Okay, so many of you have asked that what is the role of D-dimer testing in

diagnosis
of D-viti or pulmonary volumine.
So understand that D-dimer has got a very high negative predictive value because it
can get
elevated in lot of condition.
So if the D-dimer value is coming negative, that means we have 95 to 90% chance
that this
person is not having D-viti or pulmonary volumine.
But again, this testing depends upon how much you are provably suspicious about D-
viti
or pulmonary volumine.
So that is the right particular patient.
If you have a wheel score or any scoring system, if you feel that this is patient,
there is
a high chance of D-viti or pulmonary volumine.
You give an anti-coglation and then do your eco-ancity pulmonary angio for that.
But if you are suspecting low or moderate risk in that particular patient, get a D-
dimer
done and if D-dimer comes negative, that means 95 to 98% chance that this is not
having D-viti
or pulmonary volumine.
But if again it comes positive in low or moderate category, you need to do again
imaging
to rule out the things, do do it more about it.
Okay so many of you asked on the channel that how to calculate the dose of soda
bicarb
infusion if you want to give.
So understand that the dose of soda bicarb net depends or sodium bicarb net depends
on
which condition you are giving.
So doses are different in different condition.
But as a general rule, if you want to give an infusion, the formula simply form
lies,
you calculate the difference between what is your desired sort of so bicarb net and
what
is the actual and usually with targets somewhere around 15-16.
So suppose your desired sort of bicarb net is 15, actually stands so what is the
difference
5 and half of the weight of the multiply by half of the weight.
So 60 kg patient is there, multiply by 30.
So 30 into 5, 150 milli-clint and then give this total sort of bicarb net dose over
a
period of 24 hours.
So this is how you calculate the dose of sodium bicarb net.
Again, understand that the dose of bolus and other depends upon the condition in
which
you are giving.
So do read more about it.
Okay so many of you asked that once we interpret the patient in the ICU at what
level we should
fix the endotrical tube and how we will assess the appropriate level on the x-ray.
So please understand that why we want to do this.
We want the tube should be inside enough so that it doesn't come out from the
glottis
and it should not be too deep so that it stimulates and irritates the carina.
So where your cavit
this particular
Prasugel and Tikagalara. So, when to use which one. So, Sarah has told that all
three
have same mechanism of action, but the difference is Prasugel and your clopidogal
are irreversible
inhibitor of platelet while Tikagalara is reversible inhibitor platelets. Secondly,
clopidogal
being the oldest one is widely used, but in some patients you have clopidogal
resistance.
Prasugel and Tikagalara being more potent than clopidogal, so they should be used
in
high risk patient, but Prasugel should only be used in patient in which you are
doing
intervention means angioplasty or PCI. It is should never be used in medical
management
of acute coronary syndrome as a dual interpretive. While Tikagalara can be used in
medical management
as well as intervention also, but it is side effect of bronchospasm. So, you need
to take
care of it. So, do read more about it. Thank you.
Okay. So, we all know that IV adenosine is given for the termination of
supravantucleotide
cicardias, but it is important to remember that its dose depends on from which
route
you are giving means IV line, but it is peripheral line or central line also in
which patients
if it is in heart transplant patient. So, for normal patient if you are given where
kivital fossa interket line the dose is 6 mg if it does not get terminated the
ticicardia
you can repeat 12 mg and if it does not get terminated you can repeat 12 mg more.
So,
6 12 12, but if you are giving the ijb or saplivin central line the line is very
close
to the heart. So, dose get reduced to 3 mg followed by 6 mg if required followed by
9
mg if required. So, dose get reduced like that and if it is a heart transplant
patient.
So, according to up to date reference the dose is 1 mg followed by 3 mg followed by
3 mg. So, maximum of 3 doses are given. So, this is very very important go and do
read
more about it. Thank you. Okay. So, I have Dr. Shireh is with me he is a consultant
physician
and he provided a very useful tip to our members that what is the optimal level of
hb about which we should transfuse blood in ICU intensive care setting. So, first
you
need to understand that all the trials and all the studies have shown that you can
wait
up to 7 if the patient is hemodynamic stable. If you do not if the patient does not
require
any support for maintaining the blood pressure then above 7 you should not
transfuse, but
there are 3 exceptions. One if your patient is a cardiac patients in such patient
is good
to maintain about 9 if the patient is a pediatric 1 75 85 is the range or if the
patient is
active bleeding. So, in such patient keeping hb about 9 is justified, but if the
patient
is hemodynamically stable up to 7 you can wait to transfer hemoglobin. Thank you to
up to stage for this do read more about it. Okay. So, other than all the things
which
you see in the x-ray like identification right or left like that you should always
check
the exposure of the x-ray because then the exposure is not correct you will not be
able
to interpret it correctly. Now, as you can see here this is the x-ray which is the
outside.
Now, to check the exposure just see if your spine is visible you can count that.
Now,
this was the outside x-ray now you can see this x-ray. Now, this x-ray seems to be
bad,
but the problem is it is under expose you cannot see count the spine while when we
repeated
the x-ray if you can come closer you can see we can now count spine and now these
two x-rays
are more or less similar. So, whenever you check the x-ray always look at the
exposure
if the spine is not visible it is under expose and if it is too dark it is over
expose. So,
for adequacy you will you need to be just able to count the spine. So, read more
about
it. Thank you. Okay. So, many of the new journeys or the new
refugents feel that for fluid resuscitation central line is necessary. So, this is
a myth
for fluid resuscitation if you have a good intricate of 16, 14 or 18 because they
are
good enough for fluid resuscitation because the length of these intricate are small
while
in central line the limit is good, but the length of the even length of the
capacitor
is long. So, this creates a resistance. So, for fluid resuscitation if you have a
good
16, 14 or 18 gauss canula they are called large bore canals and they are fair
enough
for fluid resuscitation. So, do not get worried do a fluid resuscitation and then
take central
line for other purposes you want do read more about it.
Okay. So, one of the number asked on the channel that when we are celebrating
magnesium for
preeclimcia or for any other reason what are the things we can monitor clinically.
So,
clearly you can measure three things one is your respiratory the patient is going
to
respiratory depression or loss of deep tendon reflexes if the deep tendon reflexes
are going
down or the urine output is going down. So, if the patient is developing bredipnea
if
the patient is developing loss of deep tendon reflexes or the patient is developing
alling
area it is a sign that we are learning in magnesium toxicity or magnesium overdose.
So, by this you can monitor them clinically do read more about it. Thank you.
Okay. In a pregnant female who present into the third remester and she develops
caesar.
So, it can be obviously due to eclimcia but you should always keep two
differentials more in it.
One is press syndrome means due to high blood pressure posterior reversible and
chiflopathy syndrome
she can have developed this because of uncounted and controlled blood pressure and
the second thing
is venous sinus thrombosis. Renous is an hypercogulable state. So, at times patient
presence in the
last remester with venous sinus thrombosis. So, these two differentials should
always be kept in mind
in a patient in a pregnant female who present with caesar in the third remester
other than
eclimcia. Do read more about it. Okay. So, one very important tip is whenever you
see
a A B G of a patient and it is showing high and high and high metabolic acidosis
and your
lactates are normal but still you are seeing high and high and high metabolic
acidosis.
So, two conditions which needs to be kept in mind is one is your diabetic
ketoacidosis,
other one is your starvation ketoacidosis. I will call it ketoacidosis. Usually we
will have a
lactate didn't because the liver is not able to metabolize the lactate. So, but if
a patient is
having high and high metabolic acidosis with normal lactates always think of
diabetic ketoacidosis
or starvation ketoacidosis in such patient. So, this is very useful in the issue.
Do read more
about it. Thank you. Okay. So, one very good question is on the channel whether
amidora
infusion can be made in Dextrose 5% or normal saline. So, it should always be made
in Dextrose 5%.
The reason being the literature says that the chloride ions in the normal saline
makes the amiduron incompatible and it makes it precipitate in the solution.
And also in Dextrose solution also the amiduron remains stable for only for 12
hours. That's why
you must have seen that the infusion of amiduron is made for 12 hours, 12 hours, 12
hours. It's
not made for straight away for 24 hours. So, that's the correct amidora infusion
should be made in
5% Dextrose and only 12 hour infusion should be made and then you can again make a
12 hour
more infusion. Do read more about it. Thank you. Okay. So, when somebody asks you
whether it's a
low voltage ECG or not and why it is important. So, low voltage ECG is important
because
along with many differential it is one of the findings which you've seen
pericardole fusion
or cardiac tamponade. Pericardole fusion means the fluid around the heart so that
the heart is
not able to come properly and it can lead to hemodynamic instability shock and
mortality also.
So, one of the findings we see in this is a low voltage ECG. So, what did you buy
low voltage ECG?
