ACE Review - Pulm Flashcards
Cause of neurogenic pulm edema
Sympathetic discharge
When does neurogenic pulm edema occur
Within 12 hrs. As as soon as 4 hrs
Common cause of neurogenic pulm edema
Head trauma
in a tension pneumo, where should a large bore needle be placed
mid clavicular 2nd intercostal
in a tension pneumo, where should a chest tube be placed
mid clavicular 6th intercostal
If an abg had an air bubble in it,how would the pao2 and paco2 be affected
Increased pao2 and decreased paco2
How does the pao2 increase bc of an air bubble?
Air fio2 is 0.21, thus partial pressure is 160mmhg(.21x760). O2 will diffuse into blood that only has an o2 partial pressure of 60-100 if pt is on room air
How does the paco2 decrease with an air bubble.
Same idea. Air partial co2 pressure is 0.04%
how many steps are there in lung injury when aspiration occurs
two steps
what is the first step of aspiration lung injury
loss of type 1 alveolar cells leads to pulmonary edema
what is the second part of aspiration lung injury
lung acute reactive airway disease
what is the first goal of aspiration
provide oxygenation and
what is the recommended tx for liquid aspiration
suction with a large bore catheter
should you do bronch lavage with liquid aspiration
no, it will push the contents down further
should you give antibiotics
no, because you are now making the patient more prone to vent assoc pna with resistant bacteria
should you give steriods
no, because it has been shown to increase risk of mortality in criticlly ill patients
what patient would benefit cpap
patients suffering soley from hypoxemia, like osa
what patient would benefit from bipap
pts suffering from hypercarbia or mixed hypercarb/hypoxemia
4 most common reasons for bipap
postop thoracic / ab surgery, pulm edema 2ndry heart failure, acute copd exacerbation, immunosupression
6 contraindications to bipap
ams, decreased resp drive, aspiration risk, untreated pneumothorax, hemodynamic instable, refusal
What is the leading cause of
TRALI
What are the other 2 major causes for transfusion associated mortalities
TAS - Transfusion Associated Sepsis, ABO Hemolytic transfusion reactions
what component makes transfusion more likely to have TRALI
plasma components
what is an example of plasma rich component
plateletes…it is 1000x more likely than prbc
what is the percent of death by trali
5-10%
what is the mechanism of action of trali
neutrophils are sequestered in the lungs…they are then triggered by high concentration of leukocyte antibodies
what kind of donors have higher likely hoold of giving blood components with high chance of trali
female multiparous pts bc they have developed more HLA antibodies
what kind of compenents have multiparous female donors have shown to increase risk of trali
ffp and plateletes, cryo and prbc not shown much difference
where does angioedema occur
mucocutaneous tissues primarily in lungs and bowel
who are prone to angioedema
hereditary…those who lack c1 easterase inhibitor enzyme
what drugs are associated with angioedema
pcn and sulfa drugs
what drugs causes pseudo-angioedema
NSAIDS…bc they inhibit prostaglandin synth
what is the most common cause for angioedema admission to ER
ACE inhibitors 17-38%
what is the moa for ace-I causing angioedema
it accumulates bradykinin that causes increase in vascular permeability
what 3 drugs are used to treat angioedema
epi, benadryl, steriods
how long should a pt with angioedema be followed
at least 24 hours bc relapse can occur
do patients with hereditary cause of angioedema have any preventative meds for acute angio tx
epsilon-aminocaproic acid and danazol(steriod)
does lasix cause angioedema
no
what is the calculation for static compliance of the lungs
tidal volume/ Plateau pressure minus peep
what is the purpose of static lung compliance
it is to test the elasticity of the respiratory system
when is static lung compliance measured
at the end of inspiration when lung volume is kept constant
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what can increase pulmonary hypertension
hypercarbia, acidosis, hypoxia
what is ards
oxygenation problem 2ndry non cardiogenic protienacious pulmonary edema
what has been assoc with decrease mortality in pt w ards
prevention of ventilator associated lung injury
what are the ventilator goals for decreasing ards assoc vent mortality
less than 6cc/kg of predicted body wt tidal volume and peak pressures less than 30mmHg
should we target to get a Pao2/Fi02 over 300 for ards pt
no
what may be used to help oxygenation in ards pt
peep
should high peep pressure be used in ards pt
no, may cause barotrauma…hi peep not recommended
