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112 Cards in this Set
- Front
- Back
what is the CNS mechanism of asthma? (3)
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1.allergen-induced immunological response
2.abnormal ANS regulation 3.imbalance b/t excitatory (bronchocontraction) and inhibitory (bronchodilation) neural input allowing mast cells to interact w/ ANS |
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what are 4 airway characteristics of asthma?
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1. bronchial hyperreactivity
2. airway inflammation 3. hypertrophy of smooth muscle 4. reversible expiratory airflow obstruction |
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is asthma obstructive or restrictive? -and- is asthma irreversible or reversible?
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expiratory obstruction of airflow; reversible
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age incidence in children & adults?
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children < 5; adults > 40, smokers w/ emphysema or chronic bronchitis
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what endothelium and cardiac disorders associated w/ asthma?
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subendothelial fibrosis & cardiac toxicity due to treatments
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explain allergen-induced immunologic rxn associated w/ asthma.
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1. antigen exposure
2. synthesis & secretion of IgE antibodies 3. release of histamine, interleukins, tumor necrosis factor,leukotrienes, prostaglandins, & platelet-activating factor from mast cells 4. airway inflammation, contraction, and hyperreactivit 5. eosinophils infiltrate airways hrs after allergen exposure 6. further release of chemical mediators |
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what are the 3 classic manifestations of asthma?
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1. wheezing
2. coughing w/ copious yellow sputum 3. dyspnea |
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reason for wheezing?
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turbulent airflow thru narrowed airways
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during wheezing, what is an omnious sign?
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it abruptly stops = complete obstruction of airways
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what could single monophasic wheezing that's consistent represent?
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focal airway obstruction (e.g. foreign body aspiration, neoplasm, etc.) and not asthma
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can coughing be the only symptom of asthma?
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yes
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what is dyspnea dependent on?
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obstruction of the airflow
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what other pathologic state can dyspnea mimic?
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angina pectoris
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what's the typcial functional exhaled volume of asthmatic patient?
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< 35% normal
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during severe attacks how much can FRC increase?
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1-2 liters
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what happens w/ TLC during asthma attack?
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usually remains normal
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how long can residual anomalies of PFTs persist following an attack? are symptoms present?
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several days after attack; no symptoms present
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are FVC increased or reduced? why?
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reduced; because airways close prematurely toward end of maximal expiration
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what do abg's reflect with mild asthma?
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normal abgs
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what do abg's reflect with moderate asthma? why?
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hypocarbia & respiratory alkalosis; because of initial hyperventilation
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what do abg's reflect with severe asthma? why?
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hypercarbia; common cause is muscle fatigue
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what happens with your v/q & o2 in severe asthma?
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severe v/q mismatch and decreased o2
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name 3 diagnostic tests for asthma.
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cxr, ekg, & bronchodilator responsiveness
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what does cxr show w/ asthma?
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hyperinflation of lungs
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what does ekg show w/ asthma?
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right heart failure & ventricular irritability during acute attack
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what is benefit of bronchodilator responsiveness test?
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provides supportive evidence when asthma suspected
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what does bronchodilator responsiveness test show w/ asthma?
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=/> 15% increase in airflow
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why would you get false (+) or false (-) w/ bronchodilator responsiveness test?
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because of the episodic nature of the disease
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name 10 differential dx for asthma.
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1. tracheobronchitis
2. sarcoidosis 3. RA 4. CA 5. croup & other upper airway diseases 6. hx of intubation 7. hx of trauma 8. hx of surgery 9. chf 10. pulmonary edema |
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name 5 different types of asthma.
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1. allergen-induced
2. excercise-induced 3. aspirin-induced 4. occupational 5. infectious |
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Which asthma type is this?
1. IgE mediated 2. most common 3. allergic rhinitis or dermatitis (may be present) 4. genetic 5. release of mediators |
allergen induced asthma
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what's the physiology behind exercised-induced asthma?
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changes in heat & water in tracheobrachial tree during humidification of large volumes of air
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what's another name for exercised-induced asthma?
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"thermal induced-asthma"
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who most commonly suffers from exercise-induced asthma? and why?
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children & young adults b/c of high levels of physical activity
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what drugs should sufferers of aspirin-induced asthma stay away from?
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ASA, NSAIDS (especially tordal)
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what physical feature is often seen with suffers of aspirin-induced asthma?
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nasal polyps
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what's the underlying cause of aspirin-induced asthma?
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1. blockage of cyclooxygenase-mediated conversion of arachidonic acid to prostaglandins
2. formation of leukotrienes |
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how many agents have been noted for occupational asthma?
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250 different agents
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what are the 2 types of occupational asthma?
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IgE dependent and non-IgE dependent
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what's the difference b/t the 2 types of occupational asthma?
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IgE dependent: longer latency periods b/t exposure & symptoms
non-IgE: brief intervals b/t exposure & symptoms |
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what are 3 common agents that cause occupational asthma?
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chlorine
ammonia latex |
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what's the underlying cause of infectious asthma?
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acute inflammatory disease secondary to viruses, bacteria, or mycoplasma organisms
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what were the past therapies for the prevention and control of asthma?
