Respiratory System Disorders – Comprehensive Study Notes

Lung Anatomy

• Right lung: three lobes (upper, middle, lower) - Right lung is where you most commonly get Aspiration PNU

  • Right main (primary) bronchus is shorter, wider, and more vertical → higher risk that aspirated material, foreign bodies, or vomitus will enter the right middle & lower lobes.

• Left lung: two lobes (upper & lower) - Only two to make room for the heart

  • Left main bronchus more curved → ↓ aspiration risk.

• Clinical connection

  • When assessing aspiration pneumonia, first auscultate right middle‐lobe area (5th ICS, right mid-axillary line).

  • Post-stroke, dysphagic, or intoxicated patients = highest aspiration risk.

Goblet Cells & Mucous Production

• Location: entire respiratory epithelium + portions of GI tract.

• Function: secrete mucin → combines with water → mucus layer.

• Ultrastructure

  • Prominent rough ER & Golgi → high protein synthesis for mucin.

  • Secretory vesicles migrate to apical membrane & exocytose.

• Clinical relevance

  • Goblet-cell hyperplasia occurs in chronic bronchitis → excess sputum.

  • Cystic fibrosis: defective Cl⁻ transport → dehydrated mucus → impaired ciliary clearance.

Mechanics of Breathing (Ventilation)

• Inspiration (active) - The pressure decreases on inspiration because the space inside the lungs is increasing

  • Diaphragm contracts & flattens; external intercostals lift ribs.

  • Thoracic cavity length & diameter ↑ → intrathoracic & intra-alveolar pressure ↓ below atmospheric.

  • Air flows into alveoli until pressure equilibrates.

  • Parietal pleura pulls visceral pleura, ensuring lung expansion.

• Expiration (mostly passive)

  • Diaphragm & intercostals relax.

  • Elastic recoil of lungs + ↓ thoracic volume → intra-alveolar pressure ↑ above atmospheric.

  • Air flows out to atmosphere.

• Ventilation graphic: p. 276 Fig 13.2 (see linked video for kinetic animation).

Control of Ventilation - CO2 is what stimulates the Medulla to breathe

• Neural centers

  • Medulla oblongata → sets basic rhythmic drive.

  • Pons (pneumotaxic & apneustic areas) → fine-tunes length of inspiration & expiration, smooths transitions.

• Chemoreceptor feedback

  • Central (medullary) receptors

  • Sense ↑ \text{CO}_2 (hypercapnia) & ↓ pH in CSF.

  • Acute hypercapnia/acidosis → powerful stimulus to ↑ rate & depth.

  • Peripheral (aortic & carotid bodies)

  • Respond to ↓ \text{O}_2 (< 60 \text{ mm Hg}) & ↓ pH.

  • Become dominant “hypoxic drive” in chronic hypercapnia (e.g., COPD).

• Practical implications

  • COPD patients may rely on \text{O}2 levels to breathe—excessive \text{O}2 administration can blunt drive.

  • Sedatives, opioids, or tranquilizers further depress medullary center—use cautiously.

Lung Volumes & Capacities - Do not need to know the totals

• Tidal Volume (TV): 500 \text{ mL} – quiet breathing in/out.

• Residual Volume (RV): 1{,}200 \text{ mL} – air left after max exhalation.

• Vital Capacity (VC): 4{,}600 \text{ mL} – max air moved in one breath (IRV + TV + ERV).

• Total Lung Capacity (TLC): 5{,}800 \text{ mL} – VC + RV (all air in lungs).

• Clinical pearls

  • Emphysema ↑ RV & TLC (air trapping).

  • Restrictive diseases ↓ VC & TLC.

Perfusion & Ventilation–Perfusion (V/Q) Matching * for effective gas exchange you have to have effective Perfusion and Ventilation

• Perfusion: blood flow through alveolar capillaries.

• Optimal gas exchange requires both adequate ventilation (V) and perfusion (Q).

• Nursing exam Q (PE):

  • Pulmonary embolism impairs perfusion while ventilation is preserved → option C.

Oxyhemoglobin & Gas Transport Bright red blood is Artery Deoxygenated blood is Dark colored

• \text{O}_2 binds to Fe²⁺ on hemoglobin → oxyhemoglobin (bright red arterial blood).

• In tissues: ↓ PO₂, ↑ \text{CO}2, ↑ H⁺ (Bohr effect) → Hb releases \text{O}2 → venous blood dark/bluish-red.

• Significance

  • Pulse oximetry estimates % saturation.

  • Severe anemia: normal saturation but ↓ total \text{O}_2 content.

