2-late phase rxn- airway inflammation and cough and sputum production
3- airway hyperresponsiveness- wheezing in a variety of stim that would normally have little effect
What cellular mechanisms are involved in an asthma attack?
mast cell activation, degranulation with d/c of mediators (histamine), synthesis of arachidonic acid derivatives (PGD and leukotrienes- both bronchoconstrictors), cytokine release (stimulates IgE production and reactivates mast cells)
What does trypase do?
Trypase is a type of protease, it detaches epithelial cells from basement membrane, results in debris in airway, and airway narrowing
What is the significance of the deficiency of the enzyme alpha-1 antitrypsin in emphysema?
enzyme that inhibits protealysis (anti protease) is deficient, so elastin is lost and replaced with collagen
What is the best indicator of asthma severity at home?
-increased elastin breakdown in the alveolus and destruction of alveolar septa
-portions of alv-cap bed destroyed which increases volume of air in resp zone
-exp difficult b/c of loss of elastin recoil
-hyperinflation of alv causes lg air spaces (bullae) and air spaces adj to pleura (blebs) to develop
What values are you likely to see in a pt with emphysema?
Increased RV, FRC, TLC
All due to air trapping
What are the major differences between type A and B respiratory failure?
type A- "pink puffers," emphysema, low PCO2
type B- "blue bloaters," chronic bronchitis, elevated PCO2
both have same effects but diff patho
What 2 mechanisms are believed to be responsible for hypercapnia when delivering O2 to a pt with COPD?
1- vent depression by O2
2- altered V/Q relationship
giving O2 can worsen V/Q mismatch, HPV inhibited, alv open, but O2 in alv still low
How would you best differentiate btw type a and b COPDers?
COPDers have huge alv and large RV, this means they have greater diffusing capacity, right?
WRONG! It is not effective area for gas exchange!
What constitutes COPD treatment?
smoking cessation, inhaled bronchodilators, corticosteriods, antibiotics for infections, O2, and ventilation PRN
What should the PaO2 be maintained at for a COPDer?
80-90 mm hg as this reduces long term mortality
Should you give a COPDer O2 to get their PaO2 to the desired level?
In the periop period, yes, even if they are becoming apneic.
How does lung volume reduction surgery help to improve COPD?
Removes the part of the lung that is overdistended and unable to participate in normal gas exchange. This improves V/Q balance. This part of the lung could have been compressing normal lung tissue and it improves the effective gas exchange area.
Why might you be unable to maintain a COPDer on spont vent during anes?
During anesthesia the responsiveness to CO2 decreases, COPDers already have a decreased responsiveness to CO2, so might need controlled vent
What TV and RR would you want for a COPDer? What about exp phase?
High TV, low RR, long exp phase
Why might you not want to use N20 in a pt with COPD?
It will expand the airspace, esp bad for an emphysema pt with blebs and bullae
Should you try to normalize your blue bloater's CO2 level on the vent?
No, maintain CO2 level, they have no CO2 sensitivity, and the bicarb has been increased to maintain pH
-If acutely lower CO2, will cause alkalosis
Should you try to normalize your blue bloaters pH?
Would you expect a COPD pt to have a A-a gradient?
Yes, likely a large A-a gradient. You can't be sure the amount of exhaled CO2 = PaCO2.
How does anes affect the upper airway muscles assoc with resp? and how can we fix it?
-Causes obstruction of the pharyngeal airway (so use ETT, LMA, or oral airway to keep it open)
-Soft palate falls against posterior pharyngeal wall and occludes nasopharynx (tongue falls back and occludes glottis), correct it with forward mandibular thrust
How does anes affect the lower reps muscles?
-Depression of IC muscles
-Diaphragm function is well preserved
-Excitation of abd muscles
-Result is paradoxical muscle activity, diaphragm moves down on inspiration, but upper rib cage is drawn in towards lung due to depression of IC muscles
How does anes affect FRC? CC?
