Alterations of Pulmonary Function

Pulmonary Disorders

What do pulmonary function tests measure?

• Pulmonary function tests measure:

  • lung volume

  • capacity

  • rates of flow

  • gas exchange 

• Obstructive: when air has trouble flowing out of the lungs due to airway resistance  

• Restrictive: when air has troube flowing into the lungs

  • when lung tissue or chest muscles cant expand enough 

Obstructive Disorders

• ↑ resistance to air flow during exhalation 

• airway obstruction is worse with expiration 

• more force is required to expire a given volume of air

• emptying of lungs is slowed

• V/Q mismatch

• Dyspnea and wheezing

• examples: 

  • asthma, chronic bronchitis, emphysema 

Restrictive Disorders

Restrictive:

• ↓ expansion of the lungs

• alterations in the lung tissue, pleura, chest wall

• ↓ compliance of lung tissue

• examples: 

  • pulmonary fibrosis, acute respiratory distress syndrome, atelectasis, TB, pneum.  

Pulmonary Function Tests 

Obstructive Disorders 

• ↓ FEV1, FEV1/FVC 

• ↑ RV, FRC, TLC

Restrictive Disorders

• ↓ TLC, VC, FEV1, FVC, RV

• FEV1/FVC can be normal or elevated

COPD

• caused by mucous plugs and narrowed airways

  • air trapping and hyperinflation of alveoli on expiration

• during inspiration, airways are pulled open allowing gas to flow past the obstruction

• enhanced chronic inflammatory response

Chronic Bronchitis

• Hyper secretion of mucus and chronic productive cough

  • hypersecretion: ↑ goblet cells

  • cough: cilia eradication & impaired movement 

• Inflammation d/t inspired irritants or a URI

  • Infiltration of neutrophils, macrophages, and lymphocytes into bronchial wall

  • chronic inflamm → chronic bronchitis

  • chronic inflamm → causing edema and spasms

• airways collapse early in expiration trapping air in distal portion of lung

• chronic hypoxia → kidney produces erythropoietin → polycythemia → ↑ RBCs → cyanosis

• chronic hypoxemia → vasoconstriction of pulmonary arteries → pulmonary hypertension → right-sided heart failure (cor pulmonale)

Chronic Bronchitis Clinical Presentations

• Clinical Presentation:

  • Hypoxemia, hypercapnia, respiratory acidosis 

  • spirometry: FEV1/FCV < 70%

Emphysema

• Destructive changes in alveolar walls w/out fibrosis

• ↓ lung elasticity: ↓ recoil, ↑ compliance

  • ↑ workload of breathing

  • passive expiration becomes difficult

• abnormal enlargement of airspace in distal terminal bronchioles

• hyperinflation of lungs → ↑ TLC

• destruction d/t proteolytic enzymes

• air trapping in lungs d/t ↑ airway resistance w/ collapse of small airways

  • hyperexpansion of chest

• loss of surface area for gas exchange → hypoventialtion → hypercapnia

smoking → emphysema

• proteolytic enzymes are released from inflammatory cells ← activated by smoking and air pollution

• neutrophils activated → release granules (rich in protease)

  • protease destroy alveolar septa

  • bullae develop in lung tissue

• no v/q in later stages

• a1Antitrypsin (protective enzyme) → inhibited by smoking

  • made in liver

  • inhibit proteases

  • mutation in a1-antitrypsin gene → cause COPD

COPD - Clinical Signs

• ↓Chronic Bronchitis:

• blue bloater

• obese

• hypoxemia and hypercapnia

• ↑ hematocrit

• cor pulmonale

• ↑ secretions

Emphysema

• pink puffer

• weight loss

• mild hypoxemia, no hypercapnia initially

• hyperventilation initially, hypoventilation and hypercapnia noted in later stages

• ↓ secretions

Oxygen Therapy in COPD

• severe hypoxemia and CO2 retention → administer O2 with caution → can ↓ stimulus to breathe

  • central chemoreceptors → dont act as primary stimulus

  • peripheral chemoreceptors take over → sensitive to change in PaO2

  • do not exceed 60 mmHG → stimulus to breathe decreases

Asthma

• chronic inflammatory of bronchial mucosa 

  • bronchial hyperresponsiveness (inflammation)

  • constriction of airways

  • variable airflow obstructive that is reversible

• airway inflammation

  • mucosal edema, secretion of mucus, inflammation

• stimuli 

  • allergic asthma (extrinsic) - IgE - mediated simulation of mast cells 

  • non-allergenic (intrinsic) - no history of allergies 

  • exercise induced 

• innate and adaptive immunity response to antigen in airway 

• immediate and late responses 

  • peaks 30-60 mins, lasts 1-2 hours

  • begins 4-8 hours last hours or days

Acute Asthmatic Responses

• antigen binds to mast cell → releases inflammatory mediators → induces broncho spams, edema, and mucus secretions → eosinophils activated → damage to respiratory epithelium → airway obstruction 

Status Asthmaticus

Sever bronchospasms

• bronchospasms not reversed 

• ↓ ventilation, ↑ hypoxemia 

• ↑ PaCO2 → acidosis

• asthma becomes life threatening

  • signs of death: silent chest & PaCO2 > 70 mm Hg

Restrictive Lung Disorders

• acute or chronic

• the greater the decrease in lung volume, the greater the severity of the disease

