Meeting-20250207_163848-Meeting Recording

2025 年 2 月 7 日, 上午 08:38
3 小时 18 分钟 40 秒

Asst. Prof. Dr. Muhammad Junaid Farrukh 0:03

Are wait, let me see. Am I recording already or not?

Koh Siew Hua 已开始听录

Asst. Prof. Dr. Muhammad Junaid Farrukh 0:21

So we will be covering some conditions under cardiovascular system. So
Systemwise body system wise we will see different types of conditions
and diseases like cardiovascular diseases then endocrine system we will
touch and see some of the important conditions under endocrine
disorders. Then we will have gastrointestinal disorders.
So GI disorders is I think 6 hours, the most, heaviest 1.
Then we have musculoskeletal diseases, nervous system disorders, blood
disorders, haematological disorders, renal functions, pulmonary diseases,
and finally a general topic which is medicine management in the aged
population. So basically from head to toe, we will be covering all kinds of
system and important diseases related to that.
And some of those topics we will cover through the case studies. So like
every subject.
We will be having three case studies under this course, one from
cardiotopic, one from Renaltopic and one from pulmonary topic.
And as usual, the there's also similar your previous courses, the CBL
discussion and presentation is the heaviest 30% and the case report is
15%, followed by the final examination which is 55%. OK, so from here
you can secure maximum of your internal marks by preparing.
Nice slides, less spelling and errors.
And try to practise it before you come and present in the class. So like this
you will easily secure maximum marks in your.
Internal assessment so that when it comes to final examination, the
pressure on you will be less.
OK, so the reference books are mentioned here. We will be using the Piro
and Femicotherapy case books and the CPG guidelines. So in each topic I
will tell you that this guidelines or what references to follow and majority
of the information I already put in the slides.
So if we take a look at the teaching plan.
So our classes will be on Thursdays and Fridays 4, so 4 Thursdays are
involved and the rest of the classes will be on the Fridays only. And this
course will only be taught by me. No other lecturer will be involved.
So today, so now I'm giving you the course briefing and we will start with
cardiovascular system first. OK. So each system there will be some
diseases, we will focus more attention to that and some of the topics will
be minor topics. I will tell you that this one we will not go in too much
details.
Then week two, no lecture. So like this, we will try to follow this and we
will go with our own pace. When you guys are OK, we will proceed. If too
much for that day, we will take breaks and stop. So it is all manageable
between us and then in our week three I will share the first case
discussion with you.
And we will follow the sequence according to the teaching plan. Then you
see you have a big break from week four, week five, week six. So no
lecture is there. And then after that Gap, week seven, we will continue the
remaining lectures.
Associate presentation you have quite long time to prepare.
Then case 2, then one week gap for this presentation, then case 3 and
then finally case 3 presentation.
And final three weeks are also of no lecture, is there?
OK, so this was the introduction about the courses.
And the lecture topics which we will be covering.
OK, so let's.
Start.
Our first topic, which is about the cardiovascular diseases, OK, so
cardiovascular diseases, all the diseases related to heart and
cardiovascular system.
So like always there, you may see some of the information is not in your
hands, out handouts or not being uploaded. So that is, you know some
extra information. Sometimes I like to share or sometimes I want to
explore, you know, explain something more.
Information which we have already studied, I just don't want to make your
slides heavy so I can explain here. And if you want to refer it again, you
can always, you know, watch the downloaded videos.
OK. So in cardiovascular diseases, what we will be focusing on will be the
most common condition which is hypertension, then followed by your
acute coronary syndrome, ischemic heart disease, angina, unstable
angina, myocardial infarction, it is all clumped under acute coronary
syndrome or we also call it as CAD, which is coronary artery disease.
And some of the topic like atrial fibrillation.
We can cover under case studies in the form of case studies as well. OK,
so the format will be the same that first we will learn about the
introduction to that disease and then what are the common sign and
symptoms on the diagnosis part. We will not push much attention just
overall that OK, these are the diagnostic tools because diagnosis is mainly
the.
Task of the doctor or physician. But we should know that what which are
being used.
So when they share the information with us, we are aware of that, that
these are the tools which are used for diagnosis and then main focus will
be on the pharmacotherapy part that what are the goals of therapies,
what are the drugs involved and then background information, what is the
classification of this drug and then we zoom into the clinical practises
guidelines. So sometimes we can compare.
Different country guidelines also like if Malaysia guidelines say this.
What European guidelines says what Canadian guidelines says or
American guidelines says, what are the similarities or what are the
differences, you know like that?
OK, hypertension. So we already know hypertension is the elevated blood
pressure when your blood pressure is high, we call it hypertension. So
what, what is the normal blood pressure reading? Can anyone tell me?
What is a normal reading of blood pressure?
No one knows the normal how much.

Koh Siew Hua 8:06

And it's.
Very hundred 2480 millimetre mercury.

