Respiratory Physiology
Part II: Respiratory Physiology
Volume Changes and Pressure Changes Affecting Air Movement
Learning Objectives:
Describe the normal pressures: atmospheric pressure, intrapulmonary pressure, and intrapleural pressure.
Relate Boyle's Law to inspiration and expiration events.
Compare the pressure differences in the outside atmosphere.
Explain the roles of respiratory muscles and lung elasticity in generating volume changes for airflow in and out of the lungs.
List physical factors influencing pulmonary ventilation.
Pressure Relationships in the Thoracic Cavity
Air molecules move creating atmospheric pressure.
Atmospheric pressure at sea level = 760 mm Hg, pushing mercury up a tube represents 1 atm of pressure.
Intrapulmonary pressure (Ppul) varies: rises to push air out and lowers to bring air in, eventually equalizing with atmospheric pressure.
Intrapleural pressure (Pip) is slightly negative, as the visceral pleura (moist with pleural fluid) adheres to the parietal pleura, maintaining lung expansion and inflation.
Atelectasis and Pneumothorax
Atelectasis: Collapse of the lung due to blockage (e.g., respiratory bronchiole blockage, pneumonia).
Pneumothorax: Air enters the intrapleural space, causing intrapleural pressure to equal atmospheric pressure, preventing lung inflation.
Pulmonary Ventilation
Boyle's Law:
If the container volume decreases, pressure increases; if the volume increases, pressure decreases.
Inspiration:
Thoracic cavity enlarges, pressure decreases, and air rushes in.
Diaphragm contracts and flattens.
During large breaths, external intercostal muscles raise the chest.
Expiration:
Thoracic cavity decreases, pressure increases, and air exits.
Diaphragm relaxes, and abdominal organs rebound upward.
For forceful expiration, abdominal and internal intercostal muscles collapse the chest.
Physical Factors Influencing Ventilation
Lumen diameter of bronchioles influences airflow:
Irritants cause bronchoconstriction via parasympathetic reflexes and histamine release during allergies.
Asthma can lead to bronchial spasm and potentially fatal airway constrictions.
Epinephrine (via sympathetic reflex or injection) causes bronchodilation.
Alveolar surface tension: Surfactant prevents alveolar walls from sticking together:
Low surfactant leads to Infant Respiratory Distress Syndrome (IRDS); insufficient surfactant in premature infants results in impaired gas diffusion.
Adult Respiratory Distress Syndrome (ARDS): occurs due to gas exchange problems from complications like drowning.
Compliance: Refers to lung elasticity; decreases with age or tissue damage (e.g., fibrosis).
Respiratory Volumes and Capacities
Learning Objectives:
Explain various lung volumes and capacities.
State information gained from pulmonary function tests.
Definitions of Respiratory Capacities and Volumes
Tidal Volume (TV): 500 ml; volume of air inhaled and exhaled at rest.
Inspiratory Reserve Volume (IRV): 3100 ml; volume forcibly inhaled above TV.
Expiratory Reserve Volume (ERV): 1200 ml; volume forcibly exhaled after TV.
Residual Volume (RV): 1200 ml; volume of air remaining in lungs after forced expiration.
Vital Capacity (VC): ; indicates the volume of air that can be forcibly exhaled.
Forced Vital Capacity (FVC): instruct patients to take a deep breath and exhale forcefully; a high FVC indicates no obstruction.
If FVC is lower than normal, it suggests restrictive airway disease (e.g., asthma).
Forced Expiratory Volume in 1 second (FEV1): Volume exhaled in the first second of FVC; should be about 80% of total VC.
Graphing Respiratory Capacities and Volumes
Visual representation of various lung volumes:
IRV, TV, ERV can be graphically depicted with total capacity visualized.
Gas Exchange and Diffusion
Learning Objectives:
Describe differences in atmospheric air and alveolar air composition.
Gas Composition and Partial Pressures
Total atmospheric pressure = 760 mm Hg:
Nitrogen (N₂): 80% or 597 mm Hg.
Oxygen (O₂): 20% or 160 mm Hg.
