Cardiopulmonary disease Exam 1 Review

Asthma prevalence rates

• 25 million asthmatics in U.S.
• Prevalence varies around the world.
• More common in urban than rural areas.
• Prevalent in poverty and large minority populations.
• Higher among minorities.
• Most cases develop at early age

-Higher in children than adults; boys > girls in childhood; women > men in adulthood.

Bronchiectasis presented clinically

-Chronic Cough
• Sputum Production
• Large amounts
• Purulent
• Foul smelling
• Dyspnea
• Clubbing
• Hemoptysis

• Most commonly, crackles, rhonchi, wheezing,heard upon
auscultation.
• Digital clubbing
• Cyanosis
• Plethora
• Wasting, and weight loss.
• Nasal polyps and signs of chronic sinusitis may also be present.
• In severe cases, findings are consistent with cor pulmonale. Right-
sided heart failure may be observed, including peripheral edema,
hepatomegaly, and hypoxia. This can ultimately lead to progressive
respiratory failure.

Risk factors for developing asthma

Genetics: family history of asthma, family history of atopy

Age/gender: Boys <20 years old, Women ≥ 40 years old

Exposure: Cigarette smoking, cleaning agents (occupational), chemical fumes (occupational), environmental tobacco smoke, exhaust fumes (occupational), fires (occupational), industrial spills (occupational).

Bronchiectasis X-ray findings/CT scan

X-RAY: increased pulmonary markings, honeycombing, atelectasis, and pleural changes, Dilated bronchi, linear hyperlucency, and parallel markings emanating from the hila are seen in cylindrical bronchiectasis.

CT SCAN: there is absence of bronchial tapering as it reaches the periphery of the lung, the bronchial internal diameter’s width is greater than the adjacent vessel, and the bronchi are visualized in the peripheral 1–2 cm of the lung fields

Bronchiectasis

An abnormal, irreversible dilation of one or more bronchi due to extensive inflammation and destruction of bronchial wall cartilage, blood vessels, elastic tissues, and smooth muscle

Complications of asthma

• Occur most often when asthma is uncontrolled
and during exacerbations
• Interference with activities of daily living
• Respiratory failure
• Death
• Circumstances increasing risk of death from asthma
• Previous intubation/mechanical ventilation from
asthma
• ICU admission for asthma in past
• Two or more hospitalizations from asthma in past year

• Death (continued)
• Circumstances increasing risk of death from asthma
(cont’d.)
• Three or more ER visits for asthma over past year
• Comorbidities
• Poor adherence to treatment
• Use of > two MDI canisters of SABA per month
• Low socioeconomic or urban residence (lack of
medical care)
• Sensitization to aeroallergen Alternaria alternate

Complications: These complications include, but are not limited to, interference with activities of daily living, respiratory failure from severe acute asthma, and death.

What is the process of asthma, and which medications treat each major sign/symptom?

caused by airway inflammation, bronchoconstriction, and mucus plugging, leading to coughing, wheezing, chest tightness, and dyspnea.

• Wheezing / Bronchoconstriction → Bronchodilators

• SABA: Albuterol, Levalbuterol

• LABA: Salmeterol, Formoterol

• Anticholinergics: Ipratropium, Tiotropium

• Coughing / Inflammation → Anti‑inflammatory meds

• ICS: Fluticasone, Budesonide, Beclomethasone

• Systemic steroids: Prednisone, Methylprednisolone

• Leukotriene modifiers: Montelukast

• Airway inflammation → Corticosteroids

• ICS for long‑term control

• Oral steroids for exacerbations

• Mucus production → Hydration + steroids

• Hydration

• Airway clearance

• ICS/systemic steroids
  (No mucolytics — may worsen bronchospasm)

• Chest tightness / SOB → Bronchodilators + steroids

• SABA for immediate relief

• ICS for long‑term control

Long term meds for management of asthma

• Inhaled corticosteroids (ICS)
• Anti-inflammatory
• Prevent future severe exacerbations
• Dose depends of severity
• Inhaled long-acting beta-agonist (LABA)
• Used in combination with ICS for long-term control
and prevention of asthma symptoms
• Formoterol, salmeterol
• Not to take place of SABA

