Comprehensive Review of Pulmonary and Critical Care Medicine

uh a quick review on pulmonary and critical care uh we will do it over uh two or three sessions uh I'm trying to

cover the main topics uh that uh may be covered in the internal medicine board exam and the upcoming in service uh exam

in uh September uh this is a part of the blueprint from the internal medicine uh Board website uh you can see the

pulmonary disease is up uh to 10% of your exam and critical care is about another 10% uh end of life and uh

paliative care is about 3% so we're talking about uh 23% of your exam will be related to uh pulmonary and critical

uh care uh these are the topics we are going to cover in the first part we'll talk about basic physiology pulmonary

function test asthma COPD Alpha antirion pulmonary hypertension cystic fibrosis uh bronches in the second uh part next

week uh we will talk about uh other uh topics uh left uh so a little bit about physiology

uh if we talk about hypoxemia uh the aa gradient uh it depends on the age and uh the formula to calculate it there are

different formulas one of them is age divided by 4+ 4 and roughly this will give you a number between uh 5 and uh 15

uh the simple way of calculation is 150 minus partial pressure of oxygen uh plus 1.25 partial pressure of carbon dioxide

these values uh can be obtained from your blood gas uh this 150 number came from this equation uh remember this

equation has the parametric pressure uh the partial pressure of uh the water vapor and the normal F2 which is 0. uh

21 uh so remember you cannot apply this formula in every single situation if you have change in altitude or uh if the

patient is on oxygen then this can affect your a gradient if the patient is receiving oxygen this can increase your

a gradient so for example uh your a gradient can increase by 5 to 7 mm Mercury for every 10%

increase in your uh fi2 uh the opposite is right for high altitude uh because if you ascend for 1,000 ft uh the pressure

will decrease by about 24 mm Mercury if you apply this number here this will give you a lower number than 150 because

the atmospheric pressure will be lower so here the normal atmospheric pressure is about 760 if you go to Denver

Colorado it will be around 500 uh 20 uh so this will give you definitely lower uh number than 150 and this will affect

your total aa gradient uh calculation uh when you have a case of hypoxemia you can calculate your a

gradient and it helped to classify the cause uh of hypoxemia uh so you may have normal a gradient in cases of

hypoventilation uh most commonly on the floor this will be a patient on pain medication like narcotics this can

suppress his breathing and this can uh include CO2 retention and some hypoxemia but when you calculate your a gradient

in case of hypoventilation this will be uh normal in other situation when you calculate your aa gradient and uh it's

increased the cause can be a Vu mismatch or a shunt the way to differentiate is to give the patient a low to moderate

flow of oxygen and see the response if the patient respond and uh the partial pressure of oxygen increase or improve

uh this can be a vum match if not you have to think about uh shunt uh treatment will be of course uh depending

on the underlying cause but if there is a Vu mismatch you have to adjust oxygen to keep saturation if there is a shunt

you have to treat the cause of the shunt for example if you have a intrapulmonary shunt physiology because of collapse of

aluli you may need to add positive pressure if you have other causes uh causing shunt you have to Target that

like AV malformation or other uh causes we will talk a little bit more about shunt so the shunt can be anatomical

shunt or physiological shunt uh the anatomical shunt uh you have to uh suspect it uh especially if they give

you a question with a patient on very high amount of oxygen because usually the patient will be hypoxic you will try

to correct the chunt with low to moderate amount of fi2 the patient usually will not respond and you can go

even higher in the oxygen and uh the partial pressure of oxygen will not respond to your trial of increasing

oxygen so the usual question uh uh giving you a patient on 100% F2 usually maybe talking about uh shunt the shunt

can be anatomic or can be just physiological an atomic shunt it include actual shunting and you can detect that

by uh ordering to the echo with a bubble study uh you inject the bubble of agitated Salin and it goes to the Venus

side goes to the right side of the heart and you have to watch with the echo for these bubbles when it appears on the

left side of the heart if the shant is intra cardiac usually these uh bubbles will appear in the left side of the

heart soon maybe within one cardiac beat uh if there's a pulmonary shunt there is time of circulation the blood has to go

through the pulmonary circulation then the shunt happens and comes back to the uh heart so you can see this bubbles on

the left side of the heart later maybe after three or even after five beats so it's very important when you order the

2D EO with a bubble study to know when these bubbles appeared on the left side because it's not positive or negative

study it can be positive but you need to know how soon the bubbles appear on the left side to know if this chant is

intracardiac or uh through other uh abnormality in the lung like AV malformation uh which we can see as a

congenital type or in uh liver cell uh failure in advanced stage you can have uh hepatopulmonary syndrome with uh

disia and hypoxemia wors in upright position give you give you the term of plaia for shortness of breath on ight

position or oxia which is hypoxemia in the upright position the reason the hypoxemia and shortness of breath

becomes worse in upright position because this AV malformation uh tends to be localized to the lower parts of the

lung so when you sit by gravity there is more flow in the lower parts of the lung and there is more shunting and there

will be more more hypoxemia and more shortness of breath uh vacuum mismatch different uh pathologies can cause

vacuum mismatch uh interstial lung disease um pulmonary vascular disease obstructive lung disease uh very rarely

to have a diffusion as a cause of um increased a gradient because it has to be very low uh below 30% and uh rapid

heart rate so you don't have enough uh time uh for uh diffusion so the main causes will in increased uh your aa

gradient will be uh shunt and VQ uh mismatch and again you can differentiate by giving oxygen if you have shunt this

will correct will not correct if you have vum smatch uh this will respond to low to moderate amount of oxygen uh this

is a patient we received he he was 27y old male uh he had history of Chron's Disease he presented with uh hypoxia uh

shortness of breath uh this was a chest xray I mean the Parma looks clean but if you can see here there is maybe a small

nodule here another nodule on the lateral XJ maybe there is something there if you look more look on the right

copy of the diag there is something there and he underwent uh CT Ang geography to Ru out pulmonary Imp plasm

in setting of you can say not not normal xray but there is no uh pathology can explain the degree of hypoxemia uh so he

underw the CT scan uh P protocol and we can see the AV malformation a big AV malformation here with it's enhancing

another one here and we can see it here definitely with the feeding blood uh vessel the patient underwent a coiling

of the AV malformation with Improvement of his hypoxemia uh so this is an example of shunt due to AV uh

malformation uh in in this case the previous one you have to make sure it's not part of uh not a part of heriditary

