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RESPIRATORY DISEASES Hypoxemia/Hypercapnia • Hypoxemia =/= hypoxia – Hypoxia = decr’d oxygen at tissues – Hypoxemia = low PaO2 • V/Q – Ratio ventilation rate(V) compared to perfusion rate(Q) of blood through lung capillaries at alveoli – Normal (healthy) ratio = 0.8 • PaCO2 dependent on VA (alveolar ventilation rate) – If CO2 removal =/= CO2 prod'n, PaCO2 will increase – If decr’d VA (hypoventilation) incr’d PaCO2 (hypercapnia) • Ventilation not adequate to meet metabolic demands (cells producing more CO2 than lungs can get rid of) • If CO2 removed faster than produced, PaCO2 will decrease – If incr’d VA (hyperventilation), decr’d PaCO2 (hypocapnia) • Ventilation exceeds metabolic demands – Occurs with • Anxiety • Head injury • Insufficient O2 in blood (Why would you now breathe faster?) – Remember acid/base imbalances: what happens to acid/base balance if you breathe too little? What compound is increased in the blood? Why is this bad? What would your body do to compensate? So, with respect to V/Q Ratio: • If V/Q < 0.8, body has “wasted perfusion” (physiologic shunt) – Blood “shunted” past alveoli w/out adequate gas exchange – Due to impaired ventilation – PaO2 decr’d – PaCO2 incr’d – Shunting - alveolar spaces nonfunctional • If extreme physiologic shunt (if alveoli collapsed, edematous, filled w/ exudates), get extreme V/Q mismatch (V=0) • Can cause: – Severe hypoxemia – Administration oxygen does not correct • If V/Q > 0.8, called dead-space disease – Q = 0 (again, extreme V/Q mismatch; now due to no perfusion) – Ventilation not effected physiologically, BUT see incr’d work of breathing • Also hypercapnia, hypoxemia • Clinical - variable response – Hypoxemia if PaO2 = 40-50 mm Hg • Impairment of – Brain – headache, confusion, unconsciousness – Heart – tachycardia, dysrhythmias, incr’d bp – Hypercapnia • CNS depressed (headache coma) • Body fluids become acidotic Pathologies vent’n/ perfusion imbalance • Heart disease – Incr’d pressures in lung vasculature (pulmonary hypertension) • W/ valve disorders, CHF, etc. • pulmonary arteriosclerosis decr’d blood volume at lung (hypoperfusion) – So decr’d Q and V/Q mismatch • Note: not the same as incr’d perfusion • Actually, more similar to ischemia to lung tissues • Pulmonary embolism hypoperfusion – Material in pulmonary circulation “plugged” vessel – Thromboembolism most common • Often w/ thrombi from lower extremities – Same risk factors as w/ systemic thromboembolism (smoking, hyperlipidemia, hypertension, etc.) – Most common cause of acute pulmonary disease in US • ½ deaths occur w/in 2 hrs of embolism in pulmonary circulation – Pathophysiology • V/Q mismatch (decr’d Q) incr’d PaCO2 and decr’d PaO2 • Also pulmonary hypertension may result (Why?) and/or decr’d CO • Pulmonary embolism – cont’d – Clinical – severity varies • Massive – shock, chest pain, tachypnea, tachycardia • With lung infarct, see pleural pain, pleural effusion, dyspnea – What does the term infarct mean? – Treatment • Prevention – Eliminate risks associated w/ thrombus formation (stop smoking, etc.) • Anticoagulants – Prevent clot formation • Pulmonary edema – Excess fluid in lung, so decr’d ventilation – Lung usually kept “dry” by 3 mechanisms: 1) lymph drainage 2) capillary exchange 3) surfactant lining the alveoli – Predisposing factors to pulmonary edema related to 3 • Heart disease – LV failure incr’d pressures in L heart incr’d pressures in respiratory (gas exchange) capillaries – Fluid gets forced out of capillaries alveoli and between lung cells – So decr’d gas exchange ability and decr’d lung compliance – Lymph drainage compensates for awhile • Capillary injury – Injury incr’s capillary permeability fluid forced more easily out of capillaries into alveoli and between cells (as above) – Decr’s compliance and gas exchange – Injury to cap’s may be due to chemical, physical lung injury • Obstruction of lymph system – If lymph vessels or nodes blocked little/no drainage of ISF (so builds up between lung cells and into alveoli) – Again decr’d compliance and gas exchange – Clinical • Dyspnea, hypoxemia, incr’d work of breathing – Treatment • Depends