should increasing fi02 to maintain o2% greater than 94% be targeted in ards pt
no…may lead to oxygen toxicity in pt
what is the cause of hereditary angioedema
it is autosomal dominant lesion that leads to a C1 esterase Inhibitor deficiency
what is the prob with hereditary angio edema
it causes swelling of mucos membranes including those of airway and gi tract
what are 2 prophylactic meds for hereditary angioedema
attenuated androgens, antifibrinolytics
what are examples of attenuated analbolic androgens
danazol and stanozolol
whare is an example of antifibrinolytic
epsilon amino caproic acid
which is prefered for prophylactic use for hereditary angio edema
androgen steriods bc antifibrinolytics have been assoc with thrombosis
what are drugs used for acute attacks of hereditary angio edema
FFP and synthetic C1 easterase inhibitors
what are 2 examples of C1 esterase inhibitor synthetics
CinRyze and Berinert P
which is c1 esterase inhibitor can be used for acute attack
only Berinert P can be used for acute attacks
is FFP better than synthetic C1esterase inhibitor
no because it is assoc with TRALI
if patient is to get a short proceedure, and they have Hereditary angioedema…what is the recommeneded treatment
avoide airway manipulation with the following: androgens 2 days before surgery, c1esterase inhibitors 24 hrs before surgery,or ffp 6-12 hours before surgery
what if airway manipulation is required?
ideal to achieve normal c1easterase inhibitor levels, but 40-50% is ok
how to achieve normal c1 esterase levels
5-7 days of androgen steriods, FFP on day of surgery, Berinert P on day of surgery
What prostacyclin is used to treat pulm hypertension.
Epoprostenol flolan
How does epoprostenol work
It vasodilates and inhibits platelet aggregation.
How is epoprostenol administered.
It is given as an infusion.
What phosphodiesterase inhibitor is used for pulm htn
Sildenafil
What drug in obstetric patients is contraindicated in pulm hypertension
15-methylprostaglandin- it vasconstricts. This is also known as hemabate
What is the p50 in adults
26.7
Which way does the oxyhemoglobin curve shift with carbon monoxide.
Left
Which way does the oxyhemoglobin curve shift with methemoglobin
Left
Which way does the oxyhemoglobin curve shift with fetal hg
Left
Which way does the oxyhemoglobin curve shift with preggos
Right
What settings can be set for high oscillatory freq ventilatoin
Fio2, inspiratory time, bias gas flow rate, frequency, amplitude,
What are alcoholics at risk for postoperatively
Postoperative pneumonia
which way does carbon monoxide shift oxyhemoglobin curve
left because it makes the o2 that is bound higher affinity to heme group…and not get kicked out
how does carbon monoxide work
besides competing for heme, it also inhibits cytochrome oxideases
what is similar to carbon monoxide in moa
cyanide…which also inhibits cytochrome oxidases
what is the most common presentation of carbon monoxide
altered mental status
how is carbon monoxide tested for
co-oximetry
how to treat carbon monoxide posioning
high flow non rebreather o2 mask, then ett with o2, then hyperbaric oxygen
what drug inhibit hypoxic pulm vasoconstriction
inhaled anesthtic
What problem can pectus excavatum cause
The sternum can cause Compression of the right heart And cause right ventricle outflow tract compression
What kind of PFT Is seeing with pectus excavatum
restrictive pattern
What common cardiac lesion is associated with pectus excavatum
50% of patients have mitral insufficiency
If Marfan’s is associated with pectus excavatum , What must you look out for him
Aortic insufficiency aortic dissection aortic aneurysm
What is adult P 50
26.5 mmHg
What is Fetal P 50
20 mmhg
What a sickle cell P 50
30 mmhg
What is the effect called when increased CO2 causes decreased O2 affinity in hemoglobin
bohr effect
What do inhaled anesthetic gases do to the Oxyhemoglobin curve
right shift
obesity…what happens to work of breathing
increse work of breathing
obesity…what happens to frc
decrease
obesity…what happens to vital capacity
decrease
obesity…what happens to dead space
no change
obesity…what happens to closing capacity
increase
obesity…what happens to hemoglobin
increase - polycythemia
obesity…what happens to fev1
decrease
obesity…what happens to fvc
decrease
obesity…why is there less time for 100% saturation on induction
supine postion decreases frc, increases shunt fraction, and worsen vq mismatch
Myasthenia gravis…what is the oral med used in MG
Pyridostigmine
Myasthenia gravis…what test is done before surgery to check if the patient needs optimization for surgery
Pulmonary function test.
