Blood gas adventures at various altitudes

Friedrich Luft

Experimental and Clinical Research Center, Berlin-Buch

Mount Everest 8848 M

Any point in bird watching here?

Respiration is gas exchange: the process of

moving gas across membranes. Internal res-

piration: O2 to cells, CO2 away, CO2/O2 is R/Q=0.8

• Hypoxia: low tissue oxygen

– 1. Hypoxemic hypoxia (Hb not saturated; carrier)

– 2. Anemic hypoxia (1 g Hb carries 1.34 ml O2;

15 g Hb carries 20 ml O2 or 200 ml/L)

– 3. Circulatory hypoxia (stagnant, cardiogenic shock)

– 4. Histotoxic hypoxia (as in cyanide poisoning)

Hypoxia?

Carrying oxygen in the blood is not the same as hypoxia; rather it is

hypoxemia (low O2 in blood). Hypoxemia is what we clinically detect

in our measurements. The differential diagnosis is not the same.

- 1. Decreased barometric pressure (Reinhold

Messner)

- 2. Alveolar hypoventilation (not breathing)

- 3. True shunt as in anatomic shunt, intrapulmonary

fistula

- 4. A mismatch between ventilation and perfusion

at the alveolar level.

Hypoxemia?

QQ

V

35

31

Sea level 6000 M

Atmospheric

(760 mm Hg) Mouth 380

PO2 160 (21%) 79 (21%)

PN2 600 300

PCO2 <1 0.4

Alveolar air

PAO2 100 22

PAN2 572 271

PACO2 40 40

PAH2O 47 47

External and internal respiration

Prenzelberg (349 M) and 6000 M

Without hyperventilation

35

15

20 40 60 80 100 120

40

30

20

10

0

PaCO2 mm Hg

PaO2 mm Hg

Defense Zone

At altitude, when the PaO2 is <35 mm Hg, the PaCO2 is 10 mm Hg

6000 M

8000 M

The Himalayan goose has been sighted at 11 000 meters

No one knows exactly how he does it !!!

How do we measure the amount of gas in

the blood or tissue?

• Gas laws: P x V = nR x T (n moles, T °K, R constant [0.082 L/atm/mol/K°])

– P1 x V1 = P2 x V2 (Boyle)

– V1/T1 = V2/T2 (Charles)

– P1/T1 = P2/T2 (Guy-Lussac)

– Partial pressures, water in gas phase,

diffusion (Dalton), gas solubility (Henry)

PO2 160

PN2 600

PCO2 <1

PO2 160

PN2 600

PCO2 <1

1 g Hb carries 1.34 ml O2

15 g/dl Hb carries 1.34x15 = 20 ml O2

20 ml O2/100 ml blood (20 vol%)

Arterial O2 content 20 vol%

(Mixed) venous O2 content 15 vol%

O2 consumption 250 ml/min

CO = 5 L/min

O2 delivery = 1000 ml/min

Body O2 extraction 25%

Extraction

Heart 90%

Kidneys 50%

Skin 1%

etc

CaO2 = (1.34 x Hb x SaO2) + (0.003 x PaO2)

O2 200 ml/LO2 150 ml/L

Thank you Professor Fick

Würzburg ca. 1871

„Mixed“

Fick‘s Principle

CO (5 L/min) = 250 ml/min

CaO2 (200 ml/l) - CvO2 (150 ml/l)

CO (5 L/min) = 200 ml/min

CvCO2 (540 ml/l) - CaCO2 (500 ml/l)

PvCO2 PaCO2

CO2 elimination

RQ = 200 CO2/250 O2 = 0.8

Ventilation and perfusion: VA/Q relationship

lower lobes under ventilated and over perfused

Total VA/Q = 1

Pa

PLA

Pcwp Q=0

3. Pa > Pc > PA

2. Pa > PA > Pc

1. PA > Pa > Pc

PA

PA

PAZone

Zone

Zone

Zone 3 lies

under LA

„West“ Zones in a ventilated patient with a Swan-Gans catheter

VA/Q = 1 VA/Q = 0

VA/Q = ∞ VA/Q = 0

Ventilation/perfusion match and mismatch

O2CO2

O2CO2

O2CO2

V/Q

Ratio

1 (perfect unit)

<1

>1

Venous admixture

PaO2 PaCO2 n or

Dead space ventilation

PaO2 PaCO2

When dead

Space >50%

Asthma

Chronic bronchitis

Pulmonary edema

Pneumonia

Atelectasis

Capillaries „around“

PE

Dead space

increased:

Emphysema

Heart failure

Pulmonary

embolism

PEEP

Anatomic shunt and „patho“physiological shunt

COPD, asthma, pulmonary embolism, acute and chronic

heart failure, pneumonia are all VA/Q problems

CcO2

CaO2

CvO2

Qs = CcO2-CaO2

Qt CcO2-CvO2

Qt (total) = Qc + Qs (Qc = perfect, Qs = shunt)

Qc

Qs

Hb

O2O2

O2 O2

Hb

O2O2

O2

O2

Cell

Sat 100%Sat 75%

VO2 = Q x Hb x 13.4 x (SaO2 - SvO2)

Arterial saturationVenous saturation

28 40 100 28 40 100PO2 PO2

Oxygen demand

Hemoglobin-oxygen saturation curve

PaO2 60 mm Hg, Sat = 90%

Venous blood

Arterial blood

Nanga Parbat

2,3-Diphosphoglycerate binds with greater

affinity to deoxygenated hemoglobin, thus

enhancing the ability of RBCs to release

oxygen near tissues that need it most.

2,3-DPG is thus an allosteric effector.

