alterations in respiratory function

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  1. What is ventilation? What is tidal volume?
    what increases respiration?
    What decreases it?
    • Ventilation: Movement of air to the lungs to maintain oxyganation, and the removal of CO2.
    • Tidal V: amt of air taken in (inspiration), amt of air going out (expiration).
    • When CO2 increases or O2 and pH decrease = increase in respiration.
    • when CO2 decrease, or increase in p = will decrease respiration.
  2. What factor affect alveolar ventilation?
    • Neurological control of ventilation (ponse and medula- Brain stem)
    • Mechanical factors (the ability to inspiration and expiration).
    • Deadspace and distribution of ventilation (everything that affects that alveoli ability to exchange gases)
  3. What forces are included in the work of breathing (mechanics)?
    • Elastic forces: Lung recoil due to elastin, collagen, fibrin.
    • Surface forces: surface tension due to water-air interface.
    • Airway Resistance: Primarily determined by airway radius.
  4. What is anatomic dead space? Alveolar dead space? Physiologic dead space? Alveolar ventilation?
    • Anatomic DS: Volume of gas not used in gas exchange.
    • Alveolar DS: Ventilated, but underperfused or unperfused alveoli.
    • Physiological dead space: the sum of anatomic and alveolar dead spaces.
    • Alveolar ventilation: (tidal v - dead space) x rate.
  5. What is ventilation and perfusion? what's there importance?
    • V: amount of air move in and out of the lungs - amt of air that goes from the mouth to the alveoli.
    • Q: Amt of blood flowing through the lungs - the ability for the heart to pump blood to the lungs.
    • Importance: there must be adequate V/Q matching to oxygenated the blood.
  6. What are ventilation-perfusion abnormalitites?
    • Image Upload
    • Low V/Q: due to impaired ventilation.
    • Shunt (very low) V/Q: blocked ventilation, collapsed alveolus.
    • High V/Q: impaired perfusion (PE) alveolar dead space.
  7. What's Hb affinity? What does a shirt to the right mean? shift to the Left? examples of what could cause them?
    • Affinity: How easy does O2 hook up to Hb.
    • Right shift: decreased O2-hb affinity. (low pH, high pCO2, high temp, etc)
    • Left shift: increased O2-hb affinity. (high pH, low pCO2, low temp)
  8. What are the alteration in pulmonary function?
    • Hypoventilation: Insufficient air to the alveoli to provide O2 and remove CO2. It is influence by the rate and depth of respiration. -- high CO2 = increased respiration -- causes: opioids, surgery of thorax or abdomen, etc.
    • hyperventilation:  Low pCO2 (hypocapnia), blow off CO2 -- causes: pain, fever, anxiety, high altitude, obstructions, etc

    hypoxemia: Deficient blood O2, due to poor diffusio n at the alveoli or anemia wit low arterial O2 and low hb saturation.   

    • hypoxia: Decrease tissue oxygenation. Four types:
    • Hypoxic-hypoxia:PaO2 decreased despite normal carrying ability (high altitude) 
    • Anemic-hypoxia: Decreased O2 carrying capability, low Hb (sickle cell anemia)
    • Cicularoty-hypoxia: Low cardiac output, O2 carrying capacity is normal, but blood flow is reduced. (blood loss, hemorrhaging)
    • Histotoxic-hypoxia: toxic subtance leads to the inability of tissue to use available O2 (cyanide poisoning).