Myasthenia gravis…what to look for in pulmonary function test
Vital capacity…they should have a vital capacity greater than 2 liters…or else that means that they will most likely end up intubated post thymectomy
Myasthenia gravis…ok, you got a low vital capacity…what should you do
Plasmapheresis
Myasthenia gravis…how should the patient be induced
Rapid sequence because they are at high risk for aspiration.
myasthenia gravis…how do these patients respond to succinylcholine
They are more resistant
Myasthenia gravis…why are they resistant to succinylcholine
Because the antibodies occupy most ach receptors…thus only a few ach receptors left for succ to work on….
Myasthenia gravis…how do they respond to nondepolarizing mm relaxants
They are more sensitive…only the few ach receptors left over need to be blocked
Myasthenia gravis…are neuraxial anesthesia contraindicated?
No…actually they help. They decrease the use of narcotics…and thus less chance of respiratory depression by narcotics
Myasthenia gravis…what are the 4 indicators of postoperative ventilator dependance
- Pyridostigmine dose greater than 750 daily. 2. Vital capacity less than 2.9liters, 3. MG for greater than 6 years 4. Coexisting copd
Myasthenia gravis…what other treatment can be used before surgery to decrease chance of postoperative intubation
Immunoglobulin administration
Beach chair…what happens to alveolar dead space in this position
There is increase alveolar dead space
Beach chair…what is the mechanism for increased alveolar dead space
It causes more dead space at the apex of the lungs…and also positive pressure ventilation causes decrease preload
Trali…what are 4 criteria
Onset within 6hrs of transfusion, hypoxia, chest X-ray bilateral infiltrate, pulm artery occlusion pressure below 18mmhg
Trali…how do u know there is hypoxia
Pao2/fio2 ratio less than 300, or spo2. Less than 90 on room air at sea level
Trali…what is the treatment
Supportive with oxygen supplementation
Axillary roll. What is the purpose
To prevent the head of the humerus from compressing the brachial plexus…to prevent brachial artery occlusion.
Axillary roll. Where should it be placed…
Caudal to the axillary pulse.
Axillary roll. What danger can be caused if it is placed to cephalad
Brachial nerve injury, arm ischemia, compartment syndrome
Axillary roll. What is a common complaint in people using axillary roll
Nondependant shoulder pain.
Axillary roll. What is a treatment for Nondependant shoulder pain
Interscalene block. ..but ketorlac is the first line treatment.
Sepsis. What are the 4 goals of early goal directed therapy for sepsis patients
Cvp 8-12, map 65-90, central venous oxygenation greater than 70.
Sepsis. What if you cannot get central venous oxygenation above 70?
Transfuse to get the hematocrit above 30
Sepsis. What kind of shock is septic shock
Distributive shock
ards. what is the treatment
low tidal volumes to prevent vent associated trauma
ards. what treatment may improve hypoxemia
prone positioning
Preoxygenation. Where does the extra oxygen go to
Frc
Preoxygenation. Does that affect the hypoxic pulmonary vasoconstriction
No. It does not alter it.
Preoxygenation. Does it affect the second gas effect.
No it does not alter it.
Preoxygenation. Does it alter diffusion hypoxia
No it does not alter it.
Preoxygenation. What is the second gas effect.
It is the high concentration effect of one gas that causes the increase in concentration of another gas.
