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ALTERATIONS IN PULMONARY FUNCTION
Boyle's Law - ANS - Pressure and volume are inversely related. Decrease in volume - Increase in presure and Increase in volume- Decrease in pressure Dalton's Law - ANS - In gas mixture, the pressure of ea. gas is directly proportinal to the precentage of that gas in the total mixture. In a mixture of gas each individual gas contributes a partial pressure to the total pressure. What is the percentage of O2 in the atmosphere? - ANS - 21% Pathway of air through the respiratory system? - ANS - Nasal and Oral cavities. 2. Pharynx 3. Trachea 4. Bronchi 1,2,3 5. Bronchioles 6. Teminal Bronchioles 7. Alveoli Where do the lungs sit in the chest cavity? - ANS - The apex sits slightly above the clavicles (collar bones) and the base of the lungs rest on the diaphragm How many lobs are in the right side of the lungs? - ANS - 3 lobes - Superior, Middle and Inferior (going from top to bottom) How many lobes in the left lung? - ANS - 2 lobes (Superior and Inferior) Origins of gas exchange in the lungs? - ANS - Alveoli The wall of the aveoli are made up of what kind of epithelium? - ANS - Simple quamous type I cells
Cough - ANS - a productive reflex that clears the airway A protective reflex that cleans airways with an explosive expiration to remove foreign particles Dyspnea - ANS - Shortness of breath Labored breathing Caused by increased airway resistance Signs: flared nostrils and use of accessory muscles. Surfactant (phospholipid) - ANS - prevents collapse of the lungs Contraction of the diaphram and external intercostals increases the size of the thorax - ANS - Inspiration pO2 moves from - ANS - High to low pressure Volume of air inspired or exspired during normal quiet breathing - ANS - Tidal Valume (Vt) Inspiratory Reserve - ANS - IRV the volume inspired during a very deep inhalation Range is 3100 ml Abreviation for Expiratory Reserve - ANS - ERV Expiratory Reserve amount 1200 ml Shortness of breath when patient lies down? - ANS - Orthopnea
Pleuritic Pain - ANS - Sharp stabbing pain associated with breathing caused by disorders affecting the pleura, airways, and chest wall Clubbing - ANS - Boulbous enlargement of the end of fingers and toes due to chronic hypoxia Abnormal Sputum - ANS - Change in color, oder, consistency, and amount of sputum Abnormal sputum can give us what information - ANS - information about a disease and its progress Pulmonary Edema - ANS - Excessive fluid in the lungs. Usually caused by heart disease Aspiration Pneumonia - ANS - an infectious process leading to collapse and consolidation of lung tissue Bronchiectasis - ANS - persistant infections due to dilated bronchial blebs caused by obstruction, immunologic iency, or abnormal function of cilia Pleural effusion - ANS - Fluid in pleural spaces causing the lungs to collapse partially or fullydue to pressure by effusion Empyema - ANS - Pus in the pleaural space (infected/exudative pleural effusion) Pleurisy (pleuritis) - ANS - Inflammationof the pleara (usually viral) causes friction rub; stabbing pain Fibrosis - ANS - Remodeling of connective tissue in the lung
Chest wall restriction - ANS - Compromised ventilation due to deformity Flail chest - ANS - When one or more ribs is broken in one or more places Toxic Gas Exposure - ANS - results in inflammatory damage to the airways and plumonary edema Pneumoconiosis - ANS - Black Lung- fiberous tissue or nodules in the lungs due to inhalation of dustparticles from work such as silica, coal, clays, cement Allergic alveolitis - ANS - Lung inflamation due to inhaled allergens such as mold, grains, pollens, feathers. Like bronchiolitis but farther down in the lungs All disorders that result in ARDS do what to the alveolocapillary? - ANS - Injury, causing severe pulmonary edema nd markedly reduced compliance of the lung First step in ARDS - ANS - injury of the pulmonary capillary endothelium and alveolar epithelium What is cental to the development of ARDS? - ANS - Neutrophils which release a battery of inflammatory mediators such as Proteolytic enzymes, O2 free radicals, and proinflammatory cytokines What kind of cells make up 90% of the alveoli and allow gas exchange to take place? - ANS - Type I epithelial cells Tension Pneumothorax - ANS - : Site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing during expiration (intrapleural pressure > atmospheric pressure)