Arterial oxygenation

• Hemoglobin-dissociation curve (Hb is a magnet for O2)

• Curve shifts to the right with: increased [H], increased PaCO2,

increased T, increased 2,3 DPG

• Curve shifts to the left with: decreased [H], decreased PaCO2,

decreased T, decreased 2,3 DPG

• Know the Pa50 (28 mm Hg at 50% Sat) and the mixed venous PvO2

(40 mm Hg at 75% Sat)

Shifted Hb-O2 curve to left Hb is more sticky,

Shifted Hb-O2 to right, Hb is less sticky,

left is good for lung, right is good for tissue

Dissolved O2 3%100

Christian Bohr and the Bohr effect

Blood O2 consumption 200 ml/L, 1000 ml/min

Hypoxemia is due to:

1. Decreased barometric pressure (Reinhold Messner)

2. Alveolar hypoventilation (not breathing)

3. True shunt as in anatomic shunt, intrapulmonary fistula,

capillary membrane (ARDS, rarely pulmonary fibrosis)

4. Shunt effect (VA/Q mismatch) This is most common

Hypoxemia review to this point: PaO2 problems

Va = alveolar volume, Vt = tidal volume,

Vd = deadspace volume

RR = respiratory rate, MV = minute ventilation

Normal MV 6 L

VA = 4 L

VD = 2 L

VA = VE (1-Vd/Vt)

VdAlveolar ventilation

and the PaCO2

Va

Vt

Minute ventilation

also called VE

(total) ventilation

Vt≈500 ml

Va Vd

The hyperbolic relationship between PaCO2 and

the alveolar ventilation.

You can now estimate the alveolar ventilation

from any PaCO2 value

More importantly, you now gain great

insights into pathophysiological mechanisms

relevant to gas and acid-base problems

(and also know more than most professors)

Please comprehend this!!!

Alveolar ventilation: PaCO2 problems

expressed anatomically or -

physiologically

• VE = VA + VD (alveolar ventilation + dead space ventilation)

• VA = k (CCO2 x total expired air)

PaCO2

• Clearance formula (ClCr = UCrV/PCr)

• Amount of blood „cleared“ of CO2 per min is ~ 4 L

• PaCO2 can increase from increased production, decreased alveolar ventilation, or increased dead space

Causes of alveolar hypoventilation

Respiratory center

Ventilatory motor nerves

Neuromuscular junction

Ventilatory muscles

Thoracic cage

Lungs

Airways, blood vessels, deadspace

VA/Q relationship

Coma

ALS

Myasthenia

Polio

Trauma

Bad COPD

pH 7.4

[H] 407.20

60

7.60

20

PaCO2 80 mm Hg

(respiratory)

HCO3 24 mmol/l

(metabolic)

Acute respiratory acidosis

This pan must change!!7.00

100

~0.3 mmol

per mm Hg

pH 7.4

[H] 407.20

60

7.60

20

PaCO2 80 mm Hg

(respiratory)

HCO3 37 mmol/l

(metabolic)

Chronic compensated respiratory acidosis

7.00

100

The alveolar gas equation:

and the A/a gradient

• PAO2 = PB-PH2O x (FiO2) - PaCO2/RQ

• PAO2 = 760-47 x (0.21) - (PaCO2/0.8)

• (760-47)x0.21=150

• 150 - (1.25xPaCO2)

• 150 - 50 = 100 mm Hg

• PAO2 = 150 - (1.25xPaCO2)

• A-a = 100 - PaO2 in mm Hg (< 10 mm Hg)

Dope addict, „found down“, T 34°C, BP 90/65 mm Hg,

HR 100 min, RR 4 min

• pH = 7.12

• PaCO2 = 80 mm Hg

• PaO2 = 29 mm Hg

• HCO3 = 22 mmol/L

• AG = 18

• Acid-base disturbance?

• Acute or chronic?

• Structural lung disease

present? (A-a gradient)

• Why the slight increase

in AG? Does the HCO3

fit for solely acute

respiratory acidosis?

• 150-(1.25x80)=50

63 year old chronically ill woman admitted at 17:00

on Friday with dx of pneumonia. Smoker, possible

chronic bronchitis. 48 hr dyspnea, fever, cough,

right sided chest pain on inspiration.

No cyanosis, skin warm and dry, Temp. 39o C,

rales bilat. Chest xray alveolar pattern in right

middle and lower lobes. WBC 17,500,

yellow sputum, Gram stain, + diplococci

Smoker with pneumonia

FIO2 0.21 BP 140/100

pH 7.51 P 126/min

PaCO2 28 mm Hg RR 36/min

PaO2 46 mm Hg Hb 7 g/dl

What is her HCO3?

What is her SaO2?

What is her A-a gradient?

Clinical information and blood gas slip

29 = 24x28 = 23.7

HCO3

PAO2 = 150 - (1.25xPaCO2)PAO2 = 150 – (1.25x28) = 150-35 = 115, A-a gradientIs 69 mm Hg. Apparently a major example of admixture

Questions about the last patient

• What is the O2 carrying capacity in the blood?

(Hb 7 g/dl; SaO2 80%)

• What is her cardiac output?

• What is the acid-base disturbance present here?

• What is internal and external respiration?

• What is the definition of respiratory failure and does

this patient have it?

• What is this patient´s alveolar ventilation?

• Where is this patient´s oxygen saturation curve?

• What should be done therapeutically for this patient?

0.8x1.34x7=7.5 ml/100 ml blood

High (we hope)

“Partial” respiratory insufficiency

40% increase

Left

Supplemental O2; address anemia

Chronic respiratory alkalosis; Alv. Vent. 16 L/Min

Blood gases above 8000 M

148 ml/L

SAT 52%

PO2 28

mm Hg

1657 Otto von Guericke

demonstrated the power

of atmospheric gases

Thank you!