Note
Studied by 13 people
A&P II RESPIRATORY SYSTEM
Major functions of RESPIRATORY SYSTEM: supply body with O2 for cellular respiration and dispose of CO2, a waste product of cellular respiration
Respiration involves four processes
Respiratory system
PULMONARY VENTILATION (breathing): movement of air into and out of lungs
EXTERNAL RESPIRATION: exchange of O2 and CO2 between lungs and blood
Circulatory system
TRANSPORT of O2 and CO2 in blood
INTERNAL RESPIRATION: exchange of O2 and CO2 between systemic blood vessels and tissues
Also functions in olfaction and speech
22.4 Mechanics of Breathing
Pulmonary ventilation consists of two phases
Inspiration: gases flow INTO THE LUNGS (inhalation)
Expiration: gases FLOW OUT OF LUNGS (exhalation)
Pressure Relationships in the Thoracic Cavity
Atmospheric pressure (Patm)
Pressure exerted by AIR surrounding the body
760 mm Hg at SEA LEVEL = 1 atmosphere
Respiratory pressures described relative to Patm
NEGATIVE RESPIRATORY PRESSURE: LOWER than Patm
POSITIVE RESPIRATORY PRESSURE: HIGHER than Patm
ZERO RESPIRATORY PRESSURE: EQUAL to Patm
Intrapulmonary pressure (Ppul)
Pressure in THE LUNGS
Also called intra-alveolar pressure
Fluctuates with breathing
Always eventually equalizes with Patm
Intrapleural pressure (Pip)
Pressure in PLEURAL CAVITY
Always a NEGATIVE pressure (<Ppul and <Patm)
Usually always 4 mm Hg less than Ppul
Fluid level must be kept at a MINIMUM
Excess fluid pumped out by LYMPHATIC SYSTEM
If fluid accumulates, positive INTRATHORACIC pressure develops
Lung COLLAPSES
Transpulmonary pressure = PPul – Pip
Pressure that keeps the LUNGS INFLATED
PNEUMOTHORAX → air enters pleural cavity, disrupting the negative pressure causing lungs to collapse
Pulmonary Ventilation
Consists of INSPIRATION and EXHALATION
Mechanical process that depends on VOLUME changes in thoracic cavity
Volume changes lead to PRESSURE CHANGES
Pressure changes lead to flow of GASES to equalize pressure
BOYLE’S LAW - Relationship between pressure and volume of a gas
Gases always fill the container they are in
If amount of gas is the SAME and container size is REDUCED, pressure will INCREASE
Pressure (P) varies INVERSELY with volume (V)
Expiration
QUIET expiration normally is PASSIVE PROCESS
Inspiratory muscles relax, thoracic cavity volume decreases, and lungs recoil
Volume decrease causes intrapulmonary pressure (Ppul) to increase by +1 mm Hg
Ppul > Patm so air flows out of lungs down its pressure gradient until Ppul = Patm
FORCED expiration is an ACTIVE PROCESS → uses oblique and transverse abdominal muscles, as well as internal intercostal muscles
INTRAPULMONARY PRESSURE - Pressure inside lung DECREASES as lung volume INCREASES during inspiration; pressure INCREASES during expiration
INTRAPLEURAL PRESSURE - Pleural cavity pressure becomes more NEGATIVE as chest wall expands during inspiration. Returns to INITIAL VALUE as chest wall recoils
VOLUME OF BREATH – During each breath, the pressure gradients move 0.5 LITERS (500 mL) of air into and out of the lungs
Physical Factors Influencing Pulmonary Ventilation
Three physical factors influence the ease of air passage and the amount of energy required for ventilation:
AIRWAY RESISTANCE
ALVEOLAR SURFACE TENSION
LUNG COMPLIANCE
1. Airway resistance
FRICTION: major nonelastic source of resistance to gas flow; occurs in airways
Relationship between FLOW (F), PRESSURE (P), and RESISTANCE (R):
F = ΔP / R
ΔP – pressure gradient between atmosphere and alveoli
2 mm Hg or less during normal quiet breathing
2 mm Hg difference sufficient to move 500 mL of air
Gas flow changes INVERSELY with resistance
Resistance in respiratory tree is usually insignificant for two reasons:
Diameters of airways in first part of conducting zone are HUGE
Progressive BRANCHING of airways as they get smaller leads to an increase in total cross-sectional area
Any resistance usually occurs in MEDIUM–SIZED BRONCHI
Resistance disappears at terminal bronchioles, where DIFFUSION is what drives GAS movement