In ECG you see these there are limb leads and there are chest leads. So, limb leads
are 1, 2, 3,
UBL, ABF and UVR and chest leads are prechordial B1 to B6. So, if all the complexes
in the limb leads
are less than 5 mm and if all the complexes in the chest leads are less than 10 mm
either of the two
then we call it as a low voltage ECG and you should always rule out pericardole
fusion
temperature by 2D to cartography in such cases do read more about it. So, very good
question
asked on the channel that whenever you want to supplement potassium we should give
in normal
saline or half normal saline but not in dextrose because it will not serve other
purpose. It is
correct because what happens whenever there is a hyperglyceome or dextrose in the
intervascular
compartment the body secretes the insulin to move the sugars from intervascular to
the intercellular
compartment along with that it also moves potassium from intervascular to the
intercellular compartment.
So, if we give potassium with dextrose what will happen in saline we get secreted
it will lower
the sugar level as well as lower the potassium level because the potassium will
move inside the
cell from intervascular compartment. So, if we want to give dextrose also and
potassium also
give dextrose amylthane in a separate thing and give potassium in a separate thing
in
normal saline half normal saline. So, it will maintain and if you will get give
dextrose and
potassium simultaneously it will not raise the potassium level but it will maintain
the
potassium level in the blood as it is do read more about it. So, whenever you are
seeing a
patient of acute coronation in room and you are looking at the ECG especially in
esti-segment
elevation am I always try to look at lead avr. Lead avr is usually negative in all
the ECGs
and in the am I also but if avr is showing elevations esti-segment is elevated or
the lead is positive
that means this lesion is very proximal either it is in the left menotry or very
proximal already
and in hospital modality is very high in such patients and these needs to be
tackled very aggressively.
I will show with comparing two ECGs both are am I patient you can see this but here
the lead is
avr is negative here is this an am I but lead is negative but in avr here you can
see that the
esti-segment is elevated and the patient also develops bundle branch block. So,
this is a patient
who is more severe who is in LVR who is in shock and may require IVP. So, next time
you see an
esti-segment elevation am I do give a look on lead avr thing. Okay, so, one of the
embers are
on the channel that how much potassium we can give by peripheral line and how much
potassium we can
give a central line. So, according to literature and the clinical practice via
peripheral line we
can give 10 milli kilo an per hour maximum 20 milli kilo an hour via central line
up to 20 milli
kilo an hour and 40 milli kilo an hour maximum in case of emergencies. Having said
that when we
want to infuse potassium more than 10 milli kilo an hour or at times 5 milli kilo
an hour always
always use infusion pumps because etcetera which needs to be monitored very
carefully.
In our setup we prefer extra jugular which is a peripheral line which is a good
line
when we want to give by infusion pumps. Also, if it is not possible you can dilute
potassium in
100 ml of dilutant and I sort of extro the half normal saline or 500 ml of dilutant
and then
keep again give by a peripheral line. Hope this clarifies during more about it. So,
I got a very
interesting question on the channel that whether vasopressants or anatrophs should
be used in or
should be diluted in normal saline or extra 5 percent. So, I reviewed all the
literature which
is available up to date, textbook and manufacturing levels and there are no head to
head studies
comparing the efficacy and compatibility of both the dilutions. But having said
that all the
literature is favoring that the compatibility and efficacy is more with dextrose 5
percent
compared to normal saline for these anatrophs and vasopressants. Also, some studies
have also
reviewed that even if we give this dextrose 5 percent to patients who are diabetic
or who are
in ketoacidosis it does not make change, it does not harm to the patient or it does
not increase
in the hyperglycemia. So, to conclude we should or I would recommend that making
vasopressant anatrophs in the D5 percent is a better option as compared to normal
saline.
Do read more about it. Okay, so you must have read or heard that giving too much
percent of
0.9 percent normal saline can cause metabolic acidosis. So, which type of metabolic
acidosis
can cause? It causes normal anion gap metabolic acidosis and what is the reason? It
is because
of the chloride content. That is why the other term for nagma is hyperchloramic
metabolic acidosis.
You see in the normal saline the chloride content is 154 millimoles per litre while
in half normal
saline 0.45 it is 77 millimoles per litre while in the RL it is only 111 millimoles
per litre.
So, if you give these fluids the chloride content will be less and the normal
anangia
metabolic acidosis transfer development will be less and that is true for balanced
crystalloids also.
But remember this metabolic acidosis never to severe in practical sense and also
whenever
your patient is hemat dynamically unstable we need the fluid to retain in the
intra-vascular
compartment. So, you can give normal saline safely do read more about it. Okay, the
festival season
approaching and hospitals may receive burn injury patients. So, what is the initial
fluid
resuscitation strategy in such patients? So, for initiating we have two formulas.
One is
parkman formulas which says that 4 ml per kg into total body surface area of the
fluid should be
given. Half of which should be given in first 8 hours and the rest should be given
in the next
16 hours. In modified rookies formula say that 2 ml per kg into total body surface
area should
be given in first 24 hours. Review have said that total in modified rookies those
amount of
fluid which you are giving is less but it is not buzzing half. And mind you all
these formulas
applicable only for second, third and fourth degree one, first degree one where
there is no
blistering are excluded from this and still the crystalloids are the choice of
fluid for fluid
resuscitation. The maintenance will depend upon what is the third spacing how much
is the urine
or pore what is the blood pressure. So, this is important do read more about it.
Thank you.
Okay, so in 2010 the AHA changed this guidelines from A, B, C to C, A, B. So,
air withering circulation to circulation air withering. Why this change happened?
Two reasons. Suppose assume a patient holds its breath for 1 or 2 or 3 minutes,
that it can hold comfortably but if the circulation stops or there is hypertension,
suddenly the patient fell down or become unconscious. So, circulation is more
important.
So, by shifting from A, B, C to C, A, B chest compression starts and the blood flow
restore
very fast and that is only 18, 20, 20 second delay in initiating the airway which
is which
can be taken care of. Secondly, the H in A, B, C by opening them out, by standard
thinking,
giving mouth to mouth breathing or taking out the mouth that H is removed and
immediately the
chest compression started very fast. But remember that this CAB is not applicable
in case of children,
in case of esphyxial arrest, drug abode pose or near drowning among adults in that
ABC is still
followed. So, do read more about it. Thank you. Okay, so a very good question was
asked by Dr.
Ankit today. Today is his birthday also. So, he asked that whenever we see patients
of
heart failure, some of the institutes or some consultants and BNP and some sent
anti-probNP.
So, what is the difference between these two? So, understand that it is an
atyutectic type
which the heart secrets whenever the heart wants the viruses to happen. So, it
secrets pro-probNP,
then it gets converted into probNP and after that it gets divided into two parts.
One is anti-probNP
and other is BNP. So, the biologically active molecule is BNP which is biologically
active and
it gets cleared fast also. While anti-probNP is biologically inactive and it gets
cleared passively.
So, it remains elevated for a longer period of time in the blood. So, whenever in
the
doubt anti-probNP remains elevated in the blood for a longer period of time. So, it
can pick
the heart failure early, but there are no head-to-head trials between these two,
but it helps at times.
So, do read more about it. So, what is the role of aluminium in ICU? So, if you go
through the
textbook you will see the indications, but they will fall in rolling two
categories.
One in homodynamically unstable patients in which you have after even after giving
lots of
fluid and waste of pressure and steroid blood pressure is not picking up, then we
need to
maintain the on-cotic pressure. For that we can use aluminium in the sequence.
Secondly, in patients which we have leaky capillations in the on-cotic pressure,
like in serotic patients, in the angle shock patients. Wherever there is anisarca
and there
is a leaky capillations in the room, there the aluminium is useful to maintain the
on-cotic pressure.
It has got no nutritional value in terms of patient care in the ICU. We do not give
allowing for nutritional value and just for the saying the lab report has come,
aluminium in is low in it, we do not get. Only when the patient is in wood and is
unstable
or when there is a leaky capillate syndrome sort of picture. Do read more about it.
Okay, so one very interesting fact, suppose we have patient of acute coronavirus
syndrome and
the patient at ST segment elevation am I and we have decided to thromblize with
streptocyanis.
So, one thing we should always inquire is whether there is a previous exposure of
streptocyanis or the patient has been previously thromblized with streptocyanis
before, because
streptocyanis is an animal protein and it induces the antibody production in the
patients after
first exposure. The antibody development takes somewhere around 3 to 5 days to
develop and remain
in the body for years. So, the literature which I read got the references from
every literature.
It is a relative contraindication that if the patient has a previous exposure to
streptocyanis
more than 5 days 2 or 5 years. So, if there is a patient as a previously been
thromblized
streptocyanis, this time we should use a different agent because the chances are
they have used the
same streptocyanis in such patient, there may be enough electric reaction or the
reduced efficacy
due to antibody production. Do read more about it. Okay, so when you decay patient,
what are the
end points of the treatments? I mean till when you will continue on fluids and
insulin and other
supplements. So, understand this that in decay what is happening because of the
lack of insulin,
the body is not able to utilize the glucose in utilizing proteins and fat and that
is why they
are getting converted into ketones. So, we need to supplement insulin but because
we supplement
insulin, the patient will end in hyperglycemia sugars will get down. So, we
supplement dextrose.