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bronchodilators
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what was the problem w/ using bronchodilators for prevention and control of asthma?
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mask underlying inflammatory process by relieving symptoms but allowing continued exposure to allergens
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what happens initially w/ ABGs after tx w/ bronchodilators? and what's the cause?
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PaO2 initially decreases
2nd to relief of vasoconstriction in poorly ventilated areas |
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why is the initially drop in PaO2 w/ bronchodilator tx tolerated?
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due to greatly enhanced airflow
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what is the current preferred first line tx for asthma?
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corticosteriods
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what caused the switch from bronchodilators to steriods for prevention and control of asthma?
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asthma now recongnized as chronic inflammatory process
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why do bronchodilators work for asthma?
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beta-agonist causing dilation of bronchial smooth muscles
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what are 2 current uses for bronchodilators?
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1. prevention of exercise-induced asthma
2. relief of symptoms when anti-inflammatory therapy is insufficient |
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what should happen to FEV after drug treatment for asthma?
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FEV should return to 50% normal
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name 6 drug therapies for asthma.
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1. anti-inflammatories
2. cromolyn 3. leukotriene inhibitors 4. bronchodilators 5. anticholinergics 6. methylxanthines |
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what drug therapy is most effective at controlling chronic symptoms of asthma?
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corticosteriods
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via which route are corticosteriods typically administered?
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inhaled
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how long does it generally take for inhaled corticosteriods to take effect?
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several months after tx airway hyperresponsiveness is reduced
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what drug regimen is associated w/ decreased risk of death from asthma?
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regular low-dose inhaled steriods
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name some drugs w/in the inhaled steriod class for tx of asthma.
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beclomethasone
budesonide fluisolide fluticasone triamcinolone |
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are inhaled steriods water soluble or lipid soluable? and what's the advantage of this property?
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highly lipophilic
allows for rapid entery into airway cells |
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what's the mechanism of action of inhaled steriods?
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inhibts gene transcription for cytokines during asthmatic inflammation
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how much of the inhaled steriod is swallowed? and is this a problem?
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most (~80%)
no, b/c the drug is still systemically absorbed following the first pass effect |
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what are 4 side effects of inhaled corticosteriods?
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1. hoarseness
2. candidiasis (elderly) 3. glossitis 4. pharyngitis |
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do inhaled steriods effect metabolism? or pituitary-adrenal function?
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no evidence
little to no effect even at high doses |
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how does cromolyn work?
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inhibits release of chemical mediators from mast cells
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what the disadvantage of cromolyn?
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not effective once bronchospasm is present
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in relation to anti-inflammatory therapy: how are leukotriene inhibitors used?
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with or substituted for anti-inflammatory therapy
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which types of asthma do leukotrienes play a role in?
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aspirin induced
excercise induced allergen induced |
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how do bronchodilators work?
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a. stimulate beta 2 receptors
b. increase cAMP c. tracheobronchial smooth muscle relaxation |
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r/t steriod therapy: how are bronchodilators typically used?
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in combination w/ steriods
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which bronchodilator is most selective beta 2 agonist?
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albuterol
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name 5 side effects of bronchodilators.
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1. SNS stimualtion
2. tachycardia 3. cardiac dysrhythmias 4. intracellular shift of K (hypokalemia) 5. down regulation |
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how do anticholinergics work in the tx of asthma?
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blocks muscarinic receptors in airway smooth muscle decreasing vagal tone
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which respiratory disease process are anticholinergics more effective in ?
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COPD
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give an example of an anticholinergic for tx of asthma.
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ipratropium (Isuprel)
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give 2 examples of methylxanthines for tx of asthma.
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aminophylline
theophylline |
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what are the potency level effects of methylxanthines control?
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modest anti-inflam
bronchodilator effects < beta 2 agonist |
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what measurements are important during tx w/ methylxanthines?
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blood therapeutic levels
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what is status asthmaticus?
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un-resolved life-threatening bronchospasm
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what are 4 effective tx of status asthmaticus?
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1. repeated doses of inhaled beta 2 agonists
2. iv corticosteriods 3. supplemental oxygen to keep sat > 95% 4. broad-spectrum antibiotics |
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give 2 examples of IV corticosteriods.
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cortisol
methylprednisolone |
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what ABG parameter warrants tracheal intubation and mechanical ventilation during status asthmaticus?
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PaCO2 > 50 due to resp fatigue despite aggressive treatment
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are low or high peak pressure needed for intubated status asthmaticus patients? why?
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high peak pressures
in order to deliver adequate TV despite bronchocontriction |
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what's the disadvantage of OR vents when managing status asthmaticus patients?
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too much compressible volume wasted on circuit to deliver adequate TV w/ such high pressure
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what's the benefit of high gas flows w/ status asthmaticus patients?
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shorter inspiratory time
greater exhalation time lower PEEP |
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is hypercarbia positive or negative w/ status asthmaticus patients? why?
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positive
can reduce barotrauma |
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when is general anesthesia required for production of bronchodilation? and what inhalational agents are beneficial?
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very ill patients
halothane, enflurane, isoflurane |
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name 6 preop evaluation goals for anesthesia mgmt of asthma patients.