oric tesia uh because these patients can have AV malformation and these patients with AV malformation they have uh higher

incidence of a stroke because of this uh shunt uh this is another patient uh this is another example of anatomical sht uh

we had her for evaluation of possible pulmonary hypertension uh she was 37 no past medical history uh doing the right

heart CF her Superior vinaa saturation was 95% uh she underwent CT and geography with a 3D reconstruction and

we can see the left pulmonary veins joining the left nominate veins so definitely she has a shun um partial

anomalous pulmonary Venus return the only blood vessel from the left side of the the left lung uh joining the left

atrium was here Crossing in front of the descending uh aorta and these are different Imaging showing the left

pulmonary vein joining uh the left in nominate vein she underwent surgery with uh Improvement of her symptoms

indication for surgery was enlargement of the right and uh Atrium and right ventricle and there are other indication

we have to see how much shunt she has and uh if she has large amount of shunt this will qualify you for surgery as as

well together with uh symptoms uh so when you have a case of hypoxemia you can look at the carbon

dioxide if carbon oide dioxide is elevated this can be a case of hypoventilation you can look for causes

make sure the patient is not receiving narcotics uh or uh there is uh nothing affecting the central nervous system

causing hyperventilation if your carbon oxide is okay and your oxygen is low you can calculate your a gradient your a

gradient if it's slow uh you can think about shunt and VQ match and you can give low to moderate amount of oxygen

see the response for oxygen if it improve it can identify VQ mismatch if it doesn't uh you can think about

sh uh next we will talk about uh oxyglobin dissociation curve uh there is what's called 3060 6090 rule uh so at if

you do your blood gas the partial pressure of oxygen at 60 mm Mercury will be almost equal to uh 90% saturation on

on your pulse oximeter if this rule doesn't apply you have to think about carbon monoxide poisoning or mid

hemoglobinemia the the the presentation will be different in carbon monoxide you will have a pulse oximeter reading

forcely elevated because it cannot differentiate between oxyhemoglobin and carboxyhemoglobin while your blood gas

will show a low partial pressure of oxygen in hobia it's the opposite so uh you will find your uh pulse oximeter is

low while your blood gas is normal this is important in in case of you can get a question with carbon monoxide poisoning

they will give you a patient and they will give you history of exposure and they will give you the pulse oximeter is

98 % and the blood gas showing P2 of 40 so this goes with carbon monoxide poisoning if it's the opposite mmia case

uh this is frequently asked because myoglobinemia can be performed secondly to benzoin therapy uh not therapy penan

spray which you use for local uh um uh anesthesia when you perform broncoscopy or te or AGD uh if you give too much

spray of benzocaine that can produce MOG gmia and this can present on the pulse oximeter while you in the endoscopy

Suite as hypoxemia and then you will do the blood gas and the blood gas will be normal so you will get a case and the

patient is undergoing broncoscopy he received benzocaine uh spray and uh you started the procedure now the

oxygenation is uh pulse oximeter give you reading about 80% there is good air entry you don't suspect Nemo thorax you

do the blood gas and your po2 is 200 so in this case you should consider M uh hemoglobin and you should know the

treatment uh for both uh carbon monoxide um uh poisoning and mommia we will go over it but just also you should

remember the causes of right and left shift uh for your oxygen dissociation curve uh it shows up in in the exam uh

on many occasions uh if you want to remember it by exercise you need more oxygen with exercise your body

temperature rise your CO2 is produced uh lactic acid is produced so you'll have more acidosis so if you want to remember

it this way when you exercise there is right shift uh for the oxygen uh dissociation care so exercise will uh

will do this shift increase temperature acidosis or if you want to remember it by pneumonics here the C stands for

increase CO2 increase acid which is lactic acid or acidosis uh 23 DPG exercise all of these causes with the

temperature can cause right shift which will allow easy dissociation lift shift will be different uh uh which cause

difficult dissociation of the oxygen and this is another pneumonic uh to remember uh if you get a case of carbon

monoxide uh again your pulse oximeter will show a false elevated reading uh when compared to your blood gas uh you

should know the indications for treatment if you have end organ damage like severe acidosis Cardiac Arrest uh

seizure or coma this will be indication for Hyperbaric oxygen therapy if you have carbon uh the uh the monooxide

carbon monoxide level elevated above 25% this is another indication in case of pregnancy the number goes down to 20%

and the other indication will be a fetal distress uh so you should remember this indications hyper paric oxygen will

decrease uh your uh total time or or half life of the carboxy hemoglobin uh from 90 minutes uh to about 30 minutes

uh in cases of methemoglobinemia the treatment of methylene blue uh the treatment can be given if the patient is

symptomatic or the level is above 20% uh remember don't give too much because giving too much methy uh methylene blue

can cause a hemolysis uh then we will go uh to pulmonary function test uh pulmonary

function test is complicated more than two three slides but I will try to give you a simple way just to detect

obstruction restriction and to answer the the question if they require you to identify any of these abnormalities in a

setting of lung pathology uh so we have the fvc or the forced vital capacity and this is the maximum amount of air

exhaled after maximum inspiration uh we have uh F1 which is the volume of air exhaled during the first second uh of

your fvc uh your total lung capacity is equal to your residual Volume Plus the vital capacity just to remember numbers

remember 80% and 70% 80% is uh the number for uh normal uh absolute levels so your total L capacity should be more

than 80% your fv1 should be more 80% uh 70% number is is for ratio so fv1 over fvc should be more than 70% if it's less

than 70% uh this can indicate obstruction by gold criteria uh response to

bronchodilator always remember that uh you should have increas in F1 by by 12% and 200 cc so this is not or you should

qualify for both 200 cc and 12% to read the ponary function test first you can take a look at the total L

capacity to make sure if there is a restriction or no and then to the ratio uh to determine if there is a

instruction then uh you can look uh into the diffusion so for example here we have different cases if we take a look

first at the total L capacity above 80% normal normal and the DLC was normal so this is

a normal uh pulmonary function uh if you look at the second one TC 110 maybe there is some hyperinflation the ratio

is below 70% so there is some obstruction the dlco is decreased it's below uh

80% and the fv1 is decreased as well so that can be obstruction we can see this pattern in a case of

inys uh third case TLC about 100% normal There is mild reduction in the ratio here there is some obstruction dco is

normal or a little bit elevated about 80% uh if A1 is low this can qualify for uh obstructed pattern can be asthma uh