So, somewhere we maintain sugar somewhere around 180 to 200 till the time your
ketones gets
negative the body stops utilizing adipose tissue and protein. So, how will you
check it?
You will check it by urine ketones, they may be falsely negative but in here you
need to check
it's ABG. In ABG, if high-end metabolic acidosis goes away, that means your goals
are achieved.
Normal a line get can persist because of fluidization but if the ABG shows no
asthma that is your endpoint in treating decay. Do read more about it. Thank you.
Okay, so if any patient presented with acute onset lower limb weakness which is
symmetrical
in pattern or all four limbs weakness which is symmetrical and you suspect Gullian-
Barrison-Dohman
suspicion. So, always check the potassium level before labeling this patient as GBS
or moving forward
because hypokalemic periodic paralysis can present with acute all four limb
weakness
in such patient. Secondly, in geriatric question especially those who are on
statins or have some
viral infection, always check CPT total, Gritin-Posokanase levels because if these
are too high, they can
also mimic the all four limb weakness sort of pattern. So, always when you suspect
GBS,
check potassium level mandatory. Secondly, if in doubt, check CPT total also. Do
read more about it.
Thank you. Okay, very interesting question also on the channel. What to do if only
IgG
antibody is positive in geriatric infection, NS1 and IgM antibodies are negative.
So,
understand this, DIGU is called by four strains of viruses, fly virus, NS1 to four.
So,
a NS1 antigen is positive. It can become positive from day one to day nine on
infection. It's an
acute infection. If IgM antibody is positive, then it's also acute infection
because they start
developing with heart to heart. They remain elevated for three weeks up to six
months. So,
it's acute infection. But if only IgG is positive, other two are negative that
there are two chances.
Either it's a past infection because antibody rise from day four to day five and
remain related
for years. But if your patient is infected by a different strain of DIGU this time
and also,
if you have UHG showing features of DIGU, H-O-TPT is elevated, your patient has
clinical science
and symptoms. There is a leaky capillate syndrome. It may happen because of
secondary
infection type of virus this time. IgG antibodies are elevated strongly this time.
So, it can happen
patient having acute infection. Do read more. Okay, so what is the difference
between a
support which is given by a Biapap machine and a support which is given by an NIV
machine on
the ventilator. So, Biapap is a bi-level positive value pressure and NIV machine is
a non-invasive ventilation. So, there are two main differences. One, the Biapap
machine,
you can give approximately up to 60 percent of the Biapap 5.2 while from an NIV,
you can give up
to 100 percent of the Biapap 5.2. Second major difference is on a Biapap machine,
the mass which
you are using on the patient, the Biapap mass is a vented one. Means there is an
exhalation
port. So, the air goes in and then the air comes out to the exhalation port on the
Biapap
mask. While an NIV, the mask is non-vented one. The inhalation goes through a
tubing and the
exhalation also goes to the ventilator. So, you need to be careful which mask you
are using and
the on Biapap there is a single tubing which is used on an NIV. There are double
tubings which
are used. So, do read more about it. Thank you. Okay. So, whenever a patient has
pneumothorax,
phantase, pneumothorax or in trauma, the patient has pneumocephalus, then why we
provide high-flow
oxygen by the mask or with a oxygen reservoir? Why provide high-flow oxygen to such
patients?
The reason is because the air which is there in the plural cavity in the brain is
in the
composition, in the composition is same as the eta of our atmosphere which contains
lots of
nitrogen which is non-observable. High-flow oxygen replaces the nitrogen from that
air mixture
and which makes the air absorption 4 to 5 time or 3 to 4 times faster. So, it
causes very fast
resolution of the pneumothorax and pneumocephalus for that matter. But, K-I should
be taken that
this should not be given for COPD patients, high-flow oxygen because it can depress
their
respiratory diets. So, do read more about it. Why high-flow oxygen is given for
patients with
pneumothorax and pneumocephalus and how it helps in absorption of the pneumothorax
and pneumocephalus.
Thank you. Okay. So, a very good question was asked by one of the members on the
channel,
the member's name is Dr. Fusant. He asked that in cerebral edema, when we should
use 3%
celline and when we should use many talk. So, the answer is very simple. As a
thumbnail,
you should remember that if your patient is having cerebral edema with
hypertension,
3% celline should be preferred and if your patient is having cerebral edema with
hypertension,
where diuresis will help, then we should prefer monetol. 3% cellines can be given
as
continuous infusion or boluses and its sodium should be target somewhere around 150
to 155,
beyond 160, it should not go and monetol is always given as boluses. So, do read
more about it.
Thank you. Okay. So, whenever we have a patient of head injury or any surgery,
brain surgery,
neurosurgery, he comes to ICU for monitoring and the patient is on ventilator like
that.
So, usually such patients are not down sedated patients. So, in such patient, if
you see
bradycardia with hypertension, not hypertension, means bradycardia with
hypertension, race blood
pressure, not hypertension, then it is a sign of race the ICP intracamial pressure.
If you see bradycardia with hypertension, it is not that sign, but bradycardia with
hypertension,
BP accelerating 180, 200 and your heart rate goes to 50, 45 like that. It's a sign
of race
the ICP. People's dilation will come later on. So, we should act promptly to reduce
the ICP and
find out the cause. It is also known as a cushion reflex. So, whenever you have a
patient in ICP or
post of neuro-maintaining, one ventilator, especially on ventilator, do read more
about it and look
for it. Thank you. Okay. A very good question was asked by one of the members on
the channel that
what would happen if we ventilate or intubate and ventilate a patient of severe
metabolic acidosis?
So, basically it's all about pH, maintaining the pH in the body. So, whenever a
patient
has severe metabolic acidosis, the patient tried to exhale CO2 so that the pH comes
to normal. So,
the patient will be technique that's breathing at respiratory rate of 2530 and this
wash out the
PCO2 somewhere around 2020 to 24 and this picking the pH too close to normal
7.27.3. But as soon as
you put the patient on ventilator, what happens you said to normal ventilatorate
and now the PCO2
becomes 35 to 40. So, the compensation is lost and as soon as the compensation of
respiration is lost, the pH becomes asymptotic, it's purely metabolic acidosis, pH
drops to
706.9 and this causes a sudden cardiac rate. So, in such patient when you intubate
and ventilate,
make the respiration rate 24 to 26 initially and then you can adjust, do read more
about it.
Okay. So, one very interesting fact is what is the difference between sinus
tachycardia
on atrial trichardia for 2emol specific focal atrial trichardia. So, just remember
one thing,
whenever the beat is originating from the AC node in the itia, it will you call it
sinus
tachycardia, sinus tachycardia and if the beat is originating from the itia, but
other than the
AC node, it will you call as atrial rhythms like focal atrial trichardia, atrial
fibrillation,
atrial flutter, multifocal atrial trichardia. We don't call it sinus fibrillation,
sinus flutter
like that. So, any beat which is originating from the AC node will be a sinus
tachycardia,
any beat which is originating from the itia other than the AC node will be call as
atrial rhythm.
How do you do identify? Do check three, check three leads. One is your limited to
the AC node
or sinus beat will be upright in it. It will be inverted in AVR and in lead V1, it
will be biophasic.
Other it will be it will show different it will do read more about it.
Okay. The question which is asked today on the channel is why IV adenosine is given
through a
rapid I push and given in the cubital way. Basically, adenosine is used to
terminate
super ventricular tachycardia of some type. It slows down the conduction of the
you know that it has to reach it fast because as soon as you give it, it gets
metabolized by
the endothelial cells in the blood vessels and it has a very short half line. It is
0.6 to 10 seconds.
So, it gets metabolized very fast. So, the way of giving it is you connect an
intercal,
then connect the try way from one side you give the adenosine and then y20cc ml ns
you push it
very fast. So, the idle way is doing it and the vein should be as near as possible
to the heart.
So, cubital vein is very near to the heart that is why it is given through this and
if you have
central line then it has it is preferred to the cubital vein. So, because it has a
very short half
line it is given to the nearest vein which is close to the heart. Do read more
about it. Thank you.
Okay. So, today's question was asked on the channel that what will happen if we
give calcium
you will connect by rapid IV push. So, if you give calcium you will connect by
rapid IV push,
it will cause vasodilatation, hypotension, bradycardia, any type of arrhythmia. So,
it should never be given as a rapid IV push. You can remember it by rule of 10, 10,
10,
so 10 ml of calcium you will connect in a 10 ml syringe over a period of 10
minutes.
So, this is a easy tool to remember. So, do read more about this calcium IV rapid
push. Thank you.
Okay. So, Dr. Arushi has asked me a question. Sir, what are shockable and non-
shockable rhythm?
So, it is very easy to understand. See, when you are giving shock to the heart you
want that
the heart should come still and then start functioning or beating normally. So,
there are only two
rhythms which are shockable. One is ventricular techecardia and ventricular
fibrillation. This
ventricular techecardia fibrillation, the heart is beating like in a fibrinating or
witty type of manner. So, you need to shock the heart and so that it becomes still
and then start
functioning beating normally. While non-shockable rhythm is acesterly, it is
already still so you
don't need to give shock and the other is PEA, pulse-less electrical activity.
