Respiratory System: Chapter 21–23 Lecturr
Exam Context and Webinar Announcements
Sandra announced an EKG interpretation webinar with voice-over PowerPoint format; intent to help with reading EKGs and heart blocks.
Tandrika offered to share a recorded dysrhythmias session if given the link; facilitator agreed to distribute it after obtaining the recording.
Discussion of exam logistics: exam date is soon (next week). Instructions emphasize not sharing content prematurely and preparing with study questions likely to appear on the exam.
Listed topics/questions students anticipated on the exam: hemoglobin synthesis; red blood cell degradation; hemopoiesis; anemia; platelets; hypertension; acute arterial occlusion; deep vein thrombosis (DVT); oxygen/hemoglobin dissociation; myocytes; tuberculosis; cardiac action potential; neuromuscular disorders; mitral valve disease; congestive heart failure (CHF); second-degree heart block; shock types; calcium ions in myocardial contraction; conduction system; myocardial infarction; carbon dioxide transport; dispersion/conduction principles; respiratory anatomy and physiology; functional residual capacity; hypoxia; DVT; asthma; pulmonary function tests; cystic fibrosis; low cardiac output; and more.
Emphasis on connecting exam content to foundational physiology, clinical practice, and real-world relevance (e.g., recognizing when to escalate to emergency care).
Session ends with a plan to resume the last chapters and provide content lists for study.
Chapter 21: Respiratory Function and Alterations in Gas Exchange
Fetal development timeline
Lung development begins around day 26 of gestation.
By ~25 weeks gestation, fetal lungs are developed enough to allow respiration.
Anatomy: upper vs lower airways
Upper: nasopharynx, oral pharynx, large laryngeal/pharyngeal structures.
Lower: trachea, bronchi, bronchioles.
Pulmonary circulation and perfusion
Pulmonary circulation brings the entire cardiac output from the right ventricle to the alveoli for gas exchange via pulmonary arteries.
Blood becomes oxygenated in the alveoli and returns via pulmonary veins to the systemic circulation.
Aging and respiration
Aging leads to variations and changes in respiratory structure and function.
Lung volumes and capacities; dead space
Dead space is air in respiratory tract segments that does not participate in gas exchange:
Anatomic dead space
Physiologic dead space (composite of anatomic and alveolar dead space)
Alveolar dead space is air reaching alveoli that do not participate in gas exchange.
Minute ventilation and alveolar ventilation
Minute ventilation = volume of gas inhaled/exhaled per minute.
Alveolar ventilation concerns the portion participating in gas exchange; some air is wasted in dead space.
Gas exchange area and barriers
Diffusion occurs across the alveolar-capillary membrane; barriers include surfactant layer, alveolar membrane, interstitial fluid, and capillary membranes.
Surfactant
Surfactant reduces surface tension to prevent alveolar collapse (atelectasis).
Composition: ~90% lipid and ~10% protein.
Diffusion and concentration gradients
Gas diffusion is driven by concentration gradients (high to low): O2 moves from alveolar air (high O2) to blood (low O2); CO2 moves from blood (high CO2) to alveolar air (low CO2).
Transport of oxygen and carbon dioxide
Oxygen transport forms:
Dissolved in plasma: ~1.5\%
Bound to hemoglobin: ~98.5\%
Carbon dioxide transport forms:
Dissolved in plasma
Bound to hemoglobin (carbaminohemoglobin)
Bicarbonate ions \mathrm{HCO_3^-} (major form, via the carbonic acid-bicarbonate buffering system)
Hemoglobin and oxygen carrying capacity
Hemoglobin carries the majority of oxygen; dissolved O2 is a small fraction.
Partial pressures and diagnostic tests
Arterial blood gas (ABG) assesses O2 and CO2 levels and acid-base balance; used to diagnose respiratory failure and gas exchange abnormalities.
Chest X-ray and pulmonary function tests (PFT) assist in diagnosis and monitoring.
Respiratory control: neural and chemical regulation
Neural control centers: medulla oblongata and pons regulate breathing, heart rate, and blood pressure.
Medulla oblongata: primary autonomic control; integrates signals to breathing and heart function.
Pons: regulation of breathing patterns, sleep, and sensory input.
