N4S1 Critical Care: COPD, PAH

COPD

Irreversible lung and airway damage that obstructs airways and makes it hard to breathe.

Emphysema

COPD type where alveoli become damaged and enlarged; destruction of alveolar walls → ↓ surface area for gas exchange.

Chronic bronchitis

COPD type with inflammation of large airways, airway narrowing, and excessive mucus production; cough is the most common symptom.

Loss of elasticity

Loss of elastic recoil in airways and alveoli contributing to airflow limitation in COPD.

Inflammation & scarring

Chronic inflammation in COPD causes scarring (fibrosis) and narrowing of airways.

Thick mucus

↑ goblet cells and enlarged mucus glands produce thick mucus, causing mucus plugging and impaired ciliary clearance.

Destruction of alveolar walls

Leads to enlarged airspaces, air trapping, and impaired gas exchange in emphysema.

↑ Dead space

Alveolar destruction increases physiologic dead space → ↓ oxygen diffusion → hypoxemia.

↓ Pulmonary capillary bed

Loss of capillary bed from alveolar destruction → ↑ pulmonary vascular resistance → pulmonary hypertension.

Cor pulmonale

Right-sided heart failure from pulmonary disease; signs include dependent edema, distended neck veins, and liver pain.

Chronic cough

Common early symptom of COPD; may be intermittent or unproductive.

Sputum production

Chronic and persistent sputum production especially in chronic bronchitis.

Wheezing

Common lung sound in COPD due to airway obstruction.

Cyanosis

Bluish skin or lip discoloration from hypoxemia seen in advanced disease.

Dyspnea

Progressive shortness of breath, worse with exertion and possibly at rest in advanced COPD.

Weight loss

Occurs due to difficulty eating and increased work of breathing in advanced COPD.

Accessory muscle use

Recruitment of accessory muscles for breathing over time in COPD patients.

Barrel chest

Chronic hyperinflation in emphysema causing an increased anteroposterior diameter.

Supraclavicular retraction & shoulder heaving

Signs during inspiration in hyperinflated emphysematous lungs.

Alpha-1 antitrypsin deficiency

Genetic risk factor causing imbalance of proteinases > antiproteinases and lung parenchymal damage.

Tobacco smoke

Major risk factor; exposure accounts for an estimated 80–90% of COPD cases.

Secondhand smoke

Recognized risk factor for COPD.

Occupational exposure

Dust, chemicals, and fumes at work increase risk for COPD.

Air pollution

Environmental contributor to COPD development and progression.

Increased age

Normal aging causes ↓ vital capacity and ↓ FEV1 and accelerates COPD incidence.

Proximal airway changes

↑ goblet cells and enlarged submucosal glands → mucus hypersecretion in proximal airways.

Peripheral airway changes

Bronchioles <2 mm develop wall thickening, peribronchial fibrosis, exudate → obstructive bronchiolitis.

Parenchymal changes

Alveolar wall destruction → loss of alveolar attachments and ↓ elastic recoil impairing gas exchange.

Pulmonary vasculature changes

Chronic inflammation → vessel-lining thickening and smooth muscle hypertrophy contributing to PH.

Spirometry

Pulmonary function test used to evaluate airflow obstruction (FEV1/FVC) and bronchodilator reversibility.

FEV1/FVC ratio

Spirometric ratio used to determine presence of airflow obstruction in COPD.

Pulse oximetry

Noninvasive measure of oxygen saturation (SpO₂) used in COPD and PH monitoring.

Chest X-ray/CT scan

Imaging to detect lung changes from COPD (e.g., hyperinflation, structural changes).

Arterial blood gas (ABG)

Blood test to measure PaO₂ and PaCO₂ for oxygenation and ventilation assessment.

Exercise testing

Tests whether oxygen levels drop with exertion and helps evaluate exertional dyspnea.

ECG

Assesses heart function and can help rule out cardiac causes of dyspnea.

AAT blood level

Blood test to check alpha-1 antitrypsin levels for deficiency screening.

Genetic testing

Blood tests to detect genetic causes (e.g., AAT deficiency) for early onset COPD.

Pneumonia risk

COPD can trap bacteria leading to increased risk of pneumonia.

Hypercapnia

↑ PaCO₂ (CO₂ retention) can occur in COPD and requires monitoring.

Hypoxemia

↓ PaO₂ (low oxygen) commonly seen in advanced COPD and PH.

Respiratory failure

Severe complication of COPD when gas exchange is insufficient.

Pneumothorax

Possible complication from COPD (collapsed lung).

Polycythemia

Secondary increase in RBC count from chronic hypoxemia in COPD.

Smoking cessation

Single most cost-effective intervention to prevent COPD and stop progression.

Inhaled bronchodilators

Medications to open airways and relieve airflow obstruction in COPD.

Inhaled corticosteroids

Reduce airway inflammation; used in COPD management/exacerbations.

Oxygen therapy

Used to improve PaO₂, relieve hypoxia, and reduce pulmonary vasoconstriction.

Pulmonary rehabilitation

Program to reduce symptoms, improve quality of life, and increase participation.

Systemic corticosteroids

Used during COPD exacerbations to reduce inflammation.

Antibiotics in COPD

Prescribed for frequent bacterial infections and to prevent exacerbations.

Lung volume reduction (LVR)

Surgical/valve procedures to reduce trapped air in severe COPD candidates.

Diuretics in COPD

Used to reduce fluid overload, decrease cardiac workload and oxygen demand.

