Patho Week 5 9/29/2026

Pulmonary Function and Gas Exchange

Which structures conduct air?

Nasopharynx, oropharynx, larynx, trachea, bronchi + terminal bronchioles

Which structures perform gas exchange?

Respiratory bronchioles, alveolar ducts + alveoli.

How does pulmonary circulation differ from systemic circulation?

It is a low-pressure system that carries blood to the lungs for gas exchange.

What are ventilation, perfusion, and diffusion?

Ventilation = air reaches alveoli. Perfusion = blood reaches alveolar capillaries. Diffusion = O₂/CO₂ cross the alveolar-capillary membrane.

What factors decrease O₂ diffusion?

↓ Surface area + thick membrane + low alveolar O₂ + poor ventilation + poor perfusion.

What determines alveolar O₂ tension?

Barometric pressure + water vapor + FiO₂ + adequacy of ventilation.

What is normal adult tidal volume?

About 400–500 mL per breath.

What is lung compliance?

Ease of lung expansion; ↓ compliance means stiff lungs + ↑ work of breathing.

What are FVC and FEV₁?

FVC = total air forcefully exhaled; FEV₁ = air exhaled in the first second.

How do emphysema, pneumonia, and PE impair gas exchange differently?

Emphysema destroys surface area. Pneumonia fills/thickens alveoli. PE blocks pulmonary perfusion.

What is a V/Q mismatch?

Ventilation does not match perfusion → oxygenation decreases.

What is low V/Q?

Blood reaches poorly ventilated alveoli (wasted perfusion); examples: pneumonia

What is high V/Q?

Air reaches alveoli with little blood flow (dead space); classic example: PE.

What is the normal overall V/Q ratio?

About 0.8 because normal perfusion is slightly greater than ventilation.

What is a shunt?

Blood reaches alveoli that receive little/no air (example: fluid-filled alveoli in pneumonia).

What is dead space?

Alveoli receive air but little/no blood flow (example: pulmonary embolism).

How do hypoxemia and hypoxia differ?

Hypoxemia = low O₂ in arterial blood (↓ PaO₂). Hypoxia = inadequate O₂ reaching/being used by tissues.

How does the body initially respond to hypoxemia?

Hyperventilation → ↓ PaCO₂ + ↑ pH.

Can tissue hypoxia occur with a normal PaO₂?

Yes. Anemia = not enough hemoglobin to carry O₂. Poor cardiac output = not enough oxygenated blood reaches tissues.

What are early versus late findings of hypoxemia?

Early = restlessness + anxiety + tachypnea + tachycardia + diaphoresis. Late = confusion + cyanosis + decreased LOC.

What findings suggest chronic hypoxemia?

Polycythemia + clubbing + cyanosis + pulmonary hypertension.

How does chronic hypoxemia cause polycythemia?

Low O₂ → kidneys release erythropoietin → bone marrow produces more RBCs.

How does chronic hypoxemia cause pulmonary hypertension?

Low alveolar O₂ → pulmonary vasoconstriction → ↑ pulmonary vascular resistance → ↑ pulmonary artery pressure.

How do shortness of breath and dyspnea differ?

SOB = patient reports difficulty breathing. Dyspnea includes observable increased work of breathing (accessory muscles

How do bradypnea, hypoventilation and hypopnea differ?

Bradypnea = slow rate; hypoventilation = inadequate ventilation with CO₂ retention; hypopnea = shallow breaths.

What does hypoventilation do to ABGs?

CO₂ is retained → ↑ PaCO₂ → respiratory acidosis.

What is the difference between tachypnea, hyperpnea, and hyperventilation?

Tachypnea = rapid rate. Hyperpnea = deeper breathing. Hyperventilation = breathing removes too much CO₂ → ↓ PaCO₂.

What is Kussmaul breathing?

Deep, rapid breathing used to compensate for metabolic acidosis.

What are agonal respirations?

Gasping, ineffective breaths indicating a life-threatening emergency.

How do normal breath sounds differ?

Bronchial: expiration longer; bronchovesicular: equal; vesicular: inspiration longer + softer.

What do type I and type II alveolar cells do?

Type I = thin cells used for gas exchange. Type II = produce surfactant → ↓ surface tension → prevent alveolar collapse.\

What is hypoxemic respiratory failure?

PaO₂ ≤60 mm Hg from inadequate oxygen transfer.

What is hypercapnia?

Elevated arterial CO₂, usually from hypoventilation; it can cause respiratory acidosis.