ARDS Pathologic Lung Changes (first two): - ANS - 1. Difuse epithelial cell injury with increased alveolar-capillary permeability > fluid, plasma proteins, blood cells shift from vascular compartment to alveoli and interstitium (sits in alveoli)
- Alveoli cell damage leads to edema fluid, surfactant inactivation, and formation of hyaline membrane and alveolar collapse...leads to impaired gas exchange ARDS Pathologic Lung Changes (second two): - ANS - 3. neutrophils accumulate early in course and play a central role: synthesize and release variety of inflammatory mediator including:
- proteolytic enzymes
- toxic oxygen species
- they cause increased inflammatory response > injury to capillary endothelium and alveolar epithelium (further damage and more problems with gas exchange)
- As disease progresses:
- work of breathing becomes greatly increased as lung stiffens and becomes more difficult to inflate
- impaired gas exchange and profound hypoxia ARDS: Clinical Manifestations: - ANS - 1. Rapid onset: 12-18 hours of initiating event
- Increased RR
- Marked hypoxemia (profound! even with respiratory therapy...know numbers!)
- Signs of respiratory failure (increase in PCO2 and decrease in PO2)
- Chest Xray shows diffuse bacterial infiltrates of the lung tissue without cardiac dysfunction
- Multiple organ failure: particularly kidneys, GI system, CNS, CV system (because of lack of O2) ARF: Hypoxemia and Hypercapnia numbers and reasons: - ANS - 1. Hypoxemia: PaO2 < 60 mmHg
- Hypercapnia: PaCO2 > 45 mmHg Respiratory acidosis usually present...too much CO2=acidosis
Hypoxemia: result of inadequate oxygen exchange between alveoli and capillaries Hypercapnia: result of inadequate alveolar ventilation Asthma...what is it? - ANS - Chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, and epithelial cells
- inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning
- Episodes are usually associated with widespread, but variable airflow obstruction that is often reversible, either spontaneously or with treatment
- Inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli Asthma: Classification (and 4 steps): - ANS - Based on clinical severity, not on underlying pathophysiology Step 1: Mild intermittent
- Symptoms 2x/week or less; <=2x/week at night Step 2: Mild persistent
- symptoms > 2x/wk but < 1x/day; >2x/month @ night Step 3: moderate persistent
- daily symptoms/ > 1x/wk @ night Step 4: Severe persistent
- continual symptoms/ frequent night time symptoms Asthma: Clinical Manifestations: - ANS - -during remission, individuals asymptomatic with normal PFT (pulmonary function test)
- During partial remission, they are asymptomatic, but have abnormal PFTs
- Increased work of breathing
- Increased interpleural and alveolar gas pressures can cause decreased alveolar perfusion (this leads to uneven ventilation-perfusion relationships > hypoxemia)
- Hyperventilation > decreased PaCO2 and increased pH Asthma: Risk Factors: - ANS - 1. Genetic predisposition (1/2 cases develop in childhood)
- Allergen exposure
- Urban residence
- Exposure to air pollution and cigarette smoke
- recurrent respiratory viral infections and other allergic diseases (allergic rhinitis) Atelectasis...what is it?: - ANS - -Incomplete lung expansion; collapsed alveoli
- primary: present at birth; lung never inflated
- secondary: acquired (more common) Atelectasis: Clinical Manifestations: - ANS - -Dyspnea, cough
- Tachycardia, tachypnea
- cyanosis, hypoxemia (measured by pulseox)
- Decreased chest expansion