Preoxygenation. What is diffusion hypoxia.
During extubation. When a patient begins to breaths room air, and nitrous oxide is discontinued, hypoxemia then develops.
Lung mechanics. What is elastance.
Inward recoil of the lung.
Lung mechanics. How is elastance and compliance related
Inverse of eachother
Lung mechanics. What are the components of total lung compliance.
Lung paranchyma and chest wall compliance
Lung mechanics. What conditions decrease compliance.
Fibrosis. Pulm edema. Consolidations
Lung mechanics. What condition is increase compliance.
Emphysema.
Lung mechanics. What does general anesthesia do to compliance.
Decrease compliance
pneumonectomy. what is a complication that can mimick ards
postpneumonectomy pulm edema
pneumonectomy. what side of operation is at risk for pppe
right side
pneumonectomy. what kind of fluid management is associated with pppe
excessive fluid resuscitation
pneumonectomy. what peak pressures are associated with pppe
peak pressures greater than 25mmhg
pneumonectomy. what pt factor can cause increase in pppe
alcohol abuse
pneumonectomy. what is the rate of pppe in a lobectomy
1-7%
pneumonectomy. what is the rate of pppe in a total pneumonectomy
4-7%
pneumonectomy. what is the mortality of pppe
30-100% regardless of lobectomy or pneumonectomy
carbon monoxide. which is the order of anesthetic gases that make carbon monoxide over dessicated soda lyme
desflurane>enflurane>isoflurane,sevoflurane>halothane
carbon monoxide. which co2 absorbant has higher carbon monoxide production if dessicated
baralyme more than sodalyme
Plateau pressure. When is this measured
At the middle of an inspiratory hold.
Plateau pressure. What does it represent
Pressure in the small airways and alveoli
Plateau pressures. How do you measure pressures of the large airways and trachea.
It is not plateau pressure but it is the peak pressure.
Plateau pressure. What can it be used to measure.
The static compliance of the respiratory system.
Compliance. How do you calculate static compliance.
Tidal volume/(plateau pressure - PEEP)
Compliance. How do calculate dynamic compliance.
Tidal volume /(peak pressure - PEEP)
Mediastinal mass. What 3 symptoms can u see with this
Orthopnea, chest pain. Superior vena cava syndrome.
Mediastinal mass. What dangers can occur after muscle relaxant.
Compression Of tracheal bronchial tree after relaxation.
Mediastinal mass. Would tracheostomy be useful in this case.
No. Because the obstruction may be distal to the tracheostomy.
Mediastinal mass. How would a pt be optimized for surgery.
Radiation or chemo to reduced the size of the lesion.
Mediastinal mass. How should anesthesia be given to the pt.
Pt should be kept spontaneous.
Mediastinal mass. What should you have ready when induction of these pt
Rigid brochoscope. To visualize and ventilate through.
Mediastinal mass. What should be done for these pt with your use of muscle relaxants.
It should be avoided.
Mediastinal mass. How is the pt positioned for awake fiber optic.
Semifowler position.
Mediastinal mass. What should you have ready if there is tracheal tree bronchial obstruction.
Be able to intubate with reinforced tube, have a ventilating rigid bronch, have cardiopulmonary bypass available.
Mediastinal mass. What should you have ready if there is pulmonary artery obstruction
Avoid negative ionotrops and have cardiopulmonary bypass available.
Mediastinal mass. What should you do to IV line if there is superior vena cava syndrome.
Place IV lines in the lower limbs.
pulmonary hypertension. what factors can increase pulmonary hypertension
hypoxia, hypercapnea, acidosis, peep, hypOthermia
pulmonary hypertension. what agents can be used to decrease pvr
phosphodiesterase inhibitor, nitric oxide, prostaglandins, btype naturetic peptide
pulmonary hypertension. how does milrinone work
inhibits phosphodiesterase III in the heart, increasing cAMP, influx of calcium, improve ionotropy, pulm and systemic vasodilation
pulmon hypertension. how does nitric oxide work
it acts to increase guanylate cyclase activity…thus increase cGMP on smooth cells…thus pulm vasc relax
pulmonary hypertension. how does b-naturetic peptide work to decrease pvr
it increase cGMP like nitric oxide
pulmon hypertension. how long does b-naturetic peptide work
around 18 minutes
pulmonary hypertension. what kind of prostaglandins work for pulm htn
pge1 and pgi2
Aspiration. What should be done when there is gastric content seen in the oral pharynx
Head down position. Suction of gastric. Content. Intubation. Suction of ett.
