alterations in respiratory function.txt

• 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.

• 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)

• 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.

• 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.

• 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.

• 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.

• 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)

• 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.

• Vascula: Pulmonary HTN or embolism.
• Obstructive.
• Restrictive
• Infectious.

• It is the elevated P in the pulmonary arteries.
• 2 types: primary (rapidly progressing), secondary (result from known disease process)
• CM: (dyspnea on exertion and paroxysmal nocturanal dyspnea) exercise intolerane, fatigue, syncope, cor pulmonale (Rt sided failure), chest pain on exertion.

• 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.

• Carcinomas - most common one being adenocarcinoma.
• High mortality, usually less than 1 yr.
• CM: 10 - 25 % cases are asymptomatic.
• Types: extra or intra-trhoracic.

• 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.

• Bronchiectasis.
• Bronchiolitis.
• Cystic Fibrosis.
• Acute tracheal obstruction.
• Epiglottitis.
• Croup syndrome.

• 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.

• 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.

• 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.

• 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.

• 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

• Asthma.
• Acute bronchitis.
• Chronic Bronchitis.

• 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.

• 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).

• 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.

• (it is the loss of radial traction, damage in the alveoli) 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.

• 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.

• Lung parenchyma disorders.
• Pleural space disorders.
• Chest wall disorders.
• Infection/inflammation of the lung.
• CH: decrease tidal volume, which is the amt of air that goes in and out in each breath.

• 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)

• 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.

• 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.

• 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)

• Kyphoscoliosis
• Ankylosing spondylitis
• flail chest

• Deformoty of chest wall resulting from kyphosis or scoliosis, which, most of the time, is congenital.
• It leads to V/Q mismatch, and pt is not able to take deep breaths.
• Complications: The higher the deformity, the greater the compromised respiratory status.
• CM: rapid, shallow breaths, chest wall deformity, etc.

• Chronic inflammation at the site of ligament insertion in the spine or sacroiliac joints. Progressive, inflammatory disease affecting the vertebrae and ribs.
• Causes: are unknown.
• Patho: Respiration is affected by limited lung expansion caused by pulmonary fibrosis w chest wall muscle atrophy, which can develop in bronchiectasis.
• CM: oain in the low or mid-back, stiffness,
• Tx: breating and mobility exercises, NSAIDs.

• results from multiple rib fractures as a result of trauma, which causes chest instability and decreased lung expansion on inspiration.
• Causes: car accident where chest hits the steering wheel.
• CM: trauma, SOB, cyanosis, pain on inspiration, etc.

• ( it involves an abnormally enlarged gas-excahnged system and the destruction of alveolar walls) It is the inflammation of the bronchioles, alveoli, interstitial tissues caused by an infectious agent.
• Etiology: Infectious and noninfectious agents.
• Bacteria: strep, staph, H. influenzae
• Viruses, Fungi, Protozoa, Parasites.
• Patho: Microbial agents enter the lung, multiply and trigger pulmonary inflammation, usually when defenses are compromised.
• Alveoli air spaces fill with exudative fluid (except in viral).
• CM: fever, chills, cough/sputum, elevated WBC (not in viral)

• Viral: nonproductive cough, low grade fever, normal WBC, no consolidation, Minimal V/Q change, minimal change in x-rays, less severe, no antibiotics.
• Bacterial: Productive cough (yellow green or brown), high fever, elevated WBC, consolidation (dull, e-->a), change in V/Q (low V/Q shunt), infiltrates in xrays, yes antibiotics.

• It is a type of pneumonia caused by the acid fast bacillus Mycobacterium tuberculosis, which infects lungs and lymph nodes through inhalation of small droplets (expelled with cough, sneeze, or talking) containing bacteria. 
• Classifications: Primary and reactivating.
• patho: entry of mycobateria into the lung tissue, spreads via lymph and blood, multiply in pulmonary alveoli, could cause inflammation and become fibrotic, or stay dormant for yrs.
• CM: night sweats, low-grade fever, cough, positive PPD and + acid fast bacilli (sputum), etc

• the majority are viral by RSV (respiratory sinvactol virus).
• CM: Malaise, watery conjunctivae, all others.
• Usually self-limiting in 5-7 days.

Collapse lung -- alveolar dead space.