Which tests commonly evaluate pulmonary disease?

ABG, cultures, imaging, capnography + PFTs; invasive tests include bronchoscopy, thoracentesis and lung biopsy.

When should PFTs be avoided?

During acute respiratory illness because results may not reflect baseline lung function.

What is thoracentesis?

Needle/catheter removal of pleural fluid for diagnosis and/or symptom relief.

What ABG pattern suggests hypoventilation?

↓ PaO₂ + ↑ PaCO₂ + ↓ pH (respiratory acidosis).

What is hypoxic pulmonary vasoconstriction?

Low alveolar O₂ causes pulmonary vessels to constrict.

What is the purpose of hypoxic pulmonary vasoconstriction?

Redirect blood toward better-ventilated alveoli.

What can chronic hypoxic pulmonary vasoconstriction cause?

Pulmonary hypertension → right-heart overload → cor pulmonale.

Acute Respiratory Failure

What is acute respiratory failure and what ABGs support it?

Sudden failure to oxygenate blood and/or remove CO₂. PaO₂ <60 and/or PaCO₂ >50 with acidemia may support the diagnosis.

How do hypoxemic and hypercapnic respiratory failure differ?

Hypoxemic = gas-exchange failure → ↓ PaO₂. Hypercapnic = ventilation failure → ↑ PaCO₂ + respiratory acidosis.

What findings suggest worsening respiratory failure?

Severe dyspnea + accessory-muscle use + low SpO₂ + restlessness/confusion. Fatigue + rising PaCO₂ + decreasing LOC = impending failure.

Why is a rising PaCO₂ dangerous in a patient who was breathing rapidly?

Respiratory muscles are tiring → ventilation is failing → CO₂ is no longer removed.

A patient’s PaO₂ and PaCO₂ are both low. What is happening?

Hypoxemia is stimulating tachypnea/hyperventilation → extra CO₂ is exhaled.

A patient’s PaO₂ remains low while PaCO₂ rises. What is happening?

The patient is tiring → hypoxemic and hypercapnic respiratory failure is developing.\

Pneumonia

What is pneumonia and how does it cause hypoxemia?

Inflammation of alveoli/bronchioles → fluid and exudate fill alveoli → ventilation decreases while perfusion continues → low V/Q → ↓ PaO₂.

What increases pneumonia risk?

Virulent organism + large exposure + weak host defenses. Other risks = age

How do bacterial and viral pneumonia differ?

Bacterial = neutrophils/purulent exudate fill alveoli → productive cough + consolidation. Viral = mainly interstitial inflammation → often dry cough; may lead to secondary bacterial pneumonia.

How do CAP, HAP, and VAP differ?

CAP = community-acquired. HAP = hospital-acquired. VAP = ventilator-associated.

What findings suggest pneumonia?

Fever/chills + cough/sputum + dyspnea + tachypnea + crackles/decreased breath sounds + low SpO₂ + pleuritic pain.

Why do crackles occur with pneumonia?

Air moves through fluid-filled alveoli or causes collapsed alveoli to reopen.

What is consolidation?

Normally air-filled alveoli become filled with inflammatory material → lung tissue becomes dense/solid → ventilation decreases.

What are the major complications of pneumonia?

Atelectasis + pleural effusion/empyema + abscess + sepsis + ARDS + respiratory failure.

A pneumonia patient becomes confused

hypotensive

How is pneumonia diagnosed and treated?

Chest X-ray may show infiltrates/consolidation. SpO₂/ABGs assess oxygenation, CBC may show leukocytosis, and sputum culture identifies bacteria. Treatment supports oxygenation and targets the cause; bacterial pneumonia requires antibiotics

Tuberculosis

What causes TB and how is it spread?

Mycobacterium tuberculosis spreads through airborne droplets from active pulmonary/laryngeal TB. Crowded

What is the TB disease pathway?

Organisms multiply → cell-mediated immune response → granuloma forms → infection becomes latent or active.

How do latent and active TB differ?

Latent = organisms contained, no symptoms, not contagious. Active = organisms multiply, damage tissue, cause symptoms, and pulmonary TB may spread

What can reactivate latent TB?

Weak immunity from HIV, cancer, malnutrition, older age, or immunosuppressive medications.

What findings suggest active pulmonary TB?

Chronic cough + hemoptysis + weight loss + anorexia + malaise + night sweats. Not every patient has every symptom.

What are pulmonary, extrapulmonary, and miliary TB?

Pulmonary = lungs. Extrapulmonary = outside lungs. Miliary = TB spreads through blood to multiple organs.