- diminished breathing sounds
- intercostal retractions over involved area during inspiration (retractions in muscles between ribs when breathing in)
- fever leukocytosis BOOP: - ANS - Bronchiolitis Obliterans Organizing Pneumonia (inflammation of the bronchioles and lungs)
Brief description of pulmonary edema: - ANS - water in the lungs Brief Description of Ventilation-Perfusion (V/Q) - ANS - Abnormalities: V-amount of air getting into the alveoli Q-amount of blood perfusing the capillaries around the alveoli An abnormal V/Q ratio is the most common cause of hypoxemia. Normal ratio is 0.8-0. Bronchiectasis Clinical Manifestations: - ANS - sputum smells foul bad breath, hypoxemia, cyanosis, clubbing, chronic cough, easily fatigued, SOB, gets worse with exercise (DOE), wheezing, weight loss Bronchiectasis....what is it?: - ANS - Destruction and widening of the large airways May be congenital or acquired Bronchiolitis Obliterans: - ANS - VERY RARE, deadly, a fibrotic process that occludes airways and causes permanent scarring of the lungs...further complicated by BOOP Bronchiolitis...what is it?: - ANS - Most common in children Inflammatory OBstruction of bronchioles Causes of Atelectasis: - ANS - 1. Airway obstruction followed by absorption of air from dependent alveoli
- Lung compression: external pressure on portion of lung causing alveoli collapse
- (tumor, mucus plug, fluid or air in pleural space, abdominal distension, scoliosis, pleural effusion)
- Increased recoil of lungs due to loss of pulmonary surfactant
- very large tidle volumes
- no expiration pause
- alternating periods of deep and shallow breathing and apnea. Signs: Cyanosis Chronic Bronchitis Clinical Manifestations: - ANS - 1. SOB
- Excessive Bronchial secretions
- Productive cough with gray sputum (carbon)
- Prone to resp infections
- Polycythemia (resulting from hypoxemia) Chronic Bronchitis...what is it?: - ANS - -Airway obstruction caused by inflammation of major and small airways
- Edema and hyperplasia of submucosal glands...produce lots of sputum
- Hypersecretion of mucus in large airway (earliest feature)
- repeated infections from mucus
- Only airways....NOT alveoli...smaller airways effected first Chronic Bronchitis...what symptoms diagnose it?: - ANS - Presence of chronic productive cough for > or = to three months in each of > or = to 2 consecutive years (other causes of chronic cough excluded) Clinical Manifestations of Alterations of Pulmonary Function (10): - ANS - 1. Dyspnea/Orthopnea
- Kussmaul respirations
- Cheyne-Stokes respirations
- Hypoventilation/hyperventilation
- Cyanosis
- Clubbing
- Cough
- Hemoptysis
- Abnormal Sputum
- Pain Clinical Manifestations of Flail Chest (5): - ANS - 1. Pain
- Dyspnea
- Asymmetrical chest expansion
- Hypoventilation
- Hypoxemia COPD (Chronic Obstructive Pulmonary Disease) What is it? - ANS - 2 things that are signs....: - Disease state characterized by presence of airflow obstruction that is not fully reversible
- Chronic Bronchitis
- Emphysema The conditions often coexist
- increases in severity as time goes on, however, good management can help maintain optimal functioning COPD: Risk Factors: - ANS - 1. Cigarette Smoking*
- 80 - 85% of COPD patients have a history of smoking
- As many as 50% of smokers may have undiagnosed COPD
- Occupational Chemicals and Dust
- Air Pollution
- Infection
- Heredity (Alpha Antitrypsin (AAT) Deficiency)
Direction of trachea base shift in Tension Pneumothorax: - ANS - Inspiration > Away Expiration > Further Away Emphysema (what is it in general in relation to COPD): - ANS - Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles (alveoli) with destruction of their walls and without obvious fibrosis Emphysema...what is it and major anatomic changes: - ANS - -Abnormal enlargement of air spaces distal to the terminal bronchioles (alveoli) and destruction of alveolar walls and capillary beds
- Different from chronic bronchitis because it is in alveoli, not airways
