RS 3060 - COPD (part two), Asthma, CF

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Rehabilitation Sciences
Rehabilitation Sciences 3060A/B
Bert Chesworth

COPD II / Asthma 11/26/2013 8:58:00 PM COPD II: True or False Questions: 1. Anesthesia impairs central respiratory regulation and tone of respiratory muscles 2. At high doses, some anesthetics globally depress muscular activity and reduce the respiratory effort 3. Release of inflammatory mediators by some anesthetic agents produces bronchospasm, resulting in hypoxia, hyperinflation and air trapping 4. Dry anesthetic gases and prolonged mechanical ventilation may impair normal mucociliary mechanism and lead to atelectasis from mucus- plugs 5. There is a risk of aspiration pneumonitis with general anesthesia when airway reflexes are reduced all true! - if going into surgery and getting general anesthetic, these are the normal risks - we care about COPD because: we deal with people going through surgery patients, post-operatively we should care what they‟re lungs are like we should avoid the negative effects (i.e. pulmonary exacerbation) i.e. by clearing anesthetics out of body after surgery Known adverse effects of anaesthesia: pneumonia, respiratory failure (usually defined as the need for mechanical ventilatory support), bronchospasm, atelectasis, hypoxaemia, exacerbation (or flare-ups) of underlying chronic lung disease Ventilation Review: Abnormal ventilation-perfusion - top left: normal, normal V/Q - top right: hyper-reactivity causing bronchospasm  restricting ventilation (i.e. asthma); Low V/Q in asthma, no pathology in alveoli bronchospasm restricts ventilation - bottom left: mucus plug could block ventilation, (i.e. chronic bronchitis); Shunt (Very Low) V/Q in chronic bronchitis, mucus plug could block ventilation - bottom right: (instead of impaired or blocked ventilation…) alveolar destruction, removed capillary bed; damage on blood side (i.e. emphysema); High V/Q if you take away the alveolar wall, you take away the capillary bed on the other side COPD in nutshell: - left side: patients with primarily emphysema - right side: patients with primarily chronic bronchitis - y-axis: degree of bronchial inflammation or alveolar destruction - average patient with COPD is sitting in middle of 2 curves of more/less bronchial inflammation (chronic bronchitis) and alveoli destruction (emphysema) Asthma: - clinical syndrome characterized by increased narrowing of tracheobronchial tree - most remarkable feature: episodic attacks of wheezing, shortness of breath (dyspnea) ***(COPD in contrast: shortness of breath on daily basis, every minute) - take-away epidemiology (prevalence) is that it is very common: 14 to 15 million in U.S., 3 million over age 12 in Canada Etiology: - cause of airway hyper-reactivity is unknown - possible suggested factors: genetic predisposition environmental pollutants (i.e. dust, molds, second-hand smoke, pollens, etc.) - airways that are hypersensitive to: allergens, RT infections, respiratory irritants, cold weather, emotional stress, exercise, chemical substances *** GROUPED below: Categories of Provocative Factors: category 1: allergens (dust mites, animal dander, wood dust, etc.) category 2: physicochemical agents (i.e. exercise, cold air, respiratory tract infection, ingestants i.e. drugs to treat other conditions) category 3: mediators of smooth muscle contraction (physiologic or pharmacologic)(i.e. histamine) Pathology: - airway narrowing occurs because of: bronchospasm of smooth muscle inflammation of bronchial mucosa increased bronchial secretions - this increases resistance to airflow (hard to breathe in)  causes air trapping and hyperinflation air trapping mechanisms (one of the four ventilation abnormalities diagrams on previous slide): the one depicting hyper-reactivity and bronchospasm - bronchospasm and mucus hypersecretion (due to allergic reaction) narrows airway and prolongs turbulent airflow creating wheezing wheezing is sound of air over mucus plugs that are only partially obstructed; and over airways that have lost their shape/structure - two pathological responses: early and late Early Response: - antibodies bind to foreign substance (allergen/antigen) on surface of mucosa in airway - this presence triggers an inflammatory response release inflammatory mediators to “fuel the fire” (i.e. histamine), causing: smooth muscle constriction of airways mucosal edema mucus secretion Late Response: - 4-8 hrs after Early Response (could be up to 24 hours): inflammatory cell recruitment causes 2nd wave of inflammatory mediator release causing „more‟ bronchospasm, edema and mucous secretion eventually causes: epithelial damage & impaired mucociliary function (this is usually a consistent mechanism in everyone, with control over mucus creation; cilia sweeps to mouth/nose to clear out) from toxic inflammatory effects, which may aggravate bronchoconstriction & mucous production via autonomic pathways - if ongoing for years: chronically increased numbers of inflammatory cells may lead to „long-term‟ changes in airway - such as: goblet cell hyperplasia (make more mucus; talked about in chronic bronchitis lecture) airway wall remodeling subepithelial fibrosis smooth muscle hypertrophy (bronchospasm a lot = working a lot) - first two boxes represent the early asthmatic response: potentially reversible! leads to the “Early Effects” characteristic of asthma: smooth muscle constriction, mucosal edema, mucus secretion (again, there is a reversibility of abnormal pulmonary function tests at this point) - late asthmatic response (4-8 hours later): about 50% of patients more bronchospasm, mucosal edema, mucus secretion leads to the “Late Effects”: as you persist with this chronic asthmatic state, more inflammatory cells hallmark feature: hyperreactivity direct relationship between inflammatory cell # and hyper-reactivity of bronchial tree eventually can lead to: epithelial damage (goblet cell hyperplasia), impaired mucociliary function, airway fibrosis, smooth muscle hypertrophy as walls thicken, paths narrow, effort is greater Normal vs. Acute Asthmatic Lung - diagram B shows: shortness of breath: increased resistance from mucous plugs, thickened edematous airway walls leads to hyperinflation work of breathing increases greater muscular effort detected by intercostal spindle stretch receptors increasing symptoms of shortness of breath wheezing: smooth muscle constriction and mucus hypersecretion/retention causes turbulent airflow … take this and put it into a classification system (below) … Asthma Classification: *exacerbations are flare-ups Step 4: severe persistent continual symptoms; frequent exacerbations; l
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