another case we can look at the TLC TLC 54% which is reduced the ratio here is 91% which is actually inre

inreased your dco is decreased and your fv1 is low this can qualify for restrictive disease you have decrease in

fv1 and FC in restrictive disease as well but the pattern is is different so the total uh ratio will be increased in

restrictive disease while it's decreased in obstructive uh because of the component which is affected more in the

obstruction fv1 affected more restriction you may have fvc affected more and this can give you either low

ratio in case of obstructive disease like inisa or higher ratio in case of restrictive uh disease and the last

example here this is another example TLC is decreased this is a little bit increased dlco is normal this can be

restrictive and it can be extrathoracic uh because DLC o is normal again you have to do the interpretation

in clinical setting you have to associate that with the patient symptoms the Imaging pathology and and so

on uh you have to identify the abnormal pattern of your pulmonary function uh test C or the flow volume Loop so this

is a normal one there is inspiration and expiration in inisa there is scooping or tailing uh so this is usually with

severe obstruction in restrictive lung disease such as fibrosis it looks like the normal Loop but it's a little bit uh

smaller and shifted it can give you uh different picture as witch head but basically you should

be able to remember this scoping or tailing in case of empyema with severe obstruction different algorithms to do

interpretation for uh pulmonary function test you can take a look at the spirometry if you have uh low fv1 fvc

ratio think about obstruction low fvc of low total lung volume think about restriction normal spirometry you can

think about asthma if there are symptoms consistent with asthma and you can do what's called metap challenge test and

we will uh touch based on that questions so you have a 68y old uh Hispanic male admitted to the ICU acute

respiratory distress chest xray obtained bilateral infiltrates DC elevated what's the most likely

diagnosis a b c d what D so D is the is the right answer so

dlco it can increase with alular hemorage uh it can increase with polycythemia sometimes with asthma and

this is a quick pneumonic for EUR obstructive lung disease including asthma prones chronic bronchitis and um

empyema uh you have to remember also this other pattern of the flow volume Loop especially this uh two here uh we

saw the previous one the normal flow volume Loop has more curve in the inspiratory portion and expiratory

portion uh when you have this curve with cut off of the inspiratory limb and expiratory limb you have to think about

fixed obstruction they will give you a patient uh with repeated uh intubation and they will give you uh that she was

diagnosed with uh severe asthma nothing is working she continues to weas despite treatment and uh they did pulmonary

function test they will give you numbers if V1 if VC and they will give you the actual Loop and the they will ask you

what's the next step or what maybe the diagnosis and in this case if you see this flow volum loop with cut off of the

inspiratory and expiratory limb you you have to think about tral stenosis especially with a repeated history of

intubation so the next step you may do broncoscopy to see if there is a real stenosis or no and if the patient is

very symptomatic you can uh pursue different kind of treatment other than keep adding steroids and inhaler uh the

other test question will be the cut off of the inspiratory limb of the flow volume Loop usually this happen with a

vocal cord dysfunction they will give you a similar presentation uh patient with resistant asthma or severe asthma

nothing is working patient is weing and she's getting multiple courses of steroids with no uh Improvement and this

uh Curve will give you the clue about the diagnosis there is inspiratory cut off uh this goes with vocal cord

dysfunction uh the Third Lop which is expiratory cut off it can happen with intrathoracic TR Malaysia

most commonly they give you a question about TR stenosis or vocal core dysfunction these numbers here represent

the 50% ratio so you compare this area to this area uh in fixed obstruction this will be equal and this will give

you a number of one uh in case of um inspiratory cut off this area will be longer than this area and that's why you

have ratio more than one here the opposite the ratio will be less than one or uh some books will say less than

0.3% uh this is explanation why you have inspiratory cut off or expiratory cut off depending on the site of the Legion

in thoracic versus intrathoracic it depends uh on the atmospheric pressure intrathoracic pressure and uh the

intra-airway pressure uh during inspiration and expiration this will give you uh uh an

idea about the pathogenesis or how this uh inspiratory and expiratory cut off

happens but if you want to remember quickly for the test extra with inspiration intra with expiration so

intra with X extra with in so that's that's a way to remember it quickly for for your uh

test uh so vocal cord dysfunction uh a lot of times it's diagnosed as resistant asthma or severe asthma uh the diagnosis

is difficult you have to either visualize the vocal cord adduction with laringoscopia or you have to uh find the

classic inspiratory uh cut off which is difficult to find especially if the patient is not uh having the attack

during the acute attack you may give uh some uh helium oxygen mixture or uh CPAP but uh basically the treatment is speech

therapy uh behavioral therapy and a lot of patients beh have depression you should Target that as well uh this is a

case we had a patient presented with multiple history of intubation resistant asthma severe asthma multiple courses of

steroids nothing is helping the flow volume Loop inspiratory and expiratory cut off we thought about uh stenosis

because of multiple intubation uh but we did the broncoscopy and she had vocal core dysfunction but this was atypical

she had inspiratory and expiratory vocal core dysfunction so this is during inspiration the vocal Cordes are

abducted and this is diagnostic this is called a posterior uh gtic shink so they have preserv it posterior gtic shink

which is this opening diamond shape and during expiration she still has some abduction but it's better and that's why

when we did the ratio it was more than one uh goes with vocal cord dysfunction plus we saw the vocal cord and she

didn't have evidence of uh stenosis and when she was breathing not sure if this is uh working

here yeah I had a video um audio recording for uh the strier that she had during

breathing but it was evident that it's coming from the upper Airway and uh not from the