2. Alveolar surface tension
SURFACE TENSION: the attraction of liquid molecules to one another at a gas-liquid interface
Tends to draw liquid molecules closer together and reduce contact with dissimilar gas molecules
Resists any force that tends to increase surface area of liquid
Water, which has very high surface tension, coats alveolar walls in a thin film
Tends to cause alveoli to SHRINK to smallest size = COLLAPSE
SURFACTANT is body’s detergent-like lipid and protein complex that helps reduce surface tension of alveolar fluid
PREVENTS ALVEOLAR COLLAPSE
Produced by type II alveolar cells
3. Lung compliance
Measure of CHANGE in lung volume that occurs with given change in transpulmonary pressure
Measure of how much STRETCH the lung has
Normally high because of:
DISTENSIBILITY of lung tissue
SURFACTANT - decreases alveolar surface tension
Higher lung compliance means it is EASIER to expand lungs
Compliance can be diminished by:
NONELASTIC SCAR TISSUE replacing lung tissue (fibrosis)
Reduced production of SURFACTANT
Decreased FLEXIBILITY of thoracic cage
22.5 Assessing Ventilation
Several RESPIRATORY VOLUMES can be used to assess respiratory status
Respiratory volumes can be combined to calculate RESPIRATORY CAPACITIES, which can give information on a person’s respiratory status
Respiratory volumes and capacities are usually abnormal in people with pulmonary disorders
SPIROMETER
Respiratory Volumes
TIDAL VOLUME (TV): amount of air moved into and out of lung with each BREATH
Averages ~500ml
INSPIRATORY RESERVE VOLUME (IRV): amount of air that can be inspired forcibly beyond the tidal volume (2100–3200 ml)
EXPIRATORY RESERVE VOLUME (ERV): amount of air that can be forcibly expelled from lungs (1000–1200 ml)
RESIDUAL VOLUME (RV): amount of air that always REMAINS in lungs
Needed to keep LUNGS FROM COLLAPSING
Respiratory Capacities - Combinations of two or more respiratory volumes
INSPIRATORY CAPACITY (IC): sum of Tidal volume (TV) + Inspiratory reserve volume (IRV)
FUNCTIONAL RESIDUAL CAPACITY (FRC): sum of Residual Volume (RV) + ERV
VITAL CAPACITY (VC): sum of TV + IRV + ERV
TOTAL LUNG CAPACITY (TLC): sum of ALL lung volumes (TV + IRV+ ERV + RV)
Dead Space
ANATOMICAL DEAD SPACE: does not contribute to GAS EXCHANGE
Consists of air that remains in PASSAGEWAYS
~150 ml out of 500 ml TV
ALVEOLAR DEAD SPACE: space occupied by nonfunctional alveoli
Can be due to collapse or obstruction
TOTAL DEAD SPACE: SUM of anatomical and alveolar dead space
Pulmonary Function Tests
Spirometry can distinguish between:
Obstructive pulmonary disease: increased airway resistance (example: bronchitis)
TLC, FRC, RV may increase because of hyperinflation of lungs
Restrictive disease: reduced Total Lung Capacity due to disease (example: tuberculosis) or exposure to environmental agents (example: fibrosis)
VC, TLC, FRC, RV decline because lung expansion is compromised
Pulmonary functions tests can measure RATE of gas movement
FORCED VITAL CAPACITY (FVC): amount of gas forcibly expelled after taking deep breath
FORCED EXPIRATORY VOLUME (FEV): amount of gas expelled during specific time interval of FVC
FEV1: amount of air expelled in 1st SECOND
Healthy individuals can expel 80% of FVC in 1st second
Patients with obstructive disease exhale less than 80% in 1st second, whereas those with restrictive disease exhale 80% or more even with reduced FVC
Alveolar Ventilation
MINUTE VENTILATION: total amount of gas that flows into or out of respiratory tract in 1 minute
Normal at rest = ~ 6 L/min
Normal with exercise = up to 200 L/min
Only rough estimate of respiratory efficiency
22.6 Gas Exchange
Gas exchange occurs between LUNGS and BLOOD as well as BLOOD and TISSUE
EXTERNAL RESPIRATION: diffusion of gases between blood and LUNGS
INTERNAL RESPIRATION: diffusion of gases between blood and TISSUES
Both processes are subject to:
Basic properties of gases
Composition of alveolar gas
Basic Properties of Gases