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1. plan that prevents/blunts obstruction of airflow
2. h&p 3. understand: disease & effectiveness of tx 4. listen to pt's lungs 5. PFT (before & after bronchodilator therapy), ABGs, CXR |
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what 5 drug types may be given to an asthma patient preop? and what concerns are present?
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1. opioids (watch
ventilatory effects) 2. anticholinergics (watch for increased viscosity of secretions) 3. H2 receptor antagonists (watch for bronchoconstriction due to blocked bronchodilating effects of H2) 4. bronchodilators (should be continued up to induction) 5. corticosteriods (supplementation may be needed for larger surgeries, esp w/ possibility of adrenal suppresion by drugs used to tx asthma) |
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what's the effect of ASA, NSAIDS, etc during postoperative period?
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ASA, NSAIDS may produce adverse effects (asthma attack) in pts w/ asthma so use w/ caution
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what's the #1 goal of induction and maintenance for asthma pts?
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depress airway reflexes w/ anesthetic drugs to avoid bronchoconstriction in response to mechanical stimulation
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name one factor that would precipitate bronchospasms during intubation.
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inadequate depth of anesthesia to suppress airway reflexes
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what is an alternative to intubating? why?
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regional anesthesia
will avoid intubation & instrumentation of airway |
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what's the + or - benefits of propofol w/ asthma pts?
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+ = bronchodilating effects
- = use only if hemodynamics are stable |
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what's the + or - benefits of ketamine w/ asthma pts?
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+ = sympathomimetic effects for those actively wheezing
- = do not use in increased ICP, etc. |
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what's the + or - benefits of thiopental w/ asthma pts?
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+ = doesn't cause bronchospasms
- = doesn't suppress airway reflexes enough for instrumentation which may acutally trigger bronchospasms |
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what is metabisulfates and their significance to asthma pts?
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preservative found in generic propofol
may cause bronchospasm |
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which volatile gas is the most effective bronchodilator? and at what MAC?
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halothane
MAC < 1.7 |
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which 2 volatile agents are less pungent? which 2 are more pungent? and why is this important?
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halothane & sevoflurane < isoflurane & desflurane
less pungent = less coughing and bronchospasms |
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what's the importance of lidocaine for induction in asthmatics? and when should it be given?
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blunts airway relexes
1-3 minutes prior to DVL & intubation |
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why is albuterol so important during intubation/maintenance phase?
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it's most effective at blunting airway responsiveness to intubation
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which NMBA is best for asthma pts?
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anyone that is less likely to cause histamine release
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what is the effect of atricurium on histamine release & the airway of asthma pts?
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large increases in histamine release
severe broncospasms following administration |
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what is the effect of sux on histamine release & the airway of asthma pts?
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mild increases in histamine
there's been no evidence of increased airway resistance w/ sux |
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what effect can anticholinesterase drugs have on the airway of asthma pts? and what's the underlying cause?
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bronchospasms of smooth muscles of airway
due to stimulation of postganglionic cholinergic receptors in airway smooth muscles |
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what blunts the effects of anticholinesterase drugs on the smooth muscles of the airway?
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anticholinergic drugs given w/ them during reversal of NMBAs
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name 5 facts for ventilatory managments during surgery on asthma pts.
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1. slow inspiratory flow
(for optimal V/Q ratios) 2. allow sufficient time for exhalation (to prevent air trapping) 3. avoid PEEP (it can impair adeq exhalation along w/ narrowed airways) 4. humidification (to reduce transmucosal heat loss that can trigger bronchospasm) 5. maintain hydration w/ liberal IV fluids (aid in expulsion of secretions) |
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what are 2 possible extubation plans for asthma pts?
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1. deep extubation (b/c airway reflexes are still suppressed)
2. awake extubation (but continuous lidocaine 1-3 mg/kg/hr to minimized airway stimulation may be needed) |
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what's important to note regarding the admin of ASA, NSAIDS, etc in asthma pts postop?
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use caution b/c adverse asthma attacks are possible
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name 4 ways to manage intraop bronchospasms in asthma pts.
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1. bronchospasm NOT due to
acute asthma exacerbation will respond to deepening of anesthesia with volatile agents OR NMBAs 2. bronchospasm due to acute asthma exacerbation will respond to deepening of anesthesia with volatile agents but NOT NMBAs 3. beta 2 agonists, i.e. albuterol, thru T- connector (for bronchospasms after deepened anesthesia) 4. corticosteriod therapy (for bronchospasms after deepening of anesthesia & bronchodilators) |
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does albuterol have a synergistic or additive effect w/ volatile agents?
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additive
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what's the onset of therapeutic action for corticosteriod theraphy?
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at least 3-4 hrs after administration
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what is the conflict regarding emergency surgery and asthma pts?
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conflict b/t airway protection from aspiration & production of bronchospasms w/ awake intubation
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compare the use of bronchodilator therapy and regional anesthesia for EMERGENCY surgery in asthma pts.
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bronchodilator therapy - insufficient time for benefit
regional anesthesia - may be best option if possible for superficial or extremity injuries |