Diaphragmatic breathing

Nursing intervention to improve ventilation efficiency in COPD patients.

Pursed-lip breathing

Technique taught to help control dyspnea and improve exhalation.

Effective coughing

Nursing instruction to assist secretion clearance and airway hygiene.

Postural drainage w/ percussion & vibration

Respiratory physiotherapy used if prescribed to mobilize secretions.

Avoid bronchial irritants

Patient education to avoid cigarette smoke, aerosols, extreme temperatures, and fumes.

Oxygen therapy goal (COPD)

Raise PaO₂ ≥ 60 mmHg and achieve SaO₂ ≥ 90%.

Long-term oxygen therapy (LTOT)

Recommended ~15 hours/day for eligible COPD patients.

LTOT indications

PaO₂ ≤ 55 mmHg or SaO₂ ≤ 88%, cor pulmonale, secondary polycythemia, or impaired mental status.

Oxygen therapy types

Continuous (24 hr), exercise-induced, and intermittent (for ADLs/exertion/sleep).

Monitor SpO₂ & RR

Nurse monitors respiratory rate and SpO₂, aiming to keep SpO₂ ≥ 90% at lowest flow.

ABG indications in COPD

Get ABG when SaO₂ ≤ 88% or if hypercapnia is suspected.

Risks of excess O₂

Excess O₂ can suppress CO₂ chemoreceptors → ↓ respiratory drive and CO₂ retention.

V/Q mismatch risk

Excess oxygen may worsen ventilation–perfusion mismatch and cause hypercapnia.

Pulse oximetry limit

Pulse oximetry does not measure PaCO₂ (does not detect CO₂ retention).

Contributing factors to CO₂ retention

Neurologic impairment, electrolyte imbalance, opioids, sedatives.

Pulmonary Hypertension (PH)

Condition with high blood pressure in pulmonary arteries that can cause right heart failure.

PH diagnostic thresholds

Pulmonary arterial pressure >25 mmHg at rest or >30 mmHg with exercise.

PH clinical presentation

May present initially with exertional dyspnea and is often clinically silent early.

WHO PH classification

Five groups based on mechanism: Group 1 PAH, Group 2 left heart disease, Group 3 lung disease/hypoxemia, Group 4 CTEPH, Group 5 unclear/multifactorial.

Group 1 PAH examples

Idiopathic, heritable, drug/toxin-induced, connective tissue disease, HIV, portal HTN, congenital heart disease.

Group 2 PH

Due to left heart disease: systolic/diastolic dysfunction or valvular heart disease.

Group 3 PH

Due to chronic lung diseases and/or hypoxemia such as COPD, interstitial lung disease, or sleep apnea.

Group 4 CTEPH

Chronic thromboembolic pulmonary hypertension from thromboembolic occlusion of pulmonary vasculature.

Group 5 PH

PH with unclear or multifactorial mechanisms (e.g., hematologic, systemic, metabolic disorders).

PH pathophysiology

Endothelial dysfunction, vascular smooth muscle dysfunction, hypertrophy and intimal/adventitial proliferation.

Pulmonary vascular resistance mechanisms

Caused by vasoconstriction (hypoxemia/hypercapnia) or reduced vascular bed (embolism).

RV effects of PH

Increased pulmonary pressure → RV hypertrophy, dilation, and eventual right ventricular failure.

Systemic effects of PH

Passive hepatic congestion leading to hepatomegaly and right upper quadrant pain.

PH early symptom

Shortness of breath during daily activities (e.g., stairs, shopping) — often the first symptom.

PH respiratory signs

Decreased breath sounds, tubular breath sounds, crackles, and reduced diaphragmatic excursion.

PH cardiac signs

Substernal chest pain, tachycardia, syncope/near-syncope, displaced apical impulse, RV lift, murmurs.

PH systemic signs

Fatigue, weakness, anorexia, abdominal pain, occasional hemoptysis.

Right-sided heart failure signs

Peripheral edema, ascites, jugular venous distention (JVD), liver engorgement.

PH initial evaluation

History & physical, check JVD, palpate liver, inspect edema, auscultate heart/lungs, measure SpO₂.

Chest X-ray in PH

May show enlarged central pulmonary arteries and attenuation of peripheral vessels; RA/RV dilation.

Pulmonary function studies in PH

May be normal or show mild ↓ vital capacity, ↓ compliance, or ↓ diffusing capacity.

ECG in PH

May show RV hypertrophy, right axis deviation, tall P waves, tall R waves anteriorly, ST/T changes.

Echocardiogram in PH

Doppler echo estimates systolic PAP and evaluates RV/RA size, thickness, and function.

Right heart catheterization

Gold standard to confirm PH; measures pulmonary artery pressure, mean PAP >25 mmHg confirms PH.

V/Q scan in PH

Detects blood clots and ventilation-perfusion mismatch suggestive of CTEPH.

Pulmonary angiography

Identifies filling defects in pulmonary vasculature (pulmonary embolism).

Chest CT in PH

Used to identify clots and other lung conditions contributing to PH.

Polysomnogram (PSG)

Sleep study to evaluate for sleep apnea as a contributor to PH.

Six-minute walk test

Functional test to evaluate exercise tolerance and oxygen desaturation in PH.

Blood tests in PH

CMP and CBC assess organ function, metabolic status, and infections.

Anticoagulation in CTEPH

Anticoagulants prevent formation of new clots; do not dissolve existing clots.

Pulmonary Endarterectomy (PEA)

Surgical removal of thromboembolic material; curative option for suitable CTEPH patients.