ARDS acute respiratory distress syndrome you need four things for it to be ARDS or ards one
it needs to be acute meaning something happens and all of a sudden you have ARDS within hours
two days number two you need to have bilateral pulmonary infiltrates on chest imaging whether
that's a chest x-ray or a cat scan of the lungs and then three because you have these pulmonary
infiltrates you have low oxygenation specifically in order to meet the criteria you need a po2 to
fio2 ratio of less than 300 it used to be 200 but now it's 300 and then the fourth thing that you
need for it to be ARDS is some kind of evidence to say that this is not due to the left side of
the heart in other words this is non cardiogenic pulmonary edema going on so let's dive a little
deeper into each one of those and talk a little bit more about the idea let's dive a little deeper
into ARDS we mentioned the low oxygenation in order to calculate this you'll need an ABG to
measure the po2 in the arterial blood normally a healthy person is going to have a po2 of 100 or so
then you take the fio2 which is the percentage of oxygen the patient is breathing room air is
21% without be zero point two one if you have them on 100% oxygen that would be one point zero zero
so for me and you right now our po2 taffyta ratio would be 100 divided by zero point two
zero which comes out to about five hundred so of course you and I are nowhere near meeting the
ARDS threshold of less than 300 used to be 200 but now it's 300 the third requirement to meet
ARDS criteria is having bilateral pulmonary infiltrates on chest imaging so check out this
chest x-ray from a patient of mine on this chest x-ray you see that the endotracheal tube tip is
right around here ideally you want that to be 2 to 4 centimeters above the karana the Quran
is right here and this tip appears to be about 4 centimeters above that so this is good enough
position here this is the central line here and the right internal jugular looking at the
diaphragm and it costophrenic angles don't see any fluid there or here so no pleural effusions the
heart looks normal in size I wouldn't say there's any cardiomegaly and then the obvious here is the
pulmonary infiltrates so pretty extensive on this side pretty extensive on this side this
is a hetero G this is a heterogeneous pattern if it's homogeneous the entire lung parenchyma would
be white there are areas of black hair so this is definitely a heterogeneous pattern sometimes
ARDS it can progress to a homogeneous pattern but this is classic ARDS looking but doesn't tell
the whole story if I showed this chest x-ray to you without any clinical context you'd say
this could be pulmonary edema due to left-sided heart failure and I'd say yeah it could be just
about anything so there needs to be some kind of evidence to suggest that these pullman infiltrates
are non cardiogenic in nature so it's best to get an echo to see if there's anything wrong with the
left side of the heart if that's the case it's easy to say that this is non cardiogenic pulmonary
edema the waters get muddied when someone has left-sided heart dysfunction because it's not
like CHF patients are excluded from getting ARDS but for board purposes I wouldn't expect them
to give you a muddied case like that in the old days you need to do a pulmonary arterial catheter
ization meaning a swan-ganz catheter in order to determine the pulmonary capillary wedge pressure
if the wedge pressure is less than 18 millimeters mercury it means the pulmonary edema is not
cardiogenic but today if there's not any evidence of left-sided heart failure on echo we can say
that this is not cardiogenic pulmonary edema it's good enough there is one diagnosis out there that
is actually impossible to differentiate from ARDS unless you do a specific test the disease is
called acute eosinophils pneumonia and the only way to differentiate it from ARDS is by doing
a bronchoscopy that demonstrates more than 25% of sinha fills and the BAL broncho alveolar lavage
alright so back to this chest x-ray this x-ray by itself just tells you that there are extensive
bilateral infiltrates so you need to know the clinical context based on the patient's history
and other clinical clues if a patient with this x-ray is a young person who vaporized and had
acute inhalational injury you're thinking ARDS or if it's a young person who aspirated or if
they sustained a trauma or a septic shock you're thinking ARDS on the other hand if it's an older
person with a cardiac history and they have a high BNP level or at low ejection fraction you
know it's going to be cardiogenic pulmonary edema the most common causes of ARDS are aspiration
pneumonia severe sepsis inhalation injuries other causes include near drowning severe trauma severe
pancreatitis transfusion of blood products and fat embolism why do they cause ARDS
I don't know we just know that somehow it caused this crazy chaotic inflammatory response within
the lungs during this chaos there's damage to the alveoli and surrounding capillaries which
leads to excess protein and fluid accumulation in interstitial and alveolar spaces that means
decreased lung compliance increased VQ mismatch and increases in shunt and dead space ventilation
and not that you would ever biopsy someone would air yes because they're too sick for that but if
you did the histology would show diffuse alveolar damage patients with ARDS are at high risk of
mortality which increases with ARDS severity with that said mortality is usually the result
of the underlying disease itself that triggered the ARDS rather than refractory hypoxemia the
severity of ARDS is important because it's going to determine how we manage patients in severity
is determined by the po2 DeFeo T ratio to be more specific it's the ratio that you calculate while
they are mechanically ventilated with a peep of at least five but let's not get caught up into
my new show because let's say you get the ABG before they're intubated it's not like you're
gonna say well I can't calculate the severity of ARDS because they're not intubated with five so
