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PHED 644 – Advanced Exercise Physiology II LECTURE 5 Ventilation & Respiration
Terminology :
Respiration --the process involved in supplying the body with oxygen and disposing of carbon dioxide
Involves four distinct processes:
- pulmonary ventilation : movement of air into and out of the lungs
- external respiration : gas exchange between the blood and air-filled chambers of the lungs
- transport of respiratory gases : transport of O 2 and CO 2 between the lungs and the tissue cells of the body
- internal respiration : gas exchanges between systemic blood and tissue cells
Lung Volumes and Capacities:
Tidal Volume (VT) --volume of gas moved during quiet breathing --500 ml
Inspiratory Reserve Volume (IRV) --volume of air that can be forcefully inhaled above a normal tidal volume inhalation --1900-3100 ml (female v. male)
Expiratory Reserve Volume (ERV) --volume of air that can be forcefully exhaled after a normal tidal volume exhalation --700-1200 ml
Residual Volume (RV) --volume of air remaining in the lungs after a forced exhalation --1100-1200 ml
Total Lung Capacity (TLC) --max. amount of air contained in lungs after a maximum inspiratory effort (TLC = IRV + VT + ERV + RV) --4200-6000 ml
Vital Capacity (VC) --maximum amount of air that can be expired after a maximal inspiratory effort (VC = IRV + VT + ERV) --3100-4800 ml (~80% TLC)
Inspiratory Capacity (IC) --maximum amount of air that can be inspired after normal expiration (IC = IRV + V (^) T) --2400-3600 ml
Functional Residual Capacity (FRC) --volume of air remaining in the lungs after a normal tidal volume expiration (FRC = ERV + RV) --1800-2400ml
Mechanics of Breathing (Pulmonary Ventilation):
Two Phases of Pulmonary Ventilation:
- inspiration ( movement of air into the lungs)
- expiration (movement of air out of the lungs)
Pressure Relationships in the Thoracic Cavity :
--respiratory pressures are always described relative to atmospheric pressure ( P atm) ~760 mmHg at sea level
--i.e., negative respiratory pressure indicates that pressure is below atmospheric pressure (-4 mmHg: 760 – 4 = 756 mm Hg); positive respiratory pressure indicates that pressure is above atmospheric pressure; and a respiratory pressure of 0 mmHg is equal to atmospheric pressure.
Intrapulmonary Pressure ( P alv) --pressure inside the alveoli of the lungs
Intrapleural Pressure ( P ip) --pressure within the pleural cavity
Intrapleural pressure is always negative relative to both P atm and P alv (~4 mmHg less). --forces in opposition: a. the tendency of the lungs to recoil b. surface tension of the alveolar fluid ( surfactant ) c. expansion of the chest wall
--pleural fluid secures the parietal and visceral pleura together (e.g., like a drop of water between two glass slides) ⇒ negative intrapleural pressure --to maintain this relationship, the level of pleural fluid must remain minimal (excessive fluid in the intrapleural space produces a condition of positive pressure in the pleural cavity – atelectasis , or lung collapse)
It is the transpulmonary pressure ( P alv – P ip ) that keeps the airspaces of the lungs open (or, from collapsing)
Airway Resistance --the major non-elastic source of resistance to gas flow is friction, or drag, encountered in the respiratory passageways.
Q = ∆P/R
NOTE: the factors determining gas flow in the respiratory passages and blood flow in the CV system are equivalent.
∆P = P (^) atm - P (^) alv
Normally, very small volume differences in pressure produce large changes in the volume of gas flow. The average pressure gradient during quiet breathing is 2 mm Hg or less, and yet it moves 500 ml of air in and out of the lungs with each breath.
Resistance in the respiratory tree is determined by the diameters of the conducting tubes. As a rule, airway resistance is insignificant because: a. the diameters of the airways of the initial part of the conducting zone are huge, relatively speaking. b. gas flow stops at the terminal bronchioles (where the airway diameters might start to become a problem) and diffusion takes over as the main driving force of gas movement.
Bronchiolar smooth muscle is, nevertheless, sensitive to neural and chemical influence. --chemical irritants and inflammatory chemicals (e.g., histamine) can cause bronchoconstriction, i.e., asthma attack --epinephrine dilates bronchioles and reduces airway resistance
Mucus, infectious material, and tumors are also sources of airway resistance.
Surface Tension
At any gas-liquid boundary, the molecules of the liquid are more strongly attracted to each other than to the gas. This unequal attraction produces a state of tension at the liquid surface.
Surfactant --a detergent-like lipoprotein produced by type II alveolar cells --interferes with the cohesiveness of the water molecules; as a result the surface tension of alveolar fluid is reduced ⇒ less energy is required to overcome these forces to expand the lungs and prevent alveolar collapse
Lung Compliance ( C L) --the ease to which lungs can be expanded (distensibility)
--a measure of the change in lung volume that occurs with a given transpulmonary pressure.