Neuroreceptors:
Central chemoreceptors respond to arterial CO2/pH changes; drive ventilation adjustments.
Peripheral chemoreceptors (carotid bodies, aortic bodies) respond to O2 and CO2 changes; particularly sensitive to hypoxemia.
Proprioceptors in skeletal muscles, tendons, joints influence movement and breathing.
Baroreceptors in the aortic arch and carotid sinus monitor BP and inform respiratory adjustments.
Hering-Breuer reflex: prevents overinflation of the lungs by signaling to stop inspiration.
Environmental factors and chemoreflexes influence respiration and pH homeostasis.
Pulmonary blood flow and ventilation distribution
Distribution of blood flow (perfusion) is uneven and affected by body position and exercise.
Ventilation distribution is also affected by gravity and body position; ventilation is greater at the base of the lungs when upright.
Ventilation-perfusion ratio ($V/Q$) assesses the efficiency of gas exchange; typically, ventilation and perfusion are matched in healthy lungs.
Hypoxic pulmonary vasoconstriction redirects blood flow away from poorly ventilated regions to better-ventilated regions to optimize gas exchange.
Gas exchange and diffusion barriers
Gas exchange mainly occurs by diffusion driven by a concentration gradient.
Diffusion can be impeded by barriers such as surfactant integrity, alveolar-capillary membrane thickness, and interstitial fluid.
Hypoxemia, hypoxia, and respiratory failure concepts
Hypoxemia: low blood oxygen levels; often reduces O2 delivery to tissues.
Hypoxia: tissue-level oxygen deficiency.
Acute respiratory failure: failure of gas exchange with hypoxemia and/or hypercapnia; clinical features include shortness of breath, cyanosis, confusion, and fatigue.
Respiratory function testing: spirometry and ventilatory metrics
Forced Vital Capacity (FVC): the amount of air that can be forcibly exhaled after full inspiration.
Tidal Volume (VT): normal volume of air displaced during normal breathing.
Inspiratory Reserve Volume (IRV): additional air that can be inhaled after a normal inspiration.
Expiratory Reserve Volume (ERV): additional air that can be exhaled after a normal expiration.
FVC = VT + IRV + ERV
Forced Expiratory Volume in 1 second (FEV1): volume exhaled in the first second of a forced expiration (key for obstructive disease assessment).
Total Lung Capacity (TLC): maximum amount of air the lungs can hold.
Functional Residual Capacity (FRC): the volume of air remaining in the lungs after a normal exhalation.
Bronchial provocation testing (e.g., methacholine): assesses airway hyperreactivity; methacholine is a muscarinic receptor agonist used to induce bronchospasm in controlled testing.
Practical clinical implications and exam relevance
Recognize differences between upper and lower airway involvement in respiratory disease.
Understand how V/Q mismatch drives symptoms and need for targeted therapy.
Identify when ABG and imaging are indicated, and how PFTs differentiate obstructive vs restrictive disorders.
Be able to interpret spirometry results and the significance of FVC, FEV1, and the FEV1/FVC ratio in diagnosis.
Grasp the role of surfactant and alveolar mechanics in preventing atelectasis and maintaining gas exchange.
Appreciate the importance of oxygen delivery, CO2 elimination, and acid-base balance in clinical assessment.
Chapter 22: Obstructive Pulmonary Disorders
Core concept
Obstructive disorders are characterized by increased airway resistance, which can be due to inflammation, airway wall changes, airway lumen obstruction, or external compression; many are reversible or variable in reversibility.
Asthma
Types and clinical variants
Adult-onset and pediatric-onset asthma; many pediatric cases improve with age.
Exercise-induced asthma; obesity-related asthma; eosinophilic asthma; neutrophilic asthma (a subset of severe asthma).
Pathogenesis and mechanisms
Denudation of airway epithelium with loss of ciliated cells; mucus hypersecretion; basement membrane thickening; edema; mucous plugging.
Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes) and mast cell activation.
IgE-mediated allergic mechanisms (atopy, allergic rhinitis, eczema) with genetic predisposition.
Allergen exposure triggers mast cell degranulation and release of mediators leading to bronchospasm and mucosal edema.