on cause Obstructive Respiratory Diseases • incr’d resistance to air flow and decr’d vent’n • Due to obstruction – In lumen of airway (ex: incr’d secretions w/ asthma) – In airway wall (ex: inflamm’n at bronchial epithelium w/ asthma, chronic bronchitis) – In structures surrounding smooth muscle (ex: contraction bronchial smooth muscle w/ asthma) • Most common obstructive diseases: chronic bronchitis, emphysema, asthma – Difficult expiration Chronic bronchitis • Inflammation of bronchi • Most common obstructive disease • Caused by – Irritants (dominant – cigarette smoke) – Also infection • Chronic bronchitis leads to: – Increased mucus secretion – AND thickening of mucus – AND thickening of bronchial mucosa layer (w/ hypertrophy & hyperplasia of bronchial epithelium) • Body’s compensations for chronic irritation – Tries to guard cells that make up airways from irritation – Get diffuse obstruction – Lung defense mechanisms compromised • Cilia impaired • Thickened mucus can’t get rid of invaders – Find incr’d acute respiratory infections – Pathophysiology • Airways collapse w/ expiration • V/Q mismatch • PaCO2 incr’d (hypercapnia); hypoxemia – Clinical • Wheezing, shortness of breath • Exercise tolerance decr’d • Productive cough (sputum coughed up) • Incr’d risk respiratory infections – Treatment • Prevention -- STOP SMOKING • Bronchodilators open lumen • Expectorants decr mucus thickness Emphysema • destruction of alveolar walls, so decr’d elastic recoil of alveoli – Causes decr’d ability to expire – Note: obstruction not due to physical substance causing blockage; rather obstruction to gas exchange, air movement due to change in lung tissue • Genetic predisposition • Pathophysiology – Destruction of alveolar septa (shared cell membr between 2 alveoli) – Large air spaces develop (bullae) – Airways enlarge • Clinical – Dyspnea on exertion developing to dyspnea at rest • No cough; little sputum (REMEMBER: no incr’d mucus) • Tachypnea (incr’d rate of breathing) – Treatment - as per chronic bronchitis • Together, chronic bronchitis + emphysema = Chronic Obstructive Pulmonary Disease (COPD) or Chronic Airway Obstruction (CAO) Asthma • Inflammatory disease • Reversible – Unlike chronic bronchitis + emphysema • Bronchospasm + mucus hypersecretion + swelling w/ inflamm’n – Bronchospasm = prolonged contraction bronchial smooth muscle • Obstruction of air flow • Due to: – Hyperactive immune response to allergens • Prod incr’d amounts of IgE • Bind mast cells in airways • Much histamine released • Hyperactivated immune, inflammatory responses • Also, bronchospasm, incr’d mucus and edema w/ incr’d capillary permeability • Due to (cont’d) – Neural dysfunction with dysfunctional autonomic nervous system response • Disrupted or hyperactive irritant receptors (?) • Bronchospasm, perhaps also due to mast cell involvement (so all histamine effects noted above) • Common in children – Approx 50% of all asthma cases – Remission common (as adults) when asthma begins in childhood • Pathophysiology – Vascular congestion, edema – Formation of thick mucus impaired ciliary function – Incr’d work of breathing – Hyperventilation • Clinical – Wheezing, nonproductive cough, tachycardia, mucus formation • Treatment – Eliminate cause of attack – Drugs to reverse bronchospasm Restrictive respiratory disease (extrapulmonary) • Lung tissue is normal, other disorders affect ventilation • Chest wall restrictions – Work of breathing incr’s and ventilation decr’s • Hypoventilation, hypercapnia, hypoxemia • Impaired lung defenses – “Stagnant” air (doesn’t move out of body as it should) – If contains microbes or invaders, incr’d risk of infecting airways -- more time to grow, replicate – Due to • Chest wall deformities • Fat overlaying chest muscles in very obese patients • Neuromuscular diseases (ex: polio, muscular dystrophy, others) – Dyspnea – Patients more susceptible to lower resp tract infections – Over time, can respiratory failure • Intrinsic restrictions – – Acute or chronic – Chronic • Chronic Intrinsic Restrictive Lung Disease (CIRLD) – Excessive fibrous/connective tissue deposits in lung » Lung injury scar tissue formation » Lung stiffness, so