Exam II - reactice airway V Flashcards

1
Q

What is the increased reactivity seen with smoking?

A

coughing, laryngospasm, bucking, bronchospasm, wheezing, breath holding

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2
Q

Why do smokers have a chronic productive cough?

A

smoking decreases ciliary motility and increases sputum production

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3
Q

When should smokers stop smoking before surgery?

A

-ideally they should stop smoking 30 days prior to surgery otherwise no real benefit

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4
Q

What carboxyhemoglobin levels are seen in smokers and non-smokers?

A

normally <1%; in smokers can be as high as 8-10%

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5
Q

What effect does carboxyhemoglobin have on the heart?

A

negative inotropic = decreased contractility

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6
Q

Smokers develop obstructive disease which can lead to what physiologic effects?

A
  • V/Q mismatch, gas trapping, flattened diaphragmatic configuration, barrel chest deformity.
  • two to six-fold increase in postop pneumonia development and PPC (post-op pulmonary complications)
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7
Q

Before surgery what should you assess for with smokers related to pulmonary status?

A
  • Make sure no active pulmonary infection

- Give bronchodilator before surgery if they normally take one

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8
Q

What are post-op complications seen in smokers and what is the biggest determinate of PPC?

A
  • pneumonia and atelectasis
  • increased mucous production
  • operative site is the single most factor of determinants of PPC (non-laparoscopic upper abdominal procedures , followed by lower abdominal and thoracic procedures)
  • epidural analgesia best
  • operations > 3 hours associated with higher rates of PPC
  • advanced age
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9
Q

What could you do to treat decreased radial traction (airways collapsed and not held open) on small airways reduces cross-sectional area in patients with COPD or with decreased lung volume secondary to obesity, surgical manipulation, excessive lung water, or splinting?

A

Recruitment maneuver (PEEP)= close pop off valve on bag to increase pressure then squeeze bag and force air in distal airway

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10
Q

What are signs of inadequate post-op ventilation

A
o	tachypnea
o	anxiety
o	dyspnea
o	labored ventilation
o	increased SNS activity (tachycardia, HTN)
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11
Q

What effects can be seen from not smoking for one night?

A
  • reduces heart rate, blood pressure and circulating catecholamine levels, decreases carboxyhemoglobin levels.
  • However, it may increase their risk of PPC (Postoperative Pulmonary Complications) due to increases in mucous
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12
Q

What is Asthma?

A
  • chronic disease char by “chronic airway inflammation, reversible exp airway obs with airway narrowing in response to bronchial hyperreactivity”
  • periods of remissions and exacerbations
  • permanent changes in airway anatomy (airway remodeling) magnify the inflammatory response
  • Asthma is *Reversible COPD is not
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13
Q

Precipitating factors of asthma

A
airborne allergens
medications (histamine releasing, aspirin, sulfa agents, NSAIDS)
pollution
exercise
occupational
infection
emotional stress *
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14
Q

What is the most common the of asthma?

A
  • *allergic asthma is the most common type particularly in children
  • IgE mediated
  • usually history of allergic diseases, positive skin reactions, ↑
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15
Q

What is the pathogenesis of allergen-induced asthma?

A
  • in predisposed atopic individuals, antigen exposure leads to synthesis and secretion of specific immunoglobulin (E), antibodies.
  • Family history of allergic disease
  • IgE affixes itself to plasma cells in the bronchial smooth muscle in the wall of the airway. Once this occurs, there is a release of mediators from granules in the mast cells.
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16
Q

What are the mediators released from granules in mast cells once IgE attaches to bronchial smooth muscle in airway?

A
  • **histamine
  • **slow releasing substance of anaphylaxis (SRSA)
  • leukotrienes (potent spasmodic; proinflammatory substances)
  • interleukins
  • eosinophilic chemotactic factor (ECF-A)
  • bradykinins

All of the above compounds increase inflammation, increased smooth muscle tone and hyperactivity. Eosinophils infiltrate the airways during the hours following allergen exposure and leads to the release of mediators

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17
Q

Can you treat bronchial smooth muscle bronchoconstriction with muscle relaxant like we do with laryngospasms?

A
  • No

- treat with bronchodilator or beta agonist

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18
Q

What is another name for allergic-induced asthma?

A

Extrinsic asthma- external source

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19
Q

What are Curschmann’s spirals seen with with extrinsic asthma?