Lance um asthma versus COPD ver versus overlap syndrome with asthma you may have variable Airway obstruction uh CPD

you have more persistent Airway obstruction and now there is a syndrome with overlap between asthma and uh C CD

uh can be seen as well uh treatment of asthma is dynamic you have to assess the patient uh determine severity of the

asthma start your treatment uh step up or down depending on uh symptoms uh and this is a step up protocol uh that you

should be familiar with so step one you can use short acting when needed uh step two you can add Loos inhal cortico

steroid step three you add uh long acting beta Agonist on top of the low do inhale corticosteroids step four you

increase your uh inhal corticosteroid to medium to high uh plus the lava and step five you can add other uh treatments uh

like short courses of steroids oral map which is ante uh uh anti and also you have to focus on

avoiding smoking weight uh loss and uh exercise and such so this is important the Step Up therapy and you have to keep

it and ass the patient later the patient is doing okay you can uh do a step uh down uh to control the

symptoms uh symptom control you ask about the daytime symptoms night symptoms and uh the frequent use of

inhalers and uh activity uh limitation by uh symptoms and you can uh put the patient in one of these categories

depending on how many questions they will Mark as yes and then the asthma severity itself you can classify it as

mild and moderate and severe uh mild usually is controlled by step one or two moderate controlled by step three and

severe requires step four uh or five uh now we have uh bronchial thermoplasty which can be used in advanced cases uh

we do uh broncoscopy with a thermoplasty of different segment and this decrease the uh uh emergency room visits for

these people with frequent exacer Pati uh for asthma but we have to select uh the patient carefully uh for

this I'm trying to advance okay exercise induced asthma uh you

shouldn't avoid exercise even if you have exercise induced asthma the treatment usually is prophylactic

treatment with a short acting beta Agonist before the exercise if they ask you in the board should the patient stop

exercise the answer is no uh long-term control is not required just short acting beta agon to when needed before

exercise if you want to diagnose it you can do exercise test and you have to stress the patient to above 85% of the

heart rate uh expected and in this case you can measure the fv1 and you will have about 15% reduction in your fv1

reactive Airway syndrome is different think which may look like asthma in the question they will give you a single

exposure uh to irritant as usually it can be like chlorine and then the patient will have frequent episode

which looks like asthma in this case you treat it as asthma you can do methol challenge test as well if you are not

sure asthma and pregnancy uh 1 third of the patients gets better one3 stay the same one/

third may do uh worse uh principles of treatment uh for pregnant women are the same uh as for non pregnant um actually

asthma attacks uh carry more risk for the fetus more than the medications we give for asthma uh control uh even some

side effects which were thought to be a side effect of the inhaled uh steroids or other medications now are thought to

be due to the effect of hypoxemia and not the medications uh the most studied inhal corticosteroid is bide in case of

pregnancy uh if you have a patient uh with asthma recently diagnosed she's not an inhaler it's prefer to start pide if

the patient is on different inhal the steroid and her asthma is controlled symptoms are controlled you can just

continue with the medications uh she's receiving even if it's different than uh pite uh Senter syndrome you will have a

patient with asthma uh nasal allergy nasal polyps and history of aspirin uh allergy or asthma can be precipitated by

aspirin or other nonsteroidal uh drugs and you can uh do aspirin desensitization in controlled

setting in the ICU and liquid Trine agents can help with the symptoms uh most common three causes of chronic cuff

include asthma and uh upper award syndrome used to be called a postnasal drip syndrome and uh gear so you should

Target these three issues and take good history uh to make sure what's causing this chronic cuff uh asthma can present

in in a way uh the patient just has chronic cuff it's called cuff variant asthma and this can be difficult to

diagnose sometimes and you may need to do a meolin challenge test meolin challenge test you give the patient

multiple inhalers of escalating doses of meolin and you measure your fv1 after each inhalation and see uh at what dose

your fv1 will drop by uh 20% uh so in normal individual you will keep es you keep giving escalating Doses and the F1

will start to at certain level but in asthmatic patients or patients with Airway hyperactivity this drop will

happen earlier and you can take a look at what does this uh 20% drop happen and then you can uh say if it's normal or

mild or moderate uh or severe and this can be a helpful way to diagnose uh cases of asthma which uh

doesn't present with classic picture on the pulmonary uh function test uh another question patient asmatic

longstanding severe asthma evaluated from neonet fever fatigue skin rash uh respiratory symptoms uh 4 weeks ago she

started taking lrin receptor antagonist tapping off her oral prone chest exay shows bilateral infiltrate CPC showing

gly cytosis with exophilia what's the best Next Step a b c d

so we we will stop the liot Trin receptor antagonist uh you have to know that uh liot Trin modifiers uh were

associated with ch St syndrome in patients with asthma especially when you try to titrate uh the cortico steroids

it's not known is it the the loten medication is is the cause or just by titrating the steroids you are unmasking

the symptoms that were treated with uh corticosteroid but that's usually the situation this is a differential

diagnosis for a patient who has wheezing presented with enopia infiltrate on the X-ray make sure it's not infection and

then you have to go through your differential diagnosis it can be allergic Bronco pulmonary osis uh it can

complicate asthma cystic fibrosis it can cause Central bronches finger and glove appearance on the CAT scan IG level will

be very high above 1,000 and the treatment is steroid plus or minus itraconazol can be used as a steroid

sparing agent but the main treatment is steroid so we have to think about that if you have a case of resistant asthma

the patient keeps coming and nothing is working make sure he's not developing allergic Bronco pulmonary aspergillosis

should be in the differential chronic xenophilic pneumonia usually uh middle-age women they will have the

photographic negative of uh congestive heart failure so more peripheral uh opacities on the chastic ray one third

they don't have peripheral xenophilia the other third differential is sh stuss Rome Panka will be positive they may

have GL nephritis very high zils up to 80% of their white count uh L syndrome you have to think about medications if

they have a component of allergy to medications or parasitic uh infections uh in case of ler syndrome uh it's

called Simple pulmonary xenophilia treatment is just stop the offending drug or treat the underlying uh

parasitic infection tropical pulmonary inopia will be the last one but it's not common here it's number to vishia B

cofty and you will have very high IG and positive antifilarial antibodies this is a photographic

negative uh of chronic exophilic pneumonia uh in heart failure you will see the opacity more as that Wing

appearance this is more at the periphery uh so that's why it's called photographic negative of pulmonary edema

uh chronic isic pneumonia is different from acute exophilic pneumonia acute exophilic pneumonia you will have uh

Pati patient who is a smoker and he will come crashing with hypoxemia and acute picture of illness and they will not

have peripheral isia uh COPD uh the classification still the same mild moderate severe and very

severe depending on uh the cut off points of 80% 50 and 30% but the treatment uh changed recently and the

classification so now you have to put your patients in one of these categories a b c and d depending on the underlying

symptoms and the risk for exacerbation it may look complicated but we will dissect it and make it more easy uh

patient in group a they have low uh risk and less symptoms so the symptoms here uh you go this way there's more symptoms

you can use two scales the cat scale or the MRC scale here on that uh uh side this is the exertion risk here this is a

golden classification so patients in a they will have low uh risk and uh less symptoms in B they will have low risk

but more symptoms because we go this way C they will have uh high risk and less symptoms and B they will have high risk

and more symptoms it it can look complicated but basically your symptoms increase when you go this way

exacerbation risk is increasing here and severity of uh COPD this is the MRC scale but I just wanted you to remember

uh walking slower or to stop because number two is the defining number between uh mild symptoms and severe

symptoms so basically you can put your patient in one of these categories if you remember three questions uh first

you have to assess symptoms then you assess risk you assess symptoms by asking the patient if if he has to stop

uh because of shortness of breath or if he has to walk slower because of shortness of breath If he if he answer

yes he's already above two so now you are putting him in in the patients with more symptoms which can be uh uh b or uh