Asst. Prof. Dr. Muhammad Junaid Farrukh 8:12

120 by 80 is considered as the normal blood pressure. Correct? OK. So
when we go into further, the definitions of hypertension or the staging of
hypertension, you may see some variation among different sources and it
can vary from country to country. Like CPG, Malaysia has different cut off
values for the staging and the American or the European guidelines, they
follow some.
Slightly different cut off for the staging.
So for your final exams, we will always follow the Malaysian guidelines and
the Malaysian cut off points to standardise it. OK, so in general.
The persistent elevation of blood pressure of more than 140 and 90 is
considered as hypertension.
So what is blood pressure? Blood pressure is basically a combination of
cardiac output and the systemic vascular resistance. OK, what is
systemic? Vascular resistance that in our blood vessel, when the blood is
flowing, how much pressure is being exerted from the?
Vessels, all the vescular walls. So this thing combined into blood pressure.
So in easier words, how to you know, remember what is blood pressure? It
is the cardiac output and the resistance or the pressure exerted by the
walls, the vessels.
OK, so let's see further theory about the blood pressure. It is the force of
the blood against the walls of the arteries. So consider this. This is the
artery or the vein vessel inside is the blood is flowing. So whatever the
pressure it it will exert on the outer walls the walls of the vessels.
And then in a person, this actually varies with different activities across
the day, night and from one day to another. So all this pressure consistent
throughout the day for the nonhypertensive person also like if you don't
have hypertension still there will be fluctuations in our blood pressure
which depends on our activity. You know of course if we are at resting
state, if we are sitting calmly.
On our chair, the blood pressure will be different, but when you start doing
some activity normal activity there will be slight change in the blood
pressure.
Compared to, let's say you are doing some exercise, you go to treadmill,
you do running, then suddenly you will see the hard disc pumping very
fast. You feel the blood coming on your face so that the blood is
increasing in that state. So it depends on different activities. The blood
pressure will never be the same in all kinds of our activities.
OK. And then?
One or two incidents of, you know, the blood pressure can be increased. It
is not considered that you have developed hypertension. So hypertension
is when consistently your blood pressure is high and then you have to
take two separate readings average and you know then for doctor then
only you will be qualified as a hypertensive case. If you have only one
reading and that also.
You know on and off and it is not consistent, then it is not up hypertension
stage.
And then what is the benefit of controlling this blood pressure, so lowering
the blood pressure just even 5 millimetre of mercury can significantly
lower the chance of developing serious health problems? OK, so.
The question is if patient has developed the high blood pressure, what will
be the effect on the person's body OK.
So I will explain that later. Let's see some of the classification. So this is
according to the American Heart Association. So according to that, so 120
by 80 is considered normal. So this one all guidelines agree upon that. So
from 1:20 to 1:30 and less than 80, it is considered as elevated blood
pressure.
So it is not under any staging, so this is just elevated blood pressure for
stage one of hypertension. When you have 1311439.
And 8289, so diastolic.
Then for stage two is 140 and above.
Or 90 or higher in the diastolic range and hypertensive crisis is normally it
is 180 and above.
So later we will study in detail that what is hypertension crisis, what are
different types of hypertensive crisis and how to manage it.
OK, so this is the according to Malaysia, the CPG guidelines. So here you
see that stage one is 140 and above and 1:30 to 1:39, we still consider it
at the pre hypertension or at the risk of hypertension. So see, this is the
difference between the American guidelines in which 13239 is already
stage 1, whereas in Malaysian guidelines.
Only 140 and above will be considered as stage 2 and so on.
Stage two stage 3 like that.
OK, so of course it will depend on the healthcare setting and the doctors
that what guidelines they follow, but the more strict control we the more
better outcome the patient will be.
OK, so this is our revision to what happens in the renin NGOs, Tencent
aldosterone system, RAAS system. Basically this is the system which is
responsible to regulate the blood pressure.
OK, so we may discuss hypertension topic in detail because later on in
heart failure, the drugs will be the same. So we will not go in detail under
the heart failure chapter. So let's see some of the basics and background
information for the hypertension. So what happens is that after the NGO
Tencinogen which is released by the liver and then and this
angiotensinogen is converted by Rennin Kidney release, the renin.
And it is converted into Angiotensinine 1 and this angiotensin one is
convert by the ACE enzyme into angiotensin 2 and you here you can see
that when angiotensinine one is converted.
Into endogenous in two you can see that basal constriction the vessel is
getting narrower so vessel is getting narrower. The pressure blood
pressure will increase.
OK. And on the other hand, the aldosterone is also being released and this
stimulates the reabsorption of sodium and water. So in this way the
normal.
Water regulation and sodium water retention and regulation is being
managed by this RAAS system. So when we the body feels that they need
to conserve the water then it will cause vasoconstriction. When they feel
that blood pressure is now going high, it needs to come down
immediately. The enzymes will stop and.
Vasodilation will occur so this will do automatically on its own.
OK, wait.
So.
First, arterial blood pressure is right.
Regulated by pressure neurons called battle receptors located in the
aortic arch and carted sinuses.
So for example, if blood pressure falls too low, those baroreceptors can
send signals to the adrenal medulla, causing release of catecholamines
and thus increase in sympathetic activity through activation of alpha and
beta receptors.
So activation of beta one receptors causes increase in heart rate and
stroke volume.
And thus increase cardiac output, which leads to increase in blood
pressure. On the other hand, activation of A1 receptors on smooth muscle
causes vasa constriction and thus increase in vascular resistance, which
again leads to increase in blood pressure. Now another major system
involved in blood pressure regulation is the renin angiotensin aldosterone
system.
So we also have better receptors in the kidneys that respond to fall and
blood pressure or reduction of blood flow.
By releasing enzyme called renin.
Additionally, renin secretion is also stimulated by sympathetic activation
of beta one receptors in the kidneys. Now renin is necessary for the
production of Tensing 2.
Is a very important vasoconstrictor which constricts systemic blood
vessels, thus increasing peripheral resistance.
Angiotensin 2 also constricts renal blood vessels and stimulates a a
dosant secretion which leads to sodium and water retention, thereby
increase blood volume, cardiac output and ultimately increase blood
pressure.
OK, so when your blood pressure is increased it also reduce the blood
supply to the kidney.
Yeah. So then kidney release more renin and then the angiotensin and
aldosterone system will be there and it will further cause the narrowing of
the arteries and patient will develop hypertension.
1st.
OK, so hypertension now there are various methods or various causes that
how a patient can develop the hypertension. So we divide it into two, one
can be primary or essential hypertension and other is secondary
hypertension. OK. So what is primary hypertension which is majority of the
time you know 90 to 90% of the case is.
Of primary hypertension, whereas only 5 to 10% of the cases are from the
secondary causes, so primary cause include that when patient has some
genetic factor of the hypertension or they have family history of the
hypertension.
The parents mother's side or father's side. It is in the generation, so we
call it family history of hypertension and 3rd can be by their own.
Lifestyle factors. So smoking, alcohol, dietary patterns, all those things. So
these all are included under primary hypertension whereas secondary
hypertensions are those secondary diseases or conditions which are
indirectly contributing to increase in blood pressure.
So here we can see some of the examples and comparison that what is
primary and what is secondary hypertension.
OK, so like I discussed with you, primary hypertension cause is either a
genetic cause or it can be by family history or it can be through lifestyle
factors.
In the secondary hypertension, it is due to some other diseases. It can be
like kidney disease. It can be some hormone fluctuations or hormonal
disorders or it can be caused by some drugs or some medications.
OK. Then in terms of onset, the primary the hypertension develops
gradually over year, whereas the secondary hypertension, hypertension
can develop suddenly.
And often at younger age.
And the risk factors for primary include family history as the person age,
ageing is also.
You know, phenomena so in elderly patients we see that most likely they
can develop the hypertension. Why? Because of the physiological changes
in the body, the elasticity of the.
Vessels is reduced the cholesterol component in the body is high water
content go low. So these are the normal ageing phenomena.
Obesity is one of the risk factors.
Salt intake. So obesity. Also, we know that due to the deposition of the
cholesterol there will be narrowing of these. We will study this in detail
importance of cholesterol in coronary artery disease and salt intake. So it
will disrupt the salt and water regulation. So when we have more salt
more water retention will be there more volume will be there and it will
you know.
Increase the blood pressure.
That smoking it also causes you know, vasoconstriction. Stress is also
vasoconstrictor and sedentary lifestyle. When you don't do exercise
indirectly, it will cause in you obesity.
OK, So what conditions are causing the secondary hypertension?
Kidney disorders. Hormonal imbalance like Cushing's syndrome or
hyperthyroidism.
OK. Hyperthyroidism. You all know when your thyroid levels are high. So it
will cause the hypertension, whereas Cushing's syndrome, what is
Cushing's syndrome? Can anyone recall what is a Cushing syndrome?
I.
What happens at it? What?
Or.
It is involved here, which one of the?
Hormone.
The Cushing syndrome is basically when.
Your cortisol level, cortisol level, are very high, OK normally, especially
when a patient is on long term of steroid treatment. So this can lead to
Cushion syndrome.
Then the other condition is obstructive sleep apnea. OK, sleep apnea
means that patient feels shortness of breath. Apnea means shortness of
breathing while sleeping. So obstructive sleep apnea while the patient is
sleeping, they feel difficulty in breathing.
So this also leads to hypertension indirectly and then drugs related
medication induced hypertension. There are many drugs later on we will
see, but the common ones can include your birth control pills, the oral
contraceptive pills and your pain killers and saves.
OK, so symptoms, the primary hypertension, usually asymptomatic in the
early stages may lead to headache, dizziness, blurred vision if severe
cases. Whereas in the secondary hypertension, the kidney disease may
cause the swelling hormonal disorder may cause weight gain. So again,
the symptoms will depend on what is the cause if let's say kidney is the
cause.
We will see the symptoms or the.
You know, silence symptoms related to kidney related origin volume
overload will be there. Edoema Formation will be there, which means
kidneys are not functioning properly and the hormonal disorders.
Like, say, Cushing's syndrome or hyper hyperthyroidism, these are most
likely we can see the changes in the weight.
Or even, let's say, diabetes also, so we can see changes in the weight. OK,
for the treatment for primary hypertension. So starting with the lifestyle
modification because here you see lifestyle fact, one of the main will in
the primary hypertension, so diet, exercise, weight loss, all these things
are done. And then if still not.
Controlled then we start NP hypertensive medications for those
medications which control your blood pressure.
Whereas for secondary hypertension, so since secondary hypertension is
developing due to another cause, the secondary caused. So we need to
treat that cause first. We're treating the underlying condition, it helps to
control blood pressure along with antihypertensive drugs because of
course that condition cannot be cured immediately. You have to start the
therapy to treat that underlying cause.
But at the same time, we need to give some medication to the patient so
that the blood pressure can be lower down.
So people with very high blood pressure, usually about 180, which we
classify as hypertensive crisis later on, we will discuss about that and they
can severe some of the common symptoms of hypertension, which
includes your headache, chest pain, dizziness.
Difficulty in breathing, cutting. So these are, you know, common examples
of elevated blood pressure. But blood vision changes.
This needs extreme blood pressure.
Confusion. So this is also associated with when the blood pressure is very
high, extremely high nose bleed, sometimes Nosebleed or sometimes.
Blood shed in the eye. We can see the patients there. The capillaries in
the eye, they burst and there is redness or red patch in the eye. So this is
also happens in persistently elevated.
Blood pressure and at the.
Higher level, very high blood pressure. So these are the common silence
symptoms in the extremely elevated blood pressure. According to who
World Health Organisation.
OK, so this is again the same common symptoms of hypertension,
including the one the patient can experience at mild mildly elevated
hypertension and as well as an extreme hypertension cases. OK. So just
now I already identified those things. So let me revise it again. For
example, headache, dizziness.
This woman, nausea, vomiting.
Be associated in in the earlier stages of the hypertension.
Whereas blood in urine, bloody vision, Nosebleed these kinds of extreme
symptoms are associated when the blood pressure is very high.
Let's say they have some persistent headache and they just take
painkiller panadol for the headache. For the temporary relief, and they're
not investigating that. Why I am feeling headache every day, so if the
patient will be ignorant then the body you know will have this adverse
effect on the other body organ system. So the first thing like your vital
organs like.