What do PPD and QuantiFERON show?

TB infection and an immune response. They do not prove active disease or distinguish active from latent TB.

How is active pulmonary TB diagnosed?

Chest imaging + sputum AFB smear + sputum culture. Culture confirms TB and checks medication resistance.

How is extrapulmonary TB diagnosed?

Culture/test the affected tissue, wound, or body fluid.

What complications can TB cause?

Lung destruction/cavities + TB pneumonia + pleural effusion/empyema + respiratory failure + organ involvement.\

Chest Pain

How does pleuritic chest pain differ from cardiac pain?

Pleuritic pain = sharp and worse with deep breathing/coughing. Cardiac pain = usually pressure/heaviness and does not directly change with breathing.

What pulmonary conditions can cause pleuritic chest pain?

Pneumonia + pleuritis + pulmonary embolism + pneumothorax + pleural effusion.\

Restrictive Disorders

Types of restrictive lung disease?

• Aspiration

• Bronchiectasis

• Atectasis

• Broncholitis and bronciolitis Obliterans

• Pulmonary Edema

• ARDS

What is the easiest way to remember restrictive lung disease?

“Bear hug” → lungs cannot fully expand → ↓ compliance + ↓ lung volume → difficult inhalation.

How do restrictive and obstructive lung disease differ?

Restrictive = bear hug (hard to expand/inhale). Obstructive = breathing through a straw (hard to push air out/exhale).

What happens during restrictive lung disease?

Inflammation, fluid, alveolar collapse, or fibrosis → lungs become stiff → ↓ compliance and lung volume → rapid shallow breathing + hypoxemia.

What findings suggest restrictive disease?

Progressive dyspnea + tachypnea + dry cough + hypoxemia ± cyanosis/clubbing.

What PFT changes suggest restrictive disease?

↓ lung volumes/FVC with a normal or ↑ FEV₁/FVC ratio.

Why is wheezing often absent in restrictive disease?

The main problem is stiff lung tissue, not narrowed airways.

What is lung compliance?

Compliance decreases with edema, inflammation, fibrosis, or alveolar collapse.\

Aspiration

What is aspiration and who is at risk?

Food, fluid, saliva, vomit, or gastric contents enter the lungs. Risk = decreased LOC, dysphagia, stroke, sedation, seizures, vomiting, or weak gag reflex.

What happens after aspiration?

Material enters lungs → obstruction/chemical injury → inflammation → impaired gas exchange.

What findings and complications can aspiration cause?

Sudden coughing/choking + wheezing/crackles + dyspnea + low SpO₂. Complications include pneumonia, bronchiectasis, ARDS, respiratory failure, or death.

What complications can aspiration cause?

Aspiration pneumonia + bronchiectasis + ARDS + respiratory failure + death.\

How is aspiration evaluated?

Focused respiratory assessment + SpO₂ + chest X-ray; ABG if severe and swallowing evaluation if dysphagia is suspected

Bronchiectasis

What is bronchiectasis and how does it progress?

Repeated infection/inflammation destroys airway support → permanent bronchial dilation → mucus trapping → more infection.

What can cause bronchiectasis?

Recurrent infections, chronic aspiration, airway obstruction, cystic fibrosis, or immune problems

What findings strongly suggest bronchiectasis?

Chronic cough + copious foul-smelling sputum + recurrent infections + possible hemoptysis.

Why may bronchiectasis sputum smell foul?

Mucus remains trapped → bacteria multiply → pus forms.

How does bronchiectasis differ from chronic bronchitis?

Bronchiectasis = permanently dilated/damaged bronchi with copious foul sputum. Chronic bronchitis = chronic mucus-producing airway inflammation related mainly to irritants/smoking.

Is bronchiectasis restrictive or obstructive?

Primarily obstructive because damaged, mucus-filled airways limit airflow. Severe disease may cause mixed changes

How is bronchiectasis diagnosed?

History of recurrent infection/copious sputum + chest imaging; CT shows permanently dilated bronchi.

Atelectasis

What is atelectasis and what causes it?

Incomplete expansion/collapse of alveoli caused by shallow breathing, immobility, mucus obstruction, compression, pneumothorax, abdominal distention, or surfactant loss.

Why are postoperative patients at risk for atelectasis?

Pain + sedation + immobility → shallow breathing → alveoli collapse.

How does atelectasis cause hypoxemia?

Blood reaches collapsed alveoli with little/no ventilation → low V/Q → ↓ PaO₂.