Exam 4 Obstructive lung disease part III Marlea Flashcards

1
Q

Major risk factors for Development of postop pulmonary complications
- pt related (5)

A
  • Pt related:
    -age>60yo
    -ASA class>II
    -CHF
    -preexisting pulmonary disease (COPD)
    -cigarette smoking

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2
Q

Major risk factors for Development of postop pulmonary complications
- Procedure related (4)

A
  • Procedure related
    -emergency surgery
    -abdominal or thoracic surgery, head/neck surgery, neurosurgery, vascular/aortic aneurysm surgery
    -Prolonged duration of anesthesia >2.5hrs
    -general anesthesia

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3
Q

Major risk factors for Development of postop pulmonary complications
- Test procedures (1)

A
  • Albumin level of <3.5g.dL

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4
Q

Perop strategies to reduce post-op complications

A
  • encourage cessation fo smoking for at least 6 weeks
  • treat evidence of expiratory airflow obstruction
  • treat respiratory infection with abx
  • initiate patient education regarding lung volume expansion maneuvers

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5
Q

Intraoperatvie strategies to reduce post-op compications

A
  • use minimally invasive surgery (endoscopic) techniques when possible
  • consider regional anesthesia
  • avoid surgical procedures likely to last more than 3 hours

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6
Q

Postoperative strategies to reduce post-op complications

A
  • institute lung volume expansion maneuvers (voluntary deep breathing, incentive spirsmetry, continuous positive airway pressure)
  • maximize analgesia (nerve blocks, neuraxial opioids, PCAs)

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7
Q

Smoking cessation:
- ~20% adults smoke, of whom ____ - ____ undergo surgery with GA
- this offers a window of opportunity for a ____ ____ and encourage the pt to stop smoking
- Evidence shows that the earlier the intervention, the more effective in reducing ____ ____ complications

A
  • 5-10%
  • smoking intervention
  • postop complications

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8
Q
  • the maximum benefit of smoking cessation usually isn’t seen unless smoking has been stopped for ____ weeks prior to surgery
  • smoking is the simgle most important risk factor for developing ____ and ____ caused by lung disease
  • the American Society of Anesthesiologists has a ____ ____ ____ and provides resources to help practitioners encourage smoking cessation
A
  • 8 weeks
  • COPD and death
  • Stop smoking initiative

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9
Q
  • The adverse effects of carbon monoxide on O2 carrying capacity and nicotine on the CV system are ____
  • Nicotine causes ____ effects on the heart for ____ - ____ min
  • E1/2 of carbon monoxide:
A
  • short lived
  • sympathomimetic; 20-30min
  • 4-6 hours

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10
Q
  • within ____ hours after smoking cessation, the P50 increases from ____ to ____ and the plasma levels of carboxyhemoglobin decrease from ____ to ____
  • whats the caveat?
A
  • 12 hours; 22.9 to 26.4mmHg; 6.5% to 1%
  • Despite favorable effects on plasma carboxyhemoglobin concentration, short-term abstinence from cigarettes has not been proven to decrease the incidence of postoperative pulmonary complications

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11
Q

What does cigarette smoking cause?

A
  • mucous hypersecretion, impairment of mucociliary transport, and narrowing of small airways
  • may also interfere with normal immune responses and thus the ability to respond to pulmonary infection following surgery

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12
Q

How long does it take to see lung improvement after smoking cessation?

A
  • it takes weeks of no smoking to see improved ciliary and small airway function, and decreased sputum production
  • return of normal immune funation requires at least 6 weeks
  • some components of cigarette smoke stimulate hepatic enzymes
  • it may take 6 weeks or longer for hepatic enzymes to return to normal

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13
Q

Things to help with smoking cessation

A
  • optimal timing of quitting before surgery is 6-8 weeks, if a pt is scheduled for surgery in <4 weeks should be advised to quit and offered behavioural support and pharmacotherapy
  • Nicotine replacement therapy
  • sustained release bupropion (started 1-2 weeks before smoking is stopped)

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14
Q

Although long term smoking cessation offers clear advantages, what are the disadvantages in the immediate postop period?