Stimulus of Breathing & Hypercapnia vs Hypoxic Drive

• Normal: slight ↑ \text{CO}_2 (hypercapnia) → strongest respiratory stimulant. - TOO much CO2

• Chronic hypercapnia (e.g., COPD)

  • Central receptors become insensitive → peripheral chemoreceptors take over.

  • Patient depends on low \text{O}_2 to breathe.

  • Oxygen therapy must be titrated to maintain \text{SpO}_2 ≈ 88–92\%.

Manifestations of Respiratory Disease

• Hypercapnia: headache, drowsiness, CO₂ narcosis.

• Cyanosis: bluish skin/mucosa due to >5 \text{ g/dL} deoxygenated Hb. - When the Patient is Blue

• Adventitious Breath Sounds

  • Wheeze → small airway obstruction (asthma, COPD). Wheezing = Asthma

  • Stridor → upper airway obstruction (croup, foreign body). Stridor = gasping or choking

  • Rales/crackles → serous fluid (pulmonary edema) or pneumonia. Crackles = Fluids

  • Rhonchi → coarse, low-pitched, thick mucus (bronchitis). Rhonci = Bronchitis

• Altered patterns

  • Kussmaul respirations: deep, rapid, compensatory for metabolic acidosis. PH related

  • Labored/prolonged expiration → obstructive pathology.

Pleural Membrane & Pleural Space Disorders

• Anatomy: visceral pleura (lung surface) & parietal pleura (thoracic wall) with lubricating fluid.

• Negative intrathoracic pressure keeps lungs expanded.

• Pleural effusion: fluid accumulation → restricts lung inflation. ( lungs cannot inflate due to fluid around the lung)

  • MC symptom: pleuritic chest pain worsening on inspiration (answer B).

  • May require thoracentesis.

• Pneumothorax: air entry → loss of negative pressure → lung collapse.

Atelectasis (Alveolar Collapse)

• Pathophysiology

  • Obstructive: mucus plug, tumor –> air distal to blockage absorbed.

  • Compressive: external mass, pleural effusion, post-op abdominal splinting.

  • Surfactant deficiency ↑ surface tension.

• Post-operative risk: within 24–72 h (esp. abdominal surgery) due to hypoventilation & pain.

• Clinical presentation

  • Small area → asymptomatic; large → dyspnea, tachycardia, tachypnea, chest pain, mediastinal shift, asymmetric chest rise.

• Management: incentive spirometry, early ambulation, bronchoscopy for mucus removal.

Pneumonia

• Definition: infection‐induced inflammation → alveolar exudate (‘infiltrate’ on CXR).

• Categories

  • Community-acquired (CAP): Streptococcus pneumoniae MC; also viral.

  • Hospital-acquired (HAP): >48 h post-afremitus, Staphylococcus aureus (incl. MRSA). Staph is the most common cause

  • Aspiration: GI or oral bacteria; multiple lobes; common in impaired gag reflex.

  • Viral: Influenza A/B, RSV – begins upper airway, descends.

  • Atypical “walking pneumonia”: Mycoplasma pneumoniae.

• Pneumococcal pneumonia specifics

  • Localized to one/more lobes, can glue pleural layers (adhesions).

  • S&S: sudden high fever, rales, pleuritic pain, productive “rusty” sputum, leukocytosis, confusion in elderly.

  • Vaccine (PCV13, PPSV23) available.

• General clinical picture

  • Cough (± sputum/hemoptysis), fever/chills (maybe absent elderly), pleuritic chest pain (Chest pain related to breathing), dyspnea, tachypnea, ↑ tactile fremitus, dull percussion.

Asthma

• Chronic hyper-reactive airway disorder with reversible bronchoconstriction.

• Triggers: allergens, viral infections, exercise, GERD (nocturnal), occupational, cold air.

• Pathophysiology

  • IgE-mediated mast-cell release → histamine, leukotrienes → bronchoconstriction, edema, mucus.

  • Each attack ⇒ airway remodeling (smooth muscle hypertrophy, basement membrane thickening).

• Clinical features

  • Expiratory wheeze, prolonged expiration, cough, chest tightness, use of accessory muscles, pulsus paradoxus in severe attack.

• Peak-flow meters assess severity; step-up therapy (SABA, ICS, LABA, LTRA, biologics).

• Humorous meme: “It ain’t easy wheezy bein’ wheezy when you pass a smoker.”

Chronic Obstructive Pulmonary Disease (COPD)

Overview

• Umbrella term: chronic bronchitis + emphysema ± hyperreactive airways.

• Primary cause: cigarette smoking (also chronic wood-smoke, alpha-1 antitrypsin deficiency).

• Shared features: airflow limitation non-reversible, chronic inflammation, progressive.