flow volume loops. what is the positive y axis
expiration
flow volume loops. what is the negative y axis
inspiration
flow volume loops. what is the x axis.
measurement of the lung volume
flow volume loops. what is the capacity as demonstrated by the width of the loop
vital capacity
flow volume loops. what are 2 characteristics to look at when describing lesions
intra vs extrathoracic. fixed or variable
flow volume loops. what do you see with a fixed airway obstruction
both values of extra and intrathoracic flows are decreased (the y values are decreased)
flow volume loops. what do you see wiht a variable extrathroacic obstruction
you see a decrease in the inspiration flow value (less negative y value)
flow volume loops. why do u see dampened inspiration flow with a variable extrathoracic obstruction
because during inspiration, a variable extrathroacic obstruction causes obstruction. but during expiration, the positive intrathoracic pressure releaves and resolved the variable obstruction…thus almost normal expiration flow loop
flow volume loops. what do you see with a variable intrathoracic obstruction.
you see decrease amplitude on the positive y axis…aka the expiratory flow is decreased in amplitude.
flow volume loops. why do you see a dampened expiratory flow loop with variable intrathoracic obstruction
because when you expire, the positive intrathoracic pressure will cause that mass or obstruction to clamp down on airways and decrease expiratory flow. however, during inspiration, the negative intrapleural pressure will pull up on the obstruction and help have a normal inspiratory flow
flow volume loops. what is unilateral paralyzed vocal cord considered as for an obstruction
variable extrathoracic obstruction
flow volume loops. what is special about the V25-75% of the flow volume loops
this portion is not effort dependant..but is independant of the patients effort
flow volume loops. what disease has alterations of the v25-75% area of the expiratory limb
copd…this is a dease of the small airway disease that is obstructed intrathoracic….these small airways is not dependant on pt effort to get obstruction
flow volume loops. what does a restrictive lung look like
a very narrow skinny loop
flow volume loops. why is it skinny loop vor restrictive lung disease
because there is a decrease in lung capacity…but the inspiratory and expiratory flows are normal
flow volume loops. what is a restrictive lung disease loop an inverse of?
it is an inverse of a fixed obstructive leison
mediastinal mass. what must be available
rigid bronchoscope to intervene when intubation cannot ventilate
mediastinal mass. what if the pt does not have svc compression…should u still place a central line above the diaphram?
no…bc the svc may be clamped in these cases…so u need ivc access.
mediastinal mass. what population of pt are at highest risk for airway compromise
pediatric pts
Tongue. Motor.
Hypoglossal. Cn12
Tongue. Taste. Posterior 1/3
Glossylpharyngeal. Cn9
Tongue. Taste. Anterior 2/3.
Cn7. Chordatymapni branch.
Tongue. Taste. Epiglottis and Root.
Cn10.
Tongue. Sensation. Anterior 2/3
Cn5. Mandibular v3 portion
Tongue. Sensation. Posterior 1/3.
Cn9. Glossylpharyngeal.
atelectasis. what IV agent does not cause atelectasis
ketamin
obstructive lung disease. what is decreased
max breathing capacity, max midexpiratory flow rate, fev1/fvc ratio
obstructive lung disease. what is increased
residual volume, total lung capacity
obstructive lung disease. what happens to vital capacity
normal
obstructive lung disease. what happens to total lung capacity
increased but can be normal
restrictive lung disease. what is decreased
vital capacity, total lung capacity, residual volume
restrictive lung disease. what is increased
fev1/fvc ratio…it can be normal as well
restrictive lung disease. what happens to max breathing capacity
normal
restrictive lung disease. what happens to max mid expiratory flow rate
normal