Your kidneys. The kidney will start to damage your cognitive function.
Your brain. It will start to.
The vision decline or loss heart diseases will, you know, start to develop
peripheral artery disease will be there.
OK, so why all this thing is happening again? The main concept in
hypertension is when blood pressure is increased, there is a narrow
narrowing of the artery, which means the amount of blood reaching all of
these vital body organ, it is reduced and then in turn it is causing all those
complications and symptoms.
OK, so these are the details of the all list of drugs.
Which can be associated of increasing the blood pressure.
OK, so it's we already discussed this, then the stimulants like
methylphenidate and vitamins, so these are the CNS stimulants, drugs. So
why we need to know all these things. So let's suppose patient come in
the history of blood pressure that oh from last 2-3 weeks, I'm having a
headache. So we need to we need to see the patient medication history.
Because the high blood pressure may be due to the patient medication
which they are taking. So by adjusting the dose maybe we can solve the
issue of hypertension, substitute the drug, reduce the dose of the drug
like this. But if we ignore or if we do not take the patient medication
history and we keep on adding antihypertensive drugs, we may not able
to solve the issue because the causative agents will.
Maybe still in the patient current prescription. So first we need to make
sure that patient is not taking all of these medications.
OK. And this doesn't mean that if these drugs are involved, then we have
to stop those drugs, especially when it comes to the mental health related
drugs, like your antidepressants or hormone related drugs. So because
you don't.
We have to see the risk versus benefit if patient depressive disorder,
bipolar disorder, you know, general anxiety disorder is very high. That risk
factor is very high. We cannot simply stop these drugs. Then we have to
play around with the first, make sure that patient is at the lowest possible
dose.
Then we can see that can we switch this drug and then at the same time
we can introduce antihypertensive drugs to the patient. So it is all case by
case basis of the patient and then then we have some over the counter
medications or health supplements or sometimes even our dietary
ingredients which might be responsible for increasing blood pressure. So
this again?
Why this heading is separate so when we are taking patient history?
We make sure to ask these question as well because let's suppose patient
is out addicted to caffeine. They have two to three or four cups in a day
and patient comes to you and complain that I have headache,
palpitations, increased heartbeat is there. When you check the blood
pressure is high then. Oh then you can start. You know, antihypertensive
drugs to the patient. But if we are not identifying.
That the main reason can be patient dietary patterns like caffeine itself,
caffeine can cause increase in blood pressure.
Or these herbal supplements like ginseng or even, you know, jinco by
Luba. All these memory enhancing supplements. What's the mechanism?
Affection of those memory enhancing supplements that it increase the
blood flow. So when it increase the blood flow patient may develop, you
know, high blood pressure. And then this same joint ward also it is you
know.
Associated with blood pressure and at the same time this Saint John Ward
has.
A lot of drug interactions with other prescription medication and your
energy drinks, like your Red Bull and what else monster drink? So all
these things, they also can be associated with the blood pressure. So we
while history taking, we have to make sure that patient current
medication as well as patient over the counter medication and lifestyle do
not have any conflicting things.
Or a risk factor for patient high blood pressure.
OK, sometimes patient, let's say on medications or without medications,
they may complain. A sudden spike of blood pressure that, oh, suddenly
my blood pressure is increased or suddenly, you know, oh, my headache
is there. Palpitation is there. So why there can be some triggering factor
such as caffeine. So let's suppose during exams students suddenly the.
Caffeine intake is high so that can cause a sudden spike. Spike means
elevation of the blood pressure or suddenly you have some trauma, a
stress or anxiety.
So that can also cause some sudden spike in blood pressure then smoking
smoking normally will. You can say a person who smokes is regularly
doing it, so we rarely see some sudden spikes in smoking unless the
number of the cigarettes or the amount of nicotine or tobacco which the
patient is consuming is increased suddenly. Then yes, we can see some
sudden spike.
OK. Any health complications during pain? So in pain, the physiological
response of the body, we may see some you know?
Spike in the blood pressure. Sudden dehydration. Uh, huh? So we know
just now. We discussed in the RAAS system the remnants aldosterone
system. So which regulates the sodium and water level. So when there is
suddenly drop off the water then sodium retention will be high and this
will increase in the blood pressure.
So thyroid complications, so we already discussed that thyroid
hyperthyroidism, these thyroid related disorders we can cause the blood
pressures.
The medication so all the medications here, especially the OTC drugs, the
N SEDS drugs, which you take sometimes so they can cause.
Sudden spike, then drug use and abuse so the drug abusers, you know
who are taking illicit drugs.
Narcotics. Heroin. You know, other illicit drugs can be natural, can be
synthetic. They can cause blood pressure. Spike, especially when the the
patient is intoxicated. Stage when they overdose with these drugs. So
then the spikes can happen.
And then the dietary habits again, when the person is taking it
consistently and in moderate amount, we may not see such spikes. But
when we sometimes over eat, you know, today I'm feeling very happy.
OK, Double Burger 2 cold drinks make it large. So all these will give you
extra calories to you and patient will feel more heavy. So this can also in
turns give.
Extra blood pressure spike because your sugar content suddenly is high
because you consume more than what you need.
Then alcohol and other caffeine, all these things, they can also cause a
blood pressure spike, physical activity or lack of activity, right? Mostly it
happens in physical activity in which you can see sudden blood pressure
spike. Like I shared with you. When we go to the gym. Suddenly when we
are on the treadmill, so your body is the workload on the body is
increased.
The oxygen demand is increased as a result. What happens? The heart
needs to beat fast to compensate. Compensate with the oxygen
consumption or oxygen demand and as a result of this the blood pressure
will also increase. And how come lack of activity can increase your blood
pressure?
Can someone tell me if you're not doing anything chilling? Relaxing. Can it
give you a blood pressure spike? How? How is that?
I.
OK, so simply when you are inactive and you are like of activity for so
many days, this is not for like you are taking rest for a while. Just like I
gave you the example of exercise because you are doing physical activity
for a short period of time but this lack of activity is related to when you
are lazy throughout the time when you are lazy throughout the you know
week or month and prolonged so prolonged lack of activity indirect.
Lee will cause you increased weight gain and all those sedentary life
changes then indirectly it will increase the blood pressure. OK, so these
are the sudden causes of the blood pressure, which as a healthcare
professional we should be aware of. Let's say some patient walk into the
pharmacy.
Oh, I have a high blood pressure and then you check that. Oh, blood
pressure is high and the patient may, you know, claim that throughout the
week I did not feel anything. The blood pressure was very consistent. I
don't know why suddenly I got this.
So we when we are taking the patient history, then we can ask any of
these question that did you have caffeine or what did you eat recently. So
maybe one of these factor is causing that sudden spike of blood pressure.
OK. So in terms of diagnostic, I'll go with him.
So this is the source is Canadian Journal of Cardiology.
So the cut off values which are used are for non diabetics the.
Automatic arterial blood pressure or semi automatic blood pressure. So
first let me tell you what is that. OK, there are two to three methods of
measuring your blood pressure. It depends on your blood pressure.
Apprentice. It can be half automated in which the digital metre is there,
but you still need to pump the air inside. So this is known as half
automated device.
Ice then we have non automated device call as non AOBP, non automated
blood pressure device. The old ones the mercury kind of blood pressure
device or the needle kind of blood pressure device. So these are known as
non AOBP and then we have fully automated devices which are called as
AOB.
Automated device for blood pressure like now these days we have in
pharmacy have in pharmacies and at home.
And some are. You wrap it around your wrist or your finger, although the
accuracy is not that high as compared to the arm one. OK, so this was
your background for what is non ao BP and what is Ao BP OK so for the
nondiabetics AOBP is preferred and it if it is 135 to 85.
You consider this no hypertension and for the diabetics, if it is more than
130 / 80.
Then we consider this hypertension.
And out of office, may meant the abbm is preferred. The daytime mean is
135.
And the 24 hour mean is 130 and then if it is still no then it can be white
code hypertension which means any of these values or patient is
nondiabetic nondiabetic that condition is not there. So sometimes patient
may have fear of the hospital setting and they may appear in the increase
in blood pressure. So we call it as white coat hypertension.
OK, so this diagnostic algorithm you don't need to memorise in detail.
For us, we will just follow the staging of the hypertension as blood the CPG
guidelines.
Yeah. So this is the risk stratification of the blood pressure.
That at what blood pressure level and what existing comorbidities like Tod
means target organ damage like when left ventricular hypertrophies that
when your heart is enlarged.
Then other example can be retinopathy of your eye or patient has protein
urea in the urine.
OK, so TOC target organ complications like heart failure, renal failure, and
RF is the additional risk factors like smoking or the triglycerides are high
family history, et cetera.
OK, so when you see this table, so we have to match the blood pressure
reading and what is the status of their coexisting condition then based on
the presence or absence of that condition we can classify the patient as
low, medium or high category. OK. So once we have this data then we can
see that oh if my patient is in the low category then the management is
we encourage.
Lifestyle changes first.
We encourage the patient to do healthy living that if the patient is in the
medium category, then healthy living plus we can do the drug treatment
and then high and very high of course we follow the same.
So this algorithm is as per your CPG guidelines. So when we measure the
blood pressure, if let's suppose blood pressure is immediately more than
160, we start with the drug treatment. And this again, please mind be
mindful that these readings are not one or two readings. It is when the
blood pressure is established or persistently elevated.
You know, two readings, 2. Two to three readings.
Two occasions apart, all those you know, protocol of measuring the blood
pressure.
And then what if the patient blood pressure is between 1:30 to 1:59? Then
we have to see how much cardiovascular risk factors are there. The low,
medium, high category. So if patient is in that low, medium, high
category.
Just based on our previous table, sorry, then we start the drug treatment.
And if it is in the low or intermediate level, so first we follow up or we start
with the non pharmacological management. So basically both of these
recommendations are similar.
And then if after the follow up, if the blood pressure is less than 140, so
you still continue the lifestyle changes.
And ask the patient to follow up for the next six months and if it is more
than 140, which according to CPG is stage 1 hyperroduction already. Then
we start the drug treatment.
OK, So what non pharmacological management options we have which we
can advise the patient to start.
OK, so first of all, of course, sedentary lifestyle is the main cause.
Patient is overweight, patient is diabetic. So all of this lead to more you
can say BMI of the patient. So for this we can encourage the patient to do
physical activity and to do the weight control and the diet control.
OK. So in terms of physical activity, the 1:50 to 300 minutes of the
moderate intensity is required or 75 to 150 minutes of vigorous activity
each week. So again, all these things are very general and we have to see
our patient condition when we.
Recommend these exercises to the patient. OK? Why I'm saying this
because let's suppose your patient.
Is having arthritis problem or they have some other musculoskeletal
disorder or they are extremely overweight that they cannot do these kinds
of exercises? Then we have to tailor make those exercises for those
patients. So this physical activity in.
Like instead of going to the gym, we can recommend them to go do the
swimming, you know, or do other alternate exercises. Do cycling instead
so that there is less pressure on the knees of the patient. OK, so in terms
of weight control, the recommendation is that a four KG reduction in body
weight, it can significantly reduce up to.
4.5 mercury readings of the blood pressure.
OK. And for the diet?
So we will advise the patient to increase the green vegetable diet,
increase the fruit content and and reduce the salt and fat. OK, so more
precisely, according to who? Less than five gramme per day of salt is
needed. So and this is a habit you know so ask the patient to change their
habit and especially not to use the uncooked salt.
You know the salt which we put in our.
Food while we are cooking it is less harmful as compared to let's say we
have French fries on those French fries. We are sprinkling the salt, so this
added salt is very extremely harmful for the blood pressure.
OK, then five serving of the vegetables and two serving of the food daily.
So this is for the dietary requirement.
And then if the patient is smoker, so we know that smoking is one of the
risk factors, so smoking says.
Should be done so and this one. Also, we know that smoking cessation
cannot be done immediately. Patient need to cut down or reduce the
smoking. OK, why patient cannot do smoking cessation abruptly? Can
someone tell me?
And also to check you are you all alert listening to me or not?
Why smoking cessation is not done abruptly and if we do, what will be the
effects?
I.
Wang Jia Tong.