Chronic Bronchitis (“Blue Bloater”)

• Diagnostic criteria: productive cough ≥3 months/yr for ≥2 consec. yrs.

• Pathology: mucus gland & goblet cell hyperplasia → thick sputum, airway narrowing.

• S&S: cyanosis, chronic hypoxia, cough, wheeze/rhonchi, digital clubbing, peripheral edema (cor pulmonale).

• Pulmonary vasoconstriction → pulmonary HTN.

Emphysema (“Pink Puffer”)

• Pathology: permanent enlargement & destruction of distal airspaces, loss of elastic recoil.

• Consequences: air trapping, ↑ RV/TLC, hyperinflated ‘barrel’ chest, flattened diaphragm, prolonged exhalation, accessory muscle use.

• Often thinner pt, relatively well oxygenated (pink) but dyspneic.

Pink Puffer vs Blue Bloater Table (key distinctions)

• Pink: ↓ BMI, less cardiovascular co-morbidities, more dyspnea, hyperinflation, ↓ diffusion capacity.

• Blue: ↑ BMI, metabolic & cardiac co-morbidities, OSA overlap, chronic bronchitis predominance, ↑ exacerbations, higher IL-6 & CRP.

Changes in Breathing Stimulus

• Chronic \text{CO}_2 retention → chemoreceptor desensitization.

• Peripheral \text{O}2 sensors drive respiration → keep \text{SpO}2 low-normal.

• Caution with high-flow \text{O}_2, sedatives, opioids.

Mnemonic for Alveolar Changes

• P – pursed-lip breathing

• I – increased chest (barrel)

• N – nonproductive cough (emphysema)

• K – keep tripod position

• B – big & blue (blue bloater)

• L – long-term cough with sputum

• U – unusual breath sounds (rhonchi, wheeze)

• E – edema (peripheral)

Pulmonary Edema

• Most common etiology: left-ventricular failure (LVF).

  • LV can’t eject → blood backs into LA & pulmonary veins → ↑ hydrostatic pressure → fluid leaks into alveoli.

• Presentation: severe dyspnea, orthopnea, pink frothy sputum, diffuse crackles.

• CXR: bilateral perihilar “bat-wing” opacities.

• Acute management: high-flow \text{O}_2, diuretics (furosemide), nitrates, morphine, treat LV dysfunction.

Pulmonary Embolism (PE) A blood Clot going on vacation to the Lungs

• Clot lodges in pulmonary arterial tree; usually from lower-extremity DVT or right atrial thrombus (a-fib).

• Pathophysiology: perfusion blocked → V/Q mismatch (V normal, Q zero) → hypoxemia.

• Clinical spectrum: asymptomatic micro-emboli to massive saddle embolus causing sudden death.

• Classic triad (only in ~10\%): dyspnea, pleuritic chest pain, hemoptysis.

• Signs/Sx by size

  • Small: transient chest pain, cough, mild dyspnea.

  • Large: sudden dyspnea, tachypnea, pleuritic pain ↑ with cough/deep breath, hemoptysis(couhging blood + fever, hypotension, syncope.

• Diagnostic work-up: D-dimer, CT angiography, V/Q scan, lower-extremity Doppler.

• Prevention: early ambulation, SCDs, anticoagulation post-op.

Ethical, Philosophical & Practical Considerations

• Smoking cessation remains the most effective COPD prevention—public health priority.

• Vaccination (influenza & pneumococcal) ethically imperative in at-risk groups to curb morbidity/mortality.

• Balancing oxygen therapy: do no harm vs relieving hypoxia in COPD; monitor ABGs & SpO₂.

• End-of-life discussions in severe COPD & pulmonary fibrosis—address quality of life, advanced directives.

Quick Review Questions & Answers

1. PE affects which V/Q component? → Perfusion impaired; ventilation preserved (C).

2. Commonest symptom of pleural effusion? → Sharp chest pain worsened by inspiration (B).

Key Equations & Figures (expressed symbolically)

• Ideal gas flow during inspiration: Q = \dfrac{\Delta P}{R} where \Delta P = P{atm} - P{alveoli}.

• Minute ventilation: \dot V_E = TV \times RR.

• Alveolar gas equation: P{A\,O2} = (P{atm} - P{H2O})F{i\,O2} - \dfrac{P{A\,CO_2}}{R} (useful in V/Q mismatch).

External Resources & Videos Mentioned

• Ventilation animation: https://www.youtube.com/watch?v=NM3PK5qy9uA

• Asthma cartoon explanation: https://www.youtube.com/watch?v=zSSoYmQS6Ng

  • Use for visual learners; embeds pathophysiology in humorous context.