & PaO2Dangers of Hypercapnia – lowers PAO2 & PaO2

An elevated PaCO2 will lower the PAO2 and as a result will lower the PaO2

PAO2 = FIO2 (BP-47) – 1.2 (PaCO2) =.21 (760-47) – 1.2 (40) = 150 – 48 = 102

Assuming 10 mm (A-a) O2 difference, PaO2 = 92 mm Hg

PAO2 = FIO2 (BP-47) – 1.2 (PaCO2) =.21 (760-47) – 1.2 (60) = 150 – 72 = 78

Assuming 10 mm (A-a) O2 difference, PaO2 = 68 mm Hg

Page 17: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

An elevated PaCO2 will lower the pH, as predicted by the Henderson-Hasselbalch Equation.

HCO3

pH ~ ------------ PaCO2

Dangers of Hypercapnia – lowers the pHDangers of Hypercapnia – lowers the pH

Page 18: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

An elevated PaCO2 will lower the pH, as predicted by the Henderson-Hasselbalch Equation.

HCO3

pH ~ ------------ PaCO2

Dangers of Hypercapnia – lowers the pHDangers of Hypercapnia – lowers the pH

Normal

24 mEq/l7.40 ~ ------------ 40 mm Hg

Respiratory Acidosis

24 mEq/l7.23 ~ ------------ 60 mm Hg

Page 19: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Basic Metabolic Panel from venous blood (BMP)

Na+ 140 mEq/LK+ 4.0 mEq/LCl 95 mEq/LHCO3 35 mEq/LBUN 20 mg%Creatinine 1.1 mg%

HCO3 and PaCO2 are 2 of 3 components in the H-H equation:

What does HCO3 by itself reveal

about PaCO2?

HCO3

pH ~ ------------

PaCO2

Page 20: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Any venous HCO3 can reflect virtually any value of PaCO2. Shown here is venous HCO3 of 35 mEq/L , plotted on graph of H-H equation.

The range of possible PaCO2 values is below 20 to above 100.

Page 21: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Abbreviated H-H equation:

Knowing just one parameter doesn’t tell you the acid-base state; you need at least two of the three values in H-H equation!

HCO3

pH ~ ------------ PaCO2

Page 22: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

 Effect of 1 liter decreases in alveolar ventilation on PaCO2, when VCO2 = 200 ml/min

High PaCO2 increases the slope of change for any further decrease in VA

VCO2 x 0.863

PaCO2 = --------------- VA

A one-liter decrease in VA when PaCO2 is 40 mm Hg will increase PaCO2 to 52 mm Hg.

The next one-liter decrease in VA will increase PaCO2 to 75 mm Hg…

And the next 1 liter decrease in VA will increase PaCO2 to 133 mm Hg!

High PaCO2 is dangerous!

VA (l/min)

PaC

O2

Dangers of Hypercapnia – Dangers of Hypercapnia – less reserve if there is less reserve if there is further hypoventilationfurther hypoventilation

Page 23: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCO2 of 60 mm Hg is not ‘just 50% higher’ than 40mm Hg. A high PaCO2 also:

Lowers PaO2 at any given Bar. Press.PAO2 = PIO2 – 1.2(PaCO2)PAO2 > PaO2

Makes patient acidotic pH ~HCO3 PaCO2

Increases the slope of change for any further decrease in VA.

Graph of: VCO2 x 0.863

PaCO2 = ------------- VA

For VCO2 of 200 and 300 ml/min

VA (l/min)

PaC

O2

Dangers of Hypercapnia – summaryDangers of Hypercapnia – summary

Page 24: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

You cannot assess PaCO2 clinically – Why not?

50-year-old man with COPD:

respiratory rate 35/minute; agitatedBP 170/104 mm HgPulse 105/minuteGood breath sounds

Is he hyperventilating? Hypoventilating? No way to tell clinically.

At bedside can’t determine if PaCO2 high or low because:

VCO2

x 0.863PaCO2 = ------------------------

VA =

f(tidal vol. –

f(dead space vol.)

You don’t know:- VCO2- tidal volume- dead space volume

Page 25: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Case – 73 yo woman in hospital

Intern called to bedside at 11 pm because “she is agitated.” She was previously calm all day.

Respiratory rate 20 (mild tachypnea). Lungs clear. Intern assess “hypreventilation” and prescribes Valium to “calm her down.”

45 minutes later patient stops breathing, is emergently intubated.

(continued)

(continued)

Check of her lab work shows that 2 days earlier, on hospital admission, her venous HCO3 was 35 mEq/L (normal up to 29).

ERRORIntern didn’t think of hypoventilation in setting of

agitation. VCO2

PaCO2 =--------- VA = f(tidal vol.) – f(dead space vol.)

The only parameter known to intern was frequency of breathing (fast). Knowing just ‘f’, it is impossible to reliably gauge if patient is hyperventilating or hypoventilating. High HCO3 (not noted by intern) was certainly consistent with latter. Without check of ABG, Valium should not have been given!

Trying to assess PaCO2 clinically can lead to fatal or near fatal errors!