Wang Jiatong 49:44

Yeah.

Asst. Prof. Dr. Muhammad Junaid Farrukh 49:46

Why we do not ask the patient to suddenly cut the smoking? Why we
gradually taper it off?

Wang Jiatong 49:54

Because it will change the patients.
May.
I top police.

Asst. Prof. Dr. Muhammad Junaid Farrukh 50:05

Metabolism correct and dependence because the patient take nicotine,
the body is dependent on it, when suddenly you stop giving nicotine
patient will have withdrawal symptoms. The body will show craving for the
nicotine.

Wang Jiatong 50:08

Yeah.
Asst. Prof. Dr. Muhammad Junaid Farrukh 50:24
OK, very good answer. Thank you.

Wang Jiatong 50:26

Yeah.

Asst. Prof. Dr. Muhammad Junaid Farrukh 50:30

OK. So in terms of smoking cessation, what options we have?
Yeah, for smoking cessation.
So as we just discussed, we cannot suddenly cut off the smoking
behaviour of the patient because of this withdrawal effects. So basically
we need to give them nicotine replacement.
So we can slowly control the nicotine and over the period of time we can
taper it off. So for nicotine replacement, there are a lot of varieties now
available. We have nicotine patches.
Then we have nicotine gums.
And then we have nicotine spray are also now available.
And then the E cigarettes are there.
Vipping.
So like this we can provide several alternate options to the patient so that
they can be.
Stay away from the harmful effects of the smoking, which includes the
tobacco component.
The tar component, the carbon monoxide component and the same times
their body will not crave for the nicotine, and similarly alcohol intake. So
ask the patient to lower down and cut down and taper off the frequency
and volume of the alcohol. So for healthy men and women drinking no
more than two standard drinks on any day and no more than four or
anyone occasion.
Ideally you will ask to slowly taper it off and change their habit.
OK, treatment strategies and treatment targets for patients with
hypertension.
So these are already what we have discussed based on how strong is the
evidence. So lifestyle recommendation is strong evidence. Yes we know
patient at low CVD risk with persistent blood pressure and P hypertensive
therapy should be started. OK. This is a strong evidence.
Operation at moderate CVD risk with persistent blood pressure.
More than 140.
And the hypertensive should be started. Yes, you know. So of course,
when you see 160, yes, you start the anti hypertensive therapy. Then
even when it is more than 140 and patient has the CVD risk also then the
antihypertensive drugs should be started.
But then once decided to treat patients with uncomplicated hypertension,
should be treated to a target of less than 140. Yes, this is our goal of
therapy. Then in selected high cardiovascular risk population. When a
more in intense treatment can be considered aiming to target less than
120 blood pressure.
Intellectual high cardiovascular respiration, where our treatment is being
targeted less than 120 close follow up operation is recommended.
To identify treatment related adverse effect including hypertension.
Syncope, electrolyte abnormalities, acute kidney injury. OK, so this means
that those patients who have high cardiovascular risk like patients with
diabetes.
Or patient with diabetes with high proteinuria. So these so these kind of
population, the blood pressure control is very strict in such kind of
population. So when the blood target is very strict which is 120 or less
than 120 or even between 1:20 and 1:30, it is quite narrow window. So we
need to be make sure that patient do not develop hypertension.
That in in order to lower that blood pressure, the blood pressure is not.
Go very low.
Good that they develop syncope. Syncope means fainting. Now that blood
pressure is so low, that patient is now unconscious. So strict monitoring
has to be done when our target is very strict.
So impatient with uncomplicated hypertension, a SARB calcium channel
blocker, thadde or first time treatment. Yeah. So CPG also says the same.
The balance between efficacy and safety is less favourable for beta
blocker than other first line anti tensive.
Ace inhibitors and ARVs are not recommended in combination you to
increase risk of the adverse effect.
OK, so now let's see the recommendation by the CPG. What are the key
points once we identify a newly diagnosed patient with hypertension,
what are the medication choices which we have and how should we start?
So first of all, they say that the first line monotherapy, it includes all the
drug classes ASARBCCB.
Diuretics. OK, so 1234.
We have 4 choices.
This can be given. ARB can be given, CCB can be given, or diuretics can
be given.
So any of them, they are considered as first line drug.
And beta blockers are not recommended as first line.
OK. But still like if you see some European guidelines, they can like beta
blocker can be a first line. But according to Malaysian guidelines, beta
blockers are not considered as a first line option unless patient has some
really cardiovascular related complications.
So if after a sufficient period of time which is up to six weeks with
monotherapy, the blood pressure is still not controlled, then the options
are the dose of the initial drug can be increased.
The drug can be substituted with another drug.
Or a second drug can be added.
OK, so let's suppose normally what if we see in these guidelines is
inhibitors or ARBS. These are the safest choice and they are considered as
the first line drug. OK, first line drug is ace.
Slash ARB.
OK, so when let's say you started the patient on as inhibitor and after six
weeks patient come back that Oh my blood pressure is still high then what
to do? Can you immediately in let's say #2 is we add the calcium channel
blocker?
OK, so this will be the combination therapy. But before adding the second
drug, what we need to cross check is the dosing.
Is this doors already optimised?
Because maybe initially we start at the low dose of a particular agent and
later on based on the response of the patient, we slowly increase, we call
it dosage optimization.
So if the dose is not optimised and you see that the blood pressure is not
controlled, then you add another drug.
So all this decision is case by case basis because there are pros and cons
of.
Both situations. OK, what are the pros and cons? Let's suppose patient is
on one drug.
And the blood pressure is not controlled.
If you add another drug, calcium channel blocker.
The now the patient will be exposed to two drugs and the adverse drug
effects of two drugs may appear in that patient. OK. On the other hand,
when we are increasing the dose, maybe dose relative side effect can also
appear. So this is all case by case basis. Normally as a general or you can
say for general recommendation we always go for the dose optimization
first first we ensure.
The first drug which we started the dose is optimised. Let's say initial dose
was 5MG for the patient. Now it should be 10 or 20MG depending on
whatever drug the patient is taking. If the dosage is optimised and still the
patient is not responding to the drug then we go for the combination
therapy.
OK, so which according to the guidelines now again?
You will.
Question that after we start the ACE inhibitor.
Second choice should be calcium channel blocker or diuretics. What
should be the second choice? So again it is up to the healthcare
professional depending upon the underlying condition. If patient has any
heart failure related condition, fluid overload related condition we can give
diuretics, but if no fluid overload related symptoms then calcium channel
blocker should be the second line of drug.
And then let's suppose.
Even after combination therapy, the patient is still not responding or blood
pressure is partially controlled, not fully controlled. Then third drug can be
added diuretic.
Only on 4th number. The beta blocker will come.
Unless patient has some myocardial infarction, coronary artery disease
like that in that condition, beta blocker may be started earlier. Otherwise,
if patient do not have any cardio comorbidities, then this beta blockers are
the last line of choice.
So far everything clear.
Students everything clear so far?