D then you ask the patient about the risk of exacerbation by if asking if the patient had two or more exacerbation the

last year or one single hospitalization if he answer yes he is at high risk for exacerbation and you look at F1 if it's

low than lower than 50% he is high risk what about if you get low risk here and high risk in the other question you take

the higher risk and you use it for classification so just three questions will help you to classify a b c d first

ask about simp symptoms if the patient has to stop of or if he has to walk slower because of shortness of breath

second risk of exacerbation by uh history of hospitalization last year history of exacerbation and finally your

fv1 uh level treatment we don't use uh chloride

ammonium anymore unless you're taking your BS in 18 uh 68 or 86 now we use other inhalers so uh you can

classify your uh category of treatment depending on the category of the risk uh uh of exacerbation and symptoms so

patients in group a uh they can just take short acting bet Agonist uh Group B they may take lava or Lama which is

anticor energic or long acting bet Agonist Group C you will add inhal corticosteroid gr D you can add uh the

inhal cor corticosteroid with lava and uh L so s sa lama lama uh long acting inhalers uh just

remember uh there are new inhalers coming every uh year uh couple of years ago we only had C metrol and forol other

inhalers came out uh also uh we had only tirop and other inhalers are coming out which are long acting anticolic just

remember the side effects of long acting anticolic with the bad effects with narrow angle gloma urine retention and

the most common effect is dry Mouse but I want you to remember the side effects which can be severe especially if you

have a patient with history of glucoma uh don't combine long acting and short acting anti cgic uh oral

treatment in in certain cases we can use a thein after we use every other uh single therapy and still the patient is

symptomatic you have to be careful because of drug drug interaction neurotherapeutic level can cause seizure

cardiac arisia you have to monitor your level uh you have to remember macrolite and focon which is the most frequent

medications given for CD patient with exacerbation or infection they can interact with your theophine level and

increase it so if you have a patient on theophine you admit him to the hospital you start giving him focon for pneumonia

you have to remember this flocon may increase your therapeutic LEL or of theophine and the other way if you start

a patient on theopen the hospital and the patient is receiving fluocinolone and you think your liver is a

therapeutic you discharge him with the same dose and he finished the course of fluocin the level of the focon will be

uh lower uh so you have to remember this drug drug interaction uh Ro uh rast is a phosph

trace four inhibitor it's it's called Dad risp it's oral treatment it can be used for obese patients with COPD uh

chronic bronchitis type not empyema and uh history of frequent exacerbation it can decrease the weight

as well uh so it can help with obese patients with COPD who qualify for that treatment neck which is in acetal there

is conf conflicting results some trials show that it decreased the oxidant stress and help with COPD exacerbation

other trials trials didn't show uh benefit it's not part of the standard standard of therapy uh surgical

treatment you have long uh uh long voice production uh surgery now we we we conducting trials to try to do that uh

by broncoscopy by putting into bronchial valve uh to do some volume uh reduction uh but the main trial was published in

New England Journal of Medicine 2003 and it show uh benefit for the patients who has a baseline low Exercise capacity and

predominant upper uh loop um uh uh disease uh so remember number 20% if you are above 20% F1 dlco up L predominance

and you have good Exercise capacity uh you will not qualify still because of the exercise you should have low

Exercise capacity and you should maximize your rehab before referring the patient for that uh very low number will

uh put you in a lung transplantation category but you have to refer your patient before they H this number

because once they reach these numbers they will be high risk uh for uh surgery improving survival stopping smoking and

uh oxygen therapy you have to remember the indications for oxygen in in COPD uh the longer you give the oxygen the

better the survival the two main trials uh were done this is a combined data from both trials better survival with a

longer uh duration of uh oxygen smoking sensation you have different uh categories to choose in between just

remember the side effect in the board uh you shouldn't use will butterine if you have a risk of seizure and you shouldn't

use chanics or vernin if you have a history of depression a quick difference here CD4

is the main inflammatory cells in asthma cd8 in COPD uh asthma is mainly xenophilic uh inflammatory uh uh

condition COPD is nitrophilic subgroup of asthma patient they may have neutrophilic component and these are the

groups who are not getting the benefit of corticosteroid therapy and inhaled cortico steroid the the reason I

highlighted some of these interlukin some of the new medications for asthma being developed now trying to Target the

interlan 5 and 13 especially for severe asthma uh Alpha triin just remember it's more basal predominant younger age

patient uh the most severe form is ZZ form it affect 1 to 3% of your your COPD patient suspected if you have a patient

with a lower age and there is no history of exposure it's more common in patients with picutis uh and patients with Anka C

Ana vasculitis especially anti pr3 uh treatment not everyone will get the treatment but every patient should stop

smoking and if the patient has a low level which is above uh below 80 uh milligram per dcil and have moderate

obstruction of pulmonary function test and uh stop smoker already then uh he will qualify uh for treatment uh quickly

on pulmonary hypertension uh if you have suggestive symptoms suggestive Echo you do write hard cast uh you look mainly in

the pulmonary pressure the target number we look at is 25 with rest uh sometimes we can do exercise in the cast lab to

see if this number with exercise will be above 30 uh this is the actual number most of the studies using the 25 number

or 30 with exercise you should remember your classes from 1 to 5 one purely arterial with uh HIV connective tissue

disease and Venus will be secondary to a LIF side disease class three will be secondary to hypoxia such as an

intertial lung disease COPD obstructive sleep apnea uh thrombotic uh stage four uh the only thing I want you to remember

don't choose a calcium channel blocker unless they will give you a positive vasor activity test on the exam uh vasor

activity test to be positive your pressure should fall below 40 and uh should fall more than 10 mm your heart

cardiac output shouldn't drop at least it should be stable or uh increase otherwise you may harm the patient by

adding calcium channel broker 50% of the patient who are V vasor Active in few years they will lose the vasor activity

