Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
114 Cards in this Set
- Front
- Back
Cigarette smoking releases over how many compounds
|
4000
|
|
Name some of the compounds released by smoking
|
benzene, formadehyde, CO, nicotine, acetone, tar, arsenic
|
|
Two impacts of pulmonary functions caused by smoking
|
decreased ciliary function, increased sputum production
|
|
Studies show that continuous exposure to cigarette smoke leads to
|
an increase in proteolytic enzymes
|
|
Proteolytic enzymes
|
destroy lung parynchema
|
|
Smoke exposure increases the synthesis and release of
|
elastolytic enzymes - which directly damage lung tissue
|
|
Elastolytic enzymes are synthesized and secreted from the
|
macrophage
|
|
In smoking, what causes further damage
|
reactive metabolites of oxygen - which are typically used by macrophages to kill micro-organisms
|
|
What changes does the epithelium undergo
|
increased membrane permeability and decreased surfactant production
|
|
Early effects of smoking
|
mild V:Q mismatching, bronchial problems like cough, URI, bronchitis, and reactive airway symptoms plus bronchitic disease and airway hyperactivity
|
|
Reactive airway disease means asthma, right?
|
no - reactive airways are a set of symptoms that MAY be included in asthma diagnosis but may also be environmental
|
|
Symptoms of reactive airway disease include
|
coughing, wheezing, sob
|
|
Later effects of smoking include
|
increasing V:Q mismatching due to gas trapping,
|
|
Gas trapped areas
|
increase deadspace area
|
|
Increased deadspace area cause by gas trapping causes two things
|
Low PaO2 and high PaCO2
|
|
Reason for low PaO2 and high PaCO2
|
low PaO2 - increased amounts of venous admixture
high PaCO2 - b/c of reduced CO2 elimination |
|
Normal carboxyhemoglobin levels in nonsmoker
|
1%
|
|
Carboxyhemoglobin levels can increase to what in chronic smokers
|
8-10%
|
|
Increased PaCO2 will shift curve to
|
left
|
|
Cessation of smoking of how long can decrease carboxyhemoglobin levels to near normal
|
12-24 hours
|
|
What are POPCs
|
post operative pulmonary complications
|
|
Pts with hx or pulmonary disease (COPD) will have how much risk for POPC
|
2-6x
|
|
Pts who smoke but have no hx of pulmonary disease will have how much risk for POPC
|
2x
|
|
In order to see reduction in POPC - how long before procedure must smoker stop smoking
|
8 weeks
|
|
Smokers who stop smoking 4 weeks before procedure change risk of POPC how
|
increase of 4x of having POPC - above those who never smoked
|
|
How long after abstinence of smoking does it take for mucociliary function to return
|
2-3weeks
|
|
During 2-3 weeks of cigarette abstinence - mucociliary function
|
increases
|
|
Reducing number of cigarettes smoked before procedure
|
has no benefit to decreasing POPCs
|
|
7 risk factors for POPC are
|
1. postoperative site 2. dyspnea 3. pre-existing pulmonary disease 4. smoking 5. obesity 6. aging 7. prolonged general anesthetics
|
|
Incidence of post op complications ranges from
|
6-60%
|
|
POPC include
|
atelactesis, pneumonia, pulmonary embolism, respiratory failure
|
|
Which operative sites carry the highest risk for POPC
|
upper abdominal and throracic incisions
|
|
Incisions near diaphragm often result in
|
diaphragmatic and restrictive ventilatory deficits
|
|
Upper abdominal procedures reduce FRC by
|
60-70% - peaks first day and lasts 7-10 days
|
|
Why is reported preoperative dyspnea a big risk factor
|
because it correlates to the degree of existing disease
|
|
Obesity decreases
|
FRC
|
|
Obesity increases - two things
|
work of breathing, risk of DVT
|
|
Aging causes - two things
|
breakdown of recoil capacity of the lung and increase in closing capacity
|
|
Which is the least consistent factor regarding POPC
|
general anesthesia
|
|
Regarding POPCs and surgical sites - laporascopic surgeries