DALTON’S law of partial pressures
Total pressure exerted by mixture of gases is equal to sum of pressures exerted by each gas
Partial pressure
Pressure exerted by each gas in mixture
Directly proportional to its percentage in mixture
Total atmospheric pressure equals 760 mm Hg
NITROGEN makes up ~78.6% of air; therefore, partial pressure of nitrogen, PN2, can be calculated:
0.786 x 760 mm Hg = 597 mm Hg due to N2
OXYGEN makes up 20.9% of air, so PO2 equals:
0.209 x 760 mm Hg = 159 mm Hg
Air also contains 0.04% CO2, 0.5% water vapor, and insignificant amounts of other gases
At high altitudes, partial pressures DECLINES, but at lower altitudes (under water), partial pressures INCREASE significantly
HENRY’S law
For gas mixtures in contact with liquids:
Each gas will dissolve in the liquid in proportion to its partial pressure
Amount of each gas dissolved depends on:
SOLUBILITY: CO2 is 20× more soluble in water than O2, and little N2 will dissolve
TEMPERATURE: as temperature of liquid rises, solubility DECREASES
Example of Henry’s law: hyperbaric chambers
Composition of Alveolar Gas
Alveoli contain more CO2 and water vapor than atmospheric air because of:
GAS EXCHANGES in lungs (O2 diffuses out of lung, and CO2 diffuses into lung)
HUMIDIFICATION of air by conducting passages
MIXING of alveolar gas with each breath
Newly inspired air mixes with air that was left in passageways between breaths
External respiration (PULMONARY GAS EXCHANGE) involves the exchange of O2 and CO2 across respiratory membranes
Exchange is influenced by:
Ventilation → movement of gases
Perfusion → blood flow
Partial pressure gradients and gas solubilities
Thickness and surface area of respiratory membrane
Ventilation–perfusion coupling: matching of alveolar ventilation with pulmonary perfusion
Partial Pressure Gradients and Gas Solubilities
STEEP PARTIAL PRESSURE GRADIENT for O2 exists between blood and lungs
Venous blood PO2 = 40 mm Hg
Alveolar PO2 = 104 mm Hg
Drives oxygen flow into BLOOD
Equilibrium is reached across respiratory membrane in ~0.25 seconds, but it takes red blood cell ~0.75 seconds to travel from start to end of pulmonary capillary
Ensures adequate OXYGENATION even if blood flow increases 3×
Partial pressure gradient for CO2 is LESS STEEP
Venous blood PCO2 = 45 mm Hg
Alveolar PCO2 = 40 mm Hg
Though gradient is not as steep, CO2 still diffuses in equal amounts with oxygen
Reason is that CO2 is 20x more soluble in plasma and alveolar fluid than oxygen
2. Thickness and surface area of the respiratory membrane
Respiratory membranes are very thin - 0.5 to 1 µm thick
3. Ventilation-perfusion coupling
PERFUSION: BLOOD FLOW flow reaching alveoli
VENTILATION: amount of GAS reaching alveoli
Ventilation and perfusion rates must be matched for optimal, efficient gas exchange
Both are controlled by local autoregulatory mechanisms
PO2 controls perfusion by changing ARTERIOLAR diameter
PCO2 controls ventilation by changing BRONCHIOLAR diameter
Influence of local PO2 on perfusion
Changes in PO2 in alveoli cause changes in diameters of arterioles
Where alveolar O2 is HIGH, arterioles DILATE
Where alveolar O2 is LOW, arterioles CONSTRICT
Directs blood to go to alveoli, where oxygen is high, so blood can pick up more oxygen
Opposite mechanism seen in systemic arterioles that dilate when oxygen is low and constrict when high
Influence of local PCO2 on perfusion
Changes in PCO2 in alveoli cause changes in diameters of bronchioles
Where alveolar CO2 is HIGH, bronchioles DILATE
Where alveolar CO2 is LOW, bronchioles CONSTRICT
Allows elimination of CO2 more rapidly
Internal respiration
INTERNAL RESPIRATION involves capillary gas exchange in body tissues
Partial pressures and diffusion gradients are REVERSED compared to external respiration
Tissue PO2 is always LOWER than in arterial blood PO2
40 vs. 100 mm Hg
Oxygen moves from BLOOD → TISSUES
Tissue PCO2 is always HIGHER than arterial blood PCO2
45 vs. 40 mm Hg
CO2 moves from TISSUES → BLOOD