Means the electrical
activity is there but the heart is not biggie. So, shockable rhythms are VTE and VF
and non-shockable
rhythms are acesterly and pulse-less electrical activity. So, do read more about
it. Thank you for
asking. Thank you. Okay, so whenever a patient of cervical spine surgery gets
shifted to your IC4
observation, specifically if the surgery is done on high cervical C2, C3, C4, C5,
C6 or C7 also you
can take, you need to observe two things. One, what was the pre- or power of the
patient in all
forelimbs and what is the post- or power in all forelimbs, whether it is same
decreased or increased.
Secondly, most importantly you need to see what is the type of respiration, whether
it is thoracobdominal
or abdominal thoracic because and if the patient's phrenic nerve is involved, which
roots well,
which is root value of C3 to C5, then the patient respiration will get hampered. It
will be more
of abdominal thoracic. You need to see how is the chest expansion, whether the
patient is able to
expand the chest completely or not because what happens if the patient is not able
to expand the
chest, the patient will start retaining CO2, the patient will become drowsy and
then sudden collapse.
Saturation will not fall in the early stages. So do read more about it and keep a
watch on chest
expansion in such patient. Thank you. Okay, so many of you have asked that what is
baby lung in the
ARDS. So in a very simple way understand that ARDS is a non homogenous disease.
There are patchy
areas of involvement of the lung in life. So we have two sets of ill-line in a same
patient. One,
the ill-line are electrolytic. They are inflamed and they will not open or collapse
when you are
providing the mechanical ventilation and IV. While the other set of ill-line are
almost normal,
they open and collapse like in a normal fashion. But the problem is the number of
such ill-line
are reduced. That's why in a real patient because of the less number of ill-line,
we say it's baby lung because in babies the lung ill-line are less in number.
The importance is whenever you are ventilating such patient, we need to set plyto
pressure,
driving pressure in such a manner that such baby lung ill-line or normal-line are
not damaged
in ARDS. So now hope you understand it. Read more about it. Thank you.
Okay, so we have Dr. Shilpa Saxena with us who is a pediatric nephrologist and we
have Dr.
Prayena with us. She is an intensiveist. So Dr. Shilpa underwent an injury, a root
of accident recently. So we thought of discussing a very important point in a
trauma patient.
So whenever you handle a trauma patient's especially head injuries or upper torso
injuries,
always, always, always take care of the cervical spine. Put a filler to help you
call or a hard
collar and until unless your cervical spine is clear, you can use Canadian C-spine
rule to clear
the cervical spine clinically or you have an x-ray of the cervical spine or
imaging, more
advanced imaging like CT scan of cervical spine. In her case also though we were
not having any
symptoms of cervical spine but we ruled out and get a cervical spine done so that
it's clear.
Because if cervical spine injury is missed, it can have a very catastrophic effect
on the outcome. So do read more about it. Thank you. Okay, so what is the
difference
between furisamide and torsimide? So basically there are three main differences.
One is regarding the potency. So your torsimide is 2.5 to 3 times more
potent than furisamide. So you need less milligram of torsimide required.
Second is duration of action. So the furisamide is short-acting duration of action
is 6 to 8
hours wide. Torsimide has duration of action of 12 to 16 hours. So less frequent
dosing
required. Thirdly regarding the elimination and metabolism. Furisamide is
metabolized equally
by kidney, renal and hepatic. While torsimide is metabolized majority, 50% by the
hepatic metabolism
is there, elimination is there. So you should be cautious in using in patients with
liver
failures. So these are the three main differences. Do read more about it. Thank
you.
Okay, so whenever you have a patient or blunt abdominal trauma who is being
hemodynamically stable
and he or she has been posted in the ICU for observation. So in such patient, do
give
very good importance to your heart rate. If the patient is becoming tachycardic,
inspire all the hemodynamic parameters are maintained. That means there are two
chances.
One, it can happen that patient is bleeding inside the abdomen. So now it is
blending in
compensatory shock. So there is a subtle sign of tachycardia. Secondly, it can
happen that the
patient has a bowel perforation or some other injury which has activated the serse
response
and the patient is having tachycardia. So any blunt abdominal trauma patient who is
in the ICU
for observation always watch for the heart rate. Even the patient is hemodynamic
stable.
Don't consider always as related to pain. It has a special significance. Do read
more about it.
Thank you. Okay, so one very interesting fact about furisamide is that it acts on
the
luminal side of the nephron. So if a patient is totally a neuro, not passing urine,
then
then furisamide will not work because it has to reach the luminal side of the
nephrons to act.
So if the patient is all the guric passing 5 to 10 ml of urine per hour, then
furisamide will
act but that too will in hydrosis. But if the patient is totally uric, not passing
any
urumates, it's nil per hour, then your furisamide won't act. So this is an
interesting fact while
considering the use of furisamide in intensive care. So do read more about it.
Thank you.
So today's tip is something which is we have failed on our personal experience,
although we
have got some literature mentioning this. So whenever you have finding crepes in
the chest,
there is always a confusion whether these are crepes of the cardiac failure or
whether these
are crepes of the infective eutelogy. So one tip for that which we have experienced
and tested
in our clinical practice, you can find some literature for that. Usually the
failure starts
from right side of the chest and then goes to the left side of the chest, the fluid
accumulation
if this is a cardiac failure, so because of the anatomy. So if you are finding
crepes which are
more on right side of the chest as compared to the left side, usually because of
the cardiac failure.
But you are finding the crepes which are more on the left side of the chest and
less on the right
side of the chest, usually they are of the infective eutelogy like CO2, CO2, CO2,
and infective ILD or
developing pneumonia like that. So do read more about this, this is very
interesting, thank you.
Okay so one very important question asked on the channel is how much furosemide you
can give
as an IV bolus and as an IV infusion in intensive unit specifically for fluid
overload. So furosemide
means less exercise by brand name, you know. So I went to the literature and I am
giving you the
reference of up to date for this topic. The maximum dose which can be given in a
day is 600 milligrams,
that is for sure whether IV bolus or infusion cumulative. For IV bolus if the
patient is taking
some diuretics at the home, so you can give 1 to 2.5 times of the that dose as a
bolus. Suppose
it is taking 40 B.d so it becomes 280 O.d so 8200 to 200 milligram you can give an
IV bolus and then
can wait for 2 hours if no response can you can increase the dose and give bolus.
For infusion
you can start with 5 milligram per hour and go up to 40 milligram per hour. So this
is
some interesting facts do read what about it and if you have any more literature
for this
you can post in the comments. Thank you. So today's short is about stroke. We have
this
dictum of at fast when we it comes to treatment of stroke where F stands for face
deviation,
A for arm weakness, S for speech and T for time. Time is golden management of
stroke.
But I just want to tell all the people who are involved in managing of stroke and
emergencies
that nowadays a lot of patients are coming with isolated acute vision loss, the
unilateral or
bilateral which then they turn out to be stroke. So this dictum has been now
modified as to act
not only fast but we have to act very fast where V stands for vision loss. So this
point also
should be taken in my in treatment of acute onset strokes. Okay so all those who
are listening
and all those new residents and nursing staff who have started working cardiac
units they must have
heard from your their seniors that whenever patient develops QRE pattern in the ECG
postMI
it's a bad probabilistic sign it's not good. So why you need to understand this. So
in acute
colonies in true criteria if the patient develops LBB, new onset LBB then you need
to
thromblize this patient because it is considered one of the significant forms of
MI. Similarly
if the patient develops postMI QRE pattern means right mandar branch but are done
with a QA.
Then it also causes a risk of high risk of sudden death by VTBA for different
areas.
This is because the conduction system is very well protected by the co-ordinates of
the heart
and the musculature of the heart. So if conduction systems get affected in any co-
accured co-ordinates
syndrome that means the injury is very severe and can lead to modality via VTVF and
other complications.
So do read more about it. Thank you. Okay so with me Dr. Ange today and he has read
compartment syndrome yesterday so he wanted to share a very important tip. So
compartment syndrome
means like you know calf muscle or your abdomen or anywhere in the body there is
sudden rising
the pressure and it is compressing the structures in that compartment. The pressure
cannot be released
by its own. So it is important to remember that there are three structures in any
compartment which
you need to see. One is your vascular supply other is your nerve, third is your
muscle. Most of the
time what the student sees is the vascular supply whether the vascular supply is
getting compromised,
the portion is becoming cold or there is a gangrenous water development but also
you need to see
whether there is a nerve compression is also there whether the patient is the blood
food drop
or there is a muscle injury or muscle pain is too much. So all the three
compartment
three structures needs to be looked in any compartment syndrome. This is very very
important
not just the vascular supply. So thank you Dr. Ange for sharing this tip and do
read more about
it. Compartment syndrome. Thank you. Okay so based on the duration of action
dialysis can be divided
into basically three types. One is your intermittent hemodialysis, second is your
slow low efficacy
dialysis and the third is continuous renal replacement therapy which is called
CRRT. So intermittent
hemodialysis is done between 2.5 to 4 hours, slight lower efficacy dialysis is done
between 6 to 8 hours
extend up to 9 and the CRRT is given over a period of 24 hours. So what's the
difference?
