chapter 21-22 part 1
Pulmonary System: Anatomy
The pulmonary system is anatomically divided into the upper and lower airway structures.
Upper airway structures include:
Nasopharynx
Oropharynx
Laryngopharynx
These structures constitute the CONDUCTING PORTION.
Lower airway structures include:
Larynx
Trachea
Bronchi
Bronchopulmonary segments
Terminal bronchioles
Alveoli
These structures constitute the RESPIRATORY PORTION.
Pulmonary System: Trachea and Bronchi
Blood supply comes from:
Bronchial artery system
Pulmonary artery system
Partial pressures (denoted as PA for alveolar and Pa for arterial):
PAO_2: partial pressure of oxygen in alveoli
PACO_2: partial pressure of carbon dioxide in alveoli
PaO_2: partial pressure of oxygen in blood
PaCO_2: partial pressure of carbon dioxide in blood
✅ 1. Pulmonary Artery System (Low-Pressure System)
Function: Gas exchange (oxygenation of blood)
Origin: Pulmonary arteries arise from the right ventricle of the heart
Pathway:
Pulmonary trunk → right and left pulmonary arteries → lungs
These arteries follow the bronchial tree and form capillary networks around alveoli
Oxygen level: Carries deoxygenated blood from the heart to the lungs
✅ 2. Bronchial Artery System (High-Pressure System)
Function: Supplies oxygenated blood to the lung tissues themselves (bronchi, connective tissue, visceral pleura)
Origin: Branches off the thoracic aorta (or sometimes intercostal arteries)
Oxygen level: Carries oxygenated blood
Drainage:
Most bronchial venous blood drains into the azygos and hemiazygos veins
Some also drains into the pulmonary veins, mixing with oxygenated blood
Pulmonary System: Alveoli
Alveolar cells:
Type I alveolar cells: epithelial structural cells
makes up epithelial tissues that forms a protetive lsyers/ling of body surfaces/ cavities
Type II alveolar cells:
Produce surfactant, a phospholipid.
Lowers surface tension.
Facilitates gas exchange.
Alveolar macrophages:
Phagocytize foreign particles (engulfs/absorbs bacteria)
Can be damaged by smoking and inhalation of silica.
Pulmonary System: Nervous System Control
Autonomic nervous system controls bronchi and bronchiole musculature.
Parasympathetic stimulation:
Mediated by acetylcholine.
Via the vagus nerve (cranial nerve X).
Leads to constriction of muscle.
Sympathetic stimulation:
Mediated by β2-adrenergic receptors.
Leads to relaxation of the smooth muscle.
The Breathing Process
Inhalation/inspiration
Exhalation/expiration: Normally a passive process.
The diaphragm is shaped like a parachute.
Mechanisms of Breathing
Inspiration:
Lungs expand.
Chest wall moves out.
Diaphragm moves down.
Expiration:
Lungs recoil.
Chest wall moves in.
Diaphragm moves up.
Inhalation
Inhalation involves the diaphragm and external intercostals.
Diaphragm contracts leading to increased lung volume.
Ribs elevate as the diaphragm moves downward, creating a negative intrapleural pressure.
The lungs have a natural recoil tendency; the chest wall favors the expanded state.
Exhalation
Resting exhalation is due to muscle relaxation and is a passive process.
Diaphragm rises and ribs fall, leading to decreased lung volume.
Forceful breathing involves active use of internal intercostals and abdominal muscles.
Push diaphragm up & pull ribs in, resulting in more decreased lung volume.
At the end of normal expiration, alveoli still have some gas remaining, known as functional residual capacity.
Surfactant decreases surface tension, allowing the alveoli to open easily with each breath.
Pressure Changes During Ventilation
Atmospheric pressure = 760 mmHg
At rest (diaphragm relaxed): Alveolar pressure = 760 mmHg
During inhalation (diaphragm contracting): Alveolar pressure = 758 mmHg
During exhalation (diaphragm relaxing): Alveolar pressure = 762 mmHg
Factors Affecting Breathing
Airway Resistance
Lung Compliance
Distribution of Ventilation
Neurological control of ventilation
Airway Resistance
Relationship between pressure and flow = airway resistance
Airway resistance is influenced by:
Airway radius: Resistance increases as the airway diameter decreases.