Venous blood returning to heart has PO2 of 40 mm Hg and PCO2 of 45 mm Hg
Oxygen Transport
Molecular O2 is carried in blood in two ways:
1.5% is dissolved in plasma
98.5% is loosely bound to each Fe of hemoglobin (Hb) in RBCs
OXYHEMOGLOBIN
Each Hb molecule is composed of FOUR POLYPEPTIDE CHAINS, each with a iron-containing heme group
So each Hb can transport FOUR OXYGEN MOLECULES
Loading and unloading of O2 is facilitated by a change in shape of Hb
As O2 binds, Hb changes shape, increasing its AFFINITY for O2 increases
As O2 is released, Hb shape change causes a DECREASE IN AFFINITY for O2
AFFINITY → attraction to something
FULLY SATURATED (100%): all FOUR heme groups carry O2
PARTIALLY SATURATED: when only one to three hemes carry O2
Loading and Unloading
Rate of loading and unloading of O2 is regulated to ensure adequate oxygen delivery to cells
Factors that influence hemoglobin saturation:
PO2
Other factors such as:
Blood
Concentration of BPG
BLOOD pH
CONCENTRATION OF BPG
Bisphosphoglycerate - product of glucose metabolism in RBCs
Influence of PO2 on hemoglobin saturation
PO2 heavily influences binding and release of O2 with hemoglobin
Percent of Hb saturation can be plotted against PO2 concentrations
Resulting graph is not linear, but an S-shaped curve
Referred to as an oxygen-hemoglobin dissociation curve
Influence of other factors on hemoglobin saturation
BPG is produced by RBCs during glycolysis; BPG levels RISE when oxygen levels are LOW
As cells metabolize glucose, they use O2, causing:
Increases in PCO2 and H+ in capillary blood
Declining blood pH (ACIDOSIS) and increasing PCO2 cause Hb-O2 bond to WEAKEN
Referred to as BOHR EFFECT
O2 unloading occurs where needed most
Heat production in active tissue directly and indirectly decreases Hb affinity for O2
Allows increased O2 UNLOADING to active tissues
pH Levels
Changes in respiratory rate and depth affect blood pH
Slow, shallow breathing causes an increase in CO2 in blood, resulting in a drop in pH
Rapid, deep breathing causes a decrease in CO2 in blood, resulting in a rise in pH
Changes in ventilation can help adjust pH when disturbances are caused by metabolic factors
Breathing plays a major role in acid-base balance of body
Why do people breath into a brown paper bag?
HYPERVENTILATION – increased depth and rate of breathing that exceeds body’s need to remove CO2
May be caused by anxiety attacks
Leads to decreased blood CO2 levels (hypocapnia)
Brown Bag breathing __________________________________________
Causes cerebral vasoconstriction and cerebral ischemia, resulting in dizziness, fainting
Hypoxia: inadequate O2 delivery to tissues; can result in cyanosis and is classified by cause:
ANEMIC HYPOXIA: too FEW RBCs or abnormal or too little Hb
ISCHEMIC HYPOXIA: impaired or blocked blood circulation
HISTOTOXIC HYPOXIA: cells unable to use O2, as in metabolic POISONS (ex: cyanide)
HYPOXEMIC HYPOXIA: abnormal ventilation; pulmonary disease, low levels of oxygen in air
CARBON MONOXIDE POISONING: especially from fire; Hb has a 200x greater AFFINITY for carbon monoxide than oxygen
BINDS TO ALL HEMOGLOBIN NOT ALLOWING OXYGEN TO BIND TO RBCs
Treatment → HYPERBARIC CHAMBER
High Altitude
Quick travel to altitudes above 2400 meters (8000 feet) may trigger symptoms of acute mountain sickness (AMS)
Atmospheric pressure and PO2 levels are LOWER at high elevations
Symptoms: headaches, shortness of breath, nausea, and dizziness
ACCLIMATIZATION: respiratory and hematopoietic adjustments are made with long-term moves to high altitude
Chemoreceptors become more responsive to PCO2 when PO2 declines
Results in increases in minute ventilation that stabilize in few days to 2–3 L/min higher than at sea level
High altitude conditions always result in LOWER-than-normal Hb saturation levels
Due to availability of LESS O2
Decline in blood O2 stimulates KIDNEYS to accelerate production of EPO (erythropoietin)
RBC numbers INCREASE slowly to provide long-term compensation