Clinical manifestations and assessment
Wheezing, chest tightness, dyspnea, cough; use of accessory muscles; intercostal retractions; distant breath sounds with inspiratory wheeze.
Peak Expiratory Flow Rate (PEFR) zones via spirometry: green (80–100%), yellow (50–79%), red (<50%), guiding urgency and therapy.
Status asthmaticus: life-threatening severe asthma unresponsive to bronchodilators; may require intubation.
Diagnosis and management
Diagnosis from history, physical exam, sputum examination, pulmonary function tests, blood gas analysis, chest X-ray.
Treatments: prevention and desensitization; prophylactic drugs; acute bronchodilators (e.g., short-acting beta-agonists); corticosteroids; oxygen therapy.
Maintenance inhalers for daily control; rescue inhalers for acute symptoms.
Acute bronchitis and chronic bronchitis
Acute bronchitis: acute inflammation of the trachea and bronchi; often viral or mycoplasma; cough is hallmark; usually self-limited; antibiotics only if bacterial infection suspected.
Chronic bronchitis: usually linked to smoking; chronic inflammation with goblet cell hyperplasia and mucus gland hypertrophy; productive cough; diagnosed by clinical symptoms and PFT.
Emphysema (COPD component)
Pathophysiology: destruction of alveolar walls due to proteolytic enzymes; alveolar surface area reduction; air trapping and hyperinflation; loss of elastic recoil.
Classifications by location: centriacinar (upper lobes, most common), panacinar (all lobes), paraseptal (peripheral).
Clinical features: progressive exertional dyspnea; barrel chest; clubbing (in some); weight loss; decreased breath sounds.
Bronchiectasis
Recurrent infections and inflammation lead to permanent dilation of medium-sized bronchi and bronchioles; copious purulent sputum; hemoptysis; chest radiography and CT important for diagnosis; treated with antibiotics, bronchodilators, chest physiotherapy, postural drainage.
Cystic fibrosis (CF)
Autosomal recessive CFTR gene mutation; multisystem involvement (pancreas, GI, lungs, sweat glands); copious thick mucus; recurrent infections; infertility in males;
Diagnosis: sweat test (pilocarpine iontophoresis to measure sweat chloride), genetic testing, chest imaging, pulmonary function tests.
Management: bronchodilators; chest physiotherapy; mucolytics (e.g., DNase); antibiotics for infections; nutritional support; potential lung transplant.
Acute tracheobronchial obstruction
Causes: foreign body aspiration, endotracheal tube malposition, laryngospasm, epiglottitis, trauma, smoke inhalation, post-surgical clots, tumors.
Presentation: absent or reduced air movement, inability to speak, tachycardia, cyanosis; requires rapid airway management (back blows, abdominal thrust, suctioning, possibly tracheostomy).
Epiglottitis and croup (laryngotracheobronchitis)
Epiglottitis: rapid onset; drooling, dysphagia, fever, inspiratory stridor; red/swollen epiglottis on exam; management may include airway support and antibiotics; Hib vaccine is preventive.
Croup (Laryngotracheobronchitis, “froupe syndrome”): barking cough with inspiratory stridor; management is supportive; antivirals or steroids may be used depending on severity; some cases may require supplemental oxygen or nebulized therapy.
Pneumonia and tuberculosis (TB) in the obstructive-relevant context
Pneumonia: alveolar airspaces become filled with exudate; bacterial, viral, or atypical etiologies; diagnosis via chest X-ray, sputum Gram stain, cultures, WBC count; treatment often begins with broad-spectrum antibiotics pending culture results.
TB: caused by Mycobacterium tuberculosis; dormancy possible (latent TB); Ghon complex (calcified TB complex) visible on chest radiograph; evaluation with purified protein derivative (PPD) skin test or Interferon-Gamma Release Assays (QuantiFERON); sputum culture for confirmation; multi-drug antimicrobial therapy for 6–9 months; infection control in healthcare settings.
Lung cancer (pulmonary malignancies)
Histologic types: small cell (oat cell) carcinoma and non-small cell subtypes (squamous cell, adenocarcinoma, large cell, bronchioloalveolar carcinoma).