now that we got that out of the way the severity of ARDS goes like this mild is if the po2 DeFeo
to ratio is between 200 to 300 moderate is if that ratio is 100 to 200 and then severe is if
that ratio ends up being less than 100 so besides treating the underlying disease of Ards you need
to know the things that improve it especially what improves mortality methylprednisolone aka
solu-medrol if given early for severe areas may improve ICU length of stay in a number of days on
mechanical ventilation if it does work it's because you're suppressing the inflammation
that occurs in the beginning phase of ARDS so this is the first few days of ARDS later on you
get the proliferative phase and then the fibrotic stage so like we talked about earlier the alveoli
fill up with protein and fluid this leads to at least partial alveolar collapse and decreased
lung compliance with shunt physiology so what are we to do the answer is to increase the PEEP
the positive end expiratory pressure put simply peep is the positive pressure left in the chest at the
end of expiration when the patient exhales their breath air moves out of the lungs and into the
endotracheal tube air moves this way because of differences in pressure it goes from high pressure
to low pressure so if they are exhaling and there's a valve that keeps some of that air inside
there's gonna be a certain positive pressure you simply dial that peep on the ventilator
to whatever you want increasing the peep minimizes repeated opening and closing of the distal Airways
in alveoli it also improves homogeneity of the lung parenchyma by reducing drastic differences
in regional lung compliance third it improves VQ mismatch and shunt physiology by maintaining
alveolar recruitment you're essentially popping open those alveoli what is the ideal level of
peep no one knows for sure normally when a patient without ARDS is intubated we set the peep to five
but if they have ARDS we want it to be around 10 or 15 if it's really severe sometimes we'll
go all the way to 20 you don't want it to be too high though because this increases the risk
of pneumothorax so here's a table from the ards net trial that gives a suggested peep and fio2
strategy just remember that a good rule of thumb is the more severe the Ards the higher people
are gonna want to use so increasing the peep pops open alveoli and improves oxygenation and
that's great if you're taking the boards and they ask you how would you improve the oxygenation and
you have to choose between increasing the peep or increasing the fio2 always always increase
the peep but what is the only thing that has been shown to improve mortality and ARDS yep
that's right using low tidal volumes so having a low tidal volume ventilation and increasing
the peep are the keys to managing patients with ARDS so we said in ARDS there are areas of
good lung adjacent to areas of bad lung the areas of bad lung with decreased compliance makes them
more vulnerable to volle you trauma and Barrow trauma so this is the reason why the Ards net
trial showed a significant reduction in mortality with the use of low tidal volumes current ards
goals include both a tidal volume of six MLS per king of predicted body weight in maintenance of
the lowest possible plateau pressure typically this comes out to tidal volumes in the 300 range
for women of average height and tidal volumes of 400 range for men of average height but you might
imagine that giving a patient low lung volume might not be too comfortable for them so it's
important to properly sedate patients in order to accomplish our lung protective strategy of
low lung volume ventilation and it's okay if they develop a little respiratory acidosis it's called
permissive hypercapnia that's the sacrifice we make in order to achieve our ultimate goal which
is survival now let's talk about some other things that you can do for patients with ards
recently the perceiver trial demonstrated improved mortality and ards patients with the po2 at fio2
ratio of less than 150 who are treated with early prone positioning and low lung Title VII
ventilation so why is prone positioning beneficial when we lay in a prone position the weight of the
heart is no longer compressing the posterior lung region and this allows for improved vq
matching also with positive pressure ventilation the diaphragm moves more freely in the prone
position which means better chest law compliance and better gas exchange in the lower lung fields
to get the maximum benefit proning should be done for 16 hours a day so give some appreciation to
your nurses in patients with severe refractory hypoxemia both pro and positioning and ECMO can
be considered but the evidence for using ECMO is less convincing other methods to optimize
ventilator management in arts have been suggested including using inverse ratio ventilation and high
frequency oscillatory ventilation but none of these have been demonstrated to improve
mortality in arts patients at least in adults and finally what about paralytics neuromuscular
blockade like sis atracurium is sometimes used for severe refractory or life-threatening hypoxemia
especially if there's severe vent de synchrony and ARDS paralytics may help to achieve lung
protective validation by eliminating spontaneous breaths and ventilator to synchrony neuromuscular
blockade like with sisiter koream aka tandem Beck's is sometimes used for severe refractory or
life-threatening hypoxemia especially if there's severe vent to synchrony in ARDS paralytics may
help to achieve lung protective ventilation by eliminating the spontaneous breaths and
vent to synchrony there's not enough evidence to definitively say that there's a mortality benefit
of using paralytics and the downside to using them is that there's the potential for critical illness
myopathy and neuropathy so only use neuromuscular blockade if you absolutely have to so that's all I
got for ARDS thanks for watching I like watching these videos and if you want to see some more
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