A
  • thick, tenacious spiral shaped secretions that occlude the airway (mucous plug)
  • These secretions generally reveal hypereosinophilia consistent with an allergic process either initiating or complicating episodes of airflow obstruction
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20
Q

What is another type of asthma that is not allergy induced?

A

Abnormal Autonomic Nervous System Regulation of Airway function (Intrinsic or Idiosyncratic)

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21
Q

What causes Intrinsic or Idiosyncratic asthma?

A
  • abnormal regulation of neural function
  • imbalance of between inhibitory (bronchodilation) and excitatory (bronchoconstriction) neural input
  • smooth muscle function is modulated by cyclic GMP or cyclic AMP.
  • Usually in response to noxious stimuli (cold, exercise, airway instrumentation, climate, airway illness)
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22
Q

What does an increase in cyclic AMP do?

A

-**increases in cyclic AMP result in relaxation of bronchial smooth muscle

23
Q

What does an increase in cyclic GMP do?

A

-**increases in cyclic GMP results in constriction of bronchial smooth muscle

24
Q

Stimulation of the sympathetic nervous system causes what in the lungs?

A

bronchial relaxation or bronchodilation

25
Q

Parasympathetic stimulation causes what in the lungs?

A

causes bronchoconstriction or increased bronchomotor tone

26
Q

What types of meds would you want to give to asthmatics when thinking about what the SNS & PNS do to the airways?

A
  • Give sympathomimetic agents Beta agonist ex. albuterol (beta 2 agonist Bronchodilate)
  • Or blockade of the parasympathetic nervous system ex. atropine = (anticholinergic drug/parasympatholytic will bronchodilate).
27
Q

What are the clinical manifestations of Asthma?

A

a. Bronchoconstriction/Wheezing - most common finding,turbulent gas flow through narrowed airways
b. Cough - productive or non-productive; Curshman’s spirals, frequently at night or morning ,may be the only manifestation; part in children “cough variant asthma”
c. Dyspnea - varies; may be “air hunger” patients may insist on sitting up chest discomfort while awake, FEV1 (Forced expired volume) is less than 35% of normal and a max mid-expiratory flow rate that is 20% of normal or lower

28
Q

What is exercise induced asthma?

A
  • physical activity produces airway narrowing
  • “exercise induced bronchospasm”
  • children, young adults
  • “thermally induced asthma” heat and water that develop in the TB tree
29
Q

What is nocturnal asthma?

A
  • changes in airway tones, secretions, catecholamine conc., reflux related to the supine position
  • increased incidence of asthmatic deaths after midnight and before morning
30
Q

What is Aspirin induced asthma?

A
  • aspirin and NSAIDS precipitate bronchospasm in 8-20% of adults asthmatics
  • nasal polyps
  • aspirin blocks the cyclooxygenase-mediated conversion of arachidonic acid to prostaglandins; this causes shunting of arachidonic acid toward the formation of leukotrienes
31
Q

What is occupational asthma?

A
  • chlorine, ammonia, ect.
  • latex in health care personnel
  • 15% of newly diagnosed cases in the US
32
Q

What is infectious asthma?

A
  • acute inflammatory disease of the bronchi

- viruses, bacteria

33
Q

What is COPD?

A
  • obstructive disorder (resistance to airflow during exhalation)
  • enlargement of alveolar air ducts and destruction of walls, loss of elastic recoil which leads the collapse of airways during exhalation; may also see edema or inflammation of the wall of the airway.
  • *Airway changes are irreversible
  • loss of lung parenchyma and structural support; ↑ dead space
  • most patients with COPD have chronic bronchitis, emphysema
  • chronic bronchitis and emphysema usually occur together as a result of cigarette smoking
34
Q

What is Emphysema?

A
  • Destruction of lung parenchyma with a loss of effective surface area for gas transfer; they may have relatively advanced disease with preservation of arterial tension and normal CO2 tensions.
  • **Spirometry usually shows a decrease in the FEV1/FVC ratio the hallmark of chronic airflow obstruction.
35
Q

What is FVC?

A

Forced vital capacity (FVC) is the volume of air that can forcibly be blown out after full inspiration, measured in liters. FVC is the most basic maneuver in spirometry tests

36
Q

What is FEV1?

A

Forced Expiratory volume in one second (FEV1) is the volume of air that can forcibly be blown out in one second, after full inspiration. Average values for FEV1 in healthy people depend mainly on sex and age

37
Q

What is Chronic Bronchitis?

A

proliferation and hypertrophy of the bronchial glands and reactive bronchial smooth musculature.