• Combined long-term control
• LABA and ICS
• Not to take place of SABA
• Leukotriene modifiers
• Alternative treatment option
• Oral tablet
• Montelukast, zafirlukast, zileuton

• Methylxanthines
• Alternative therapy
• Bronchodilator and mild anti-inflammatory
• Immunomodulators
• Additional therapy
• Omalizumab: anti IgE injection
• Reslizumab, benralizumab: anti-IL-5 therapy injection

primary goal of asthma

The principal goals for treatment of asthma exacerbations are to reverse airflow obstruction, correct hypoxemia (if present), and reduce the likelihood of future exacerbations

To achieve and maintain long‑term control by reducing airway inflammation and preventing symptoms and exacerbations.

Genetic causes of cystic fibrosis

If the parent is a carrier of the gene (has one normal copy “R” and one mutated copy “r”). Each child has a 25% chance of inheriting two mutated genes causing CF; a 50% chance of inheriting one normal gene and one mutated gene, making them a carrier; and a 25% chance of inheriting two normal genes.

which gene gets mutated for cystic fibrosis?

CFTR gene gets mutated

What is the purpose of spirometry in asthma, and what are we looking for?

used to diagnose, assess severity, and monitor control of asthma.
We look for an obstructive airway pattern and reversibility after bronchodilator.

Key findings:

• ↓ FEV₁ (airflow limitation)

• ↓ FEV₁/FVC ratio (obstruction)

• Reversibility: ≥ 12% and ≥200 mL increase in FEV₁ after bronchodilator

• Tracks long‑term control and progression

Purpose: confirm obstruction, measure severity, check reversibility, and monitor asthma over time.

Triggers for asthma

• Exercise
• Allergen exposure
• Viral infections

What are the gold standards for diagnosing cystic fibrosis, and what clinical signs support the diagnosis?

Gold standards:

• Sweat chloride test ≥60 mmol/L on two tests

• CFTR genetic testing

Supporting signs:
Salty skin, chronic sputum production, recurrent infections, pancreatic insufficiency, malabsorption, nasal polyps.
Newborn screening: Elevated IRT.

symptoms of cystic fibrosis

• Manifests differently in each person
• Progressive
• Earliest signs:
• Salty taste on infant skin
• Digestive issues can appear shortly after birth
• Strong chronic cough
• Thick, sticky sputum
• Breath sounds
• Wheezing
• Poor aeration

• Visual signs
• Shortness of breath/dyspnea
• Clubbed fingers
• Chronic sinusitis/rhinitings
• Malabsorption in gastrointestinal (GI) tract
• Failure to thrive
• Greasy, foul smelling stool
• Males: Sterility
• Female: Irregular menstruation, difficulty getting
pregnant

drugs used for exacerbations of asthma that are not long term

• Inhaled short-acting beta-agonist (SABA)
• Relieves acute bronchospasm
• Albuterol, levalbuterol
• Inhaled short-acting anticholinergic
• In addition to albuterol for severe exacerbation in ER
• Ipratropium bromide

Magnesium sulfate
• Bronchodilator activity
• Systemic glucocorticosteroids
• Anti-inflammatory
• Oral
• Prednisone
• Prednisolone
• IV
• Methylprednisone
•Heliox
• Decrease WOB and improve ventilation

signs of hypoxemia

Physical signs:

• Cyanosis (lips, tongue, fingers)

• Tachypnea

• Tachycardia

• Nasal flaring

• Accessory muscle use

• Dyspnea

• Diaphoresis

Behavioral/neurologic:

• Anxiety

• Restlessness

• Confusion

• Irritability

• Difficulty speaking in full sentences

Skin/circulation:

• Cool, clammy skin

• Pallor

• Delayed capillary refill

What do PFTs show in asthma, and why is a bronchodilator given during testing?

• Recommended for all patients to confirm the diagnosis of asthma
before initiation of therapy.
• Spirometry can demonstrate obstruction and assess reversibility in
patients 5 years old or more.
• Commonly shows an obstructive pattern.
• Reduced forced expiratory volume in one second (FEV1).
• Decreased FEV1 / forced vital capacity (FVC) ratio.
• Normal DLCO.
• Lung volumes normal or elevated total lung capacity (TLC) and
functional residual capacity (FRC).