Carbon dioxide (CO₂): <1% or 0.3 mm Hg.
Gas exchange leads to changes in partial pressures (PO₂ and PCO₂):
Inhaled air: PO₂ ~ 160 mm Hg, PCO₂ 0 mm Hg.
Alveolar air: PO₂ ~ 100 mm Hg, PCO₂ ~ 40 mm Hg.
At the tissue level: PO₂ ↓ ~ 40 mm Hg, PCO₂ ↑ ~ 45 mm Hg due to cellular respiration.
Factors Affecting Gas Exchange (Diffusion)
Effective diffusion occurs within approximately 0.25 seconds.
Impediments to diffusion:
Reduced surface area (e.g., emphysema), increases in membrane thickness (e.g., pneumonia), and edema can slow gas exchange.
Treatment solutions to enhance diffusion:
Increase oxygen diffusion gradient, such as constant low flow oxygen supplements.
Hyperbaric therapy can significantly raise PO₂, aiding in disease treatment and oxygen delivery to tissues, but requires limited exposure to avoid toxicity.
Transportation of Respiratory Gases in the Blood
Oxygen transport: (O₂) 98% bound to hemoglobin (HbO₂) in red blood cells.
Key Measurements:
Normal arterial PCO₂ ~ 40 mm Hg (range 35-45 mm Hg).
Hypocapnia (PCO₂ < 35 mm Hg) and hypercapnia (PCO₂ > 45 mm Hg).
Oxygen dissociation curve:
Reveals how O₂ is released from hemoglobin and impacted by CO₂ levels, temperature, and pH.
Rightward shift signifies enhanced release of oxygen to tissues.
Carbon Dioxide Transport
Forms:
10% dissolved in plasma.
20% bound to hemoglobin.
70% converted to bicarbonate (HCO₃⁻) for transport.
Carbonic acid formula:
Neural Controls of Respiration
Learning Objectives:
Describe respiratory neural controls and impacts on respiratory rate.
Neural Mechanisms
Normal respiration rates (12-16 breaths per minute) regulated by the medulla oblongata via the phrenic nerve (C3-C5) and intercostal nerves.
Factors influencing breathing rate:
Chemoreceptor detection of PCO₂, PO₂, and blood pH.
Heightened levels of CO₂ (hypercapnia) will increase respiratory rate for homeostasis.
Apnea: Temporary cessation of breathing can be voluntary.
Hyperventilation: Increased respiration can lead to hypocapnia and symptoms like dizziness.
Effects of Exercise and High Altitude
Hyperpnea: Increased breathing rate greater than normal to accommodate metabolic demand, without hypoxemia or changes in pH.
Lung Diseases and Their Consequences
Learning Objectives:
Identify causes and effects of various lung diseases: chronic bronchitis, emphysema, asthma, tuberculosis, and lung cancer.
Chronic Obstructive Pulmonary Disease (COPD)
Long term, irreversible lung disease marked by airflow obstruction leading to air trapping.
Symptoms include:
Coughing, frequent infections, dyspnea (shortness of breath), and eventual respiratory failure due to hypercapnia and acidosis.
Risk factors:
Chronic bronchitis and emphysema, often linked to smoking and environmental exposures.
Asthma
Characterized by acute bronchoconstriction, leading to obstructed airflow.
Requires management via inhaled corticosteroids and immediate bronchodilators during attack.
Chronic asthmatic conditions can progress to COPD without proper management.
Tuberculosis (TB)
Infectious disease caused by bacterial infection leading to lung damage over time.
Influenced by factors like nutritional status and immunological health.
Lung Cancer
The leading cause of cancer-related mortality in the U.S.; primarily associated with smoking.
Types include:
Small-cell carcinoma, adenocarcinoma, and squamous cell carcinoma.
Study Helper - Blank Copies for Extra Practice at Home
Make an effort to memorize the atmospheric pressures, PO₂, and PCO₂ changes throughout the respiratory process. This will enhance understanding of gas exchange dynamics in the body and set the stage for clinical evaluations such as pulmonary function tests.