Chapter 22: Respiratory System
Chapter 22: Respiratory System (Part 2) - BIOL 2402 Lecture #12
Gas Exchange in the Respiratory System
Gas Exchange Locations
Occurs between lungs and blood, as well as between blood and tissues.
External Respiration: Diffusion of gases between blood and lungs.
Internal Respiration: Diffusion of gases between blood and tissues.
Both processes are impacted by:
Basic properties of gases.
Composition of alveolar gas.
Composition of Alveolar Gas
Partial Pressure: The pressure exerted by each gas in a mixture, directly proportional to its percentage in the mixture.
Unique Alveolar Composition:
Alveoli contain more CO2 and water vapor than atmospheric air due to:
Gas exchanges in the lungs (O2 diffuses out, CO2 diffuses in).
Humidity in conducting passages.
Table 22.4: Comparison of gas partial pressures and approximate percentages in the atmosphere and in the alveoli.
External Respiration: Mechanisms
Definition: Involves the exchange of O2 and CO2 across respiratory membranes.
Influencing Factors:
Partial Pressure Gradients and Gas Solubilities:
Steep gradient for O2 between blood and lungs (
Venous blood PO2 = 40 mm Hg
Alveolar PO2 = 104 mm Hg).
Less steep gradient for CO2:
Venous blood PCO2 = 45 mm Hg
Alveolar PCO2 = 40 mm Hg.
Reason for CO2 equal diffusion: CO2 is 20 times more soluble in plasma and alveolar fluid than O2.
Thickness and Surface Area of Respiratory Membrane:
Respiratory membranes are thin, approximately 0.5 to 1 µm thick.
Total surface area of alveoli is 40 times greater than that of the skin.
Ventilation-Perfusion Coupling:
Definitions:
Perfusion: Blood flow reaching alveoli.
Ventilation: Amount of gas reaching alveoli.
Both ventilation and perfusion must be ideally matched for efficient gas exchange, controlled by local auto-regulatory mechanisms.
PO2 controls perfusion by changing arteriolar diameter; PCO2 controls ventilation by changing bronchiolar diameter.
Influences of Local Conditions:
Changes in PO2 in alveoli lead to changes in arteriolar diameters.
High Alveolar O2: Arterioles dilate (increased blood flow).
Low Alveolar O2: Arterioles constrict (decreased blood flow).
Changes in PCO2 in alveoli lead to changes in bronchiolar diameters.
High Alveolar CO2: Bronchioles dilate (increased gas exchange).
Low Alveolar CO2: Bronchioles constrict.
Internal Respiration
Definition: Capillary gas exchange in body tissues.
Comparison to External Respiration:
Partial pressures/reversal:
Tissue PO2 is lower than arterial blood PO2 (40 vs. 100 mm Hg).
Tissue PCO2 is higher than arterial blood PCO2 (45 vs. 40 mm Hg).
Venous blood returning to the heart has:
PO2 of 40 mm Hg
PCO2 of 45 mm Hg.
Oxygen Transport
Transportation Forms:
1.5% dissolved in plasma.
98.5% bound to iron in hemoglobin (Hb) in red blood cells (RBCs).
Each hemoglobin (Hb) molecule can transport up to four O2 molecules, through its iron-containing heme groups.
Oxyhemoglobin (HbO2): Hemoglobin-O2 combination.
Reduced Hemoglobin (deoxyhemoglobin, HHb): Hemoglobin that has released O2.
Saturation States:
Fully saturated: All four heme groups carry O2.
Partially saturated: One to three heme groups carry O2.
Factors Influencing Hb Saturation
Influential factors include:
PO2
Temperature
Blood pH
PCO2
Oxygen-Hemoglobin Dissociation Curve
Graph illustrating the relationship between PO2 and percentage saturation of hemoglobin.
At high PO2 (100 mm Hg), Hb is ~98% saturated.
At low PO2 (40 mm Hg), Hb is ~75% saturated.
Shape of the curve is S-shaped, indicating varying O2 binding strength at different saturation levels.
At high PO2, big changes in O2 levels cause only small changes in Hb saturation.
At low PO2, small changes in O2 levels lead to big changes in Hb saturation.
Bohr Effect in Hb
Increase in temperature, H+, and PCO2 modify the structure of Hb, decreasing its affinity for O2, enhancing O2 unloading in systemic capillaries.