A
  • increased sputum production
  • inability to handle stress
  • nicotine withdrawal
  • irritability
  • restlessness
  • sleep disturbances
  • depression

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15
Q

Bronchiectasis
- associated with
- prevalance

A
  • associated with irreversible airway dilation, inflammation, and chronic bacterial infection
  • Prevalence is highest in pts >60 with chronic pulmonary disease, COPD & asthma, and in women

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16
Q

Bronchiectasis
- S/S

A
  • Chronic productive cough with purulent sputum, hemoptysis, clubbing
  • poor ciliary activity and mucous pooling cuases a vicious cycle of recurrent bacterial infection (this causes further inflammation, airway collapse and obstruction, and inability to clear secretions)
  • when bacterial superinflection is established, its nearly impossible to eradicate

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17
Q

Bronchiectasis
- diagnosis

A
  • baseline chest XR
  • sputum culture check to determine active infection
  • CT is the gold standard - it will also show dialated bronchi

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18
Q

Bronchiectasis treatment

A
  • Treatment: abx and chest physiotherapy are key
  • other treatments = yearly flu vaccine, bronchodialators, systemic corticosteroids, O2
  • surgery is only considered when severe symptomes persist or recurrent complications

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19
Q

Cystic Fibrosis
- definition

A
  • autosomal recessive disorder of chloride channels leading to abnormal secretion production and clearance
  • affects 30,000 people in the US
  • caused by a mutation of a single gene on chromosome 7 that encodes the cystic fibrosis transmembrane conductance regulator (CFTR)

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20
Q

What does the CFTR usually do under normal conditions, and what does it do with Cystic fibrosis?

A
  • Normally, CFTR produces a protein, which aids in salt and water movement in and out of cells.
  • However, in CF, the mutated CFTR gene results in the production of abnormally thick mucus outside of epithelial cells
  • Decreased chloride transport is accompanied by decreased transport of sodium and water = dehydrated viscous secretions, luminal obstruction, and destruction and scarring of various glands and tissues
  • The end result is severe organ damage

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21
Q

What does end organ damage in CF manifest?

A
  • Bronchiectasis
  • COPD (present is nearly all CF - relentless downhill course)
  • sinusitis (chronic is pretty universal)
  • diabetes
  • cirrhosis
  • meconium ileus in children
  • azoospermia
  • pancreatic insufficiency manifests with malabsoption of fats and fat-soluble vitamins
  • primary cause of mortaility is chronic pulmonary infection

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22
Q

Diagnosing CF

A
  • presence of sweat chloride concentration >60mEq/L along with clinical manifestations or family history
  • DNA analysis can identify >90% of the CFTR mutation
  • positive sputum cultrue for pseudomonas aeruginosa is common
  • lavage usually shows high percent fo neurtophils, this is a sign of airway inflammation

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23
Q

Treatment of CF

A
  • Treatment is directed toward symptom control, pancreatic enzyme replacement, oxygen therapy, nutrition, prevention of intestinal obstruction
  • Gene therapy is currently being investigated

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24
Q

Treating CF nonpharmacoligically

A
  • We mostly want to decrease sputum retention and airway obstruction
    -main nonpharmacologic approach is chest physiotherapy and postural drainage
    -high frequency chest compressions with an inflatable vest or airway oscillation

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25
Q

CF pharmacologic treatments

A
  • CF pts have greater bronchial reactivity to histamines and other stimuli
  • So Bronchodialators can be considered if the pts are known to have beneficial response to inhaled bronchodialoators
    -a postitive response is defined as an increase of 10% or more in FEV1 after bronchodialator administration.

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26
Q
  • the abnormal viscosity of airway secretions is caused by ____
  • DNA released from neutrophils forms ____ that add to the viscosity of the sputum
  • Recombinant ____ can cleave this DNA and increase the clearance of sputum
A
  • the presence of neutrophils and their degradation products
  • long fibrils
  • human dexoyribonuclease

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27
Q
  • CF pts have periodic exacerbations causing ____
  • if cultures show no ____, a ____ to remove lower airway serections may be indicated
  • many CF pts are given long-term ____ to suppress chronic infections
A
  • increased sputum production
  • pathogens; bronchoscopy
  • antibiotics

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28
Q

CF anesthesia implications

A
  • delay elective surgeries until optimal pulmonary function is ensured
  • Vit K may be necessary if hepatic function is poor or exocrine pancreatic function is inpaired
  • humidify inspired gasses, hydration, avoid anticholinergic drugs = less viscous secretions
  • frequent tracheal suctioning
  • pt should regain full reflexes, with good Vt prior to extubation
  • postop pain control is important to have deep breathing, coughing and early ambulation

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29
Q

Primary ciliary dyskinesia
- definition

A
  • Congenital impairment of ciliary activity in respiratory tract,epithelial cells and sperm tails and ciliated ovary ducts
  • Impaired ciliary activity leads to chronic sinusitis, recurrent respiratory infections, bronchiectasis and infertility

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30
Q

Primary Ciliary dyskinesia (triad and what its called)

A
  • Kartagener syndrome
  • triad of: chronic sinusitis, bronchiectasis and situs inversus (chest organ position is inverted)

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31
Q
  • Approximately ____ of pts with congenitally nonfunctioning cilia exhibit situs inversus
  • isolated ____ is almost always associated with congenital heart disease
A
  • 1/2
  • dextrocardia