• Obstructive pattern in which the FEV1 increases more
than 12% and at least 200 mL from baseline following
administration of an aerosolized short-acting
bronchodilator.
• Improvement in FEV1 verifies reversibility.
• Lack of airway obstruction or reactivity
• Bronchial challenge.
• Positive test reflects a 20% fall in FEV1 from baseline.
• Positive test is consistent with asthma.
• Methacholine given.

• Peak expiratory flow
• Objective assessment of severity of exacerbation
• Normal values depends on gender, height, and age
• Below 200 L/min = severe obstruction

What causes thick, sticky mucus in cystic fibrosis?

CFTR mutation → defective chloride transport. Chloride cannot leave the cell → sodium and water stay inside → mucus becomes dehydrated, thick, and sticky. Leads to mucus plugging, chronic infections, and airway obstruction.

How do you classify asthma as allergic or non‑allergic?

• Allergic
• Positive allergy test
• Younger patient
• Early onset
• Seasonal variation
• Allergy triggers (grass, dust, cat, dog)

• Nonallergic
• Negative allergy test
• Normal or low IgE
• Late, adult onset
• No family history

Which diseases are classified as COPD vs. obstructive but not COPD?

COPD: Chronic bronchitis, emphysema.

Not COPD (but obstructive): Asthma, cystic fibrosis.

What primary issue occurs in Type 1 respiratory failure?

Type 1 = hypoxemic respiratory failure.

Primary issue: Low PaO₂ (<60 mmHg) with normal or low PaCO₂.

Caused by oxygenation failure (V/Q mismatch, shunt, diffusion problems). Can be acute or chronic.

What % improvement after bronchodilator shows reversibility?

A post-bronchodilator forced expiratory volume in one second
(FEV1)/forced vital capacity (FEV1/FVC) of ≤ 70% confirms that
airflow limitation exists.

Reversibility = ≥12% AND ≥200 mL increase in FEV₁.

5% and 10% = not significant.

12% or more = significant improvement (asthma).

cor pulmonale

Right‑sided heart failure caused by chronic lung disease.

due to increased workload on the right ventricle as it
attempts to deliver blood through constricted pulmonary blood
vessels.

what hypercapnia means in respiratory failure?

Hypercapnia = PaCO₂ > 50 mmHg.

Caused by ventilatory failure or pump failure leading to CO₂ retention.

Seen in Type 2 respiratory failure

What happens in chronic hypoxemia that leads to cor pulmonale?

Chronic hypoxemia → kidneys release EPO → ↑ RBCs (secondary polycythemia).
More RBCs = thicker blood, increasing pulmonary vascular resistance.
Hypoxic vasoconstriction + thick blood → pulmonary hypertension.
Pulmonary hypertension → ↑ workload on the right ventricle → cor pulmonale.

What are the effects of chronic low oxygen levels in COPD?

Chronic hypoxemia → kidneys release EPO → ↑ RBCs (secondary polycythemia) → thicker blood → ↑ pulmonary vascular resistance → pulmonary hypertension → ↑ RV workload → cor pulmonale. ABGs: low PaO₂, high PaCO₂, high HCO₃⁻ (chronic compensation).

What lifestyle changes are recommended for patients with COPD?

Smoking cessation, pulmonary rehab (exercise, breathing techniques, education), vaccinations, nutrition optimization, energy conservation, airway clearance techniques, avoiding triggers, and proper use of oxygen therapy.

What are the common characteristics of all chronic obstructive diseases (chronic airflow limitation)?

Chronic airflow obstruction (FEV₁/FVC < 70%), air trapping & hyperinflation, increased work of breathing, chronic airway inflammation, impaired gas exchange (hypoxemia ± hypercapnia), progressive long‑term disease, risk of pulmonary hypertension/cor pulmonale, and symptoms of cough, sputum, wheezing, and dyspnea.

What type of exacerbation occurs in each chronic obstructive lung disease?

COPD exacerbations:

• Usually triggered by bacterial or viral infection, pollutants, or
combination

Asthma:

• Exercise
• Allergen exposure
• Viral infections

Bronchiectasis/CF:

Infection, mucus plugging