and they will need a different agent Waring is not the long choice if there is no contraindication uh we choose the

treatment depending on the stage Niha class one we just observe uh 2 three and four we start uh choosing oral medicine

uh till stage four you may have trip uh just remember uh the hard Cal the pressure is 25 if your capillary

pulmonary W pressure is uh below 15 this is uh pure arterial hypertension if it's above 25 it's secondary to uh heart

failure in between 15 to 25 you have to calculate trans pulmonary gradient which is basically your uh mean pulmonary

pressure minus your WG pressure if you have the number above 12 it means out of proportion of heart failure so you can

still qualify for uh some therapy based on that if your number is below uh 12 uh then this is proportional to your heart

failure and we canot provide specific therapy for pulmonary hypertension and uh lastly these are uh new medications I

don't think they will show in your in service or board exam the only thing I want you to remember is rioot is newly

uh approved medication for pulmonary hypertension and uh thromboembolic pulmonary hypertension and don't

prescribe nitrate uh or uh cenil with it otherwise you can have serious side effects of uh hypo tension I think if if

they uh cover any of these this will be the main point don't prescribe cenil because cenil is most of pulmon

hypertension patients they may be on cenil and you don't want to start them on U this uh uh new medication uh if

they are taking that already I think we are done for to last last week we start started this

series of review on pulmonary and critical care uh last time we discussed basic physiology pulmonary function

testing asthma uh COPD uh vocal core dysfunction and um other uh subtopics in pulmonary uh today we will uh continue

on the second part uh I had to split this sessions on into three uh Parts the third part will be including uh uh Parts

related to high altitude medicine sleep and critical care uh review so this is the second part of the

pulmonary uh review we will uh we will start with uh pulmonary

hypertension because we went through it very quick last time and we didn't have the time to uh stress on the important

uh points so previously pulmonary hypertension used to be classified as primary and secondary this is all the

classification now you have to know the type 1 2 3 4 and five uh and you have to know which uh disease

fall in which category uh so for example type one it includes the idopathic pulmonary hypertension includes

pulmonary hypertension uh secondary to HIV secondary to connective tissue disease uh port to pulmonary

hypertension is included also in uh this category uh also drug uh induced pulmonary hypertension such as

amphetamin cocaine uh it goes under this category uh category number two is uh the Venus uh pulmonary hypertension

which is basically pulmonary hypertension secondary to left-sided heart uh disease uh type three is uh the

disease we see uh secondary to hypoxemia or secondary to primary lung disease so patients with Advanced severe COPD

Advanced fibrosis um uh or patients with severe sleep apnea they may have pulmonary hypertention uh secondary to

the hypoxemia uh we know the effect of hypoxemia on the pulmonary vascul causing vasil constriction and this can

cause elevation of the pressure uh type four is secondary to thrombo embolic disease uh if the patient had acute PE

uh later on they may develop pulmonary hypertension or a chronic thrombo embolic uh pulmonary embolism which is

more common in female or contraceptive pills uh there is certain uh category of patients young female uh they may

present later just with disia on exertion without a specific incident of acute pulmonary embolism and

they may have pulmonary hypertension secondary to this chronic thrombo embolic uh disease uh category five is

miscellaneous uh it's important to know these diseases in the work cup of pulmonary hypertension because you go

through your list and you try to roll in or out every disease uh so for example HIV testing is part of the workup

checking the liver function test is part of the workup history is very important asking about previous drug abuse any

amphetamin any cocaine or an anorogenic drugs uh you need to get a baseline idea about the pulmonary function and the

lung parena so a lot of times we do high resolution CT with the chest to make sure there is no underlying lung disease

uh we can get pulmonary function test to make sure there is no underlying severe restrictive or obstructive lung disease

which may be the cause of pulmonary hypertension if if we think the patient also uh high risk for sleep apnea uh we

can do sleep studies on uh these patients uh we can do VQ scan as well to rule out a chronic thromboembolic uh

disease uh so this is important in the work up of a patient with pulmonary hypertension uh usually the patient will

have shortness of breath someone will do an echo and uh which may suggest pulmonary hypertension uh with a strain

on the right side of the heart the patient will be referred to us we will do a Heart Care

to uh confirm the numbers and uh measure uh the pulmonary artery pressure and the W pressure and then once we confirm it

with hard c a patient has pulmonary hypertension uh we will start the work up to uh determine the cause uh usually

the pulmonary hypertension when we do the right side heart calf we look at the pulmonary artery pressure above 25 uh

with rest or 30 with exercise so if we do the hard cast and the pressure of the pulmonary artery is normal say 23 uh

sometimes we do exercise in the hard calf so the patient can carry uh some uh sailing bags or sand bag and do exercise

for a few minutes and we measure the pressure again making sure it's not increasing uh with exercise because this

can cause dis with exertion uh as well uh the important Point here is about calcium channel blockers uh because a

lot of people uh see pulmonary hypertension and think calcium channel blocker and they just prescribe it uh

and they think it's beneficial for the patient we uh do not recommend to prescribe calcium channel blockers

without what's called vasor activity test uh so during the hard calf as well we usually use inhal nitric oxide here

uh to make sure the patient is B reactive or no uh so once we inhal uh the nitric oxide the pulmonary artery

pressure to to call it positive response should drop by more than 10 mm Mercury to a level less than 40 mm Mercury mean

pulmonary arterial pressure without drop in the cardiac output so the cardiac output should remain stable or

improve uh that's why it's determin in some people if they get the calcium channel blocker because this may uh

induce a drop in the cardiac output and this will be bad for the patient that's why we need to do the vasor activity

test make sure giving these agents we can use the osine proy here we use the inhal nitric oxide and to document if

they are vasor active or no if the patient is vasor active they can benefit from calcium channel blocker but a lot

of these patients later on they can lose this vasor activity so if the patient is on calcium channel blocker and later on

he was doing okay improved symptoms and then uh symptoms deteriorate we repeat the heart C making sure the numbers

didn't go up or the patient didn't lose the positive V activity test because then these patients may need other uh

kind of uh treatment and other uh groups of medication anti ulation is not the wrong answer especially if there is no

contraindication and especially in in chronic thromboembolic disease or uh pmon hypertension uh secondary to

thromboembolism uh usually for treatment we decide about the agent of treatment uh by the New York Heart Association

classification so it's a functional class class classification class 1 2 three or four uh class one usually we

just observe the patient the class two you can start adding medicines uh oral medicines some inhalers we have once you