|
do not count
|
|
Two greatest predictors of pulmonary risk
|
1. operative site 2. reported preoperative dyspnea
|
|
Is regional anesthesia better than general about reducing POPC
|
not really - has not been established
|
|
Regional anesthesia above what level should not be employed
|
above T-6 - reduces ability to cough and deep breathe
|
|
Another strategy to reduce POPC
|
post operative analgesia - chest and upper abdominal epidurals
|
|
Opioids cause
|
respiratory depression
|
|
With use of CPAP - can reduce FRC recovery time from
|
up to 7 days to 72 hours
|
|
What percentage of unsupervised people correctly uses IS
|
10%
|
|
What is more effective than IS for FRC recovery time
|
stir up regimens - coughing, deep breathing, fluid hydration, early ambulation
|
|
People who stopped smoking >2 months, and institute aggressive pulmonary toilet have POPC rate
|
nearly equal to normal patients
|
|
Obstructive pulmonary diseases include
|
emphysema, chronic bronchitis, cystic fibrosis, bronchiectasis and bronhiolitis
|
|
Obstructive pulmonary diseases have one key commonality
|
problem with air flow
|
|
Hallmark of resistance to air flow is evidenced by what pulmonary test
|
FEV-1/FVC of less than 75%
|
|
Normal FEV-1/FVC value
|
80%
|
|
Early in OPDs what is the most reliable indicator of abnormality
|
FEF or MMEF 25-75%
|
|
OPDs all lead to
|
an increase in airway resistance, which reduces exhalation volume and leads to gas trapping
|
|
OPD breath sounds may include
|
inspiratory wheezes - due to turbulent flow
|
|
Not allowing OPD patients extra E time will cause
|
stacking of breaths and ETCO2 will increase
|
|
What is the hallmark activity of asthma
|
bronchiolar hyperactivity in response to stimuli which results in dyspnea, cough, and wheezing
|
|
Asthmatic bronchiolar obstruction has what three components
|
smooth muscle contraction, bronchiolar edema, increase in secretions
|
|
Asthma pathology - 5 things in process
|
1. exposure to causative condition or agent causes release of chemical mediators or over activity of PNS
2. Bronchial mast cells degranulate after the antigens bind to IgE 3. Histamine, bradykinin, seratonin, leukotrienes, platelet aggregating factor, prostaglandins, neutrophils and eosinophil chemotaxic factors are released 4. vagal afferent factors in bronchi are sensitive to histamine and noxious stimulus - causes reflective vagal activation which leads to 5. bronchocontriction - which is mediated by increasing cGMP |
|
Asthma PFT - moderate to severe
|
FEV-1 <50%
|
|
Asthma PFT - impending doom
|
FEV-<25%
|
|
Asthma CXR
|
air trapping, flatten diaphragm
|
|
Name things that can trigger an asthma attack
|
pollen, mold, dust mites, pet dander, exercise, temperature, infection, occupational exposure
|
|
Preop assessment of asthma
|
1. what are triggers
2. last time had attack 3. how do they treat asthma 4. take meds daily 5. take med day of surgery 6. hospitalized for asthma, intubated 7. auscultate breath sounds 8. have pt take meds with good technique |
|
If asthma pt takes albuterol tx and still has wheezes, what type of procedure should be canceled
|
elective
|
|
Aspirin-induced asthma affects what % of adult asthmatics
|
8-20%
|
|
What is onset of aspirin-induced asthma
|
15min-4hours
|
|
What is pathway for aspirin-induced asthma
|
blocks cyclo-oxygenase pathway
|
|
If pt is allergic to aspirin, don't give
|
NSAID
|
|
LOOK at ketorolac-induced bronchospasm article
|
LOOK at ketorolac-induced bronchospasm article
|
|
Aspirin pathway - inflammatory mediators promote the release of
|
arachadonic acid from the cell membrane - which is then converted to endoperoxides and leukotrienes
|
|
Symptoms of asthma - PFT
|
increased TLC, RV, FRC
|
|
Symptoms of asthma - general
|
increased work of breathing
poor V:Q = hypoxemia tachypnea = hypocapnea |