So if your patient is hemodalimically stable then you can go for interpretive
hemodialysis because
the flow the dialysis machine takes is good enough but if your patient is
hemodalically unstable
low blood pressure then you can opt for slow low efficacy dialysis or CRRT. But the
problem with
CRRT and hemodialysis is slight is they are not able to remove the solutes quickly
like hypercalemia.
For hypercalemia intermittent hemodialysis is the best one. The solute clearance is
low in
slight and CRRT but they can provide hemodinium stability. Do read more about it.
Okay so wherever
you are a patient of long bone fracture like fracture femur or fracture TBFibla and
if the
patient suddenly develops respiratory distress or the patient becomes agitated or
there is a drop
in the saturation always think of fat embolism because what happens is fat gubils
can leave the
bone marrow and then travel into the blood and can cause ARDS, fat embolism,
induced ARDS and
keflopethi sort of picture. So that is why it is very very important to stabilize
the long bone
fractures either by splints or cars and at surgery as soon as possible. How can you
diagnose it?
It is a diagnosis of exclusion you need to rule out other causes but if the patient
becomes agitated
means neuroscience or the patient will be developing the idea drop in saturations
like this or you
can have rashes and the sclera, particular rashes, axilla or pallet and in flat
lugeals in the urine.
So do read more about it fat embolism in long bone fracture. Okay with me is Dr.
Vakbakshi he is a very close friend of mine and consultant intensiveist he has a
tip for you people.
So many members have asked on our channel that at what potassium level the ECH
changes happens
in hypercalemia. So basically there is no fixed level of potassium at which the
changes appear in
the ECG. It depends on how acute the changes it like for ckd patients you may have
seen that
they are having potassium 6.56 but there is no EC changes but if it changes acutely
then the
changes appear in the ECG and what are the changes? First there will be tall T
waves then there will
gradual reduction of the P wave then there will be a broad QRS complex and then
sine wave.
So it is the rapidity which the potassium changes you may have EC changes and
potassium
layer of 5.5 acute changes happens and you may not have EC changes if it reaches
even
2.66.5 in ckd patients. So do read more about it and thank you Dr. Vakshi.
Most welcome. Okay so whenever you thrombolyze a patient of ST segment elevation MI
when we
recall it is a failed thrombolyze. So there are clinical criteria and the ECG
criteria.
The one of the most important is your patient becomes chest pain free. So that is a
different
story but when we will call it a failed thrombolyze based on ECG criteria. So 90
minutes ECG after
the start of thrombolysis some say 180 minutes but most of the literature is 90
minutes. So when
you start a thrombolysis and you repeat any ECG after 90 minutes the lead which has
shown the
maximum st evaluation in the previous ECG has shown a decrease in the 50%. If the
ST segment
elevation in that lead is not dropped by 50% then you call it say failed
thrombolyze. So the
maximum elevation, ST elevation in the first ECG and after 90 minutes should drop
by 50%
for a successful thrombolyze. If it is not it is a failed one. Do read more about
it.
Okay so today with me is Mr. Mening. She is in charge of surgical ICU and this is
her team.
And today they want to give a tip to our members that many of the patients post TKR
or some surgeries
they have fentanyl or any narcotic patches there so that the patient is pain free.
So other than
monitoring the severity of the pain of the patient in such patients you need to
always measure the
respiratory rate of the patient because narcotic can make the patient role for
respiratory patients.
So if the patient is not complaining of pain that is fine but if the patient
becomes too sleepy
usually the TKR patients are always a patient. So these patients are always in the
background.
So they can very fastly and very quickly can learn into a respiratory depression
and CO2 narcosis.
So whenever you have a patient especially obese patients with a background of USA
whenever you
put the fentanyl patches in such patient always monitor the respiratory rate. Do
read more about
it and thank you. Okay so today morning we were discussing certain things in the
ICU.
So our staff, ICU staff, rubies are in charge they come up with a small tip for our
channel
viewers that whenever you have a patient who is in multiple infusion especially on
noradling and
adeline. So if you give a certain drug and suppose accidentally or suppose because
there is a fluid
in the EU line, the infusion get flushed. So if adeline get flushed it will cause
tachycardia but
but if noradling is there and if noradling get flushed it will cause bradycardia
because it
cause intense loss of constriction and there is a reflex bradycardia. So if your
patient is
on noradling infusion and there is a sudden bradycardia after giving some
medications or
flushing something always always always think and check whether noradling has got
flushed or not.
So adeline flush will cause tachycardia but noradling if get flushed will cause
bradycardia.
Do remember about it and thank you for this.
Okay so today's sister Rata came to me and then asking very important question how
much
will he claim this there in this sort of icon injection many of you asked on the
channel.
So whenever you see when the book set is written the dose whenever the return is in
milli-coin
25 milli-kene or 50 milli-kene 1 milli-kene. So come here Dr. Vini. So don't get
confused
on the by the MG return it is written approximate concentration of soda waka is
1000 milli moles
per litre. So basically it's 1 milli-kene or 1 milli-mole per ml. So if you are
giving
25 ml of this solution that means 25 milli-kene or 25 milli-mole. So if you are
giving 50 ml
that means 50 milli-kene or 50 milli-kene. So do it more about it go and check and
you
ask it thank you. Okay so with me is Dr. Aishi she is from the emergency department
and she came to me
that we had a patient who is on dialysis and patient at dialysis catheter in C2 but
one of the ports
of the dialysis catheter is blocked. So whether we can reverse the flow and do the
dialysis.
So what happens inside the dialysis catheter the ports are arranged in this patient
one is your
proximal port and one is your distal port. Now when we do the dialysis we take the
flow from this end
and then return from this end. So the impure blood is going from this and filter
blood is coming
from this. If you reverse the flow now what will happen the blood impure blood will
go from this
end and then it will go return from this port and then again it can re-circulate
because it will
get sucked into from this port. So it will cause re-circulation and the filtration
and the impurities
will not get cleared that met efficiently. So in emergency you can do that but as
soon as you
get the opportunity to change the dialysis catheter or unblock it. Thank you.
Okay so today Sister Karyshma came to me that how much calcium is present is this
calcium
gluconate valve because when we study the books and read the books we have the dose
of calcium
is written as 9mg, 10mg, 100mg like that. So this is calcium gluconate oil and
impure and in
this calcium gluconate is 50mg per ml. Calcium lactobionate if you needed 87.5mg
but
what is important is equivalent to elemental calcium is 9mg. So you need to
remember that
what is the elemental calcium presenting this calcium gluconate valve. So 1 ml of
this
calcium gluconate valve contains 9mg of calcium elemental calcium. So 10 ml will
contain 90mg of
elemental calcium. So when you calculate the dose of calcium for infusions or other
purposes
always calculate the elemental dose of calcium contained in this sample. Do read
more about it
and thank you for asking. Okay so one very important point while choosing the
antibiotics or finalizing
the antibiotics for critically efficient in ISU other than like what is the renal
substance,
what are the liver functions but one very important point is which organ or which
place you need to
target from the antibiotics like for example polymixin B it is less nephrotoxic but
it cannot be used
in complicated UTI because it will not act there. T.G. cycling though it is a good
drug but it will
not penetrate in the lungs so it is not that much useful. Seftrag zone for example
it has
got a very good concentration in the biliary tract. So you need to also keep in
mind which target
organ you are targeting by those antibiotics and whether the penetration of those
antibiotic
will be there or not. So this is something which plays a very crucial role in
prescribing the
antibiotics for the patient intensive care unit. Do read more about it and we will
keep on posting
all different antibiotics in the air future. Thank you. Okay so all those who are
working in the ISU
and in the ER they know the term which is known as VLI, VILI, ventilator induced
lung injury.
But do you know there is one more term which is known as SILI or CILI. It means
self-inflicted
lung injury or self-induced lung injury. What happens in patients who are extremely
tachypneic
who are on ventilator or on an IV they inspire too deeply and they are very
tachypneic. So this
relates to inflammatory markers at times which causes injury to the lung
themselves. So how to
treat it? Treat the cause so that the patient's tachypnei is settled and the
respiration becomes
normal either by improving or if you are taking on the ventilator or taking control
of the ventilator
or adjusting the center of an IV. But you need to be aware of this term and I, SILI
because it
can come in the exam or in the literature which you will do read more about it VLI
and CILI and CILI.
Okay so one of the question as on the channel is which fluid we should prefer in
diabetic
ketoacidosis. It's a normal SILI or 0.45% SILI and now half normal SILI. So
basically we need
to understand two things. One the decay patients are severely knee-headed usually.
So and they are
because of that they are demodynamically unstable. So initially we should
resuscitate with normal
SILI because the patient is demodynamically unstable and the normal SILI the
maximum fluid will remain
in the intellectual compartment among all the fluid available for the team. But
once your
hemodynamic stability is achieved you need to collect the cellular dehydration. For
that you
need to shift to 0.45% SILI. Also too much of normal SILI can cause normal and n-
gap
metabolic acidosis which will be reduced by a 0.45% SILI. You can go through the
algorithm,
beautiful algorithm given in the Harrison internal medicine book. Do worry about
it. Thank you.