38
Q

What are the characteristics of Chronic bronchitis?

A
  • Characteristics include: increased secretions, a chronic purulent cough, and an early tendency toward arterial oxygen desaturation and hypercarbia.
  • The course is characterized by acute episodes of bronchitis, bronchospasm, and fever.
  • These patients are often difficult to wean from mechanical ventilation.
  • Finally, these patients often have an increase in pulmonary vascular resistance due to the changes in arterial oxygen tension.
39
Q

What can the increased pulmonary vascular resistance seen in patients with COPD cause?

A

Right-sided heart failure and for-pulmonale (enlargement of right ventricle)

40
Q

Just about all smokers over the age of 60 have what?

41
Q

What symptoms pre-op could postpone surgery?

A
  • increased secretions, bronchoconstriction, airway irritability, coughing
  • wheezing, rales or rhonchi, fever
  • use your judgement
  • at risk for laryngospasm ⇒ pulmonary edema
42
Q

Patients with airway disease will have increased incidence of what especially during surgical stimulation, insufficient anesthesia, manipulation of the airway, drugs that precipitate bronchoconstriction?

A
  • laryngospasm
  • bronchospasm
  • coughing
43
Q

What are the 2 strongest predictors of respiratory complications post-op?

A
  1. Preoperative dyspnea, etc.
  2. Location of operative site
    - closer to the diaphragm
    - surgical time > 3 hours
44
Q

To prevent bronchospam’s in OR what meds would you give to treat HTN? What meds should you avoid?

A
  • Hydralazine 5mg increments (onset 10min.)
  • B-blockers-(none totally B1 specific B2 responsible for bronchdilation so if you block it more likely to bronchoconstrict)
45
Q

What are some drugs that given in the OR that promote histamine release that are bad for asthmatics?

A
Sodium pentothal (not used)
Morphine
succinylcholine
Atracurium
Cisatracurium
Mivacurium
46
Q

Why do anticholinesterase agents (Neostigmine, Pyrodostigmine, Edrophonium) cause bronchosapasms?

A
  • increased ACH for muscarinic receptors at endplate therefore increased risk for bronchoconstriction.
  • Pyridostigmine probably best to give to asthmatics but give slowly with anticholinergic
47
Q

Why shouldn’t the barbiturates Thiopental and Thiamylal be given to asthmatics?

A
  • the sulfur atom attached can cause histamine release

- Methohexital is better because no histamine release but is also a very stimulating drug to airway so not good choice

48
Q

What is the biggest enemy to an irritable airway seen in smokers, asthma, and COPD?

A
  • insufficient “Light” Anesthesia
  • make sure deep prior to instrumentation of the airway, introduction of surgical stimulation (incision)
  • one of the most significant precipitators of bronchospasm
  • mask or LMA preferred over intubation because not manually stimulating trachea (still risk for bronchospasm though)
49
Q

Why does H2 blockers cause bronchoconstriction?

A

bronchodilation is mediated by H2-receptors. Conceivably, antagonism of H2-receptors by antagonist drugs would unmask histamine-mediated H1-receptor bronchoconstriction leading to increased airway resistance”

50
Q

What are examples of H2 blockers that should be avoided to prevent bronchoconstriction?

A

-**Pepcid, Zantac, Cimetidine

51
Q

What do all volatile inhalation agents do to the airway?

A
  • decrease airway reflexes

- all promote bronchodilation

52
Q

Which volatile inhalation agent is ideal for asthmatics?

A
  • Sevoflurane ideal for asthmatics
  • Halothane sensitizes the myocardium to catecholamines (not used)
  • (Isoflurane, Desflurane, - most irritating)
53
Q

What dose of lidocaine should be given to decrease reflex-induced bronchospasm?

A
  • 1.5mg/kg (approx 100mg) 90sec - 3min prior to laryngoscopy. (give when you walk in the door to get it working)
  • LTA (Laryngeal Tracheal Anesthetic) injector (4cc of 4% lidocaine) applied directly to the airway/trachea prior to intubation of the trachea
  • 4% lidocaine instilled in the pilot balloon ( let sit for at least 30 minutes for saturation of cuff)
  • continuous infusion of lidocaine 1-2 mg/kg/h (not frequently done)
54
Q

Why is Ketamine a good drug for asthmatics?

A
  • sympathomimetic (↑ catecholamine release)
  • bronchodilator
  • 1-2mg/kg
  • increased secretions (give robinol)
  • can be used for induction or to deepen quickly