Pulmonary Mod. 4 Disorders Flashcards
Tissue Hypoxia
Decreased O2 in tissue
Hypercapnia
Increased PACO2 in atrial blood Caused by hypoventilation Suppression of respiration centers (DRG, VRG) Airways obstruction Damage to alveoli (emphysema)
Hypoxemia
Decreased PAO2 in arterial blood
Causes of hypoxemia
Decreased PO2 of inspired air (altitude/suffocation)
Hypoventilation (suppress. DRG/VRG)
Diffusion problem w/alveolocapillary membrane (emphysema, fibrosis, edema)
Altered V/Q perfusion ratio(most common)
Hypoxemia-Low V/Q
Inadequate ventilation of well produced areas of lung
Pulmonary r to l shunting (blood travels from r.side of heart to l.side w/out receiving O2.
Ex:
Asthma, pneumonia, bronchitis, ARDS
Hight V/Q
Inadequate blood flow in area of well ventilated lungs
PE=high V/Q
LUNG tissue can deliver O2 but blood can’t get there
Aspiration
Entry of fluids/solid into trachea/lung
Decreased level of consciousness, neuro probs, meds put at increased risk
Pulmonary Edema
Excess fluids in lungs
Main cause-heart disease
Also; tumor, fibrotic tissue, tissue HTN
Atelectasis (collapse of lung tissue)
Compressive- external pressure collapses lung (tumor, abd distension,pneumothorax)
ABSORPTIVE- air from blocked/hypoventilated alveoli absorbed into system
SURFACTANT IMPAIRMENT-increased surface tension=collapse
POST-OP ATEL- prevent w/deep breathing, exercise
Pneumothorax
Air accumulation within pleural cavity
Open pneumothorax
Air enters pleural cavity during inspiration, and leaves during expiration
Tension Penumothorax
Trapping if air in pleural cavity, build up of air pressure on pleural space collapses lung. Every breath=more collapsing. Emergency
Spontaneous Pneumothorax
Unexpected rupture of pleura, common in young males
Pleural Effusion
Fluid in pleural space(transudate, exudate, pus, blood, lymph fluid)
ARDS
Respiratory failure due to acute inflammation and alveolar change
Phase 1 ARDS
Injury triggers massive inflammatory response, surfactant inactivated, alveoli collapse
Phase 2 ARDS
Hyaline membrane become fibrous mass coating alveoli & bronchioles
Phase 3 ARDS
Respiratory failure.
Inflammatory mediators can cause secondary response to other parts of body (organs)
Obstructive Pulmonary Disease
Airway obstruction worse with expiration (wheezing)
Flow rate diminish
Diseases that cause it:
Chronic bronchitis
Emphysema
Asthma
COPD
Usually seen with chronic bronchitis & emphysema
Chronic Bronchitis
COPD
condition of excess mucus secretion and productive cough that lasts 3+ months
Patho of Chronic Bronchitis
Bronchial tubes narrowed (excess mucus production/increased risk of infec. And inflam.)
Narrow airways=traps air in lungs
Decreased alveolar ventilation
V/Q mismatch (low V/Q)
Hypoxemia
Hypercapnia
COPD Emphysema
Accum. Of air in lungs
Centriaacinar- destruction of bronchioles&alveolar ducts but not ALVEOLAR SACS
Panacinar-destruction of entire acinis
Patho of Emphysema
Damage to lung tissue (not excess mucus)
Smoking
Inhibits a1-antitrypsin (Which normally protects tissue from inflammatory)
Or genetic deficiencyof a1-antiteypsin
Symptoms of emphysema
DOE Prolonged expiration Increased WOB Poor gas exchange Barrel chest Change in static lung volume hypoxemia, hypercapnia
Asthma
Reversible obstructive lung disease
Caused by increased rxn of airways
Asthma-Hyper responsiveness of airway
Allergen triggers inflammatory response
3 pathological changes:
Bronchial smooth muscle spasm
Mucus production
Vascular congestion
Clinical signs/symptoms of Asthma
Immediate or prolonged Audible high pitched wheezing SOB decreased flow rate (FEV1/FVC<70%) Tachypnea
Restrictive pulmonary conditions
Short shallow breathing
Increased flow rate or stays the same
Static volume decrease (FVC, RV, TLC)
DOE-progress to suspend at rest
Restrictive Parenchymal Conditions
Sarcoidosis
Idiopathic pulmonary fibrosis
Pneumoconiosis
Drug induced interstitial lung disease
Sarcoidosis
Inflammation that produce tiny lumps of cells in various organs
Restrictive-extraparenchymal Conditions
Myasthenia gravis Guillain barré syndrome Muscular dystrophies Cervical spine injury Kyphoscoliosis Obesity Ankylosing spondylitis
Pulmonary Fibrosis
Excessive fibrosis proliferation in lung
Secondary complication from disease, inhalation of environmental hazard, idiopathic pulmonary fibrosis.
Patho:
Altered repair process=fibrosis and poor lung compliance
Chronic inflammation, alveoli shrink and loose elasticity
Pneumoconiosis
Pathology due to inaction if environmental hazards.
Silica, asbestos
Tuberculosis
Mycobacterium tuberculosis
Highly contagious-transmitted airborne
Patho of TB
Inflammatory process form bacteria
Immune response leads to granulomatous lesions (tubercle) which becomes necrotic. Usually remains dormant
Pulmonary Embolism
Occlusion of pulmonary vascular/capillary supply
Lung can deliver O2 but blood can’t get there
V/Q mismatch=hight V/Q ratio
Patho risk favors of PE
Venous stasis
Hyper coagulation
Damage to endothelium if blood vessels