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32
Q

Primary Ciliary Dyskinesia
- anesthesia considerations

A
  • preop: directed at treating pulonary infection and determining if significantorgan inversion is present
  • RA is preferred to GA - this decreases pulmonary complicaitons
  • with dextrocardia EKG position needs to be reversed for accurate interpretation
  • because of increased risk of sinusitis, nasopharyngeal airways should be avoided

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33
Q

Dextrocardia anesthesia considerations
- great vessels
- preggers
- double lumen ETT

A
  • Inversion of great vessels is the reason to select the left IJ vein for CVC
  • Uterine displacement in pregnant womane should be to the right to keep the baby off the IVC
  • double-lumen ETT, pulonary inversion may indicate a Right double lument tube placement (DLT)

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34
Q

Bronchiolitis obliterans
- from what?
- risk factors

A
  • results from epithelial and subepithelial inflammation leading to bronchoilar destruction and narrowing
  • risk factors: viral respiratory infections, environmental exposures, lung transplant and stem cell tansplant

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35
Q

Bronchiolitis obliterans
- S/S
- PFTs show…
- CT scans show…

A
  • S/S: nonspecific and include dyspnea and nonproductive cough
  • PFTs: usually show obstructive disease and include reduced FEV1 and FEV1/FVC ratio (this is likely unresponsive to bronchodialators)
  • CT shows air trapping and bronchiectasis in severe cases

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36
Q

Central Airway obstruction
- includes
- what percent of cancer pts are affected?
- obstruction can be from what things?

A
  • includes obstruction of airflow in the tracheal and mainstem bronchi
  • 20-30% of cancer pts can be affected
  • obstrution is caused by: tumors, granulation from chronic infections, airway thinning from cartilage destruction

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37
Q

Central airway obstruction
- Tracheal stenosis can develop after ____ either with an ETT or a tracheostomy tube
- Tracheal ____ can progess to destruction of cartilaginour rings and subsequent circumferential ____ formation
- minimize this by ____ on the ETT

A
  • prolonged intubation
  • mucosal ischemia; scar
  • using high-volume and low-pressure cuffs

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38
Q

In central airway obstruction, when does tracheal stenosis become symptomatic?
what re the S/S?

A

when lumen is decreased to <5mm in diameter
* symptoms may not develop until several weeks after extubation
* s/s of dyspnea is prominant even at rest, accessory muscles are used constantly, stridor

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39
Q

What do the flow volume loops look like in central airway obstruction?

A
  • display flattened inspiratory and expiratory curves - this is characteristic of a fixed airway obstruction
  • CT will illustrate tracheal narrowing

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40
Q

Tracheal Stenosis
- what can be used as a temporary treatment?

A
  • Tracheal Dilation can be used as temporary treatment
  • this can be done bronchoscopically with balloon dilators, surgical dilators or laser resection

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41
Q

Tracheal Stenosis
- long-term solutions

A
  • tracheobronchial stent can be temporarty or long-term
  • most successful treatment is surgical resection and reconstruction with primary re-anastomosis
  • translaryngeal intuation is necessary for this surgery

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42
Q

Tracheal resection and reconstruction procedure

A
  • distal normal trachea is opened and the sterile cuffed ETT is inserted and attached to the anesthetic circuit
  • maintain with volatile to ensure maximal FiO2
  • high frequency ventilation is helpful
  • anesthesia may be facilitated by the addition of helium to the inspired gasses
  • helium decreases the density of the gasses and may improve flow throught the stenotic trachea

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43
Q

Key points to read through

A
  • Anesthetic management of a pt with a recent URI should focus on reducing secretions and limiting manipulation of a potentially hyperresponsive airway
  • Asthma treatment is classified into immediate and long-term therapy. Immediate therapy for bronchospasm consists mainly of short-acting β-agonists, whereas long-term relief mayinclude inhaled corticosteroids & long-acting bronchodilators, leukotriene inhibitors, monoclonal antibodies, and bronchial thermoplasty
  • In asthmatic pts the goal during induction & maintenance is to depress airway reflexes and avoid bronchoconstriction
    In COPD, smoking cessation and long-term 02 therapy are the only two interventions that may slow progression
  • Drug therapies, including inhaled β-agonists, inhaled corticosteroids, and anticholinergic drugs, are managed with a goal of decreasing exacerbations
44
Q

Key points to read through

A
  • RA is preferred over GA in pts w/ COPD, to decrease the incidence of bronchospasm, barotrauma, and the need for positive pressure ventilation
  • COPD pts receiving GA should be ventilated at slow respiratory rates to allow sufficient time for exhalation, minimizing the risk of air trapping and auto-PEEP
  • Prophylaxis against postop pulmonary complications is b/o restoring lung volumes, especially FRC, and facilitating effective coughing
  • Intraoperative bronchospasm due to obstructive lung disease should be treated by deepening the anesthetic, administering bronchodilators and suctioning secretions as needed