00:00
Let’s move on. Signs and symptoms of ARDS.
Pretty straight forward now. So, once we have
got through acute type
of respiratory distress syndrome, we talked
about sepsis being a very common cause, could
be aspiration, toxic inhalation, pneumonia,
and so forth. We talked about neonatal respiratory
distress syndrome. We talked about tachypnea
and we talked about surfactant deficiency.
Most patients present similarly and present
with tachypnea, hypoxia, tachy. Early, 12 to
24 hours.
00:35
Next, well if there is a severe V/Q mismatch,
then you can expect, take a look and focus
upon a widened A-aO2 gradient. As a rule of
thumb, say that you are about to take your
exam and you feel stressed. This is what you
want to take in mind. A-aO2 gradient normal,
if you have a pathology, outside of lung.
A-aO2 gradient widened, when you have a pathology,
inside the lung. For example, is this in the
lung? Oh, absolutely. What about the chest
X-ray? I will show you that. Diffuse alveolar
infiltrate. It may, to a layman, it may, perhaps
to a novice, be confused with interstitial
lung disease. So, you need to close your eyes
and think about what an alveolar looks like
and if that is to be collapsed, then that’s
what’s going to be found
on chest X-ray. What about ABG? Marked hypoxemia.
01:33
Here, pay attention. From the very beginning,
I have been saying that that this is a pulmonary
shunt. Shunt, why it that important? Clinically,
you give oxygen, but the patient does'nt
find to be, or does'nt find significant
improvement because of the shunt. But, you
still have to give oxygen. Is that clear?
Next, mechanical ventilation indicated decrease
in pulmonary compliance. So, mechanical ventilation
indicates that the pulmonary compliance has
gotten so, so low and the lung is so very
stiff that the only method by which this patient
can now breathe is through mechanical ventilation.
02:09
Next, what about the pulmonary arterial catheterisation?
Pay attention. Where is my damage? To lung.
02:18
Is this cardiogenic or noncardiogenic damage
to the lung? Noncardiogenic. So, tell me about
your left ventricular pressure. Normal. Understood?
If you did a pulmonary capillary wedge pressure,
do you want the differential that I showed
you? Go back and take a look. The differentials
of ARDS and I gave you pulmonary edema and
I gave you the one with sepsis, in ARDS. Right?
And during that time, in ARDS, you would also
find your pulmonary capillary wedge pressure
to be normal. Be careful, clinically, these
things become very important for us.
02:55
Acute onset. Diffuse bilateral infiltrate.
Your FiO2, well, it depends. Here, on a ratio
less than 300. Definitely, your aO2 is going
to be severely compromised. When your ratio
is decreased, the numerator is decreased.
Origin of edema, not fully explained by heart failure or volume overload
With ARDS, you have to be able to manage your
patient properly, no joke, ICU. You always
try to get to correcting the underlying cause.
May be it is sepsis, maybe it is aspiration,
things we have talked about. Always look for
mechanical ventilation, if the compliance
is so low that the patient is not able to
breathe. Remember, this was a big deal in
neonatal respiratory distress syndrome where
maybe you were thinking about giving CPAP,
continued positive airway pressure or PEEP,
positive end expiratory pressure. PEEP is
used on the ventilator to splint open the alveoli,
help oxygenate, low tidal volume ventilation,
to minimize the ventilator trauma and conservative
fluid management.