Page 26: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Hyperventilating? Hypoventilating?

Page 27: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Cannot reliably assess PaCO2 clinicallyThe ONLY clinical parameter

in PaCO2 equation is frequency of breathing!!!

There is nothing in PaCO2 equation about respiratory effort, mental status, body habitus, etc.

If all you know at bedside is resp. rate, you can’t possibly discern patient’s PaCO2!!

You cannot determine at bedside if patient’s PaCO2 is high or low.

PaCO2 is determined only by factors in the PaCO2 equation:

VCO2 x 0.863

PaCO2 = -------------------- VA = f(tidal vol.

– f(dead space vol.)

VCO2 = metabolic CO2 production/minVA = alveolar ventilationf = frequency of breathing0.863 converts units to mm Hg

Page 28: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

Oxygenation Acid-BaseHCO3

PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------PaCO2

PaO2

VCO2 x .863 PaCO2 = -------------------- VA where VA = VE =

VD =

f(VT) – f(VD)

PaCO2 is key to the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base.

Page 29: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO22 and Alveolar Ventilation: Test Your and Alveolar Ventilation: Test Your UnderstandingUnderstanding

1. What is the PaCO2 of a patient with respiratory rate 24/min, tidal volume 300 ml, dead space volume 150 ml, CO2

production 300 ml/min? The patient shows some evidence of respiratory distress.

.

Page 30: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO22 and Alveolar Ventilation: Test Your and Alveolar Ventilation: Test Your UnderstandingUnderstanding

1. What is the PaCO2 of a patient with respiratory rate 24/min, tidal volume 300 ml, dead space volume 150 ml, CO2

production 300 ml/min? The patient shows some evidence of respiratory distress.

.First, you must calculate the alveolar ventilation.

VE = 24 x 300 = 7.2 L/minVD = 24 x 150 = 3.6 L/min

VA = 3.6 L/min. Then 300 ml/min x .863 PaCO2 = -----------------------

3.6 L/min

PaCO2 = 71.9 mm Hg

Page 31: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

2. What is the PaCO2 of a patient with respiratory rate 10/min, tidal volume 600 ml, dead space volume 150 ml, CO2 production 200 ml/min? The patient shows some evidence of respiratory distress.

PaCOPaCO22 and Alveolar Ventilation: Test Your and Alveolar Ventilation: Test Your UnderstandingUnderstanding

Page 32: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

2. What is the PaCO2 of a patient with respiratory rate 10/min, tidal volume 600 ml, dead space volume 150 ml, CO2 production 200 ml/min? The patient shows some evidence of respiratory distress.

PaCOPaCO22 and Alveolar Ventilation: Test Your and Alveolar Ventilation: Test Your UnderstandingUnderstanding

VA = VE – VD

= 10(600) - 10(150) = 6 - 1.5 = 4.5 L/min

200 ml/min x .863 PaCO2 = ----------------------

= 38.4 mm Hg 4.5 L/min

Page 33: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO22 and Alveolar Ventilation: and Alveolar Ventilation: Test Your UnderstandingTest Your Understanding

3. A man with severe chronic obstructive pulmonary disease exercises on a treadmill at 3 miles/hr. His rate of CO2 production increases by 50% but he is unable to augment alveolar ventilation. If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min, what will be his exercise PaCO2?

Page 34: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

PaCOPaCO22 and Alveolar Ventilation: and Alveolar Ventilation: Test Your UnderstandingTest Your Understanding

3. A man with severe chronic obstructive pulmonary disease exercises on a treadmill at 3 miles/hr. His rate of CO2 production increases by 50% but he is unable to augment alveolar ventilation. If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min, what will be his exercise PaCO2?

Exercise increases metabolic CO2 production. People with a normal respiratory system are always able to augment alveolar ventilation to meet or exceed the amount of VA necessary to excrete any increase in CO2 production. As in this example, patients with severe COPD or other forms of chronic lung disease may not be able to increase their alveolar ventilation, resulting in an increase in PaCO2. This patient’s resting alveolar ventilation is

VCO2 x .863 200 ml/min x .863PaCO2 = --------------- VA = 4.32 L/min = -----------------------

VA 40 mm Hg

Since CO2 production increased by 50% and alveolar ventilation not at all, his exercise PaCO2 is

300 ml/min x .863-------------------------- = 59.9 mm Hg4.32 L/min

Page 35: Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine Cleveland, OHIO USA larry.martin@roadrunner.com

You can’t learn this material from a lecture!!Review:www.lakesidepress.com/pulmonary/index-phys.html

index to web sites on pulmonary physiologywww.lakesidepress.com/ABGQuiz2009-Questions.htm

multiple-choice blood gas quizwww.lakesidepress.com/pulmonary/papers/eq/

tablecontents.html

4 Most Important Equations in Clinical Practicewww.lakesidepress.com/pulmonary/ABG/MixedAB.htm

Diagnosing mixed acid-base disorderswww.lakesidepress.com/pulmonary/ABG/PO2.htm

PaO2, SaO2 & CaO2 – What’s the Difference?