progress in classes you can combine some different uh classes of uh different groups of medications and finally in

class 4 or Advanced uh class three stage you may consider adding IV treatment there are different classes of medicine

uh including sopy Endo Endo receptor antagonist prostacyclin analoges and this is a a diagram about the heart calf

if you go femoral approach you will go from the femoral vein inferior vena right atrium your catheter will go to

the right ventricle pulmonary artery and then uh you reach your uh pulmonary artery branch which uh uh you can do the

wedging of your balloon so you you keep the balloon inflated and you advance it till you see the tracing change and you

know you are in a wig position so you can measure the wtge uh uh pressure uh without when you deflate the balloon

then you you are measuring the pulmonary artery pressure when you inflate it and olude the blood vessel and you will have

a continuous colum of blood from the tip of the catheter till the left atrium this will be your wedge pressure which

is reflecting the left side of the heart or the left at uh it's important to know that uh

there are classification of lung zones lung Zone one two and three we prefer the catheter to be in zone three uh this

classification relate to if you have a continuous column of blood to the left atrium or no so we can see in Z in zone

one the alular pressure is higher than the arterial pressure and Venus pressure so it's actually interrupted here so if

you are measuring a pressure actually you will be measuring the intra alular pressure uh more and it will be

affecting your reading uh this is partial Interruption so the pulmonary artery uh pressure is uh higher than uh

the Venus uh higher than the AL pressure pressure but still the alular pressure is higher than the Venus pressure so you

can see here there is effect of the intra alular pressure on your reading so this is the best position you would like

your catheter to be in uh where you have continuous column of blood and you'll be measuring uh data reflecting the left

side of the heart uh this position is the lung is not classified anatomically anatomically to Zone 1 2 and three it's

uh more uh of uh positional uh classification the most areas uh with uh dependent

blood flow so if you are standing your zone three will be most likely towards the basis if you lie down this change

depending on the distribution of the blood flow so it's it's zone three is the most dependent area uh of your lung

where you have more blood flow and continuous blood flow from uh the right uh side of the heart between the right

side and the left side of the heart the problem with with this you may get a force High reading uh say if the patient

is on mechanical ventilation and you have high peak pressure and you put your catheter and it's in zone one you can be

measuring your peep because this is the intra Alvar pressure applied by the ventilator so that's why it's important

to make sure uh it's in zone three so this is zone three uh where your uh pulmonary arterial pressure is higher

than the Venus and alular pressure uh while the alular pressure is less than the Venus side uh this graph is

important important and these numbers are important as well so we'll do the hard cast we'll give you the report that

the main pulmonary artery pressure is above 25 so this will qualify for pulmonary

hypertension and we mention in the report capillary wtge pressure so you have to know if your capillary wtch

pressure is less than 15 this is pulmonary arterial uh hypertension uh if your capillary W pressure is more than

25 this is reflecting a picture of heart failure uh which is uh group uh two uh with Venus pulmonary hypertension second

to Heart uh disease in this group between 15 and 25 we have to calculate what's called TR transpulmonary gradient

and uh this is actually the mean uh pulmonary artery pressure minus the O pressure if the number is more than 12

it means uh there is a pulmonary hypertension out of proportion of heart failure so you may still have left-sided

heart disease and on top of that you may have pulmonary arterial hypertension if this number is below 12 then uh it's in

proportion to heart failure in this case we recommend just management of the left-sided heart failure important also

to note that uh you have to pay attention of not only to the wedge pressure and Main pulmonary pressure uh

but when you get the cast report you have to look at uh the pressure of the right atrium uh because say you have a

patient he went for heart calf and uh his main pulmonary uh artery pressure is 30 uh or 35 let's say 35

and then the patient is receiving treatment and he's doing worse and then you rep repeat the hard calf and your

mean uh pulmonary arterial pressure on the repeat heart calf is 30 so the first number is 35 the second number is 30 at

the first look you may say you the patient improve but you didn't look at the right atrial pressure maybe the

right side of the heart is failing and getting dilated and that's why the pulmonary artery pressure is uh going

down but the right side of the heart pressure is going up so if you have the first calf right arterial uh right

atrial pressure is five and now it's 10 on the second heart calf patient actually may be doing worse and not uh

better any questions about the pmon hypertension uh diagnosis management care no okay uh treatments uh two new

medications came out recently uh Messi tenton and rioot um rioot is a new size of medication it's a

soluble gate Cycles um uh stimulator and uh it's approved for both uh chronic thrombo embolic pulmonary hypertension

and Pulmonary arterial hypertension last time I mentioned you have to remember the contraindication uh because it's

contraindicated to give it with nitrates and other treatments that we use commonly for palon hypertension such as

cenil I don't think this will show up in urine service or or your board because it's a new medicine but if if if there

is any question I think it's important to know uh this interaction because you may be the primary care physician of the

patient and he is already onos for pmon hypertension and you are considering adding some nitrate for heart problem so

you should be aware about this uh contraindication uh this is a patient we had uh she had horseness of voice and uh

Disney on exertion and uh this is oscopy picture and she had left the vocal cord paralysis so the next step

you do cut scan of the lung to make sure there's no Mass uh causing uh impairment of the function or

invading uh the uh LIF recurrent lenial nerve uh the CAT scan showed enlarged pulmonary artery and she underw right

side heart cat and this is not the systemic pressure this is the pulmonary artery pressure so pulmonary pressure

was 123 over 45 and was so huge it was causing paralysis of the vocal cord because it was pressing on the left

recurrent lenial nerve this is called orner syndrome orner syndrome can happen also when you have enlargement of the