|
Symptoms of asthma - bad sign
|
normal or high PaCO2 - b/c should be compensating
|
|
Name some asthma treatment drugs
|
albuterol, leva-albuterol (xopenex), pirbuterol,
|
|
How do beta 2 agonists work
|
activate adenyl cyclase which increases cAMP, which promotes smooth muscle relaxation/bronchodilation
|
|
Name a long acting beta 2 agonist
|
terbutaline
|
|
In large doses of beta 2
|
also see beta 1 effects
|
|
What effects do nonspecific beta blockers have
|
cause high airway pressures - hard to ventilate
|
|
For asthmatic patients, can use
|
specific beta blockers - but best to choose a different agent for BP
|
|
How do methylxanthines work
|
inhibit phoshodiesterase (enzymes that break down cAMP)
|
|
Methylxanthines promote
|
bronchodilation
|
|
Do methylxanthines directly or indirectly stimulate the diaphragm
|
directly
|
|
Name two methylxanthines
|
theophylline - long acting oral
aminophylline - IV |
|
Aminophylline dosing
|
loading - 5mg/kg over 20 min
maintenance - 0.5mg/kg/hr |
|
What is a narrow therapeutic index
|
ratio between effective dose/lethal dose is small
|
|
Asthma treatment - how do glucocorticoids work
|
stabilize the membrane of the mast cell
|
|
Asthma treatment - name two glucocorticoids
|
beclomethosone and tramcinolone
|
|
Asthma treatment - Advair contains
|
a steroid and a beta 2
|
|
Asthma treatment - How do anticholinergics work
|
block PNS
|
|
Asthma treatment - Name some anthicholinergics
|
atropine, robinul, ipratropium (atrovent)
|
|
Asthma treatment - If taking every day, do we use pre-op steroids for a big case
|
*** need to find the answer for this ***
|
|
How does cromolyn work
|
inhibits inflammation buy inhibiting the release of chemical mediators from mast cells (membrane stabilization?)
|
|
Can cromolyn effective for emergency bronchospasm use
|
no - needs to be used for several days before
|
|
What class of drugs are effective with mild to moderate asthma
|
leukotriene inhibitors
|
|
Can leukotriene inhibitors be used for acute situations
|
no - for long term use
|
|
What is extremely useful for pts with emotional asthmatic components
|
preoperative sedation
|
|
Although H2 blockers are detrimental, actually they
|
promote bronchodilation
|
|
What is an unexpected effect of H2 blockers
|
since H1 receptors are unopposed, they "rev up" H1 receptors - so need to have H1 blocker too
|
|
What type of drug is theophylline
|
methylzanthines - inhibit phosphodiesterase (enzyme that breaks down cAMP)
|
|
Since aminophylline has a narrow therapeutic index
|
they should have levels drawn
|
|
Reasons to draw theophylline levels
|
pt has therpeutic level, which is not toxic
|
|
Normal treatment range of aminophylline
|
10-20mg/L
|
|
Bronchospasm most likely occurs
|
in a lighter anesthetic plane and during manipulation and instrumentation
|
|
Which drugs are histamine-releasing drugs
|
pentothal, atracurium, succinylcholine, morphine, demerol
|
|
What is a special consideration for histamine-releasing drugs
|
they should be avoided or given slowly
|
|
Asthmatic considerations of ketamine include
|
sympathomimetic properties and promotes bronchodilation
|
|
Asthmatic considerations - Why can using theophylline and ketamine together be dangerous
|
theophylline can promote seizure activity and ketamine lowers seizure threshold
|
|
Asthmatic considerations - isoflurane and desflurane are airway irritants so
|
they must be increased slowly to blunt bronchospasm
|
|
Asthma - when using proper technique, how much albuterol is delivered to the lungs
|
12%
|
|
Asthma - with an ETT in place, the 12% of abluterol normally delivered to the lungs is reduced by
|
50-70%
|
|
Asthma - with an ETT in place, how much must the dose be increased
|
6-10x
|
|
Asthma - with an ETT in place, how many puffs of albuterol must be used
|
12 puffs
|