alterations in respiratory function

• 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: 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 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.

• 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