- Major anatomic changes: loss of lung elasticity, hyperinflation of lungs due to air trapping Emphysema: Clinical Manifestations: - ANS - -Dyspnea
- Barrel Chest (wider front to back rather than side to side)
- Hypoxemia
- Hypercapnia
- Protein-calorie malnutrition (hard to eat) Empyema Pleural Effusion Clinical Manifestations:- - ANS - -Toxic presentation > fever, chills, tachycardia, signs of sepsis Etiology of Pneumothorax: - ANS - -Rupture in visceral pleura and chest wall
- Rupture in parietal pleura and chest wall Eupnea: - ANS - Normal breathing
Examples of triggers of Asthma attacks (3 and specifics): - ANS - 1. Specific allergens (most common)
- house dust mite, cockroach dung, molds, pollens, animal dander, food additives
- Nonallergenic General irritants
- cold air, dry air, airborne particles, microorganisms, aspirin, exhaust fumes, perfume, cigarette smoke
- Airway Hyperresponsiveness
- exercise (EIA-exercise induced asthma), respiratory infections, unknown reaspons, sinusitis, stress Exudative Pleural Effusions: - ANS - high concentrations of WBCs and plasma proteins (protenatious; usually with infections, RA, pulmonary infarction) Flail Chest...what is it?: - ANS - -Fracture of multiple consecutive ribs in one or more places (crush injury)
- Instability of chest wall General Clinical Manifestations of Pleural Effusion: - - ANS - Vary depending on cause
- Dyspnea
- Pleuritic Pain: sharp, stabbing, worse on inspiration, hold breath and it gets better Hemothorax: - ANS - Collection of blood that should not be there, accumulation of blood in the pleural cavity (the space between the lungs and the walls of the chest) Hyaline membrane - ANS - glassy, pink appearance, scar-like, membrane that has a ground-glass appearance
PE, Embolus with infarction presentation of PE: - ANS - A portion of the lung tissue dies PE, Embolus without infarction presentation of PE: - ANS - not severe enough to cause permanent lung injury PE, Massive Occlusion presentation of PE: - ANS - Occludes a major portion of the pulmonary circulation, shock and death PE, multiple pulmonary emboli presentation of PE: - ANS - May be chronic or recurrent Pleural Effusion...What is it?: - ANS - -Abnormal collection of fluid in the pleural cavity caused by migration of fluids and other blood components through the walls of intact capillaries bordering the pleura; rate of fluid formation exceeds rate of removal Pleural Space: - ANS - the small potential space between the parietal and visceral layers of the pleura Pleural space/pleural cavity: - ANS - Area between the visceral and parietal pleura Pleuritis (pleurisy) what is it?: - ANS - 1. Inflammation of pleura
- Not a specific thing...can have with other things...associated post viral URI or pneumonia Pleuritis Clinical manifestations: - ANS - -pain that worsens with inspiration and coughing
- fever, chills Pneumothorax**...what is it?: - ANS - -Presence of air or gas in the pleural cavity (should be in lungs)
- Destroys negative pressure of pleura space and disrupts equilibrium between elastic recoil forces of lung and chest wall Polycythemia: - ANS - an increase in the number of erythrocytes and hemoglobin in the blood Pulmonary Embolism Clinical Manifestations: - ANS - -Depends on size and location
- Small emboli: chest pain, dyspnea, increased RR
- Moderate-sized emboli SOB, pleuritic pain, slight fever, productive cough, tachycardia
- Massive (often fatal) shock and death sudden collapse, crushing substernal chest pain, shock, profound hypotension, LOC, cyanotic Pulmonary Embolism...What is it?: - ANS - Occlusion of a portion of the pulmonary vascular bed by an embolus Pulmonary Embolism: Pathophysiology: - ANS - 4 different presentations of PE: Presentations of PE:
- Massive Occlusion
- Embolus with infarction
- Embolus without infarction
- Multiple pulmonary emboli Pulmonary Embolism: Risk Factors for DVT related embolism: - ANS - -Venous Stasis (pregnancy, sickle cell disease)
- Hypercoagulability