Factors that decrease airway radius:
Mucus
Bronchospasm
Stress
Pulmonary deconditioning
Age
Pattern of gas flow
Highest airway resistance is at the nose because of turbulent flow and high velocity.
Lowest airway resistance is in the small bronchioles, where turbulent flow is small.
Airway resistance is higher in the neonate than the adult.
Bronchospasm increases airway resistance.
Lung Compliance
Lung compliance represents lung expandability and ease of lung inflation.
Compliance = change in volume ÷ change in pressure
Compliance provides an estimate of airway resistance and elasticity of the lung.
Lung compliance:
Increased in neonates and young children < 3.5 years due to their chest wall flexibility.
Decreased in elderly due to:
Increased chest wall rigidity
Reduced mobility of the ribs
Partial contraction of inspiratory muscles
Loss of elastic fibers in the lung
Distribution of Ventilation
In the upright individual (vertical),
Alveoli at the apices of the lung are much larger than those at the base.
Ventilation is greatest at the bottom of the lung and decreases towards the apices.
Regional differences in ventilation are less in the supine position.
Neurological Control of Ventilation
Neural control center for respiration is located in the pons and medulla oblongata.
Efferent fibers travel from the brainstem to the diaphragm via the phrenic nerve to stimulate inspiratory muscles.
Medullary dorsal neurons stimulate inspiratory muscles (intercostals, diaphragm).
Abrupt cessation of neurostimulation allows for expiration.
Diffusion and Transport of Respiratory Gases
Diffusion: movement of gas from high concentration to low concentration areas
Barriers to diffusion:
Surfactant
Alveolar membrane
Interstitial fluid
Capillary membrane
Plasma
Red blood cells
Alterations in Pulmonary Function: Hypoventilation
HYPOVENTILATION: air delivered to alveoli is insufficient to provide O2 and remove CO2.
Hypoventilation results in increased PaCO_2.
Causes of hypoventilation:
Morphine
Barbiturates
Obesity
Myasthenia gravis
Obstructive sleep apnea
Chest wall damage
Paralysis of respiratory muscles
Surgery of the thorax or abdomen
Alterations in Pulmonary Function: Hyperventilation
HYPERVENTILATION: increase of air entering the alveoli leads to hypocapnia (PaCO_2 <35 mm Hg)
Causes: pain, fever, anxiety, obstructive and restrictive lung diseases, sepsis, high altitude, and brainstem injury
Low PaCO_2 leads to greater binding of oxygen to the hemoglobin molecule
Hypoxemia/Hypoxia: deficient blood oxygen
OBSTRUCTION v. RESTRICTION
Obstruction
Air trapping
SMALL AIRWAY
RESISTANCE TO EXPIRATION – Just can’t get out!
Obstruction, i.e., wheezing
HYPEREXPANSION on CXR
Restriction
“Compliance”
“Infiltrative”
REDUCED lung VOLUME, DYSPNEA, CYANOSIS
REDUCED GAS TRANSFER
RESISTANCE TO INSPIRATION – Just can’t get in!
REDUCED COMPLIANCE, i.e., less sponginess!
“GROUND GLASS” on CXR
General Pulmonary Disorders
When you think of pulmonary disorders think:
Inflammation
Edema
Excess mucous production
Obstructive Pulmonary Disorders: Classifications
Obstruction from conditions in the wall of the lumen
Asthma
Acute Bronchitis
Chronic Bronchitis
Obstruction related to loss of lung parenchyma
Emphysema
Obstruction of the airway lumen
Bronchiectasis
Bronchiolitis
Cystic Fibrosis
Acute Tracheobronchial Obstruction
Epiglottitis
Croup Syndrome
Obstructive Pulmonary Disorders are manifested by increased resistance to airflow.
Asthma
Characterized by:
Airway obstruction that is reversible (not completely in some patients)
Airway inflammation
Increased airway responsiveness to a variety of stimuli
Common symptoms
Wheezing
Feeling of tightness of chest
Dyspnea
Cough (dry or productive)
Increased sputum production (thick, tenacious, scant, and viscid)
Asthma: Epidemiology and Predisposing Factors
Who has asthma?