Zhang Junxiong 1:02:03

A little bit fast.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:02:06

Little bit fast, OK, let me summarise it again. OK, so here I was telling you
about treatment options of hypertension. So if you read the guidelines
guidelines says all the drug.
Is a RBCCB diuretics. They can be used as first line, so how do we choose
that which drug is more safe? So let's suppose patient the most safest
drug is ACE inhibitor. The first line drug. So we can start with ACE
inhibitor.
Has monotherapy monotherapy means only one medication and then we
wait for some response that how the patient is responding to the patient.
So normally how long we should wait six weeks four to six weeks time we
have to 1st give the medication not like after four days patient came over
my blood pressure is not.
Controlled and you gave them another drug? No. First we need to do the
optimization of the DOS and duration. Make sure that the dose is
optimised. Only then if patient is still blood pressure not controlled.
We give them second drug.
So the second drug, like I told you, if patient do not have any fluid
overload, symptoms get some channel blocker can be a good second line
drug.
If, let's suppose heart failure is there or fluid overload is there like how to
check fluid overload?
OK, so in such patients, edoema will be there.
Or swelling will be there.
Et cetera.
OK, so when we have this evidence, then we can give diuretics first. So it
is case by case basis.
OK, so this is your revision of how the medication works.
So for our renin inhibitors.
The drug example.
Is Ellis Kirin So what this drug will do? It will.
Stop the renin and.
The conversion of an angiotensinogen into angiotensin one will be
inhibited. Then we have ACE inhibitors.
For example, your keto prilin allopril lisinopril Remi April, et cetera, et
cetera. All these pril, pril, pril, pril, pril.
So what is the role of ACE inhibitors?
Ace inhibitors will block the conversion of ACE enzyme and angiotensin
one will not be converted into angiotensin 2.
K and then at the same times.
Angiotensin 2 will not be available to bind at the 81 receptors and when
the angiotensin 2 will be reduced.
Then the vasoconstriction will be reduced.
And vasodilation will be there.
OK. So basically as and ARB will block the ASN angiotensin 2 which are
responsible for causing vasoconstriction.
OK, so they will block the Visio constriction and dilation will be there.
Before the background of calcium channel blocker. So we have basically
two types of calcium channel blocker. One is the dihydro PDT, the other
one is non dihydropyridines. So the major function of dihydropyridine is
that they act on vessel muscle whereas non dihydropyridines. Their main
effect is on the heart muscles.
OK, what is the difference? One group of drug is acting on the heart.
The other drugs are acting on the blood vessels.
OK, so dihydropyridine examples include amlodipine, phalodipine, Nic,
RDP, nifedipine all of these drugs will act on the blood vessels and they
will cause the vasodilation.
OK, whereas the non dihydropyridines their main effect is on the heart
which effects their contractility, heart rate and conduction. The examples
are dilty, Asim and verapamil.
OK, then our beta blockers, so beta blockers. Also we divide into.
Selective beta blockers and non selective beta blockers, so the beta one
selective they will act on.
Heart muscles alone. OK, heart only.
Whereas the non selective ones, they will act on both hard and the vessel.
Yeah. So when on the vessel, so they will cause those vessel dilation
because the drain in angiotensin and aldosterone secretions are
decreased and their conversion will be reduced and vasodilation can
occur.
And then for the diuretics, so we have thiazide diuretic potassium, sparing
diuretic and loop diuretic, 3 different types of diuretics are there. So this
means that each diuretic, they have their own function and own
mechanism of action. So based on the 'cause that.
What is the cause of the patient? What is the issue of the patient? Then
we choose the diuretic accordingly to treat the edoema hypertension.
No heart failure like that.
OK.
So this is basically initially we discussed that what if the patient do not
have any comorbidity. So then we discussed that if patient do not have
any comorbidity, we can start with ACE inhibitor.
And then let's suppose not controlled. We can add calcium channel
blocker or third can be diuretic.
So this is all when no comorbidity.
So let's see that in special conditions or in disease condition, how the
choice of the antihypertensive can be varied. OK, so hypertension without
other compelling indication. So monotherapy is suggested and we can
use.
Any of the ASARBCCB like that?
And second line therapy will be just combination of the first line drug like
this one I told you.
But what if the patient is diabetic? Is our choice of drug changing, so it is
still a S inhibitors or ARVs?
And then combination of CCB is preferred over the thiazide like diuretic.
So even in your case study or if your patient is diabetic, we still follow the
as as the first line and CCB can be the second choice.
OK, what if patient has coronary artery disease?
So here still ACE inhibitor are our first line of drug and then beta blocker
or CCB depending upon patient angina or underlying condition.
It then, if patient has recent myocardial infarction. So in M My case, beta
blocker N is both should be given.
OK, so remember, if patient has myocardial infarction, then we have to
start beta blocker at that time as first line.
Then heart failure again. No change is inhibited. Are the first choice.
Then diuretics and use of beta blocker, it will depend on the patient
condition. If patient is showing the fluid over low sign and symptoms, then
we can immediately start the diuretics or if patient has some other.
The If we want to reduce the cardiac output or the you know the.
The cardiac load then we can use beta blocker in that condition. Left
ventricular hypertrophy is ARB, so standard therapy. No, no change.
Stroke patient ACE inhibitor. No change.
Non diabetic CKD patient. So if patient has chronic kidney disease, so
again ACE inhibitors are the first line and after that the diuretics can be
the second choice. OK, so why is diuretics here? Because now patient has
chronic kidney disease and what is the issue in kidney related disorder
patient has.
Fluid overload kind of a symptoms, so that is why instead of calcium
channel blocker.
Now we are giving ACE plus calcium general blocker. Oh, sorry. Diuretics.
K then any renovascular disease do not affect the initial treatment. It will
still be the as inhibitors.
OK, so this is just a comparison from the 2024 European Society of
Hypertension, CPG. So they also agree with the same option. We can just
cross check. So step one, so ACE inhibitor.
Or ccb. But here in the step one, they are giving the.
Combination therapy, considering that the patient is at the high risk,
because if the monotherapy if the patient is at the lower risk, so this one
also same for all the guidelines.
Beta blocker can be used as monotherapy at any step or combination. So
this is something different. So like we studied in the CPG Malaysian
guidelines that beta blockers, we do not offer it as a monotherapy except
patient has some cardiovascular conditions like myocardial infarction.
OK, rest one. No need to go through anything.
OK, so these are the drug combinations which are available in the market?
So ACE inhibitor plus calcium channel blocker, this is the most commonly
given combination or it can be a diuretic. So choice one choice two
depending upon patient underlying condition. So here do you see if
patient has heart failure or stroke conditions we give the diuretics ones,
but if patient is diabetic or other comorbidity then?
Calcium channel blocker.
Can be a good second choice drug.
OK, so ace with beta blocker when you have myocardial infarction.
Then beta blocker. Plus the CCB in your coronary artery disease.
Thai, diuretic plus, CCB, or plus beta blocker not recommended in
presence of glucose intolerance or metabolic syndrome.
OK then combination, but with care. So when we are giving one dilty as if
and beta blocker, it has to be with care due to the risk of heart block but
risk is less than with our MIL because.
Remember dil T as in is that medication which is acting on the heart,
contractility.
And beta blocker also reduce the heart contractility.
So if we give these two together the risk of heart block can be there. So
we have to monitor.
Combination to avoid ACE inhibitor and ARB increase risk of renal
dysfunction. So this combination is usually avoided in CKD patients.
OK, this flow chart is very important.
It will help you to decide that based on what underlying condition, which
of the drugs are first line or best choice like for example, in diabetes we
see ACE inhibitors are the most effective ones.
That if patient has diabetes with nephropathy still ACE inhibitors are first
choice and ARP is also first choice.
Then if patient has gout.
So ARVs can be.
More reliable this lipidemia.
Still, it can be given, then coronary artery disease. This is interesting. So
as can always be your first line and then beta blocker, here comes in,
especially in your myocardial infarction cases.
OK, then heart failure. So heart failure. You see beta blocker are there.
But with this sign. So this means that we have to only give cardio
selective beta blocker which has metoprolol, vitoprolol, nebivolol et
cetera.
OK, then asthma still ACE inhibitors are good, but beta blocker, we are not
preferring. Why? Because beta blocker can cause your Broncho spas. So
not so suitable in asthma patients.
K, the non diabetic renal impairment is inhibitors within large history
nosis.
So basically easily you can see that ACE inhibitors are.
1st and safe choice in almost all conditions, so easy for you to memorise.
OK, so Contra indications so although you know that ACE inhibitors and
ARVs they are the first line drug in almost all conditions, but except
pregnancy you cannot give ACE inhibitor in pregnancy as they are
category X contraindicated.
Or if patient has sign in symptoms of angioedema.
Or hyperkalemia and this is important thing to know when there is a
bilateral renal artery, stenosis. Renal artery stenosis means the narrowing
of the vessel. So in such conditions you should not give as or ards.
OK, then, diuretics in gout cannot give with a blocker in asthma. Cannot
give the adhadia, cannot give or heart failure uncontrolled.
Yeah. So these are some of the questions and contraindications which we
have to memorise.
OK, so take 10 minutes break, then we continue our management of
severe hypertension.

Wang Hanying 1:19:28

None.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:33:56

Hello guys we are back.
Are you all back? Please turn on your camera.
I miss you. I want to see you.

Zhang Junxiong 1:34:09

I'm back, Sir.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:34:13

Those who can, they can.
OK, so let's do a quick recap. What we have studied now. So management
of hypertension.
So 1 honeying. What will be the first medicine to start a patient if they do
not have any other diseases?
So which drug you will start?