Okay so yesterday one of the members asked on the channel what do you invest in the
lab? So the
member is a fresh medical student. So basically whenever patient undergoes eotic
wall surgery or
mitral wall surgery these walls are foreign body to the patient's body. So what
happens
the walls move like this but with due course of time there is a wear and tear and
there is
tendency of clot formation across the well leaflets. So with time if we don't give
any
antivolation the wall the club because of clot formation these wall movements get
stuck and now
there is no forward flow of blood from the heart. So the walls get stuck. That's
why these patients
tends to remain on antivolation therapy these patients especially who are on
metallic walls.
So that's why whenever patients of well-lared heart surgery comes with shortness of
breath always
keep a differential of stuck wall disease because it's an emergency and we need to
thambulae this
patient. So do read more about it and thank you for the question. Okay so today's
ICU short is very
important. So whenever you see a patient in the emergency room or the ICU who had a
history of
well-lared heart replacement whether it's a eotic wall or mitral wall and present
with shortness
of breath. So there can be many differentials like congestive heart failure, new
MI, new acute
coronation room but you should always always always keep in mind a differential of
stuck wall. So you
should try to hear the clicks on us condition at times you may not find if it's not
metallic
you should try to get eco as soon as possible to see the well-lared structure. Also
try to get
history from the attendance what was the last INR was there if he was or she wasn't
monitoring
but always keep a differential of stuck wall because you need to thrombolae this
patient
for the stuck wall otherwise this patient will not improve and succumb. So always
keep a
differential diagnosis of stuck wall in a patient of most well-lared replacement
who present
with shortness of breath. Thank you. Okay so I have seen many ICU residents
discussing with each other
that this was a patient of renal failure and somebody has given a wringer lectured
or some
junior resident or because of the nursing staff the wringer lectured has been given
to the patient and
the patient can collapse because of the hyperkalemia. So you need to understand
that how much
potassium is there in the wringer lectured. So wringer lectured has only five milli
cleans of
approximately cleans of a potassium in one liter of wringer lectured RL. So if you
have given 500 ml
of Ringer lectured, so that will contain only 2.5 milli cleans. So obviously you
need to change
it but there is no need of getting panicking if you have given 200, 300 or even 500
ml of
Ringer lectured repression with AKI. So don't be afraid of that do read more about
it go and
check the amount of potassium in the various fluids contents present in ICU. Thank
you.
Okay so whenever you encounter a patient of subarachnoid hemorrhage always try to
inquire what is the
etiology whether it's a spontaneous subarachnoid hemorrhage or traumatic
subarachnoid hemorrhage.
Why is it important because the etiology is different. In spontaneous subarachnoid
hemorrhage
usually they are due to perianulism or anilosomal bleed in which the timing of
coiling and clipping is very important. You need to as soon as possible coil or
clip the aneurysm.
While in traumatic assays the etlose difference it is due to trauma so it is not
due to aneurysm
so chances of re-bleed are less. So how do you differentiate on the city usually in
traumatic it's a peripheral sort of distribution. Oh central can be there but it's
more
as peripheral. While in spontaneous subarachnoid hemorrhage usually there is
central distribution
of blood is more and peripheral is less. This is one of the differentiating
pictures but always on
the history try to find out whether it's a traumatic or spontaneous do read more
about it. Thank you.
Okay so today one of the members on the channel asked a very interesting question
that why we call
it permissive hypercapnia and ARDS. Basically you need to understand that
ventilation means
basically we are dealing with PCO2. So minute ventilation is your tidal volume into
respiratory
rate that's what you call minute ventilation. In ARDS you need to give low tidal
volume ventilation
with high respiratory rate so you decrease the tidal volume. So when you decrease
the tidal volume
your minute ventilation gets decreased. So if minute ventilation gets decreased
your
PCO2 level starts rising in the body. So to protect the lung and to ventilate
according to
the ARDS protocol we allow or we permit the PCO2 level to rise to up to a certain
level. So that's
why we call it permissive hypercapnia. So it is allowed up to the pH of 7.15 where
the respiratory
acidosis develops up to 7.15 it's okay and if it more than that then we take the
measures to correct
it do read more about it. Thank you. Okay so whenever you see the PO2 of the
patient you always look
at the FR2 one which how much FR2 is the this PO2 is coming in a similar fashion
whenever you
see the PCO2 of the patient you should always look at the pH because if the PCO2
has risen acutely
that will change the pH of the patient. Now the resident came to me in the morning
that
PCO2 has gone up from 4950 to 71 I asked what is the pH so pH is 7.35 slightly
actually below 7.35
and I asked how in the patient so the patient was conscious following no issues
there.
As we can see the yesterday's pH was 40 and the proxy 50 and the pH is slightly on
the
alkalotic side. If you see the previously also the PCO2 somewhere around 48 and the
pH is on
the alkalotic side. So this P2 2 side neurons is somewhat close to have normal PCO2
which you
should be having so always remember this. Okay a member on the channel asked today
that what do we
mean by fluid challenge what specifically mean by fluid challenge how we should do
it. So fluid
challenge is done when you are not sure that this patient may or may not respond to
fluid whether
we should give flow to this patient or not. So it's not about giving one letter of
fluid over a
period of 10 minutes because suppose if the patient is not fluid responsive you may
land up giving
one letter positive fluid balance to the patient and it can be harmful. So it's
about 100 to 200
ml of fluid over a period of 5 to 10 minutes and monitoring the response. You need
to give
100 to 100 ml of fluid over a period of 5 to 10 minutes and you should monitor
whether the cardiac
output of the patient is included. Okay so we had a patient of pancreatitis and Dr.
Shudharpma
came to us that whether we should repeat the lapis label to see whether the
patients
pancreatitis improving or not. So lapis label more than three times the normal
range is good enough
for diagnosing the pancreatitis along with UAG and other findings but lapis level
has no role
in predicting the severity of the pancreatitis as well as their decreasing trend
does not correlate
with improving trend of the patient or improving pancreatitis. So it's once you
have diagnosed
pancreatitis then lapis level has got no role. Rather CRP levels are more important
for assessing
the severity of the patient's CRP levels increasing CRP levels of levels more than
200 or 190
predicts that the patient is having a severe pancreatitis. So remember lapis only
for diagnosis
but not for assessing severity or progenostication in pancreatitis. Thank you.
Okay so I was reading the hematodynamic chapter and the other literature because I
need to
provide a lecture on the modanamine one thing. So I came across a very interesting
question of
the member and also the answer of it. The member has answered that sir what do you
invite fluid
responsiveness in a patient? So the only accepted definition is increase in your
cardiac output
or stroke volume by 10 to 15 percent by giving a fluid challenge that means the
patient is
fluid responsiveness. So all other parameters increase in the map or increase in
the CET or
decrease in the heart rate, pancreatic cardiac. All these things are indirect
things they are not
considered as a marker of fluid responsiveness. The only accepted definition is
increase in the
cardiac output or stroke volume by 10 to 15 percent by giving a fluid challenge is
known as fluid
responsiveness. We will see in detail in the hematodynamic class which we are
planning. Thank you.
So today's question was I have one of the resident methods. The tendency in the
hydrosa should be given to septic shock patients. So there was a trial which came
out in 2022
low VIT. In this they endowed patients who were in septic shock means they were
having
sufficient a little bit of modeling support and to some patient they gave hydrosas
of
a tarmine C 50 milligram per kg every 6 early and to other patients they didn't
give anything.
It was a placebo and at the end of the trial they found that in the tarmine C group
we need
of return replacement therapy or mechanical ventilation or there was a little bit
higher
mortality. But the catch of this study was in patients whom they gave vitamin C
they didn't
give hydrocortizone or thymine which was usual practice in giving septic shock. So
this I think
was something flaw about this study but if you ask us we will give hydrocortizone
we will give
thymine and then add vitamin C into this if patient is very in septic shock do read
more about it.
Thank you. Okay so predicting invasive candidate assays is typically a clinical
judgment it is
based on the clinical scenario of the patient but to help you out there is a score
called
Candida score only four things you need to see whether they are present or absent
and in the end
you need to add them up. So the four things you need to see whether the patient is
on TPM total
parent or nutrition second whether the patient is undergone any surgery. Thirdly
whether there
is a multifocal candidate colonization like in the urine also coming in the trickle
aspirate also
coming or in the purse or something here means multifocal more than two sides
colonization is
coming of Candida. Thirdly whether the patient is in severe sepsis which translates
into septic
shock. So if one score for TPM one for surgery one for multifocal colonizations and
two for
severe sepsis. Now if you add them all if the score is less than three then it is
highly
improbable this patient to have in basic Candida assays. So this is a very good
tool do read more
about it Candida score. Thank you. Okay so today's short is very very important and
if you are
working in intensive care team or ICU you should share this short with every member
of your intensive
care emergency team whether it's a doctor or not. So basically in pregnant females
who are in the
second trimester or third trimester the normal PCO to levels in such patients is
somewhere around
30 because of the gravity uterus and the physiological changes. Now PCO2 is an an
acid so if suppose this
patient needs to get ventilated for any cause and if you target a PCO2 of somewhere
40 which is
normal in normal patients now this 40 will cause respiratory acidosis in such
patient and this
respiratory acidosis is harmful to the fetus and it will cause fetal acidosis. So a
patient who's
in the second trimester or third trimester when or she gets ventilated you should
target a PCO2
level of somewhere around 30 on the mechanical ventilator. So this fact is very
very important
do read more about this and again do share with every member of ICU in emergency.