• dyspnea, ↑ RR, ↓TV, ↓ FVC

• V/Q mistmatch → leads to hypoxemia 

Aspiration 

• passage of fluid and solid particles into the lung 

• causes dysphagia and cough reflex

  • d/t abnormalities of central and peripheral nervous system

• Rt lung → more susceptible to aspirating

  • d/t Rt main bronchus is straighter than left

Atelectasis

• collapse of lung tissue d/t external pressure 

• ↑ shunting → ↓ compliance → hypoxemia

• can occur after surgery and anesthesia

• obstructive (absorption) atelectasis 

  • gradual absorption of air from alveoli to blood d/t obstructed or hypoventialted alveoli

Bronchiectasis 

• permanent dilation of bronchi caused destruction of bronchial muslce wall and elastic tissue

  • causes airway obstruction

• occurs with chronic bronchitis inflammation

• primary symptom: productive cough

Bronchiolitis 

• diffuse, inflammatory obstruction of small airways and bronchioles 

• common in children 

• occurs in adults with chronic bronchitis and respiratory tract virus infection 

• Bronchiolitis obliterans: fibrotic process → occludes airways and causes permanent lung scarring 

Pulmonary Fibrosis 

• Excessive fibrous or connective tissue (scarring) in the lung 

  • scar tissue from active pulmonary disease or idiopathic

• Lungs become more stiff and & diff. to ventilate

  • ↓ diffusion of gases in alveocapillary membrane → cause hypoxemia

• PF = lung scarring → seen in ILD

• ↑ dsypnea on exertion, diffuse inspiratory crackles

Pneumonia

• inflammatory response in aveoli or intersitium d/t an infectious agent 

• causative microorganisms influence s/s, treatment, prognosis 

  • bacteria, virus, fungi, protozoa, parasites

• causes → when normal pulmonary defense mechanisms are compromised

  • aspiration of oropharyngeal secretions (gastric secretions & normal bacterial flora)

    • most common route of lower respiratory tract infection

  • inhalation of contaminants (virus & mycoplasma)

  • contaminated system circulation

    • bacteremia from infections in body or IV drug abuse

Pneumonia - Pathophysiology 

• Organism enters lung → multiplies and triggers → pulmonary inflammation 

• alveolar spaces fill with fluid and inflammatory cells invade site 

• acute bacterial pneumonia → significant V/Q mismatch and hypoxia d/t fluid 

• viral pneumonia → DOES NOT produce exudative fluid

Acute Respiratory Failure

• failure of gas exchange / no ventilation in alveoli → hypercapnia

  • cant oxygenate blood / eliminate CO2 → V/Q mismatch → hypoxemia

• abnormal ABGs:

  • PaO2 < 60 mm HG

  • PaCO2 > 50 mm HG

  • pH < 7.3

• labs: ↑ WBCs, ↓ RBCs

• in conditions that impair: ventilation, V/Q, gas diffusion

  • CNS, neuromuscular disease, chest wall and diaphragm disorders, airways, pulmonary parenchyma diseases

ARDS / ALI

• lung inflammation and diffuse alveolocapillary injury

• susceptible ppl → severely ill, major injuries, sepsis

• inflamm/injury from alveoloarcapillary membranes damage

  • direct damage: aspiration

  • indirect damage: shock

• hallmarks

  • severe pulmonary edema

  • “ground-glass” opacities in a CT scan

Pulmonary Hypertension

• abnormal elevation of pressure in pulmonary circulation

  • ↑ pulm. artery pressure

  • ↑ pulm. vascular resistance

• Mean pulmonary arterial pressure: > 25 mm Hg

• Normal: high flow, low pressure (9-18 mm Hg)

• Develops as primary, but also develops secondary to other conditions

  • primary: idiopathic

  • secondary: caused by hypoxemia

• PH develops → is self-perpetuating → smooth muscle hypertrophy & proliferation of vessel intima

Primary Pulmonary Hypertension

Caused by:

• Abnormal proliferation and contraction of smooth muscle 

• coagulation abnormalities 

• intimal fibrosis → pulm. artery obliteration 

• ↑ pulm. artery pressure 

  • R-heart failure

  • Low cardiac output

  • Death

Cor pulmonale 

• R - ventricular enlargement 

  • d/t hypertrophy, dilation

• Chronic pressure overload in R ventricle

• ↑ workload → causes hypertrophy, dilation and failure of ventricle

Secondary Pulmonary HTN

• develop secondary to other conditions 

• causes: 

  • ↑ pulm. venous pressure 

  • ↑ pulm. blood flow 

  • ↑ pulm. vascular resistance

    • pulm. vascular obstruction 

    • hypoxemia → vasoconstriction of pulmonary arteries 

Pleural Effusion

• presence of fluid in the pleural space

• Types:

  • Transudative: watery

  • Exudative: WBC & plasma proteins

  • Hemothorax: blood

  • Empyema: pus, infected pleural effusion

  • Chylothorax: chyle - lymph + fat droplets

Empyema

• pus in pleural space 

  • caused by blocked pulmonary lymphatics and outpouring of contaminated fluid

  • complication of penumonia, surgery, bronchial obstruction from tumor