Chapter 11 Gas Exchange & Transport Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

Chapter 11

Gas Exchange & Transport

Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

Learning Objectives

Describe how oxygen & carbon dioxide move between the atmosphere & tissues.

Identify what determines alveolar oxygen & carbon dioxide pressures.

Calculate the alveolar partial pressure of oxygen (PAO2) at any give barometric pressure & FIO2.

State the effect that normal regional variations in ventilation & perfusion have on gas exchange.

2Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

Learning Objectives (cont.)

Describe how to compute total oxygen contents for arterial blood.

State the factors that cause the arteriovenous oxygen content difference to change.

Identify the factors that affect oxygen loading & unloading from hemoglobin.

Describe how carbon dioxide is carried in the blood.


Learning Objectives (cont.)

Describe how oxygen & carbon dioxide transport are interrelated.

Describe the factors that impair oxygen delivery to the tissues & how to distinguish among them.

State the factors that impair carbon dioxide removal.


Introduction

Respiration: process of moving oxygen to tissues for aerobic metabolism & removal of carbon dioxide Involves gas exchange at lungs & tissues

• O2 from atmosphere to tissues for aerobic metabolism

• Removal of CO2 from tissues to atmosphere


Diffusion

Whole-body diffusion gradients Gas moves across system by simple diffusion Oxygen cascade moves from PO2 of 159 mm Hg

in atmosphere to intracellular PO2 of ~5 mm Hg CO2 gradient is reverse from intracellular CO2 ~60

mm Hg to atmosphere where it = 1 mm Hg


Diffusion (cont.)



There is a stepwise downward “cascade of partial pressures” from the normal atmospheric to the intracellular, for which of the following gases?

A.CO2

B.O2

C.N

D.H2O

Diffusion (cont.)

Determinants of alveolar CO2

PACO2 = (VCO2 0.863)/VA

PACO2 will increase with ↑VCO2 or ↓VA

The relationship is expressed by:

PACO2 = arterial carbon dioxide tension (mm Hg) VCO2 = rate of CO2 produced (in mL /min STPD)

VA = alveolar ventilation (mL /min BTPS)

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BTPS) (ml/min,

STPD) (ml/min,863 2

2A

COA

V

VP

CO

. .


Diffusion (cont.)

VCO2 is expressed as flow of dry gas at 0ºC & 760 mmHg

VA reported as saturated gas at body temperature ambient pressure

Factor 863 is employed to correct measurement


Diffusion (cont.) Increase in deadspace (VD) can also lead to

increased PACO2

Portion of inspired air that is exhaled without being exposed to perfused alveoli

VA = alveolar ventilation

VT = tidal volume

VD = dead space volume f = ventilatory frequency

..



All of the following can lead to an increased Paco2 , except:

A.↓ VD

B.↓ VA

C.↑ VCO2

D.↑ VD

Diffusion (cont.) Alveolar oxygen tensions (PAO2)

PIO2 is primary determinant

In lungs, it is diluted by water vapor & CO2

Alveolar air equation accounts for all these factors

PAO2 = FIO2 (PB – 47) – (PACO2/0.8)

Dalton’s law of partial pressures accounts for first part of formula; second part relates to rate at which CO2 enters lung compared to oxygen exiting

• Ratio is normally 0.8.

If FIO2 > 0.60, (PACO2/0.8) can be dropped from equation


Diffusion (cont.) Changes in alveolar gas partial tensions

O2, CO2, H2O, & N2 normally comprise alveolar gas

• N2 is inert but occupies space & exerts pressure

• PAN2 is determined by Dalton’s law

PAN2 = PB – (PAO2 + PACO2 + PH2O)

Only changes seen will be in O2 & CO2

• Constant FIO2, PAO2 varies inversely with PACO2

• Prime determinant of PACO2 is VA


Diffusion (cont.)


Diffusion: Mechanisms

Diffusion occurs along pressure gradients Barriers to diffusion

A/C membrane has 3 main barriers• Alveolar epithelium• Interstitial space & its structures• Capillary endothelium

RBC membrane Fick’s law: The greater the surface area,

diffusion constant, & pressure gradient, the more diffusion will occur


Diffusion (cont.)

Pulmonary diffusion gradients Diffusion occurs along pressure gradients Time limits to diffusion:

• Pulmonary blood is normally exposed to alveolar gas for 0.75 second, during exercise may fall 0.25 second

• Normally equilibration occurs in 0.25 second

• With diffusion limitation or blood exposure time of less then 0.25 seconds, there may be inadequate time for equilibration


Diffusion (cont.)