Thank you.
Okay so everybody who is working in the ICU must have known about nasogastic tube
which you call
as rhizal tube. So what are the indications of putting this nasogastic tube? So 99%
of time it
is only three indications. One is if your patient is mechanically ventilated and if
you are expecting
the patient going to ventilator for more than 24 hours second if you want to keep
the stomach
empty like in surgeries, abdominal surgeries, or gastric surgeries or the patient
is having
excessive omeptings then you need to put a nasogastic tube. Thirdly if the patient
is not
able to tolerate the oral fluids and you want to feed the patient then well through
entral root
you need to put a nasogastic tube when you feed the patients. Why it is important
to
know the indication because if it is there in place in a patient unnecessarily it
is non-indicated
then it increases the patient discomfort and increases the chances of aspiration.
So go and
check in your ICU what are the indications for which you have put an NG tube in a
patient.
Do read more about it. Thank you. So today we want to show you this trackway which
is put on the
tracheostomy tube. You can see here. Now whenever you put in the patient from
tracheostomy this is
very crucial and this is important. This serves three purposes. One whenever you
put the patient
on TPs there is chance of accident and some foreign particleization this prevents
that because
there are no openings in this no solid opening. So foreign body ingestion
inhalation can be
prevented. Secondly we have bypassed the oral trache vasopharynx and sarynx so
there is not
getting humidified. But through this trackway what happens when the patient exhales
this air get
absorbed and the moisture gets absorbed and heated and the heat is absorbed and the
patient when
inhales that heat and moisture will go to the patient bed so it gets humidified.
Thirdly you
can see there is an oxygen port also by which you can provide oxygen to the
patient. So this
is very crucial when you bring the patient from ventilator and on the tracheostomy
tube. Do read
more about it. Thank you. Okay so sister Kresmer just came to me and asked us how
this HME filter works.
So all those who are working in the ICU they must have seen this heat and moisture
exchange filter.
It is put in the ventilator tubing. So what happens when we put the patient on
ventilator
the bypass is the normal heated moisture exchange system of the normal human body
knows
pore of the rings straight here. What does this do is whenever the patient exhales
on ventilator
it captures the heating moisture from that breath and when the ventilator pushes
the air back to
the patient that air gets mixed with this heated moisture which is there in the
exhalation bed.
So that's why the patient receives and heated moisture exchange breath from the
ventilator.
This is how it works and do read more about it and thank you for asking this
question.
Okay so in almost all the ICUs everybody must have given DPS trial. So what should
be the ideal duration
of DPS trial whether it should be contaminated or whether it should be in two hours
from one
per day max. So in the study we have seen that that HME strip trial is as good as
120 minutes
of DPS trial. So in our practice we usually give 60 minutes of DPS trial but that
too you need to
be cautious especially in COPD patients. In COPD patients we avoid TPS trial
because they retain CO2
and COPD trials once we say that the patient is maintaining on minimum pressure
support
on spontaneous mode ventilation on venting then we did a blood do a blood test and
then we
extubate to NIV in such patients. So read more about DPS trial 30 minutes versus
120 minutes
studies show both are same but in our practice we usually do one hour DPS trial do
read more about it.
Okay so almost all those persons who are working in the intensive care only they
must
say come across medazalam and all other sopamis. So have you wondered why medazalam
can be given by
infusion but loresopam is never heard of that infusion very rarely loresopam has
been heard
as infusion. So why is it so? So basically two differences. One is loresopam is a
little bit
long acting for anything to be given infusion it should be short acting so that we
can tolerate
the dose but the most important thing is the preservative in loresopam is ethylene
glycol or
propylene glycol and it causes propylene glycol toxicity which is similar to
ethylene glycol
toxicity and there have been case report on this. So because of this propylene
glycol toxicity
loresopam is never used as an infusion in any patient. So go and check in your ICU
see the loresopam
while and fuel check what is the preservative and do read more about it. Thank you.
Okay so whenever you come across a patient of reflective hypokalemia, reflective
hypokalemia means
in spite of giving lots and lots of potassium the potassium level of the patient is
not getting
collected always suspect hypomegisemia in these patients. So what happens in the
kidney in the
cortical connecting tubules and the collecting tubules? There are channels called
ROMK. So what
these channels do they secrete potassium from the intracellular side to the
interluminal side.
So these are normally inhibited by magnesium. In magnesium deficiency these
channels are non
non-inhibited and the potassium will get excreted or secreted into the tubule lumen
and get lores.
So what you need to do either send the magnesium levels or if not available then
what you need to
do? Give 1 or 2 gram of magnesium in 100 ml of D5-NS over 1 or 2 hours along with
the potassium
and then cross check potassium levels after 12 hours. Most of the time it got
corrected.
So this is something you need to know reflective hypokalemia due to hypomegisemia.
Do read more about
it. Okay so heparin is something which is very commonly used in the ICU almost
every ICU
is heparin. So any new team member whether nursing staff or doctor or technician
should know this
very important fact that heparin comes under 2 strength. Both are of 5 ml and but
one
5 ml contains 5000 units of heparin. Other contains 25 000 of heparin. So one ml of
this
5000 contains 1000 per ml of heparin and another one can will contain which
contains 25000
5 ml it will contain 5000 per ml of heparin. So always cross check from which while
you are
taking the heparin because otherwise the dose will not be the dose which is written
in the
instructions. So do check and do read more about it.
Okay so 2, 3, 2 days back we posted a youtube shot in which we explained what is
minoka. Myocardial
infection with non-obstructive coronary arteries. So MI has happened to the patient
but when you
do the endography there is non-obstructure means all the vessels in all the vessel
could not find
the blockage more than 50%. So one of the users asked a very important question
very good question
then if it is minoka then what is Prince battle angina. So Prince battle angina
occurs due to
the coronary vessels spasm because of which the patient will angina and in the
youtube shot we
told that once you find out minoka you need to look for the causes pathophysiology
of this minoka
what is happening. So Prince battle angina is one of the pathophysiology which can
explain
your minoka. There could be other causes also like severe eutics, nurses,
hypertension,
certain drugs, shunts, myocarditis etc. So do read minoka and Prince mitral angina
again
and thank you for this question. Okay so while working in the intensive care unit
and emergency
you must have come across the patients of acute pancreatitis. So how to put in the
severity of
acute pancreatitis? So there are different scoring system one of the most common is
rinscent but
the problem with rinscent score it it takes 48 hours to get completed. So there is
one more
criteria which is known as BISAP criteria BISAP. So B stands for blood urea
nitrogen more than 25.
I stand for impaired mental status S stands for SARS systemic inflammatory response
H stands for H more than 60 and P stands for plural effusion. So one point is
assigned to every
condition which is present on admission and if the score is more than or equal to 3
then the chances of creating this patient converted to severe pancreatitis or the
complication of pancreatitis is very high. So just try any of your new patients who
will come
across try BISAP scoring BISAP. Do read more about it. Thank you. Okay so many
times we have
told you in the previous videos also that you should keep a watch on PCO2 in the
tachypneic
patients. So if the PCO2 is rising that means the patient is getting fatigued and
now is or she
is not able to ventilate properly so the PCO2 is detailing. But very important
point I would
like to mention here in a tachypneic patient especially if it is a asthymatic
patients or
GBS patients or myesthenia patient. The patients remains tachypneic even on that
tachypnea if your
PCO2 is in a high normal range like 40, 45 that is also abnormal. You should keep a
watch on it
because in a tachypne patient PCO2 should wash out it which should be somewhere
around 30,
35 but it is even high normal range like 40, 45 that means this patient require and
I will
support or respiratory muscle support because this patient is on the verge of
getting collapse.
So high normal PCO2 in a tachypneic patient is also abnormal do remember about it.
So all of you should know this term also is menoka it means myocardial infarction
with
non-obstructive coronary arteries means this patient presented with classical of MI
stelivation but when an angiography was done there is no obstructive coronary
artery disease.
Non-obstructive coronary artery disease means any lesion on the coronary
angiography is not
more than 50% of the vasalumen. So it is always a working diagnosis because you
need to work
up this patient and find any other cause which has caused estalivation or any MI in
this particular
patient but at times you are not able to find any cause then this patient is
labeled as menoka
means myocardial infarction with non-obstructive coronary artery disease. Still
these patients are
put on dual interpretive because the risk of MI is still in these patients. This is
important one
do read more about this topic just go and search menoka in text or on the net thank
you.