    Acute respiratory failure: abnormal arterial blood gases, which is dx by an arterial stick. -- causes: quadriplegia, emboli, etc. -- CM: hyoxia, hypercapnia, confusion, decreased LOC (level of conscious), dizziness.
  9. What are the types of pulmonary disorders?
    • Vascula: Pulmonary HTN or embolism.
    • Obstructive.
    • Restrictive
    • Infectious.
  10. Pulmonary HTN? CM?
    • It is the elevated P in the pulmonary arteries.
    • 2 types: primary (rapidly progressing), secondary (result from known disease process)
    • CM: exercise intolerane, fatigue, syncope, cor pulmonale (Rt sided failure), chest pain on exertion.
  11. Pulmonary Embolus? Risks?
    • It is an undissolved detached material (clot, fat emboli, eir, etc) that occlutes blood vessels. Usually come from deep veins in lower extremities.
    • Risk: immobility, trauma, pregnancy, cancer, HF, and estrogen use.
  12. What are pulmonary malignancies?  CM?
    • Carcinomas - most common one being adenocarcinoma.
    • High mortality, usually less than 1 yr.
    • CM: 10 - 25 % cases are asymptomatic.
    • Types: extra or intra-trhoracic.
  13. obstructive pulmonary disorders? patho? etiologies?
    • patho: it is caused by an increased in  resistance  as a result of changes in the radius of the airway.
    • Etiologies: 1) Obstruction of the airway lumen, 2) wall of the lumen, 3) obstruction resulting from increase P around the outside of the airway lumen.
  14. What are the pathologies in the obstruction of the airway lumen?
    • Bronchiectasis.
    • Bronchiolitis.
    • Cystic Fibrosis.
    • Acute tracheal obstruction.
    • Epiglottitis.
    • Croup syndrome.
  15. What is bronchiectasis? Etiologies? Patho? CM? Tx?
    • It is a recurrent inflammation of the bronchial walls, associated w infection and pus formation (foul smelling sputum). Usually seen in children and ppl w CF (cystic fibrosis) 
    • Etiology: dilation of the bronchial wall, obstruction of the wall formation, CF.
    • Patho: (pathology of bronchioles) Recurrent inflammation, which causes destroction of the bronchial walls, which leads to loss of ciliated epithelium, which transforms into pus formation.
    • CM: productive cough, w a foul-smell, green or yellow, hemoptysis.
    • Tx: ABX, inhaled bronchodilators, hydration and exercise.
  16. Bronchiolitis? etiologies? Patho? CM? Tx?
    • wide spread inflammation of the bronchioles due to infection. Usually occurs from winter to spring. 
    • Etiology: Viral (RSV, influenza virus a,b,c) or bacerial (just abt anything)
    • Patho: inflammation causes mucosal swelling, excessive mucous prodution, and bronchial muscle constriction that narrow the airway. usually seen in children <2, but also in adults who smoke, toxic fumes, or immunosuppresed.
    • CM: it goes from mild to fatal, wheezing/bronchospasms, crackles, increased sputum.
    • Tx: humidified O2, bronchodilators, abx, steroids.
  17. acute tracheobrongial obstruction? Etiologies/causes? CM? Tx?
    • etiology/causes: aspiration of foreign body (most often in the Lt lung), Malpositioned endotracheal tube, laryngospasm, spiglottitis.
    • CM: inability to talk, nasal flaring, dyspnea -- requires emergency treatment.
    • Tx: removal, heimlich, dusction, tracheostomy.
  18. Epiglottitis? etiology? CM? tx?
    • Etiology: inflammation of the epiglottis due to influenza B (usually) and happens to children 2 to 4yrs -- it is a medical emergency.
    • CM: rapid onset of fever, pain, difficulty swallowing, and drooling.
    • Tx: intubation, abx.
  19. Croup?etiologies? pathogenesis? CM? tx:
    • Viral inflammatory disease of the larynx, trachea, and bronchi. It is associated w upper respiratory infection.
    • Etiology: para-influenza, pneumoniae, etc
    • Pathogenesis: Infectious agent causes inflammation along entire airway, around the subglottic area. (below the epiglottis)
    • CM: barking cough is the most common manifestation.
    • Tx: Mist, hydration, steroids, O2
  20. What are the obstructions from conditions in the wall of the lumen?
    • Asthma.
    • Acute bronchitis.
    • Chronic Bronchitis.
  21. What is asthma? types? pathogenesis?CM?
    • Its a lung disease characterized by airway obstruction and inflammation that is reversible, and brochoconstriction -- increased airway responsiveness to stimuli.
    • 2 main types: Extrinsic (triggers) and Intrinsic (no history of allergies).
    • Exercise-induced asthma: Bronchospasm after the end of exercise, usually resolves in 60 mins. It is caused by the loss of water and increase o heat.  Common causes are running, joggin, and tennis.
    • Occupational asthma: Often have positive test rxn to protein allergens in the work environment.
