Physiology 1, Fall 2008, LPC

Chapter 18 – Gas Exchange & Transport

I – Diffusion & Solubility

General Scheme

O2 into blood in lungs, delivered to tissues
CO2 into blood in tissues, delivered to atmosphere in lungs

Diffusion in lungs depends on:

Partial pressure of gas (ex: PO2)
Temperature – higher temperature -> less solubility
Solubility – most important.

O2 has low solubility in H2O
CO2 more soluble in H2O than O2

II – Gas Exchange in the Lungs & Tissues

Gases flow from regions of higher partial pressure to regions of lower partial pressure (∆ pressure)

PO2 higher in alveoli than systemic venous blood in lungs, goes into blood
PO2 lower in tissues (used in metabolism) than blood, goes into tissues
PCO2 higher in tissues (generated in metabolism) than blood, goes into blood
PCO2 higher in blood than alveoli, goes into alveoli

Hypoxia = too little oxygen

Inadequate O2 reaching alveoli
Problem with O2 exchange between alveoli & pulmonary capillaries
Inadequate transport of O2 in blood

Hypercapnia = too much CO2

Low alveolar PO2 -> low O2 uptake at the lungs
Low O2 concentration in inspired air, usually because of high altitude
Lower-than-usual volumes of fresh air entering alveoli

fibrotic lung disease – thickened alveolar membrane -> loss of lung compliance

asthma – increased airway resistance decreases airway ventilation
overdose of drugs that depress CNS

Changes in alveolar membrane alter gas exchange

Requires diffusion across alveolar membrane cells and capillary endothelium

Pathology:

1. Decrease in amount of alveolar surface area for exchange

2. Increase in thickness of alveolar membrane or

3. Increase in diffusion distance between alveoli and blood

Emphysema - macrophages release enzymes that destroy elastic fibers of lung, induce apoptosis of cells, -> low elasticity, fewer & larger alveoli -> less surface area for gas exchange

Fibrotic lung disease – thick alveolar membrane -> slow diffusion

Pulmonary edema – fluid in interstitial space -> increased diffusion distance -> low O2 in low arterial PO2, PCO2 usually normal

III – Gas Transport in the Blood
OXYGEN
Most of O2 transported by blood is bound to hemoglobin (Hb)
O2 released from Hb in tissues

Amount of O2 that binds to Hb depends on:

Amount of O2 in plasma surrounding RBCs (previous heading in outline)
Number of (binding sites in) RBCs

Each Hb molecule has 4 iron molecules which bind 1 O2/iron
HbO2 binding reversible
The percent saturation of Hb refers to the percentage of available binding sites that are bound to O2. All binding sites occupied = 100% oxygenated or saturated with O2.

Hb dissociation curves show PO2 vs & O2 Hb saturation under different conditions

HbO2 binding depends on: PO2 surrounding RBC, form of Hb, metabolic activity (PCO2, pH, temperature), DPG concentration
Metabolically active tissues:

use O2, -> easier for O2 to dissociate from Hb
produce CO2, -> easier for O2 to dissociate from Hb
CO2 -> lower pH, -> easier for O2 to dissociate from Hb
more heat, -> easier for O2 to dissociate from Hb

increased 2, 3-DPG (enzyme produced under chronic hypoxia) - > easier for O2 to dissociate from Hb

CARBON DIOXIDE

Transport in blood

CO2 + H2O carbonic anhydrase>  H2CO3 -> H+ + HCO3- (70%)
CO2 + Hb -> HbCO2 (23%)
7% dissolved in venous blood

CO2 + H2O carbonic anhydrase >  H2CO3 -> H+ + HCO3-

Reaction is reversible & depends on relative concentrations of substrates

HCO3- leaves RBCs on antiport protein, = chloride shift = one Cl- enters RBC as HCO3- leaves to maintain RBC membrane neutrality.

HCO3- necessary in blood as buffer.

H+ binds to Hb. OK, unless elevated H+ (elevated CO2), then = respiratory acidosis

CO2 removal at the lungs

PCO2 in alveoli less than in plasma, above reactions reverse
Less CO2

-> less H+ on Hb & more in plasma
 -> Cl- back into RBCs -> HCO3- release
H+ + HCO3- -> H2O + CO2, CO2 free to leave plasma

IV – Regulation of Ventilation

Central Pattern Generator

Medulla automatically creates rhythmic cycles of inspiration & expiration, influenced continuously by sensory input from chemoreceptors for CO2, O2, and H+
Inspiratory neurons gradually increase stimulation, positive feedback loop -> smooth inspiration
Inspiratory neurons stop firing, respiratory muscles relax, elastic recoil of inspiratory muscles & elastic lung tissue

CO2 (pH) of cerebral spinal fluid most important chemical controller (via medulla) of ventilation

If CO2 (pH) levels chronically high, PO2 controls ventilation, can kill someone under PO2 control by administering too much O2

Decrease in PO2 detected in carotid bodies, increased signals to medulla to increase ventilation

CO2, H+ levels detected in carotid and aortic bodies send signals to central pattern generator. These close to baroreceptors involved in reflex control of blood pressure

Protective reflexes guard lungs

Cough if irritants enter airways
Reflex prevents overexpansion of lungs

Conscious & unconscious thought processes affect respiratory activities