Declining blood pH (acidosis) or increasing PCO2 results in weaking of the Hb-O2 bond, facilitating O2 unloading where it’s most needed due to metabolizing cells.
Carbon Dioxide Transport
CO2 is transported in three forms:
7-10% dissolved in plasma as PCO2.
20% bound to globin part of hemoglobin (carbaminohemoglobin).
70% as bicarbonate ions (HCO3–) in plasma.
Formation of bicarbonate results from CO2 combining with water to form quickly dissociable carbonic acid (H2CO3).
Mechanism of Bicarbonate Transport
Reaction catalyzed by enzyme carbonic anhydrase in RBCs.
HCO3– diffuses into plasma from RBCs, balanced by Cl– moving into RBCs (chloride shift).
Influence of CO2 on Blood pH
Carbonic Acid-Bicarbonate Buffer System:
Helps maintain blood pH.
When H+ concentration rises, excess H+ combines with HCO3– forming H2CO3, which dissociates into CO2 and H2O.
When H+ concentration decreases, H2CO3 dissociates, releasing H+.
HCO3– acts as an alkaline reserve of the buffer system.
Control of Respiration
Regulatory Mechanisms:
Higher brain centers, chemoreceptors, and reflexes regulate respiratory rhythms.
Neural Control:
Involves neurons in the medullary and pontine respiratory centers of the brainstem.
Medullary Respiratory Centers:
Ventral Respiratory Group (VRG): Sets eupnea (normal rate/rhythm 12-15 breaths/min).
Dorsal Respiratory Group (DRG): Integrates input from stretch and chemoreceptors, sending info to VRG.
Pontine Respiratory Centers:
Smoothing out transitions between inspiration and expiration based on demands such as vocalization, sleep, or exercise.
Factors Influencing Breathing Rate and Depth
Breathing Depth Determinants:
Activity level of respiratory centers stimulating respiratory muscles.
Greater stimulation leads to more excited motor units, increasing depth of inspiration.
Breathing Rate Determinants:
Duration of respiratory center activity.
Modifiers include:
Chemical factors (levels of PCO2, PO2, pH).
Influence from higher brain centers.
Pulmonary irritant reflexes.
Inflation reflex.
Adjustments During Exercise
Hyperpnea: Increased ventilation (up to 10-20 times normal) in response to metabolic needs.
Ventilation increases abruptly and then gradually stabilizes; when exercise stops, there is a slight abrupt decline followed by a gradual decrease.
PCO2, PO2, and pH levels remain constant.
Adjustments to High Altitude
Quick ascent to altitudes above 2400 meters may cause Acute Mountain Sickness (AMS) due to lower atmospheric pressure and PO2.
Symptoms include headaches, shortness of breath, nausea, dizziness.
Acclimatization Mechanisms:
Long-term adaptation leads to lower than normal Hb saturation due to reduced O2 availability.
Declined blood O2 levels stimulate increased RBC production via EPO.
Chronic Obstructive Pulmonary Disease (COPD)
Definition: Irreversible decrease in the ability to force air out of lungs, mainly due to chronic emphysema and chronic bronchitis.
Common features:
History of smoking in 80% of patients.
Symptoms of dyspnea (labored breathing), coughing, frequent pulmonary infections, hypoventilation.
Accompanied by respiratory acidosis and hypoxemia.
Types of COPD
Emphysema:
Permanent enlargement of alveoli leading to lung elasticity loss, requiring accessory muscles for breathing and causing hyperinflation and flattened diaphragm.
Chronic Bronchitis:
Inhaled irritants create excessive mucus in inflamed/ fibrosed mucosa of lower respiratory pathways, impairing lung ventilation and gas exchange.
Asthma
Characterized as a condition with coughing, dyspnea, wheezing, and chest tightness.
Involves an immune response causing active inflammation of airways.
Lung Cancer
Leading cause of cancer deaths in North America, with 90% related to smoking.
Main types:
Adenocarcinoma: ~40% of cases originating in peripheral lung areas, from bronchial glands.
Squamous Cell Carcinoma: 20-40% of cases arising in bronchial epithelium.
Small Cell Carcinoma: ~20% of cases with lymphocyte-like cells originating in primary bronchi with metastatic potential.