    • Drug-induced asthma: Ranges from mild rhinorrhea to respiratory arrest, which requires mechanical ventilation.
    • pathogenesis: No known single mechanism, bronchospasm, swelling, obstruction, hyperactivity of the bronchi.
    • CM: Mild to severe attacks, Wheezing, productive cough, tick mucus, intermittent symptoms.
  22. What is bronchitis? pathogenesis? CM? tx?
    • it is a temporary inflammation of the tracheobronchial tree. It could be viral, bacterial, fungal, heat, etc. -- Upper respiratory infection.
    • Patho: Airways become inflamed and narroed from capillary dilation. fluid from fluid exudation, increased mucus production.
    • CM: symptoms are due to narrowing of inflamed airways and increased mucus production. low-grade fever, sore throat, postnasal drip, substernal chest discomfort.
    • Tx: no treatment for viral, antibiotics for bacterial, codeine-containing medications (for cough, at night).
  23. What is chronic bronchitis? etiology?Patho? CM?  tx:
    • Inflammatory disorder of the airways associated with long term smoking. It is usually a chronic or recurrent productive cough > 3 months. It is irreversible when paired w emphysema!
    • Chronic bronchitis is associated with COPD type B.
    • etiology: cigarette smoking (90%), ppl w lots of infections (10%). 
    • Patho: Chronic inflammation and swelling of the bronchial mucosa resulting in scarring over time. -- CB can lead to pulmonary HTN, and eventually Rt CHF.
    • CM: ppl that wake up coughing, cyonatic, commonly associated w emphysema, polycythemia (increased RBCs)
    • Tx: smoking cessation, bronchodilator therapy, reduction to exposure of irritants.
  24. what is emphysema? etiologies? patho? CM?
    • It is the breakdown of the elastin and fiber network of the alveoli leading to alveolar destruction and formation of larger than normal air spaces. (COPD-type A). DAMAGE IS IRREVERSIBLE!
    • Etiologies: smoking, Air pollution, occupations (welding, mining, asbestos)
    • Patho: Alveolar destruction due to loss of elastic recoil which causes a decrease in surface area for gas exchange, and produces abnormal permanent enlargement of the airspaces.
    • CM: pink puffer, Progressive exertional dyspnea and DOE, increased SOB over 3-4 yrs. Thin/weight loss, pursed-lip breathing, Minimal or absenct cough.
  25. COPD-type A (emphysema) vs COPD-type-B (chronic bronchitis)
    • L: pink puffer, thin/weight loss, mild hypoxemia, no hypercarbia, few secretions, not reversible,
    • CB: blue bloater, obese, hypozemia and hypercarbia, increased hematocrit, lots of secretion, reversible.
  26. What are the restrictive pulmonary disorders?
    • Lung parenchyma disorders.
    • Pleural space disorders.
    • Chest wall disorders.
    • Infection/inflammation of the lung.
  27. Lung parenchyma disorders? types?
    • Fibrotic: they cause fibrosis of the tissues of the lung.associated with occupations i.e black lung (coal), etc.
    • Atelectatic: ARDS and IRDS.
    • Adult respiratory disease syndrome (ARDS): profound hypozemia associated with trauma, sepsis or chock. Injury to the alveoli w changes in diameter (fluid). 
    • Infant respiratory disease syndrome (IRDS): most common in premature infants (lack of surfactant which is the way to measure the ability to breath, usually using the placenta)
  28. What is pneumothorax? Hemothorax? types? CM? Tx?
    • Accumulaltion of air in the pleural space, which results in complete or partial collapse of the affected lung.
    • Hemothroax: when there is blood instead of air, usually fractured ribs.
    • Types: spontaneous, traumatic, tension, and iatrogenic (cough hard enough)
    • CM: Really SOB, absence of breath sounds when auscultating. cyanosis.
    • Tx: chest tube w negative pressure. 3 to 5 days.
  29. What is tension pneumothorax?
    • results from buildup of air under pressure in the pleural space. Air enters the plural space but cannot escape during expiration. 
    • Lung on ipsilateral (same) side collapses and forces mediastinum towards contralateral side.
    • Decrease venous return and CO.
    • It is a medical emergency.
  30. What is pleural effusion? Causes? CM?
    • Fluid or pus in the pleural cavity as result of another disease process.
    • Causes: Changes in the pleural cavity pressures (hydrostatic, colloid oncotic, and intrapleural)
    • CM: dyspnea, pleuritic pain, dry cough, decreased tactile fremitus (pt says 99, or eeee)
  31. What are the crest wall deformities?
    • Kyphoscoliosis
    • Ankylosing spondylitis
    • flail chest
Card Set:
alterations in respiratory function
2014-11-09 05:10:18
Pulmonary disorders

Obstructive Pulmonary Disorders and restrictive.
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