Normal Variations From Ideal Gas Exchange

PaO2 normally 5–1 mm Hg less than PAO2 due to presence of anatomic shunts

Anatomic shunts Portion of cardiac output that returns to left heart without being

oxygenated by exposure to ventilated alveoli Two right-to-left anatomic shunts exist

• Bronchial venous drainage• Thebesian venous drainage• These drain poorly oxygenated blood into arterial circulation

lowering CaO2

Regional inequalities in V/Q Changes in either V or Q affect gas tensions

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Which of the following choices accurately completes the statement, “anatomic shunts…”

A.are a portion of cardiac output that returns to left heart without being oxygenated

B.are exposed to ventilated alveoli

C.cause the PaO to be normally 10–20 mm Hg less than PAO2

D.are left-to-right shunts

Normal Variations From Ideal Gas Exchange (cont.)

V/Q ratio & regional differences Ideal ratio is 1, where V/Q is in perfect balance In reality lungs don’t function at ideal level

• High V/Q ratio at apices >1 V/Q (~3.3) ↑PAO2 (132 mm Hg), ↓PACO2 (32 mm Hg)

• Low V/Q ratio at bases <1.0 (~0.66) Blood flow is ~20 times higher at bases Ventilation is greater at bases but not 20 ↓PAO2 (89 mm Hg), ↑PACO2 (42 mm Hg)

• See Table 11-1

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Normal Variations From Ideal Gas Exchange (cont.)


Oxygen Transport Transported in 2 forms: dissolved & bound Physically dissolved in plasma

Gaseous oxygen enters blood & dissolves. Henry’s law allows calculation of amount dissolved

• Dissolved O2 (ml/dl) = PO2 0.003

Chemically bound to hemoglobin (Hb) Each gram of Hb can bind 1.34 ml of oxygen. [Hb g] 1.34 ml O2 provides capacity. 70 times more O2 transported bound than

dissolved


Oxygen Transport (cont.)

Hemoglobin saturation Saturation is % of Hb that is carrying oxygen

compared to total Hb• SaO2 = [HbO2/total Hb] 100• Normal SaO2 is 95% to 100%

HbO2 dissociation curve Relationship between PaO2 & SaO2 is S-shaped Flat portion occurs with SaO2 >90%

• Facilitates O2 loading at lungs even with low PaO2

Steep portion (SaO2 <90%) occurs in capillaries• Facilitates O2 unloading at tissues







Total oxygen content of blood Combination of dissolved & bound to Hb CaO2 = (0.003 PaO2) + (Hb 1.34 SaO2) Normal is 1620 mL/dL

Normal arteriovenous difference (~5 mL/dL)





Fick equation C(a v)O2 indicates tissue oxygen extraction in

proportion to blood flow (per 100 ml of blood) Combined with total oxygen consumption (VO2)

allows calculation of cardiac output (Qt)

Qt = VO2/[C(a v)O2 10]

Normal adult Qt is 48 L/min.

VO2 constant, changes in C(a v)O2 are due to changes in Qt; i.e., ↑C(a v)O2 signifies ↓Qt

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Factors affecting oxygen loading & unloading Besides shape of HbO2 curve, many factors affect O2

loading & unloading pH (Bohr effect)

Describes affect pH has on Hb affinity for O2

pH alters position of HbO2 curve• Low pH shifts curve to right, high pH shifts to left

Enhances oxygen transport• At tissue pH is ~7.37 shift right, more O2 unloaded

• Lungs pH ~7.4 shifts back left, enhancing O2 loading





Body temperature (T) & HbO2 curve Changes in T alter position of HbO2 curve

• Decreased T shifts curve left• Increased T shifts curve right• T is directly related to metabolic rate

When T is higher, right shift facilitates more oxygen unloading to meet metabolic demands

With lower metabolic demands, curve shifts left as not as much oxygen is required.





2,3-Diphosphoglycerate (DPG) & the HbO2 curve Found in quantity in RBCs; stabilizes

deoxygenated Hb, decreasing oxygen’s affinity for Hb

• Without 2,3-DPG Hb affinity is so great that O2 cannot unload

↑2,3-DPG shifts curve to right, promoting O2 unloading

↓2,3-DPG shifts curve to left, promoting loading• Stored blood loses 2,3-DPG, large transfusions can

significantly impair tissue oxygenation


Oxygen Transport (cont.) Abnormal hemoglobins

HbS (sickle cell): fragile leads to hemolysis & thrombi Acute chest syndrome (ACS), multiple causes

• Most common cause of death Methemoglobin (metHb): abnormal iron (Fe3+) cannot

bind with oxygen & alters HbO2 affinity (left shift)• Commonly caused by NO, nitroglycerin, lidocaine• Must frequently monitor for MetHb & weigh risk vs. benefit

Carboxyhemoglobin (HbCO): Hb binds CO, has 200 times > Hb affinity than O2

• Displaces O2 & shifts curve left O2 which is bound cannot unload (left shift) Treat with hyperbaric therapy



Measurement of Hb affinity for oxygen



A factor that does not significantly affect oxygen loading & loading is:

A.plasma oxygen content

B.pH

C.body temperature

D.the amount of 2,3-Diphosphoglycerate (DPG) in RBC’s

Carbon Dioxide Transport

Transport mechanisms Dissolved in blood: ~8% as high solubility coefficient Combined with protein: ~12% binds with amino

groups on plasma proteins & Hb Ionized as bicarbonate: ~80% transported as HCO3

due to hydrolysis reaction

• Majority of hydrolysis occurs in RBCs as they contain carbonic anhydrase—serves as catalyst

• HCO3 diffuses out of RBCs in exchange for Cl, called

chloride shift or hamburger phenomenon


Carbon Dioxide Transport (cont.)

