Gas Exchange Flashcards by Jill Klausner

Normal values for flow (uptake)

Resting:

Vdot CO2 = 0.2 L/min

Vdot O2 = 0.25 L/min

R = 0.8

Maximal Exercise:

Vdot CO2 = 5.6 L/min (28X)

V dot O2 = 4 L/min (16X)

R = 1.2

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Gas Laws

Boyle’s Law: P1V1 = P2V2

Charles’ Law: V1/T1 = V2/T2

Universal gas law: PV = nRT

Dalton’s law: total pressure of a gas is sum of partial pressures of each gas

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Normal partial pressures of gas in atmosphere

N2 = 79% = mmHg

O2 = 21% = 100 mmHg

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Normal partial pressure of gas in human lung

N2 = 79% = 573 mmHg

CO2 = 5% = 40 mmHg

O2 = 16% = 100 mmHg

H2O = 47 mmHg

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ATPS, BTPS and STPD

ATPS: ambient temperature and pressure, saturated; saturation with water vapor

BTPS: body temperature and pressure, saturated; saturation with water vapor (used for lungs!)

STPD: standard temperature and pressure, dry; no water vapor

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Equation to get flow (Vdot) from volume

Vdot = Volume x f_R

Vdot = Volume x rate (breaths per minute)

(Normal total minute ventilation Vdot E = 8-12 L/min)

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What is anatomical dead space?

Volume of conducting airways (gas exchange does not occur here)

(trachea, bronchi, etc)

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What is alveolar dead space?

When you have an alveolus that is not perfused, so doesn’t contribute to gas exchange (has a capillary next to it but the capillary has no blood)

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What is physiological dead space?

Anatomical dead space + alveolar dead space

Total volume of lungs that does not participate in gas exhcange

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What happens to alveolar ventilation if you have rapid, shallow breathing?

At given level of total minute ventilation, you’ll have less alveolar ventilation if you have rapid shallow breathing

This is because your dead space ventilation increases

Air stays in your alveoli and you’re “ventilating” the trachea, bronchi, terminal bronchioles, places where gas exchange can’t occur –> more wasted ventilation

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Respiratory exchange ratio (R)

R = VCO2/VO2 = 200/250 = 0.8

Note: more O2 uptake than CO2 blown off

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Alveolar ventilation (V_A dot)

V_A dot = V_E dot - V_D dot

Alveolar minute ventilation: volume of air per minute moving in and out of the alveolar compartment

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Equation for physiological dead space

V_{D(physiological)} = V_T x (P_aCO2 - P_EbarCO2)/P_aCO2

CO2 concentration breathed out into bag is less than partial pressure of CO2 in arterial circulation due to the dilution of exhaled air by the physiological dead space air

Dead space volume is 25-33% of tidal volume at rest, 10-20% during exercise and 45-50% in obstructive diesease or pulmonary vascular occlusive disease

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Equation for partial pressure of O2 in alveoli using alveolar ventilation

P_AO2 = P_IO2 - (863 x VdotO2)/VdotA

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Normal alveolar ventilation

VdotA = 4 L/min

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Hyperpnea and hypopnea

Increase or decrease in ventilation

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Apnea, tachypnea and bradypnea

No breathing, rapid (often shallow), slow breathing

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Hyperventilation and hypoventilation

Hyperventilation: Increase in ventilation out of proportion to any increase in metabolic CO2 production/flow, and therefore causes low arterial PCO2

Hypoventilation: Decrease in ventilation out of proportion to any decrease in metabolic CO2 production/flow, and therefore causes high arterial PCO2

Alveolar hypoventilation

Leads to hypoxemia and hypercapnia (too much CO2 in blood)

Seen in diseases that affect medullary respiratory center, respiratory neuromuscular function, severe obstructive or restrictive pulmonary disease

3 things that govern diffusion according to Fick’s law

1) Partial pressure gradient
2) Diffusion coefficient
3) Geometry of the interface (amount of surface area)

Diffusion of O2 and CO2 within the alveolus and across the alveolar capillary membrane

Within alveolus: O2 diffuses 18% faster than CO2 because 2 has smaller MW (diffusion is inversely proportional fo square root of MW = Graham’s Law)

Across alveolar-capillary membrane: for getting into alveoli from blood, CO2 is 19 times more diffusible than O2 in liquid phase because CO2 is way more soluble (Henry’s Law: VO2/Vol Plasma = PO2 x alpha)

Normal gas tensions

Mixed venous blood (coming into lung): PO2 = 40; PCO2 = 46

Alveolar = arterial: PO2 = 100; PCO2 = 40

Time for complete diffusion of O2 and CO2 across alveolar-capillary membrane

CO2 goes from pulm capillary to alveoli and takes <0.1 sec for Alveolar CO2 to equal arterial CO2 (as a result can set PaCO2 = PACO2)

