Resp Disorders 1

• 1) hypoventilation -> leads to hypercapnia (high CO2 in blood) and hypoxia
• 2) impaired diffusion -> leads to hypoxemia (low O2 in blood) but not hypercapnia

• depression of respiratory center
• disease of resp nerves or muscles
• thoracic cage disorders

• interstitial lung disease
• ARDS (acute resp distress syndrome)
• pulmonary edema
• pnemonia

• PO2  <60 mm Hg
• cyanosis results
• leads to impaired function of vital centers
• symptoms include agitated or combative behaviour, euphoria, impaired judgment, convulsions, delirium, stupor, coma
• hypotension and bradycardia (decrease HR and CO -> decrease BP)
• results in activation of sympatehtic system

• increase resp
• decrease nerve firing (disorientation, coma)
• decrease muscle contraction
• vasodilation in the head region - headache, warm flushed skin

• 1) pleural effusions (fluid in the pleural cavity)
• 2) pneumothorax

• hydrothorax: serous fluid
• empyema: pus
• chylothorax: lymph
• hemothorax or fibrothorax: blood

serous fluid

pus

lymph

• air enters the pleural cavity
• air takes up space, restrictin glung expansion
• partial or complete collapse of the affected lung
• a) spontaneous: an air-filled blister on the lung ruptures
• b) traumatic: air enters through chest injuries (intense pain on injured side)
• i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)
• ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation

an air-filled blister on the lung ruptures

air enters through chest injuries (intense pain on injured side)

i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)

ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation

• tracheal shift
• cardiac compression
• lung deflation

• (bronchial) asthma
• COPD i) emphysema; ii) chronic bronchitis
• bronchiectasis
• cystic fibrosis

• chest wall - kyphosis
• pleural - effusion, pneumothorax
• parenchymal - occupational, ARDS-IRDS, atelectasis

increased airway resistance = decreased airway conductance

• extrathoracic airways (upper):
• > prolonged inspirationl inspirational stridor (labored)
• > inspiratory retraction as ribs are moved outward and body wall does not expand with rib cage (= insuf expansion)

• intrathoracic airways (lower)
• > prolonged expiration with wheezing
• > rib cage retraction as ribs are pulled inward but air  does not leave lungs

• epiglottitis
• croup:
• age range 3 months - 3 years
• brought by variety of viral infection (e.g. flu)
• characterized by hoarseness, a brassy cough
• fever
• inspirational stridor
• cough is lessened by inlhation of cold air
• can lead to cyanosis, pallor in severe cases (restriction of blood flow; Hg decr.)

• acute bronchiolitis:
• incr. expiratory effects = wheezing
• brough by viral infection

• Extrinsic (atopic): allergic reaction
• Intrinsic (nonatopic): attacks precipitated by:
• physical factors
• exercise
• psychological stress
• chemical irritants and air pollution
• bronchial infection
• aspirin

• type 1 hypersensitivity
• mast cells' inflammatory mediators cause acute response within 10-20 min
• airway inflammation causes late phase response in 408 hours

• IgE interacts w/ mast cells and acts as receptors for allegens
• hisamine release triggers the change in airway walls (thicken) (from granules)

• mucus in lumen
• inflmmation and basment membrane thickening
• enlarged mucous glands
• smooth muscle hyperplasia

• 1) bronchial smooth muscle constriction
• 2) mucosal edema
• 3) hypersecretion of mucus
• others: epithelial injury, bronchospasm, edema

• 1) resp infection: epithelial damage, IgE produced
• 2) exercise, hyperventilation, cold air: lost of heat and water may cause bronchospasm
• 3) inhaled irritants: inflmmation, vagal reflex
• 4) aspirin and other NSAIDs: abnormal arachidonic acid metabolism
• treatment: anticholinergic (preventing contraction of smooth muscles)

• emphysema: enlargment of air spaces and destruction of lung tissue
• chronic obstructive bronchitis: obstruction of small airways
• bronchiectasis: infection and inflammation destroy smooth muscle in airways, causing permament dilation

• 1) inflmmation and fibrosis of bronchial wall
• 2) hypertrophied mucus glands -> excess mucus; obstructed airflow
• 3) loss of alveolar tissue: decr. surface area for gas xchange
• 4) loss of elastic lung fibers (emphysema): airway collapse, obstructed exhlation, air trapping, decr. air delivery

• 1) manage enviro
• 2) bronchodilators (Ventolin)
• 3) antihistamine
• 4) antiinflammatory (corticosteroid - Flovent) - synthesis of beta receptors therefore boost the effects of beta agonist
• beta agonist: related to CV system, mimics SNS; decr. receptors locally on smooth muscle; receptor down regulation

• 1) bronchodilator
• 2) steroid (antiinflam)
• 3) antibiotics (decr. bacteria growth in the thickened mucus)
• 4) flu shot
• 5) O2 therapy
• 6) others - quit smoking, DB & C, exercise, reposition

• emphysema: enlargment of air spaces and destruction of lung tissue
• neutrophils in alveoli secrete trypsin (digestive protein) - incr. neutrophil = incr. trpysin
• aplha-antitrypsin inactivates the trypsin before it can damage the alveoli
• trpysin damages protein, fibers, elastin in alv. wall
• alv loses radial fraction
• types: centrilobular (distended resp bronchiole) and pancinar (one lumped alv)

• breathe in deep
• chest muscle incr.
• barrel chest (narrow); lean forward when breathing
• pursed lip breathing
• dont suffer hypoxia by incr. drawing volume of air
• increase resps
• dyspnea (incr. ventilatory effot)
• use of accessory mucscles

• chronic irritation fo airways
• increased number of mucus cells
• mucus hypersecretion
• productive cough

• needs to sit upright
• tachypnea (incr. resps)
• incr. temp due to incr. metabolic demand of muscles
• cannot increase resp enough to maintain oxygen level
• cyanosis and polycythemia (incr. RBC)
• cor pulmonale from think blood, incr. work for RS of heart, RS HF