Wang Hanying 1:34:38

Ace.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:34:40

A/C E inhibitor very good. OK, where is Mayon Kong?

云骢 马 1:34:50
Oh, hello. Hello.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:34:50

Are you on call? Yes, if let's say patient has diabetes, then which
medicine? You will start the patient with?

云骢 马 1:35:06
Move.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:35:08

These inhibitors, calcium channel blocker diuretic beta blocker which one
you want to start.

云骢 马 1:35:20
Oh.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:35:27

We can.
Share the slide as well.
This box is very easy for us to decide, so you take a look at the chart and
see.
So if patient has diabetes, which of the medicine is more safe?
So diabetes either with nepropathy or without neuropathy is inhibitors and
ARVs. They are considered as safe first line option.
OK, understood.

云骢 马 1:36:15
Yeah.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:36:17

Hmm. OK, next we can see if patient has coronary artery disease. Now
here after ACE, we can give beta blockers to the patient.
SM channel here can come third. Choice is inhibitor and beta blocker can
be the first and second choice if we are talking about combination
therapy. OK, so like this so case by case basis and patient may have more
than one condition also diabetes asthma heart failure like that. So we
have to see all the pros and cons sometimes.
Because let's suppose here. If you see asthma beta blocker blockers? Not
so.
Suggested but patient have, let's say coronary artery artery disease at the
same time. So we have to see the risk versus benefit.
So in ask MA, what will be the risk that patient may develop the
bronchoconstriction.
That also can be reduced if we give the selective beta blockers.
So like this, we have to see the condition and the medication, how many
comorbidity patient has the single comorbidity, very easy for us to select
the medication for them. The more comorbidities then the risk versus
benefit on that basis we have to choose the patient.
OK. So let's continue where we left.
So the management of severe hypertension, which we call as
hypertensive crisis emergency condition, urgent condition.
OK, so from urgent and emergency, which one is more severe? If you just
see the word?
Urgent is more severe or emergency is more severe.

Wang Hanying 1:38:29

The emergency may be more severe.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:38:32

Yes, emergency is more severe. So let's see the difference.
So the urgency is defined as when a person has elevated blood pressure.
So basically in hypertensive crisis the blood pressure is above 160 above
180. In both condition the difference is only between the complications,
presence or absence of complications. So in the urgency there is no end
organ damage or no other major complications.
Whereas in hypertensive emergency they have now other complications
have developed like intracranial haemorrhage, subarachnoid
haemorrhage, acute renal failure.
Hypertensive encephalopathy. All those things.
OK, so here we can see the hypertensive urgency symptoms. So what was
the definition of urgency? Yes, it is very high blood pressure, but the
target organs have not been damaged yet.
So what will be how we differentiate urgency versus normal elevated
blood pressure? So remember previously when we discussed the common
sign and symptoms, so I told you that having headache or nausea
vomiting, these can be in normal elevated.
Blood pressure as well, but severe palpitations and nosebleeding and
shortness of breath. They are mostly associated with urgency, so if patient
has this bleeding or suddenly very severe shortness of breath or
uncontrolled heart palpitation it should give us an indication that patient is
having hypertensive urgency.
OK. The more quickly we identify urgency and urgency and emergency we
the more quickly we can give medication to the patient because the more
longer we delay.
The complications will keep getting severe.
OK. So once we identify that, oh, this is urgency which will be blood
pressure more than 160 and 180, but no evidence of target organ
damage. These are the three best options according to the clinical
practises guideline. Very easy for you to memorise. The 1st is kptopril.
Second option is nifedipine and third option is Levit.
So in majority of the cases, we prefer to give ketopril it's onset of action is
very quick.
And the patient symptoms are treated very quickly.
OK, so you can memorise any one of these doses. I think Kaptoppril is
more easier to memorise. So starting those 12 point, 5MG and then.
You can repeat it after one hour or two hours based on the patient
response.
OK. So let me just cross check with you. The PD pin is from which drug
class can anyone recall?
Kaptoppril is from ACE inhibitor so nifedipine is from which class of drug.

Koh Siew Hua 1:42:15

Ccb.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:42:16

Is CCB and labita loll so all the LOL are from?
They are the beta blockers.
OK, so easy to memorise. Captopril nippy dip pin and labbita LOL. These
are the three drug of choices to treat the urgency.
OK, now moving on to the emergency. So emergency like by the
definition, we discussed that blood pressure is more than 180.
With and organ damage, organ damage evidence is there. So what can be
the example of those organ damage? The more important vital organs,
which include your brain so it can be any ischemic or stroke there or the
other important is heart. So heart failure or any pulmonary edoema is
there.
The next important measure, organ, is your kidney.
So any acute renal failure is there or not?
Then in retina.
Any retinopathy is there or not, and then in the arteries, any aortic
syndrome or help syndrome or preeclampsia in pregnancy?
These are some of the indications which will tell us that the major organs
are involved or not involved. Once we identify that these organs are
involved, we will immediately classify our patient as this is emergency.
This is not urgency and emergency just like.
The student told.
That it has to be treated urgently, so emergencies are mostly treated with
intravenous intravenous treatment options. Injectables.
OK, so here the options are labita loll, so this is the same drug class. Easy
to remember. This is the beta blocker.
So those students who have difficulty in memorising the drug names, they
can memorise libeter role because libertarol can be used in both
conditions in urgency as well as emergency. So what is the difference that
in emergency we are giving the intravenous form of the libido loan,
whereas in urgency we are giving the oral form?
OK, so we are using it because of again quick onset of action 20MG is
injected slowly for two minutes then 40 to 80MG every 10 minutes. Based
on the response and the maximum allowed dose IS200MG and patient
should remain in the supine position and three hour after the procedure.
And caution to use the Libita lone if patient has underlying heart failure.
OK. So that's why we have multiple choices to choose, but let's suppose
patient has contraindication cannot use labita role. Then the next option is
GTN.
This trial try and it rate or Nitro give this rain.
So this one also the onset is very quick, it's fast acting between 2:00 to
5:00 minutes, the nitroglycerine can start its work, and we have to give
this initially 5 to 25 microgram per minute.
Very slow and the usual range is 100 to 200. It is preferred in acute
coronary syndrome and acute pulmonary edoema. So if your patient has
underlying.
Acute coronary syndrome or coronary artery disease, then nitroglycerin is
preferred in those kind of patients.
And same isosorbide dinitrate is also from the same group of class and it
can also be used for coronary artery disease or acute coronary syndrome
patients.
OK, the the next choice. Let's suppose the nitroglycerine is also. Have you
know some contraindications to your patient or not available or patient is
not responding to it. Next option is hydralazine. So this is direct
vasodilator.
OK, so remember why blood pressure happens? Because the constriction
of the vessels so we can give direct visual dilators such as hydralazine.
This onset is from 10 to 30 minutes, but caution is in acute coronary
syndrome.
Aneurysm and unpredictable BP lowering affect is there. So when we are
giving this we have to monitor the patient as well.
OK, so next option is the cardi pain, the cardi pain is also from the CCP
group and then S molol is from beta blocker.
Group so caution in acute heart failure and used in preoperative situation
and tachyarrhythmia.
So most commonly and the last one, the sodium Nitro Pro site is also
there. It is very quick. Normally in ICU we use the sodium Nitro Pro side.
And caution is given in heart failure patients.
And it requires the arterial blood pressure monitoring. That's why in ICU
patients, they're always on the.
Intra arterial the CVP M AP monitoring is ongoing and low dose adjustment
required for elderly. So this is also.
A good and you can say used in very severe conditions. The sodium
atropoide is used.
OK, so for easy reference either you can memorise labita LOL because
labita LOL is used in both urgency and emergency.
Or in any question. Then it's a heart failure, et cetera then.
Sodium nitrroprocyte cannot be used.
But otherwise sodium nitroprusside very good onset of action.
OK. Any questions so far?

Wang Hanying 1:49:28

So, Sir, so the therapy for urgency, three kinds of medicine or for aura.
Asst. Prof. Dr. Muhammad Junaid Farrukh 1:49:42
Yes, three kinds of oral drugs are there.

Wang Hanying 1:49:48

This this kind of message.
Used to oral, yes.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:49:54

Yes, all three are oral.

Wang Hanying 1:49:56

OK.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:50:01

OK, Li Cheng Ying, can you tell me difference between urgency and
emergency?
Or any other student.
Zan.
John, can you tell me what is the difference between a hypertensive
urgency and emergency?

Zhang Junxiong 1:50:30

The emergency is more dangerous and need to go to the hospital. The
urgency you can control it by some medical medicine.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:50:44

OK1 difference. Any other difference in terms of the damage to organs?
Maybe he 'cause you what?

Koh Siew Hua 1:50:59

Uh, for emergency there is a complication. Like the end organ damage.
For for urgency don't have just the PP array high on me.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:51:09

Yes, because sometimes the reading can be same like 180 can mean
urgency can be an emergency. But to identify emergency we will see the
evidence of end organ damage. But in urgency, the end organ damage
will not be there and that's why we can control it by giving oral
medications.
OK, So what is the common drug which is common between urgency and
emergency?
Anyone can answer that?
One medication that can be in both condition.
Wang Hanying 1:52:01
Yeah. Leopard leopard. Hello.