O2 goes from alveoli to pulmonary capillaries and takes 0.33 sec for arterial O2 to approximately equal Alveolar O2 (but Alveolar O2 always 1 mmHg higher than arterial O2 due to diffusion, and 9 mmHg higher because of venous admixture)

Factors causing diffusion impairment

1) Decreased pulmonary capillary transit time (exercise)
2) Increased diffusion path length (alveolar proteinosis, pulmonary edema, interstitial inflammation or fibrosis, pneumocystis carinii pneumonia)
3) Reduction of functioning pulmonary capillary bed (pulmonary embolism, emphysema, pulmonary vascular disease)
4) Reduced alveolar PO2 (high altitude)

What can cause reduced PO2?

High altitude Hypoxic gas mixture given to patient Alveolar hypoventilation

Can diffusion impairment affect PCO2?

NO, mostly just O2! Because any change in PaCO2 is corrected by ventilatory control mechanisms

Hypercapnia

CO2 retention PaCO2 greater than normal (greater than 40 mmHg)

Hypoxemia

PaO2 less than normal (less than 90-100 mmHg)

Oxygen content

Total amount of oxygen carried in the blood 1) Dissolved in solution (very little) 2) Attached to hemoglobin (a lot) C_aO2 or C_vbarO2 Same thing for CO2 content

How do you measure diffusing capacity of the lung?

Hard to measure PO2, so we use CO. Inhale 0.3% CO, hold for 10 sec --\> CO diffuses into capillaries --\> measure concentration of CO inhaled then exhaled to get "diffusing capacity of lung for CO"

Factors that increase or decrease diffusing capacity of the lung

Increase: body size (SA, Vc), lung volume (SA), exercise, supine (Vc) Decrease: age, anemia (theta, Vc), diffusion impairment, resection (SA)

O2 saturation (SO2)

Percentage of Hb-O2 capacity occupied with O2 Normal arterial blood: 97% Hypoxic arterial blood: 90% Mixed venous blood: 75%

Right shift of Hb-O2 dissociation curve

Increase delivery of O2 to tissue; let go of O2 easier 1) Increased temperature (exercise) 2) Increased 2,3-DPG 3) Increased PCO2 and increased [H+] (more acidic)

Left shift of Hb-O2 dissociation curve

Decreased delivery of O2 to tissure; hold on to O2 better 1) Decreased temperature 2) Decreased 2,3-DPG 3) Decreased PCO2 and decreased [H+] (more basic)

Normal hemoglobin concentration in blood

[Hb] = 15 g/100mL Note: 15 g/100mL x 1/34 mL O2/g Hb = 201 mL O2/L = O2 capacity at normal hemoglobin concentration

How do anemia and carbon monoxide poisoning affect O2 content of the blood?

Anemia: lower [Hb] means less O2 content in blood CO poisoning: CO binds to Hb molecule and actually increases affinity of Hb for O2 so it binds O2 but doesn't let it go so no O2 gets to tissues (left shift); have normal PO2 but very low O2 content of blood (bc CO binds Hb instead of O2)

Where is CO2 during transport?

5% dissolved CO2 in plasma 90% HCO3- in plasma 5% bound to amino groups of hemoglobin

What is the Cl- shift (Hamburger shift)?

HCO3- is produced in the RBC and has to get back out to plasma. HCO3- is exchanged for bringing Cl- into the cell (to maintain electroneutrality)

When does the amino group of hemoglobin bind CO2 best? (Haldane effect)

Amino group of Hb binds CO2 best when O2 is NOT bound Deoxygenated hemoglobin binds CO2 best, and so deoxygenated blood can carry more CO2 than oxygenated blood Haldane effect Facilitates loading and unloading of CO2

Bohr effect

Effect of PCO2 and pH on the Hb-O2 dissociation curve Low PCO2 and low [H+] mean higher affinity for O2 = arterial blood coming from lungs High PCO2 and high [H+] mean lower affinity for O2 = mixed venous blood in tissues (tissue have higher [H+] because of metabolism) Ability to give up O2 in tissues and bind O2 avidly in the lungs

Alveolar Gas Equation

P_AO2 = P_IO2 - P_ACO2/R

How does alveolar ventilation (Vdot A) depend on metabolic rate of O2 and CO2 (Vdot O2 and Vdot CO2) and partial pressures in alveoli (PAO2 and PACO2)?

Vdot A directly proportional to metabolic rate: if CO2 produced or O2 needed more, will increase ventilation Vdot A inversely proportional to alveolar partial pressure of O2 and CO2: if alveolar pressure of CO2 is high, won't be able to push as much out (but explanation for O2..?)

Alveolar ventilation equation

PaCO2 = 863 x (VdotCO2/VdotA)