Occurs in 5% to 12% of U.S. population
Most common chronic disease of children
High-risk populations
African Americans
Inner-city residents
Premature/low-birth-weight children
Predisposing factors
Genetic for atopy and structural (smaller airways)
Chromosomes 5, 11, 14
History of hay fever, eczema
Family history
Positive skin test reactions to allergens
Asthma: Intrinsic vs. Extrinsic
Intrinsic Asthma
Non-allergic
ADULT ONSET
Antigen-antibody reactions are not directly involved
IgE levels may be elevated
Extrinsic Asthma
Allergic
PEDIATRIC ONSET
1/3 to ½ of asthma cases
An IgE-mediated response is common
Asthma: EXTRINSIC (ALLERGIC)
Clinical Manifestations:
Elevated IgE levels
Allergic rhinitis
Eczema
Positive family history of allergy
Attacks associated with seasonal, environmental or occupational exposure
Mechanism of Action:
Immediate phase
Chemical mediators released
Normal respiratory epithelium is denuded (loss of outside layer) and replaced by goblet cells
Alterations in epithelial integrity
Increased microvascular permeability
Late phase
Epithelial damage
Asthma: EXTRINSIC (ALLERGIC) Mechanism of Action
1- Immediate phase
Initiated by exposure to specific antigen that has previously sensitized mast cells in airway mucosa
Antigen reacts with antibody on surface of mast cell
Mast cell releases packets of chemical mediator substances
2- Chemical mediators released
Histamine
Slow-reacting substances of anaphylaxis (leukotrienes)
Prostaglandins
Bradykinins
Eosinophilic chemotactic factor
Serotonin
3- Normal respiratory epithelium is denuded (loss of outside layer) and replaced by goblet cells
4- Alterations in epithelial integrity
5- Increased microvascular permeability
Mucosal edema
Inflammatory exudates
Bronchoconstriction
Leakage
6- Late phase
Arrival of recruited leukocytes signals initiation
More mediator release causes damage to epithelium
7- Epithelial damage
Hypertrophied smooth muscle
Edema
Mucous gland hypertrophy
Mucus in lumen
Bronchial Asthma: Histologic Findings
What are the 4 classical histologic findings in bronchial asthma?
Inflammation
Bronchial (luminal) narrowing
Increased Mucous
Smooth muscle hyperplasia
What is the 5th finding if the etiology is allergy?
Increased eosinophils
Asthma: Diagnosis
Physical findings
Cough
Wheezing
Hyperinflated chest
Decreased breath sounds
Radiographic finding
Hyperinflation with flattening of the diaphragm
Sputum examination
Charcot-Leyden crystals (formed from crystallized enzymes from eosinophilic membranes)
Eosinophils
Curschmann spirals (mucous casts of bronchioles)
Pulmonary function tests
Forced expiratory volumes decrease
Peak expiratory flow rate (PEFR)
REMEMBER (Nervous System)
Parasympathetic stimulation (mediated by acetylcholine) via the vagus nerve (cranial nerve X) leads to constriction of muscle
Sympathetic stimulation (mediated by β2-adrenergic receptors); leads to relaxation of the smooth muscle
Asthma: Treatment
Antigenic and nonantigenic stimuli cause mast cell degranulation
Parasympathetic nervous system stimulation via acetylcholine
Blocked by ipratropium
Chemotaxis of neutrophils and eosinophils
Blocked by corticosteroids
Histamine
Leukotrienes
Prostaglandins
Mast cell migration inhibited by corticosteroids
Blocked by mast cell stabilizers (e.g., corticosteroids, cromolyn, nedocromil)
Blocked by receptor antagonist; (e.g., zafirlukast)
Blocked by leukotriene inhibitors
Blocked by histamine receptor blockers (e.g.. diphenhydramine)
Bronchial smooth muscle cell contraction
Mucus secretion
Mucosal edema
Inhibited by β2 agonists, theophylline, muscarinic antagonists
Inhibited by corticosteroids
Target tissue
Asthma: Treatment Strategies
Avoid triggers
Environmental control
Removal of allergens
Air purifiers
Air conditioners
Preventive therapy
Desensitization (allergen specific immunotherapy)
Medications
O_2 therapy
Small-volume nebulizers
B2 agonists
Corticosteroids
Leukotriene modifiers
Mast cell inhibitors