∆VL C (^) L = -------------------- ∆(P (^) alv – P (^) ip )
--The higher the lung compliance, the easier it is to expand the lungs at any given transpulmonary pressure.
Determined by:
- distensibility of the lung tissue and surrounding thoracic cage
- surface tension in the alveoli
Diminished by any factor that:
- reduces the natural resilience of the lungs, e.g. scar tissue
- blocks the smaller respiratory passages, e.g., mucus
- reduces the production of surfactant
- decreases the expandability of the thoracic cage, e.g., obesity, weak musculature, etc.
Alveolar Ventilation :
The total volume of air that flows into and out of the respiratory tract in one minute is referred to as total or minute ventilation (VE ).
VE = f · VT
Normal respiratory rates ( f ): adults: 12-18 breaths per minute children: 18-20 breaths per minute
Not all of the air that passes into the respiratory passages actually reaches the exchange surfaces. Of the 500 ml inhaled, ~150 ml remain in the anatomical dead space. Therefore, the volume of interest is the alveolar ventilation (the amount of air reaching the alveoli each minute).
VA = f · (VT – VD)
Anatomical v. Physiological Dead Space:
Anatomical dead space (measured using Fowler’s method –see text) is a measure of lung morphology –the volume of gas in the conducting airways down to the level where rapid dilution of inspired gas occurs with gas already in the lung.
Gas Exchange Between the Blood, Lungs, and Tissues
Pulmonary Gas Exchange (External Respiration):
The respiratory membrane is considered efficient for five reasons:
- The differences in partial pressures across the respiratory membrane are substantial.
- The distances involved with gas exchange are small (~0.5 μm).
- Gases are lipid soluble.
- The total surface area is large (~140 m 2 ).
- Blood flow (perfusion) and air flow (ventilation) are coordinated.
Ventilation-Perfusion Coupling
--local autoregulatory mechanisms continuously respond to alveolar conditions
ventilation inadequate ⇒ P O 2 low ⇒ terminal arterioles constrict; blood redirected to respiratory areas where P O 2 is high
ventilation is maximal ⇒ P O 2 high ⇒ pulmonary arterioles dilate; increasing blood flow
--opposite the autoregulatory mechanisms controlling pulmonary vascular muscle is opposite that controlling most arterioles in the systemic circulation
Changes in P CO 2 in alveoli cause changes in the diameter of the bronchioles. --alveolar P CO 2 high ⇒ bronchiole dilation ⇒ more rapid CO 2 elimination; vice versa
Ventilation and perfusion is never completely balanced in every alveolus because of: a. the shunting of blood from the bronchial and coronary veins b. the effects of gravity c. the occasional alveolar duct plugged with mucus ⇒ blood in pulmonary veins actually has a slightly lower P O 2 (100 mm Hg) than alveolar air (104 mm Hg)
Capillary Gas Exchange in Body Tissues (Internal Respiration):
Blood entering tissue capillaries: P O 2 = 100 mm Hg P CO 2 = 40 mm Hg
Tissues: P O 2 = 40 mm Hg P CO 2 = 45 mm Hg
Blood leaving tissue capillaries: P O 2 = 40 mm Hg P CO 2 = 45 mm Hg
Gas Transport by the Blood
Oxygen --carried in blood in two forms: a. dissolved O 2 b. hemoglobin
Dissolved O 2 : --obeys Henry's law --for each mm Hg of PO 2 there is 0.003 ml O 2 /100 ml of blood (0.003 vol %) --thus, when P O 2 is 100 mm Hg, blood contains 0.3 ml O 2 /100 ml blood or 3 ml/L blood
If CO is 30 L/min, the total amount of O 2 delivered to the tissue is only 30 x 3 = 90 ml/min. Tissue requirements, however, might be as high as 3000 ml O 2 /min. Thus, transport of oxygen dissolved in the blood is inadequate.
Hemoglobin (Hb): --permits efficient transport of adequate O 2 --four polypeptide chains (2 α and 2 β), each bound to an iron-containing heme group --each heme can bind one O 2 molecule --oxygen loading is reversible
The hemoglobin-oxygen combination is referred to as oxyhemoglobin (HbO 2 ). Reduced Hb (Hb that has released O 2 ) is called deoxyhemoglobin (HHb).
HHb + O 2 ↔ HbO 2 +H+
Saturation refers to the percentage of available binding sites that have O 2 attached. ~96-98% when P O 2 is 100 mm Hg
Oxyhemoglobin Dissociation Curve: --describes how Hb works
"Two Faces of Hemoglobin" a. when P O 2 is high, Hb is stingy and has a high affinity for O 2 b. when P O 2 is low, Hb is benevolent and has a low affinity for O 2
The rate of Hb reversibility is regulated by: ¾ P O 2 ¾ temperature ¾ blood pH ¾ P CO 2 ¾ DPG (2,3 diphosphoglycerate), a metabolic by-product of glycolysis –binds reversibly to Hb