Asst. Prof. Dr. Muhammad Junaid Farrukh 1:52:05

Yes, labita LOL. So labita loll, oral form can be used in urgency and
intravenous form can be used to treat the emergency situation very good.
OK, so later at the end of the lecture, in the next week, please revise.
Keep on revising your basic knowledge of antihypertensive drugs. Their
mechanism of action, their drug classes like beta blockers. What are
selective, what are non selective is inhibit. What are the cap top lacinopril
for sinopril then ARVs because the same drugs will come in heart failure.
Same drugs will come in coronary artery disease, et cetera.
So these are, you know, refresh your old knowledge on that.
Let's start the next topic.
Which is acute coronary syndrome.
OK. So acute coronary syndrome or coronary artery disease, so it
encompasses the spectrum for unstable angina to non St elevation,
myocardial infarction. And finally, St elevation, myocardial infarction. So
basically this acute coronary syndrome. Later on I will show you in the
pathophysiology. It all depends that how much of the artery.
Is blocked.
By the cholesterol deposition.
K So based on the degree of occlusion.
Degree of blockage.
It can starts from angina and stable angina, non St elevation, MI and
finally St elevation myocardial infarction. So all these things we get to
know when we do the screening test, diagnostic test, ECG, all those things
to further rule out the condition.
OK, so this is again the different classification of. It's all the same coronary
artery disease, ischemic heart disease, synonyms used there, acute
coronary syndrome. So it all leads to angina. It can be STEMI and STEMI
unstable in China, et cetera.
So the main thing here to memorise is it is a degree of occlusion or
blockage. Occlusion means what blockade ish.
Blockage of the coronary artery.
How much of our coronary artery is blocked that will determine the stable,
unstable, STEMI and STEMI like that?
OK so.
Why the narrowing of the artery occurs? So we all know. Yes, it is due to
the deposition of the cholesterol which we call as plaque formation plate
builds up when we keep on having accidental lifestyle, too much oily food,
too much cholesterol, then slowly over the period of time that's circulating
high cholesterol keep.
On depositing inside our blood vessels, OK. And then it depends how
much narrowing it will cause.
And how much blockage that plague will cause? And so here in the first
example you can see this is the normal artery. There is no cholesterol
deposition. So it's quite wide. There is no narrowing in done. The blood
can flow very easily in such arteries. Then second, we have little bit
deposition of the cholesterol. That's why we call it.
Partially blocked or partially occluded. OK.
Occlusions. Meaning, like I told you, block.
So when the artery is partially blocked, it is either unstable in China or in
STEMI, whereas when the artery is completely blocked here you can see it
is completely blocked. It can be with the plague formation. It can be with
the blood clot, it can be with the you know any thrombus formation.
It will completely block the artery and the blood will flow backwards.
This condition is called as STEMI or myocardial infarction. St elevation,
myocardial infarction. OK, so why this thrombus formation occurs?
Because as a result of your cholesterol deposition, the blood is coming
with very, you know, high force. And it is exerting pressure on this plate.
So when this plate.
Is ruptured, then the clotting factors will come and all the, you know, red
blood cells and platelets, platelets will come. Come. They will make an
aggregate which is known as thrombus.
So this thrombo formation, when it will keep on floating in the vessels. So
the point where the vessel is very narrow, it can block that vessel and
then suddenly the patient will feel the heart attack symptom.
So similarly, another way of looking at this, so this is the lining of the
coronary artery, there is no cholesterol deposition in this picture. Next,
when there are cholesterol and fatty substances, slowly, slowly, they keep
on deposing in the.
Cell or the vascular lining and then sometimes calcium deposits also come
and harden the plate.
And then when the blood pressure is very high, it can damage the plate
and then as a result of that circulating plaque also it can start the
inflammatory process because when the plate is circulating, the body
defence system will get activated the body.
Defence system.
And then your inflammatory process will be there. C reactive protein will
be there and all OK. So if the degree of blockade is less than 75%, recall is
at mild blockage.
Patient may not feel even some symptoms, but it depends on patient to
patient.
But if the degree of blockade is more than 75 now, patient may
experience angina like symptoms.
K So this is again.
What we have already discussed that when the plague ruptures, the
platelet aggregations will be there and it will activate our coagulation
cascade and finally the thrombus formation will be there and that
thrombus.
When the the artery will be narrow, it will go and stuck there and cause
total blockage. And when there is a total blockage this is called as St
Elevation myocardial infarction.
OK, so same thing, it is repeating. I will not.
Go through it again.
I hope that all of you have now understanding all of the pathophysiology,
how to relate the plague formation, how to relate the rupture of that.
Platelet and how the thrombus formation is getting take place and once
the thrombus is there then it can cause emboli.
That temple I will go and stuck in the narrower part of the artery, causing
the STEMI or endstemi.
See one of your arteries in cross section with an arthrosclerosis plaque,
which is developed over the years. Thrombosis occurs following a sudden
rupture of this plaque, a clot of blood has blocked the coronary artery. It
prevents blood and oxygen from reaching the part of the heart irrigated
by this artery. This part of the heart, already injured, risks being
completely destroyed without immediate intervention.
Respect just triggering factors, clinical features.
OK.
OK, so now we understood the pathophysiology, that how the plague or
the thrombus formation or the ambulance formation is blocking the artery.
OK, So what is that resultant effect of this blockage? The impaired flow of
the blood, let's say if it is partially blocked or completely blocked then
blood cannot.
Flow. So oxygen demand there is no oxygen and blood supply to the body
and that part of the heart or artery or tissue they will get necrosis or you
know they will die depending upon the extent of the how many supply or
how much supply has been affected.
So the risk factors are primary modifiable or the secondary modifiable or
totally unmodifiable. So we know that the patient age patient gender we
cannot modify or we could not change these parameters.
Or the menopausal status of the patient, the family history of the patient.
Or there's some genotype of the personalities. But whereas the primary
modifiable factor, the first of all is dyslipidemia, which is the actual factor
which is causing that plate formation because all that plate formation is
due to the.
High levels of.
Cholesterol.
Your triglycerides.
Your LDL all total cholesterol. So this dyslipidemia is the main factor and
we have to first try to modify this dyslipidemia then the smoking because
smoking also increase blood pressure and it also causes stress to the
plate.
The you know, mechanical stress or.
Rupture the blood vessels.
Then we have diabetes, hypertension. So these all are primary modifiable
ones. Secondary modifiable ones include obesity, stress, sedentary
lifestyle.
So this also includes diet.
So in other words, sedentary lifestyle and diet, if not controlled, it is also.
Indirectly leading to dyslipidemia so they are, you know, very important
risk factors but still modifiable. So as long as the healthcare professionals
are able to counsel the patients on this, so the severity of starting from
angina until the myocardial infarction, we can prevent it.
OK, so angina for definition, what is angina? Severe chest pain is known as
angina. So angina pectoris, chest pain on exertion.
Triggered by circumstances which acutely increase the cardiac workload,
like suddenly you started some exercise, lifting some heavy objects. So
this results in increased cardiac workload and transient chest discomfort
due to the reduced oxygen supply. OK, so because due to the blocking of
the artery.
The oxygen coming here is less.
So this will cause discomfort for the patient.
OK. And this angina condition, it can be relieved by the sublingual.
Gtn and by taking the rest.
So let's try Trinitrate 1 GTN tablet under the tongue and the patient within
few minutes. They will feel better.
Because the GTN it causes your vasodilation.
OK. So like we discussed that, what are the triggering factors, mostly
exertion exertion like exercise?
Or let's say it's the patient patient went to a place and they had to take
the stairs staircase.
So staircase also for elderly people especially, it is called as exertion. They
don't need to do a specific exercise, just going down and up the stairs is a
exertion for elderly patients.
And then some environmental factors like cold weather because they
increase peripheral resistance or heavy meals increase the GI perfusion,
they can also be a triggering factors for angina pain.
OK. Acute coronary syndrome clinical features in general. So patient will
have a retrosternal chest pain which is crushing and dull in nature even at
rest.
Lasting at least 20 minutes and the normally when we ask the patients,
you know, patient, complain of the chest pain. So now this chest pain, it
can be, you know, a differential diagnosis as well chest pain because it
can be in, you know, some gastric condition as well. It can be in H pylori
infection, dyspepsia also.
So chest pain will be there. The next question, which doctors will ask, can
you please describe what is the pattern of the pain? Then if patient tells,
oh, it radiates from the arms, neck and back. So this tells us that it is
angina type pain.
And then also associated with *** shortness of breath.
OK, so difficulty in breathing, you can say also that nausea.
And vomiting. So these are the classical sign in symptoms of this ACS
attack. And then based on the ECG finding, we will get to know is it
stemile or is it nstmais? Is it St elevation or is it normal or is it non St
elevation?
OK, after ECG or the other important test for us to conduct is cardiac
enzymes. So cardiac enzymes also they are you know elevated.
In case of any cardio injury.
So when patient has this heart attack symptoms, we have to run the
cardiac enzyme test to to check that if the cardiac injury or this heart
attack was recent or old.
OK, so let's see what type of Cardiff markers we have. So one type is
troponins, one is ckmb creatinine kinase myoglobin. So which is specific
for heart.
So the troponin TN troponin one, they are the most specific and the onset
is within minutes of the chest pain, but peeked around 12 hours.
And they remain elevated for 10 days. OK, this is the important thing
which you have to memorise, that the critical thing for troponin TS are
they can be elevated up to 10 days. OK. Whereas for the ckmb.
The normal values are back in the 48 hours and the peak is 10 to 24
hours.
OK, so like this, if we see this graph, we can see that the green colour and
the purple colour they are the troponins. So once elevated it takes up to
14 days around two weeks time.
For the troponins to come back to the normal range, whereas your ckmb it
can be come back within two days 48 hours.
So let's say ckmb.
Is elevated.
Drop on in.
Drawboard men is elevated.
What that means?
Then CKMB.
Normal.
But your troponin?
Anyway, wait what that mean?
OK. Can any student tell me what is the difference between A and B?
What kind of information we can get from scenario A and scenario B?