Decreases FRC and does not return to normal until hours after the anesthetic.
Also reduced by supine position.
No affect on CC.
What factors contribute to the progressive cephalic displacement of the diaphragm?
2) anes (occurs with GA due to excitation of abd muscles)
4) surgical retractors
What causes atelectasis during anesthesia?
-compression atelectasis (transmission of abd pressure compressing lungs)
-absorption atelectasis (low volume airway and 100% O2)
How do we counteract atelectasis post-op?
How does coughing help to re-expand the airways due to atelectasis?
It generates a forceful FEV1 so the next insp is DEEP
T or F, total resp compliance is reduced during anesthesia?
T, unsure why, maybe due to atelectasis which causes the lungs not to fill and empty as a single unit
In what patients is art oxygenation most impaired during GA? Why?
Elderly (increased CC), obese (decreased FRC), smokers (CO in RBC and increased CC), lung dz
What is the avg amount of venous admixture under GA?
(normal is 1-3%)
Why is the dead space / TV ratio increased under GA?
-Increased alv dead space (everyone has alv dead space under GA)
-Increased anatomic dead space due to valves and circuit for mechanical ventilation
How should vent settings be adjusted for the increased DS / TV ratio that occurs during GA?
Increased MV by increasing TV
How might you know you have increased DS/ TV ratio?
Increased A-a CO2 gradient
As dead space increases, ETCO2 decreases
How does anesthesia affect V/Q ratio?
V/Q scatter, more scatter towards low V/Q
How does GA affect the apneic threshold?
It is increased (as anesthesia level deepens, CO2 must rise higher before there is stimulation to breath)
How does MV vary with anesthesia depth and with surgical stimuli?
Increased anesthesia depth decreases MV
Surgical stim increases MV
What happens to vent and perf in a pt in the lateral position under anesthesia?
-preferential vent of upper (non-dept) lung
con't preferential perfusion of the lower (dept) lung; (poor V/Q matching)
-normal is increased V and Q to lower lung (good V/Q matching)
What happens to vent and perf in a pt in the prone position under anesthesia?
if upper chest and pelvis are supported, resp mechanics are minimally affected
How does regional anesthesia affect the pulmonary system?
It has little effect. Hypercapnia and hypoxic drive are unaffected by it.
What are possible causes of hypoxia post op?
-residual effects of anesthetic agents on ventilatory control
-PAO2 may be reduced by the elimination of N20 in the 1st few mins of recovery, this dilutes alveolar oxgen (diffusion hypoxia)
How can we avoid diffusion hypoxia from N20 post-op? How long can we expect it to last for?
Give supplemental O2
Why does diffusion hypoxia from N2O occur?
N20 has a low BG coefficient and likes the gas phase (comes out of blood and into the alv, leaving no room for O2)
What happens if you give opioids to a pt with OSA post-op?
It worsens their OSA and makes them more likely to desat
What PFT alteration would you be likely to see as a late post-op resp change from anesthesia?
Expiratory volume remains low
What is mechanism that results in splinting?
Due to surgery close to diaphragm, hurts to deep breath, due to phrenic nerve inhibition.
Only way to eliminate pain is with thoracic epidural anesthesia (as it's a nerve problem)
What factors affect CC?
Age, lung disease
What does increased CC mean?
The airway closes at a higher lung volume, airway closure is more likely
What affects FRC?
Position (supine), anesthesia
Which is more likely to cause low FRC, obstr or rx dz?
Which is more likely to cause increased CC, obstr or rx dz?
What are indications to give pre-op steroids?
- if pt takes PO steroids daily (pt is adrenally suppressed)
-if pt had an asthma exacerbation requiring steroids in the past year
-severe bronchospasm unresolved with bronchodilators
What steps should be taken during anesthesia induction in an asthmatic?
1) block airway reflexes prior to laryngoscopy and intubation (IV lido or deep anesthesia)