UNIT 4: RESPIRATION
Dr. John Redden
Physiology and Neurobiology
University of Connecticut
LECTURE ROADMAP
Respiratory Anatomy
Histology/Microanatomy
Blood Pressure/Volume Relationships During Ventilation
Gas Exchange
Control of Breathing
Entry Point Into Respiratory Tract
Air entering the body must be:
Filtered
Warmed
Humidified
Components:
Larynx
Tracheal cartilages
Right lung & Left lung
Primary & Secondary bronchi
Trachea
Pulmonary arteries & veins
Alveoli & Alveolar ducts
Smooth muscle in bronchioles
Capillaries
Right Lung:
3 Lobes (3 Secondary Bronchi)
Left Lung:
2 Lobes (2 Secondary Bronchi)
Types:
Visceral Pleura (Surface of Lung)
Parietal Pleura (Thoracic Wall)
Function:
Contains pleural cavity (Pleural space) allowing for lung expansion during respiration
Respiratory Passages Include:
Primary bronchi, Secondary bronchi, Tertiary bronchi (1 bronchioles < 1mm), Terminal bronchioles (6500 potential pathways)
Epithelium Types:
Pseudostratified epithelia
Stratified epithelia
Cuboidal epithelial layers
Cartilage present in Trachea
Smooth muscle found in bronchioles
Types of Epithelium:
Inferior Pharynx: Stratified Epithelium
Nasopharynx, Pharynx & Lower Respiratory Tract: Pseudostratified Columnar Epithelium
Function:
Traps dust/pathogens, humidifies air
Cilia move mucus and debris upward toward the pharynx
Not found in bronchioles/alveoli (local alveolar macrophages instead)
**Components: **
Respiratory bronchioles, Alveolar ducts, Alveolar sacs
Cell Types in Alveoli:
Type I Cells: Squamous epithelium for gas exchange
Type II Cells: Secrete surfactant (chemical to reduce surface tension)
Occurs across:
Alveolar wall
Capillary wall (fused basal lamina)
Properties:
Large surface area facilitates easy diffusion of CO2 and O2 due to their lipid solubility
Type I epithelia are over 90% of alveoli for gas exchange
Surfactant is crucial as water creates surface tension risking alveolar collapse
Surface Tension Influence:
Too much makes lung inflation difficult, especially at lower volumes
Too little means no recoil leading to airway closure during expiration
Surfactant lowers surface tension thus preventing small alveoli from collapsing into larger ones
Clinical Relevance:
Respiratory Distress Syndrome: surfactant deficiency leads to instability and collapse of alveoli
Ventilation Process:
Move air in and out through Boyle’s law (closed system)
Inspiration:
Increase thoracic volume, decrease lung pressure
Expiration:
Decrease thoracic volume, increase lung pressure
Diaphragm (contracted)
External intercostals
Accessory muscles: Pectoralis minor, Scalene, SCM
Diaphragm (relaxed)
Internal intercostals
Abdominal muscles (during forced expiration)
Components:
Atmospheric pressure
Intrapleural pressure
Intrapulmonary pressure (intra-alveolar pressure)
Mechanics:
Diaphragm and inspiratory intercostals contract to create a pressure gradient
Leads to lung expansion and airflow into alveoli
Diaphragm relaxing/stopping leads to thorax recoiling, expelling air
Loss of intrapleural pressure due to trauma/lung damage
Normally, negative pressure in pleural cavity prevents lung collapse
Gas flow impacted by resistance in air passages
Physiologically:
Parasympathetic impact: constriction
Sympathetic impact: dilation
Highest resistance occurs in bronchioles
Bronchodilation & Bronchoconstriction deal with airway resistance
Gas exchange only occurs in specific lung regions:
Anatomical Dead Space:
Air in non-respiratory parts (conducting zone)
Physiological Dead Space:
Failure of respiratory zones for gas exchange, increased with aging
Measurement:
Components:
VD (dead space), VT (tidal volume), VA (alveolar ventilation)
Involves gas diffusion in lungs among O2 and CO2 transportation
Gas diffusion is dependent on partial pressure gradients
Factors Determining Partial Pressure:
Concentration of gas
Barometric pressure
Normal Air Composition:
Mostly nitrogen and oxygen, negligible CO2
At constant temperature, gas in solution is proportional to partial pressure
Implications of altitude change on gas behavior in the body
Pressure Values:
Air: Poâ‚‚ = 160 mmHg, Pcoâ‚‚ = 0.3 mmHg
Alveoli: Poâ‚‚ = 100 mmHg, Pcoâ‚‚ = 40 mmHg
Tissue: Poâ‚‚ < 40 mmHg, Pcoâ‚‚ > 46 mmHg
Transport pathways between pulmonary arteries, veins, and tissues are essential for respiration
Increased concentrations enhance solubility (O2 binds to Hb)
Important Note: CO2 is ~24 times more soluble than O2, allowing rapid diffusion and signaling for respiration
Functionality:
Donates and accepts H+ to maintain acid-base balance via bicarbonate buffering system
Impacts of hyperventilation/hypoventilation on pH, achieving acid-alkaline balance (pH 7.35 - 7.45)
Concepts:
Gas reaching an alveolus (ventilation)
Blood flow in capillaries (perfusion)
V/Q ratio is usually matched for optimal function in a healthy person
Functionality:
Rhythmic output of CNS to respiratory muscles located in the brainstem
Hypoxia triggers increased respiration and heart rates via peripheral chemoreceptors
Established by the Pre-Bötzinger complex in the medulla (an inspiratory pacemaker)
Modulated activity affects only inspiratory muscles
Primarily sensory input, mostly inspiratory neurons
Projects to other respiratory centers (Ventral & Pontine) and spinal motorneurons
Presence in CNS for CO2 monitoring (specifically H+)
Significance in respiratory control mechanisms
Located in the medulla, controls the chemical drive to breathe by processing CO2 levels
Congenital hypoventilation syndrome due to lack of transcription factor (Phox2b) in RTN, disrupting respiratory control
Facilitates transition between inspiration and respiration phases, promoting effective expiration.