Exam 4 Obstructive lung disease part III Flashcards
(44 cards)
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
CF pharmacologic treatments
* 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
* 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
* the presence of neutrophils and their degradation products
* long fibrils
* **human dexoyribonuclease**
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27
* 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
* increased sputum production
* pathogens; bronchoscopy
* **antibiotics**
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28
CF anesthesia implications
* 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
Primary ciliary dyskinesia
- definition
* 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
Primary Ciliary dyskinesia (triad and what its called)
* **Kartagener syndrome**
* triad of: chronic sinusitis, bronchiectasis and situs inversus (chest organ position is inverted)
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31
* Approximately ____ of pts with congenitally nonfunctioning cilia exhibit situs inversus
* isolated ____ is almost always associated with congenital heart disease
* 1/2
* dextrocardia
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32
Primary Ciliary Dyskinesia
- anesthesia considerations
* 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
Dextrocardia anesthesia considerations
- great vessels
- preggers
- double lumen ETT
* 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
Bronchiolitis obliterans
- from what?
- risk factors
* 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
Bronchiolitis obliterans
- S/S
- PFTs show...
- CT scans show...
* 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
Central Airway obstruction
- includes
- what percent of cancer pts are affected?
- obstruction can be from what things?
* 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
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
* prolonged intubation
* mucosal ischemia; scar
* using high-volume and low-pressure cuffs
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38
In central airway obstruction, when does tracheal stenosis become symptomatic?
what re the S/S?
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
What do the flow volume loops look like in central airway obstruction?
* display flattened inspiratory and expiratory curves - this is characteristic of a fixed airway obstruction
* CT will illustrate tracheal narrowing
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40
Tracheal Stenosis
- what can be used as a temporary treatment?
* 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
Tracheal Stenosis
- long-term solutions
* 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
Tracheal resection and reconstruction procedure
* 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
Key points to read through
* 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 may include 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
Key points to read through
* 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