Central vs peripheral origins; metastasis via lymphatics; diagnosis via imaging (CXR, CT), cytology/histology, PET-CT; treatment depends on stage and type (surgery, chemotherapy, radiation, targeted therapies).
Chapter 23: Restrictive Pulmonary Disorders
Core concept
Restrictive disorders are characterized by reduced lung volumes and capacities due to stiffness or loss of compliance, leading to impaired expansion of the lungs.
Fibrotic and interstitial lung diseases
Examples include sarcoidosis, hypersensitivity pneumonitis (expensive allergic alveolitis), occupational lung diseases (pneumoconiosis).
Hypersensitivity pneumonitis: inflammatory lung disease due to inhaled antigens; can progress to fibrosis.
Pneumocystis pneumonia (Pneumocystis jirovecii) and other parenchymal diseases (inhaled inorganic dusts) contribute to restrictive patterns.
Acute respiratory distress syndrome (ARDS) and infant respiratory distress syndrome (IRDS)
ARDS: diffuse alveolar damage with increased vascular permeability; severe hypoxemia refractory to oxygen therapy; diffuse interstitial/alveolar edema; mortality high; treated with mechanical ventilation and supportive care.
IRDS (hyaline membrane disease): primarily in preterm infants due to surfactant deficiency; presents with respiratory distress, hypoxemia, poor lung compliance; managed with surfactant replacement and respiratory support.
Pneumothorax and pleural effusions
Pneumothorax: air in pleural space causing lung collapse; spontaneous or traumatic; management includes observation, supplemental oxygen, chest tube drainage depending on size and symptoms.
Pleural effusion: accumulation of fluid in pleural space; evaluation with thoracentesis to analyze fluid; imaging with ultrasound/CT; treatment targets underlying cause and symptom relief.
Pneumonia and its restrictive associations
Pneumonia can present with restrictive-looking patterns depending on the extent of lung involvement and diffuse edema; management includes antibiotics (depending on pathogen), supportive care, and oxygen therapy.
Neuromuscular and obesity-related respiratory disorders
Neuromuscular diseases: polio, ALS, muscular dystrophies, Guillain-Barré syndrome, myasthenia gravis, kyphoscoliosis, ankylosing spondylitis; all can contribute to restrictive physiology by limiting chest wall/diaphragmatic movement.
Obesity hypoventilation syndrome: obesity with chronic hypoventilation, daytime somnolence, hypercapnia, hypoxemia, polycythemia; management includes weight loss, ventilatory support, and addressing comorbidities.
Obesity and weight management in respiratory disease
Obesity is a major contributor to respiratory morbidity; weight loss strategies (nutrition, exercise, pharmacologic agents like GLP-1 agonists) are part of comprehensive care; weight loss improves respiratory mechanics and reduces comorbidity burden.
Pneumonia and SARS/COVID context in restrictive/obstructive frameworks
SARS (2003) and COVID-19 (2019–present) are viral pneumonias with potential progression to ARDS and multi-organ involvement; clinical courses vary; vaccination and public health measures influence outcomes; clinical management emphasizes isolation, supportive care, and evolving guidelines.
Tuberculosis (TB) re-emphasis in restrictive context
TB is a chronic infectious process with granulomatous inflammation; epidemiology and infectious control considerations relevant to respiratory disorders; diagnosis via PPD/QuantiFERON and sputum cultures; standard treatment is prolonged multi-drug therapy.
Practical and clinical implications
Recognize that restrictive patterns can arise from interstitial disease, neuromuscular weakness, chest wall abnormalities, or obesity-related hypoventilation.
Diagnostic workup includes PFTs, imaging (X-ray, CT), ABG, and targeted laboratory tests to identify etiology.
Treatment prioritizes management of the underlying cause, supportive care, and preventive strategies (vaccination, smoking cessation, weight management).
Key Concepts, Formulas, and Terms to Remember (LaTeX formatting)
Gas exchange and diffusion barriers
Diffusion across the alveolar-capillary membrane is driven by a concentration gradient.