compliance decr’s – Due to: » Irritant inhalation, infection, autoimmune dysfunction – Leads to » Decr’d ventilation (harder to breathe) » Hypoxemia » V/Q mismatch – Acute restrictions • ARDS - Adult Respiratory Distress Syndrome – Due to injury to lung » Direct: inhaling toxic gases, trauma » Indirect: systemic disorder incr’d chemical mediators of infection (thromboxanes, etc.) » (Biochem’s similar to prostaglandins; patients either release in too high concentrations, or lung cells too sensitive to them) – Pathophysiology: » Acute lung inflammation » Severe pulmonary edema » Diffuse alveolo-capillary injury » Severe pulmonary edema, hemorrhage – Pathophysiology – cont’d » Get decr’d compliance, decr’d alveolar ventilation, incr’d pulmonary vasoconstriction » Fibrosis within 7 days of injury ARDS – Clinical » Rapid, shallow breathing » Marked dyspnea » Hypoxemia unrelieved by oxygen administration » Fatal in ~ 70% of cases – Treatment » Mechanical vent’n to incr available oxygen » Sedation to decr oxygen consumption » Increase C.O., give diuretics to relieve edema Lung Infections • When lung defenses decreased • Pneumonia – By bacteria or virus • Common bacteria = strep pneumoniae • Causes ~70% of all pneumonia – Pathophysiology • Pathogens multiply in lung – Overall, due to decr’d immune response in lung • Toxins released from microbes • Bronchial mucosa becomes damaged – Pathophysiology – cont’d • Inflammation/edema results • Exudate found in alveoli • V/Q mismatch (decreased V) – Clinical • Infection chills/fever/malaise • Chest edema cough, pleural pain • Dyspnea – Treatment • Antibiotics – for bacterial infection • Mechanical ventilation Atelectasis = collapse of lung (alveoli) • Two types – Compression • External pressure pushes air out of alveoli – Alveoli can’t re-expand (because of increased pressure still on lung) – Absorption • Occurs w/ obstruction, when no expiration/inspiration • “Old” air absorbed from alveolus over time, not replaced – So alveoli collapse • Seen post-operatively – Anesthetics cause incr’d mucus production obstruction – Clinical • Dyspnea, cough, fever Pleura, pleural space affected • Pleural effusion = fluid (blood, lymph) in pleural space – Can cause collapse of lung tissue • Due to incr’d pressure of fluid pressing on alveoli • Hemothorax = bleeding into pleural space • Empyema = infected pleural effusion – Seen w/ lymph blockage • Pneumothorax = air/gas in pleural space – Negative pressure in pleural space destroyed • Pressure differential nec for proper pressures, recoil – Due to trauma, secondary to thoracic surgery Lung Cancers • Bronchogenic carcinoma – Malignant tumors of mucous membranes – Larger bronchi – ~90% of all primary lung cancers – Epidemic in U.S. • ~200,000 new cases per year • Most common of all primary tumors; most frequent cause of cancer death – Most common cause of bronchogenic carcinoma: • Cigarette smoking – Heavy smokers ~25X greater risk than nonsmokers • Other causes – Environmental, occupational (breathing in noxious/traumatizing agents, such as asbestos) • Classification by histological type; each type treated differently – Non-Small Cell Lung Cancer • Treated surgically • Squamous cell carcinoma – most common – Centrally located – Remains localized – Metastasis relatively late – Associated w/ smoking – Non-small cell cancers – cont’d • Adenocarcinoma – Tumors arise in periphery of lung – Most common in women – One type = bronchioalveolar cell carcinoma » Slow growing » Weak association w/ cigarette smoking » Low survival rate » Asymptomatic w/ early metastasis – Small Cell Lung Cancer • Treatment by chemotherapy, radiation • Strongest association w/ cigarette smoking • 20-25% of all bronchogenic carcinomas • Oat cell carcinoma – Cells compressed – Rapid growth, early metastasis – Poor prognosis (<5% alive in 2 yrs) • Stages common to epithelial cancers • Irritation hyperplasia, metaplasia, neoplasia, etc. • Clinical signs/symptoms – Coughing, hemoptysis (coughing up blood), dyspnea, chest/pleural pain, atelectasis, hoarseness • Metastasis mostly through lymphatic system – Commonly adrenals, liver, brain, bone marrow • Treatment depends on tumor type, site