So everyone of you must have used calcium for any of your issues for giving to
hypercalemic
patients or patient who is any calcium deficiency but do you know that calcium
comes in two forms
one is calcium gl Hurryenate and the other one is calcium glu Attic. The difference
between calcium
gluattering and calcium chloride is the amount of calcium present in calcium glu
Brittany streamed or of the amounts of calcium present in calcium chloride or
otherwise you can
see calcium chloride contains three times the amount of elemental calcium present
in calcium
glu
so most of the issues calcium glu
because calcium glu
calcium chloride is too concentrated and it can
extra-activate from the vein and it can cause tissue necrosis but in
cases of severe hypoglycemia, calcium chloride
is being used. So do check any issue which one you are using
calcium gluconate or calcium chloride. Do read more about it. Thank you.
Okay we all know that there is a stolic blood pressure and diastolic blood pressure
and the whole body gets perfumed during systole and diastole
but you know that the cormy vessels, especially the cormy vessels,
supplying the left ventricle are perfused during the
diastolic. Why it is important? Because left ventricle is a muscular structure
and it squeezes during systole. The vessel which are traveling from
apicardium to subalducardium. The cormy vessels, they get squeezed and
therefore the blood supply is empowered. That's why when the ventricle
relaxes during diastole, the blood flow from apicardium to subalducardium and
it gets perfused. That's why it is very important that
anything which is compromising the diastolic
excessive tecicardium or low diastolic pressure like in
sepsis, we need to be more vigilant about
maintaining optimum heart rate and optimum diastolic pressure if not
then, mean arterial pressure because it is the perfusion pressure.
So this is interesting. Do read more about it. It's very very important.
Thank you. Okay so today's question is what is the
control and cut-off value of blood pressure in hemorrhagic strokes?
So basically why we want to control the blood pressure in the
intracranial blade? Because we think that if the bleepy remains high there can
chances of increasing the hematoma size or increasing the size of bleeding in
case of intracranial blade. So there was an
interact-to trial which compared blood pressure, systolic blood pressure of 180
versus 140. They found that in both the blood pressure
the hematoma size remained the same and there was no increase in the
deaths but the disability score ranking scores was better in which 140 was the
target maintain. There was another trial attached to
trial which compared blood pressure of systolic 110 versus 140.
They found that again the size remained the same but renal complications are
more in which we keep the blood pressure low at 110.
So blood systolic blood pressure somewhere around 140 and diastolic less
than 100 is a reasonable target in hemorrhagic strokes.
Do read more about it. Okay a very good question was asked by one of the
member that sir what is the difference between
pressure support above peep on ventilator and how does it correlate to
hyperpepe? So in a simplified way just understand that
a pressure which is present or applied throughout the respiratory cycle
is your e-pep or peep or seepep. This is a constant pressure which is
applied throughout the respiratory cycle. About this pressure
whatever pressure is applied during the
insprestry phase of the respiration is your called
IPep or pressure support above peep. So to understand better
I am giving the link of a little detail video in the description of this
youtube short. Do read more about it and thank you for this question.
Okay so whenever you come across a patient who has suffered
a renal insult in the ICU we usually use the term acute kidney injury
means AKI or patient was having CKD chronic kidney disease
or acute on chronic kidney disease. So acute kidney injury and chronic kidney
disease. So have you ever come across a term which is
known as acute kidney disease? Means AKD. Now so many of you must
know that but those who don't know so if acute kidney injury recovers within
seven days that is fine that we call it acute kidney injury.
But if the acute kidney injury persists beyond seven days
and gets recovered within 90 days then we call it acute kidney disease
and if the acute kidney injury persists beyond 90 days then we call it
chronic kidney disease. So between seven to 90 days we call it acute kidney
disease. This is interesting do share with your friends and do read more
about it. Thank you. Okay so today's question which was
this. What should be the loading dose of antibiotics in renal failure?
Basically you need to understand the concept of loading dose. Loading
dose is of antibiotics given so that the MIC level of the antibiotics is
released a little bit early. For example in college time if you don't
give the loading dose you start with the maintenance dose like 3MIOTDs.
It takes about five days to reach its MIC level. While if the same drug
if you give with loading dose followed by the maintenance dose
it reaches still it takes 48 hours. So loading dose is something
which is not dependent on the creating levels even if your creating levels
are high even if the patient is on dialysis then also your loading
dose doesn't require it should be given as it is and the maintenance
dose gets adjusted according to the creating or the dialysis status of the
patient. So this is important do read more about it.
Thank you. Okay so from today onwards we'll try to respond to some of the
comments by making youtube shots. So today's question was regarding thymine.
What is the dose of thymine in alcohol withdrawal or bernicase and
keflopethi? So for the prevention of bernicase and
keflopethi the dose is 100 to 200 milligram
once a day for three to five days and for bernicase and keflopethi treatment
the dose is 200 to 500 milligram thrice a day for two to seven days followed
by 250 milligram once a day for three to five days. I have taken the
reference from up to date dot com and you can also review any intensive care
medicine text and now go and check in your ICUs. What is the amount
present in one ampoule of thymine which you are giving to the patients?
Thank you. Okay so today's tip is whenever you receive an alcoholic patient
withdrawal user or a kekak sick patient or
manelar is patient always give thymine before giving dextrose to this patient.
Why it is important? Because thymine is required for many enzymes
and in the absence of which glucose get metabolized and it also acts in
pentose phosphate pathway also. If thymine is not there then your glucose
administered glucose will get converted into lactic acidosis
and also the oxygen free radicals will not get
utilized or neutralized because of thymine deficiency. So a patient can
land in bernicase and keflopethi. So always give thymine in such
patient before giving to the patients 100 mg
sufficient but some centers give 300 mg stat
and then followed by dextrose. So do read more about this
thymine before dextrose in alcoholic or malleter's patient. Thank you.
Okay we all know that propofol is very commonly used in the intensive care unit
especially in the neuro patients but whenever your
patient is on propofol infusion you should know one terminology one
syndrome which can happen is propofol related infusion syndrome which is
commonly known as pris. It can happen when your
propofol dose exceeds 4 mg per kg per hour and then fusion is beyond
48 hours though the thymine may vary but how it will present?
It can present with unexplained metabolic acidosis,
rhebdomylases, cardiovascular collapse, renal failure,
hyperlipidemia and it should be picked up early
and the infusion should be stopped and the treatment is largely supportive.
Why it should be immediately stopped because the modulate rates are little
higher in that. So whenever your patient of propofol
infusion syndrome propofol infusion if you find
unexplained metabolic acidosis in features of rhebdomylases and renal
failure always think of this entity and do read more about pris.
Thank you. Okay so we all know that acute mitotic
inflection is divided into two types one is stamming and other one is
n-stamming but academically when you will call this
stamming means st segment elevation mi on the basis of ECG.
So a patient will present with classical symptoms of chest pain or
mi and then in the ECG when you see it should be
st elevation of more than 1 mm in two contagious leads.
Means two contagious leads it should be more than 1 mm
but specifically for lead V2 and V3 if it is a female it should be more than
1.5 mm and if it is a male patient then if the age is less than 40
it should be more than 2.5 mm in lead V2 and V3
and if it is age is more than 40 then the STS segment elevation should be
more than 2 mm in lead V2 and V3. So this is
academically but for all practical purposes any patient with chest pain
and there is an STS segment elevation of more than 1 mm in two contagious lead
we call it stamming. Do read more about it. Thank you.
Okay with me is Dr. Vivek, Jitendra and Virendra also there who works as
gastro technician with our team and today they want to show a case of
Virendra basically need to understand the difference between
Mallori Vister and Virendra and Mallori Vister it is a mucosal tear in the inner
lining of the esophagus which can be managed conservatively
at times it can be life threatening for which endoscoping interventions are
required but Virendra is transmural tear the whole esophagus is tear and it is
it is life threatening which can cause media snities, demon
media stanam, septicemia and multi organ failure. So we'll show you a few
images in which they have put a self inflating
stand which was life saving. Do read more about this topic.
So this is the esophagus and this is the whole tear in the
esophagus lining. This is the vent here. Now we'll see the
vent. You can see this is self expandable metallic
strength is placed and the vent has closed.
Okay so with me is Dr. Vivek Dixip. He is a guest entologist
in our team and today while discussing he gave a very important tip
that in serotic patients where many patients when we prescribe vitamin K
injection most of the residents and staff rights injection vitamin K
1M fuel OD. So basically always you need to
write the strength of vitamin K. It comes in two strengths one is 10 mg
and one is 1 mg. So for adult 10 mg should be prescribed
and for pediatric population 1 mg is prescribed. So many times he has seen
that when the vitamin K 1M fuel is written most of the time at most not
most of the time but at times instead of 10 mg
1 mg amp fuel comes and then the effect of the dose doesn't come to
that extent. So next time whenever you write injection vitamin K
always write injection vitamin K 10 mg for adult and injection
vitamin K 1 mg for pediatric population. So do read more about this topic.
Thank you.