LIF Atrium originally described with patients with romatic fever and nital vosis when they have enlargement of the

left atrium it can cause compromise of the left recurrent lenal nerve and it can cause vness of voice uh she was

started on uh treatment and she improved and her pressure is uh is down now uh this is another case we have you have to

consider cases of congenital anomalies even in older individual uh this is an example uh 61y old female uh past

medical R of hypertension shortness of breath she had a an echo suggested possible P hypertension uh she came with

dead heart Cal so this is a normal pathway of a catheter you insert from the inferior vena goes to the right

atrium right ventricle and to the pulmonary AR we should see that path on the xray on the fluoroscopy image it

should be going here and going like this and going to the pulmonary artery we had this abnormal uh pathway here we uh did

right femoral approach so the first catheter uh crossed the midline went up came down and it went to somewhere we

didn't know where is it but it it's in in the in the in the tracing you can tell where it's going so we saw the

tracing that the catheter going into the the right atrium and the right ventricle and the pulmonary but just the pathway

was uh abnormal uh she underwent uh CAT scan with uh reconstruction and she had a heotis

continuation of the inferior vena on the left side she has a left side is superior vinaa so you have to be

considering also these variants uh when you evaluate uh the patient even uh if the patient is not in in pediatric uh

group uh second cystic fibros is um it's a chronic lung disease uh usually can be diagnosed most of our cases diagnosed

during infancy but again uh you can uh consider it in young adult if if they had mild disease and it was not

diagnosed before uh you have chromosomal abnormality in chromosome 7 and the Delta F 508 this is the most common uh

genetic abnormality in up to 77% of the patients and you will have classic picture recurrent muonium ilas in the in

you will have pancreatic insufficiency you may have liver problems and you may develop diabetes malus with the

pancreatic uh insufficiency and eventually you can develop bronches and lung disease uh

sweet chloride test if you remember the number it's above 60 you have to know they use pyoc carbon to induce it and

other causes it can be false uh positive um in other abnormalities such as hypothyroidism hypoparathyroid there

mucos acarid dois uh severe pancreatitis severe malnutrition hypog gam globin Mia so you you have to consider all of these

uh and in the criteria for diagnosis we don't take one criteria you have to have a clinical picture consistent with that

and then testing uh this medicine evapor is a new medicine and uh only uh 4% of patients have underlying um genetic

abnormality uh this medicine can work on it this is the only medicine in cystic fibrosis which Target uh the underlying

uh problem uh and uh you know in the problem in cystic fibrosis it's mainly uh transport problem between the sodium

and chloride uh in the respiratory epithelium and this medicine is targeting this underlying problem and

patients can do very well on it but again it's only 4% of the patients but you can do genetic testing uh to see

which patients will uh uh benefit from this patients usually colonized with staff hemophilus influenza later on they

will have colonization with pomonis uh The Chronic therapy you give them dnas and uh supplementation of pancreatic

enzymes some of these patients who have a chronic colonization of Sedonas you can give inhale to pryin uh these

patients also if you have a cystic fibrosis patient you will find they be getting macroides uh such as as estris

three times a week uh for anti-inflammatory effect and uh they do better with that uh chronic infection

with bosia is a contraindication for lung transplant so if you want to know anything just remember this medicine 4%

of population May benefit uh this is contraindication for lung transplant in most of the centers it's secondary to a

problem of chromosome 7 and swe chloride test uh remember number 60 uh again diagnosis don't take just a swe chloride

test and diagn a patient based on that you have to have consistent history clinical picture genetic testing and

combination of these element uh to make the diagnosis of cystic fibrosis other causes of bronch so this

is just aonic to remember the causes if you have a patient on the floor you do a CAT scan and the report say pronexis so

you have to go through a differential diagnosis uh list uh which can include cystic fibrosis uh especially if a young

adult uh allergic Bronco pulmonary aspis so can order IG uh level uh post infectious which is most common uh think

about uh if the patient has uh TB hypog globin Mia so you can order imunoglobulin

level um other rare syndrome carag syndrome if you have cytus inversus you have to think about it and Monon

syndrome uh you look at the CAT scan and uh you compare the internal diameter of the broni to the accompanying vessel and

uh from that you can say if the patient has bronis or no this is a patient we had he came with shortness of breath

fever cuff sputum production on the CAT scan you see dilation of the airway the tra is enlarged Airway enlarged these

are brones so uh this is varicose brones and cystic brones uh we did the broncoscopy and he has a lot of

diver in the airway and this was a case of mon syndrome the patient didn't have cystic fibrosis immunoglobulins were

normal and Alpha antipin was normal uh so uh this is a case of mon syndrome as an example of

bronis um interstitial lung disease um this is a a broad topic there is a about more than 200 of interstitial lung

disease uh so this is just uh trying to have all of these diseases in in one table just for the sake of your exam and

uh we have different classification for uh interstitial lung disease so if you want to classify it by the cause

inational and non incubation organic and inorganic causes so in organic caes you will have hyper sensitivity neumonitis

fosis uh inorganic Asis silicosis neosis and bosis non incubation you have other uh things like idiopathic pulmonary

fibrosis uh collagen uh uh connective tissue disease lambang myosis usually female with neorx

kyus effusion and it's associated with t sclerosis hytos X usually present with Nemo thorax sarcoidosis which we see

frequently aniv proteinosis is very rare but you have to know uh if you do BM it's p positive which is periodic acid

Chi stain you can send for that if it comes back positive and clinical picture is consist consistent with that that you

can diagnose it but it's rare go pure syndrome and you have to have the anti anti membrane antibody and usually

patients present with hesis uh another classification we like is just classified as granulomatous disease

versus non granulomatous disease and known versus unknown causes it's important to know there are known causes

that cause interstitial lung disease and we try to exclude that in the work up if a patient comes in the are consistent

with interstitial lung disease chronic symptoms restrictive pattern on the pulmonary function test most of the time

and restricted volume and some element of fibrosis or ground glass on the CAT scan uh so you have to make sure the

patient doesn't have chronic aspiration which can cause uh basal fibrosis and the patient can present as interstial

lung disease you have to ask about history of drugs such as amidone uh because these patient they they have to

be monitored with pulmonary function test if they are receiving Amidon for long period of time

especially on higher doses you have to ask about the history uh such as history of exposure for hypers sensitivity

lionitis or any organic or inorganic dust exposure so you have to ask about the occupation occupational exposure not

only now but in the past and for how long how how was the duration uh still we have unknown causes but uh again we

have to do through history physical examination and serological can work up as well to roll out connective tissue

disease related interal lung disease uh in the process of work up uh occupational interstitial lung disease

uh these are uh some uh tips for the exam hypers sensitivity Nittis can present as acute uh Subacute or chronic

when it present as chronic it may look like a pulmonary fibrosis and uh uh it's difficult uh to just differentiate

between it and the pulmonary fibrosis except for the history uh it takes different uh names depending on the

agent the patient exposed to uh but it's all of these are basically hypers sensitivity pneumonitis um you'll have

the coton dust disease if in the typical exam uh they will give you recurrence of of symptoms especially on Monday uh

morning uh asbestos exposure you have to differentiate between asbestos exposure and asbestosis so asisto exposure can