Surfactant reduces surface tension to prevent alveolar collapse; composition: \text{surfactant} \approx 90\%\,\text{lipid} + 10\%\,\text{protein}
Oxygen transport
Oxygen dissolved in plasma: \approx 1.5\%
Oxygen bound to hemoglobin: \approx 98.5\%
Carbon dioxide transport forms
Dissolved in plasma
Bound to hemoglobin as carbaminohemoglobin
Bicarbonate ion: \mathrm{HCO_3^-} (major buffering form in blood; part of the carbonic acid–bicarbonate system)
Hemodynamics and pressures (pulmonary circulation)
Pulmonary arterial pressure and pulmonary vascular resistance influence gas exchange and right heart load.
Ventilation-perfusion concepts
Ventilation-perfusion ratio: \dfrac{V}{Q}
Hypoxic pulmonary vasoconstriction diverts blood from poorly ventilated regions to better-ventilated regions to optimize gas exchange.
Spirometry and lung volumes (key equations)
Forced Vital Capacity: \text{FVC} = \text{VT} + \text{IRV} + \text{ERV}
Tidal Volume: \text{VT}
Inspiratory Reserve Volume: \text{IRV}
Expiratory Reserve Volume: \text{ERV}
Forced Expiratory Volume in 1 second: \text{FEV}_1
Total Lung Capacity: \text{TLC}
Functional Residual Capacity: \text{FRC}
Peak expiratory flow rate (PEFR) zones (ASTHMA management)
Green zone: 80\% \leq \text{PEFR} \leq 100\%
Yellow zone: 50\% \leq \text{PEFR} < 80\%
Red zone: \text{PEFR} < 50\% (medical emergency)
Oxygenation thresholds (ABG/pulse oximetry reference points)
Hypoxemia and tissue hypoxia occur when arterial oxygen is insufficient to meet metabolic needs; ABG measures P{\mathrm{O2}} and P{\mathrm{CO2}}, among others.
Key clinical concepts to connect
Hering-Breuer reflex: prevents overinflation of the lungs.
Central vs peripheral chemoreceptors: drive ventilation changes in response to CO2, O2, and pH changes.
Mucus hypersecretion and airway remodeling in asthma; IgE-mediated allergic pathways; role of eosinophils and mast cells in airway inflammation.
Surfactant deficiency in IRDS and the importance of alveolar stability for gas exchange.
TB tubercle and Ghon complex concepts in radiography and infection control.
Ethical and practical implications
Early identification and escalation to higher levels of care (ER/hospital) when patients present with potentially life-threatening respiratory symptoms (e.g., chest pain with dyspnea, cyanosis, hypoxemia).
Emphasis on patient education, smoking cessation, vaccination (e.g., Hib for epiglottitis; influenza vaccines; TB screening in high-risk populations).
Weight management and lifestyle interventions as core components of reducing respiratory disease burden (e.g., obesity-hypoventilation syndrome, COPD risk from smoking).
The clinician’s role in ensuring collaboration with specialists and appropriate use of diagnostic testing (PFTs, ABG, imaging) to guide therapy.
Quick Reference Summary
Surfactant and alveolar mechanics are essential to prevent atelectasis and maintain gas exchange.
Oxygen transport is mainly bound to hemoglobin; a small fraction is dissolved in plasma.
CO2 is transported in three forms: dissolved, carbaminohemoglobin, and bicarbonate (HCO3−).
The PEFR zones guide asthma management and escalation.
Pulmonary hypertension, PE/DVT, pneumonia, and TB require timely recognition and appropriate specialty referral when indicated.
Obstructive diseases (asthma, COPD spectrum with bronchitis, emphysema, bronchiectasis) involve reversible/irreversible airflow limitation and distinct pathophysiologies.
Restrictive diseases include interstitial fibrosis, ARDS/IRDS, neuromuscular causes, obesity-related hypoventilation, and pleural diseases.
Diagnostic tools: ABG, chest X-ray, CT, sputum culture, PFTs (spirometry), PEFR, and specialized tests (e.g., methacholine challenge).
Medical management emphasizes symptom control, prevention, and addressing underlying etiologies; emergency scenarios require rapid airway management and stabilization.
If you’d like, I can tailor these notes to a specific chapter or topic focus (e.g., only obstructive diseases, or only gas exchange physiology) or convert to a printable study guide with condensed bullet points and highlighted exam-style questions.