Hemothorax: blood accumulating in the pleural cavity

*cause: traumatic; blunt or penetrating injury to the thorax*

*leads to dyspnea d/t compression fo the lung by blood*

Pneumothorax:  accumulation of air within the pleural cavity

*healthy lungs have negative pressure between pleural layer = fight elastic recoil of lungs*

*with air entering pleural space, vaccum (– pressure) is lost  = lung recoils and collapses in whole or in part*

*more common with tall thin males*

Atelectasis: incomplete expansion or collapse of part/all of the lung

*may result in ↑ risk of infection and ↓ oxygen delivery to tissues*

*pulmonary atelectasis is most commonly encountered abnormality in chest radiological findings*

Atelectasis neonatorum/Primary atelectasis : lung that has never been inflated/has not inflated properly

> may be complete or partial

> seen in premature or other high risk births

> NB may be fatal to infant (no expansion = no oxygenation of blood)

Acquired atelectasis: a collapse of all or part of a lung that has previously been inflated?

can be:

> compressive

> obstructive

> contraction

Occurs in any space-occupying lesion of the thorax compressing the lung and forcing air out of the alveoli

> lung tissue can be compressed by adjacent structures ie: fluid (pleural effusion), pneumothorax, hemothorax, tumors, or elevated diaphragm

> also caused by puncture wounds, scar tissue, penetrating lesions and cyst rupture

Obstructive/resorptive: when communication between alveoli and trachea is obstructed; trapped air distal to obstruction is absorbed = airway collapses

> causes: foreign body, tumor, major swelling (anaphylaxis and mucous plugging)

Contraction atelectasis: local or generalized fibrotic changes in the lung tissues preventing full lung expansion

> occur 2^o d/t anaesthetics, narcotic use, musculoskeletal pain

* anaesthetics and narcotics deperess the central respiratory drive*

*pain inhibits voluntary inspiratory effort*

Fast bronchial occl. & large lung collapse: p on affected side,  dyspnea, cyanosis, hypotension, tachycardia, fever, shock

Slow-onset atelectasis: sometimes asymptomatic or with severe, hacking, non-productive cough

*depends onset of bronchial occlusion happens, size of lung area affected and presence/absence of infection*

> Acute pneumonia

> Bronchiectasis (dilation of bronchia)

> Respiratory failure

> Sepsis

> Pleural effusion and emphysema (inflammed, infected fluid in pleura)

Obstructive pulmonary disease: flow of air impeded along the airways

> 4 mechanisms: spasm of smooth mm encircling airways, inflammation/swelling of airway mucosa, excessive secretions of mucus, loss of elastic tissue normally holding smaller airways open

> spasm of smooth muscles encircling airways

> inflammation and swelling of airway mucosa

> excessive secretions of mucus

> loss of elastic tissue that normally holds smaller airways open

Restrictive pulmonary disease: dysfunction of the muscles of ventilation or decreased volume of available air from scar tissue and fibrosis

*chest cannot expand from impaired motor control of respiratory mm*

* flow of air is NOT impeded*

True or False?

Chronic Obstructive Pulmonary Disease (COPD) is reversible.

False: COPD is predominantely irreversible damage to the lung tissue

*manifestation: chronic/recurrent reduction in expiratory airflow*

*airflow limitation not fully reversible, progressive with abnormal inflammation response of lungs to inhaled noxious particles/gases*

Manifestations

> Emphysema

> Chronic Bronchitis

> Bronchiectasis

* Lung disease characterized by increased airway resistance often leading to prolonged forced exhalations*

*underdiagnosed disease*

> Cigarette smoking

> Air poluttion

> Pathophysiology: occur in large airways, small bronchioles and lung parenchyma

ie: edematous inflammed lung mucosa, thickened BM, enlargement of mucious gland, hyperplasia of goblet cells (more of them), bronchial smooth mm hypertrophy and thickening

Airway flow limitation d/t:

> Narrowed airway

> Constricted smooth mm

> Damaged airway walls/remodelling

> Inflammation

Acute and Chronic s/s

> Productive cough: worse in morning, small, colourless

> Dyspnea: significant= ocurs until the 5^th decade of life; moderate COPD = breathless after minimal exertion

> Wheezing esp. with exertion/exarcebation

*Acute exarcebations more frequent/severe with progression of disease*

> decreased fat-free mass

> impaired systemic muscle function

> osteoporosis

> anemia

> depression

> pulmonary hypertension

> cor pulmonale

Cyanosis

Pitting peripheral edema

True or False?

Overuse of accessory mm of respiration is a physical presentation of COPD.

Breathing takes more energy:

loss of elastic recoil =  forced exhalation

increased respiratory rate, muscle weakness = fatigue, loss of energy

Simple activities done by patients with severe COPD may experience which physical presentations?

> Tachypnea

> Respiratory distress

Bronchodilator: anticholinergic drug

*block Ach to keep bronchial dilated*

Anti-inflammatory medications (corticosteroids): decrease exarcebation of COPD

> Aerobic lower extremity endurance exercise: enhance performance of daily activities and reduce dyspnea

> Upper extremity exercise training: improve dyspnea, increase ADL requiring use of upper extremities

*breathing retraining techs (diaphragmatic, pursed lip breathing) can improve ventilatory pattern/prevent dynamic airway compression*

> abnormal, permanent enlargement of air spaces distal to terminal bronchioles

*chronic degenerative lung condition from loss of elasticity of lung tissue, alveolar walls destroyed and capillary beds supplying alveoli destroyed*

*small airway collapse during exhalation; impedes airflow and traps air in lungs distal to collapsed airway*

What word defines large pockets in lungs?

Bulla : large pockets in lungs (greater than 1cm to 7cm)

*can compress adjacent healthy lung tissue, impair ventilation and perfusion*

*may be surgically removed to reduce compression and avoid "bursting" leading to pneumothorax*

> smoking

> genetic defects in respiratory unit structure (small %)

> repeated respiratory infections (chronic bronchitis)

> atmospheric pollution and combination of above

Centrilobar/Centriacinar emphysema: usually occur at terminal bronchials

* most common in upper lobes*

* rare in non-smokers; almost exclusive disease of smokers*

> focal destruction of respiratory bronchiole and central portion of acinus with edema, inflammation and thickening of the bronchiolar wall

Panlobular/Panacinar emphysema: beings at alveolar duct

* found throughout the entire lung, more severe in lower lung*

* most common occurence is in smokers or group with genetic defects*

> Slow insidious onset of dyspnea

> Tachypnea: rapid, shallow breathing (difficulty inhaling air)

> Labored inspiration, forced exhalation (d/t loss of elastic recoil)

> Apex heart beat can be difficult to palpate d/t hyperinflation of lungs

Explain how emphysema patients may still maintain perfect blood O² levels?

Hyperventilating enables emphysema patients to maintain blood O² levels

*pursed-lip breathing and healthy colour = Pink puffers*

*advance stage of emphysema: patient over-ventilates, exhales audibly with pursed lips, uses accessory respiratory mm prominently*