CO2 dissociation curve Relationship between PaCO2 & CaCO2

HbO2 affects this relationship

• Haldane effect describes this relationship

• As HbO2 increases, CaCO2 decreases Facilitates CO2 unloading at lungs

• At tissues, HbO2 decreases & facilitates higher CaCO2 for transport to lungs






Abnormalities of Gas Exchange & Transport

Impaired oxygen delivery (DO2) DO2 = CaO2 Qt

When DO2 is inadequate, tissue hypoxia ensues

Hypoxemia: Defined as abnormally low PaO2

• Most common cause is V/Q mismatch Because of shape HbO2 curve, areas of high V/Q cannot

compensate for areas of low V/Q, so ↓PaO2

• Other causes: hypoventilation, diffusion defect, shunting, & low PIO2 (altitude)

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Abnormalities of Gas Exchange & Transport (cont.)



Physiologic shunt Where perfusion exceeds ventilation, includes:

• Capillary or absolute anatomic shunts

• Relative shunts seen in disease states diminish pulmonary ventilation

Relative shunts can be caused by:• COPD

• Restrictive disorders

• Any condition resulting in hypoventilation



Shunt equation Quantifies portion of blood included in V/Q

mismatch Usually expressed as % of total cardiac output:



Shunt Equation: Mixed venous oxygen content can be measured from

pulmonary artery End capillary content must be derived from additional

calculation • Using alveolar air equation & hemoglobin concentration

Deadspace Ventilation Ventilation that doesn’t participate in gas exchange

• Waste of energy to move gas into lungs Two types: alveolar & anatomic



Alveolar Deadspace: Ventilation that enters into alveoli without any, or

without adequate perfusion Disorders leading to alveolar deadspace :

Pulmonary emboli Partial obstruction of the pulmonary vasculature Destroyed pulmonary vasculature (as can occur in

COPD) Reduced cardiac output



Anatomic Deadspace: Ventilation that never reaches alveoli for gas exchange Normal individuals have fixed anatomic deadspace Becomes problematic in conditions where tidal volumes drop

significantly

• Significant % of inspired gas remains in anatomic deadspace

Expressed as ratio to total tidal volume



In face of increased deadspace, normal ventilation must increase to achieve homeostasis

Additional ventilation comes at cost: Increase in WOB Consumes additional oxygen Further adding to burden of external ventilation



Impaired DO2 due to Hb deficiencies Majority of O2 is carried bound to Hb For CaO2 to be adequate, there must be enough

normal Hb• If Hb is low:

although PaO2 & SaO2 are normal, CaO2 will be low

• Absolute low Hb is caused by anemia• Relative deficiency may be due to COHb or metHb





Oxygen delivery to the tissues (DO2) may be substantially impaired due to all of the following, except:

A.Low Hb levels (anemia)

B.V/Q matching

C.abnormal cardiac output

D.presence of Carboxyhemoglobin (COHb)




Reduction in blood flow (shock or ischemia) Hypoxia can occur with normal CaO2 if Qt is low

• May be due to: Shock

– Results in widespread hypoxia– Limited ability to compensate

Prolonged shock becomes irreversible Ischemia

– Local reductions in blood flow may result in hypoxia & tissue death, i.e., myocardial infarction & stroke



Dysoxia DO2 is normal but cells undergo hypoxia

Cells are unable to adequately utilize oxygen• Cyanide poisoning prevents cellular use of O2

• In very sick individuals (sepsis, ARDS), oxygen debt may occur at normal levels of DO2

If oxygen uptake increases with increased DO2, then DO2 was inadequate

Demonstrates low VO2/DO2 (extraction ratio), thus dysoxia



Impaired CO2 removal Disorders that decreases VA relative to metabolic

need• Inadequate VE

Usually result of ↓VT, ↓f rare (drug overdose)

• Increased deadspace ventilation (VD/VT) caused by: Decreased VT as in rapid shallow breathing or, Increased physiologic dead space, as in pulmonary embolus

• Without compensation, alveolar is lowered per minute

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V/Q imbalance• Typically, CO2 does not rise; instead, increase VE.

• If patient is unable to ↑VE, then hypercarbia with acidosis occurs

Seen in severe chronic disorders, i.e., COPD

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Chapter 11 Gas Exchange & Transport Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

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