Zhang Junxiong 2:11:48

Bkmb is no more in B.

Asst. Prof. Dr. Muhammad Junaid Farrukh 2:11:52

And troponins are high in B, right?

Zhang Junxiong 2:11:56

Yes.
Asst. Prof. Dr. Muhammad Junaid Farrukh 2:11:57
So what this means, what you will evaluate from this information?
Versus in scenario ACKMB is also high. Proponents are also high. So what
will be the difference between scenario A and B?

Koh Siew Hua 2:12:21

Meaning, in situation a, the patient is currently have a new infection virus
for.
Situation P patient is experiencing the.
Previous impression.
Is it?

Asst. Prof. Dr. Muhammad Junaid Farrukh 2:12:35

Yes, very good. OK, so lets suppose you know patient came across in the
hospital, we do the ECG and all the cardiac biomarkers test. So in a case it
means that the infarction is recent CKMB is high, it is within the 48 hours.
Then of course next question will be when was the onset of the pain chest
pain.
Etcetera. We will take the history of the patient.
But in the scenario B.
The ckmb are normal, but Troponins are telling us that may be for the
past 7 days, 8 days or one and a half week patient might have a silent
heart attack which got unnoticed, you know.
So this will tell us that patient already received the heart attack or a
myocardial infarction and.
Based on this also our choice of therapy matters. That is it a recent
infarction or is it a old one? The choice of the pharmacotherapy will be
depending on this information.
OK, so these are the details of the differential diagnosis in terms of the
ischemic cardiovascular disease, non cardiovascular disease and non
ischemic cardiovascular diseases. We will not go in the details of the
differential diagnosis.
OK, so once based on the sign and symptoms.
Where are my sign and symptoms and tables.
Yeah, here.
So after we saw that patient has complained of severe pain, then
shortness of breath, nausea, vomiting, are there one evidence 2 evidence.
Then based on the ECG report, either is it St elevation or St Depression
non St elevation.
Then cardiac enzymes. So after all these tests, we are sure that is it
angina pain, is it myocardial infarction or is it NST elevation, myocardial
infarction? Then we will narrow down our choice of the therapy.
So the goal is to relief the pain. The first thing will be patient is coming to
the hospital with the active complaint of severe chest pain. So we have to
give such a medication which can relief the pain.
Then, after the symptomatic management, you know, we call it
symptomatic management.
Symptomatic.
Or also known as initial therapy.
Then we go for early re perfusion to the infarcted artery to prevent the
infarction, like for example.
This is the plague, or this is the thrombus formation. Still it is ongoing. The
blood is flowing, lets say 90%.
Blocked it is nstami.
So we have to start the early reperfusion we have to open this blockade
as early as possible. The more we delay, there will be a chance that it can
completely block 100% block.
So we have to open the artery as soon as possible and then prevention of
the death, other complications and prevention of reocclusions like for
example you gave the initial management, you opened the block, but
then you have to give the the secondary prevention.
Which means that we have to start the medications for the patient so that
next time the reocclusion cannot occur.
OK, so this is the flow chart of the treatment of STEMI according to the
CPG guidelines. So like we discussed first, we assessed based on the sign
and symptoms. Then we assessed based on the ECG monitoring. But at
the same times we have to do the symptomatic management of the
patients. So for the symptomatic management normally.
As you know.
Easy way of remember, normally we give this.
OK, morphine for very severe pain.
And if patient is very you know, so B shortness of breath less than 92 or
94, we give oxygen.
Then of course, N is your GTN Nitro glycerin and A is for aspirin.
This is the initial protocol. While we are doing other tests even before
giving the ECG monitoring, you have to give all these initial therapies
when patient is in severe pain vomiting like that.
Sometimes lets say patient is vomiting. Also we give metoglocromite for
that.
For the vomit. So it all depends what symptoms your patient is showing.
OK, so after the initial treatment and then of course the cardiac
biomarkers, it will take time for the laboratory to send you the result.
Then the decision of re perfusion, it depends on the onset of the
symptoms. You have to ask the patient that how early the chest pain was
started. So according to guidelines, if it is within the 3 hours.
Then we will offer either PCI, which is percutaneous intervention, it is a
surgical procedure to open the.
Plot to open the occlusion or even February. No lytic therapy can be used
if you do not have the facility of the PCI because in order to do this
surgery you need expert surgeon or you have to see the patient related
factors. Lets say maybe surgery is not suitable for our patient.
Then so you can choose both either primary PCI or the FIBRINOLYTIC
therapy.
But if it is between the 3 to 12 hours then primary PCI is more preferred. If
lets say primary PCI failed then you can go for February, no latex see it is
second option.
And then lets say if patient came after 12 hours then after 12 hours then
medical therapy and anti thrombotics are preferred. Then if necessary or
if needed the primary PCI can be done. So after this initial management
the initial management and re perfume therapy has been given then we
can start the.
Con commitment therapy, or you can say to prevent the.
Uh.
How to say reocclusion? We don't want the artery to block again, so this
will be your home medication. You discharge the patient on these
medications. Secondary prevention.
OK, so for fibrino latex.
It is very important the time factor we call that door to needle time.
The more the delay, why we say because the more time lost it means
myocardium loss. So imagine this is your heart muscles. Very poor heart.
And then these are the arteries, blah blah blah. So the whole time the
arteries are blocked. Which means that in the surrounding tissue there is
no blood supply.
So the more we delay in taking the patient to the hospital and starting this
fibrinolytic the all the cardiac muscles, the myocardium, it will die.
So fibrinolytics only given if less than 12 hours from the first onset of
chest pain.
And if your patient has following the right conditions, then it is, Contra
indicated, such as previous hemorrhagic stroke or.
Ischemic stroke within the last 3 months. So if last 3 months your patient
has a stroke, we cannot give them fibrinolytic due to the side effect of.
Bleeding.
Or patient has active internal breeding.
Or any structural vehcular lesion or any intraclanial they have neoplas
neoplasia any tumour is there.
Any aortic dissection is there so these are absolute contraindication,
which means that you cannot or you should not give any fibrinolytics.
But then we have some relative contraindication case by case basis, like
for example blood pressure is very high. So first we can try the blood
pressure to come down and then we can give the.
Fibrinolytic or patient has an INR which is high, so the risk of bleeding will
be there. Any recent trauma is there pregnancy? Is there other
cardiovascular accident is there so these are relative contraindication, not
the absolute contraindications.
OK, so once you see that ohh my patient is safe and the fibrinolytic must
be given the first choice or the best choice is Ivy Strepto kinase. This drug
is suitable and.
Is considered as first line drug to be given and this is non fibrin specific
and act on plasminogen anywhere in the circulation. The half life is up to
23 hours.
The side effects can be bleeding and hypotension, and one of the
limitation of this medication is we cannot use this drug up to one year.
Because of its antigenic property, next time you give this drug, lets say
after 6 months, it can cause reaction.
Antigen antibody reaction is there so that is the limitation because lets
suppose your patient has heart attack after 5 months again then we
cannot repeat strepto kinase because of the risk of risk antigenic
property.
OK, then we have fibrin specific agents as well.
Like Lt placed in active place, they are equally effective to septokinase
and fewer reinfarctions and less incidence of the major bleeding rare
incidence of the hypertension and it do not induce the production of the
antibodies. So they are comparatively safer but equally effective 2 strepto
kinase.
The disadvantage is these are very expensive drugs.
So specially if your insurance company is not covering it, so patients you
know they feel hard to afford it and it need to be given with heparin for 48
hours to keep the A PTT within the normal range.
The side effect is intracranial hemorrhage, so it may be reserved for
patient with certain criteria, like for example, previously septokinase
already given anterior myocardial function. Is there or large myocardial
function? Is there operation is young, you know, young patients, we can
spend more money on the patient.
But if you ask the family patient, they can spend more money even on the
elderly as well.
OK, so this is the summary what we have already discussed.
So first of all, reperfusion therapy based on the timings on the flow chart,
the primary PCI is the strategy of choice.
Otherwise, we give the renolytic therapy to the patient and the
concomitant therapy includes your aspirin clopidogrel. So dual antiplatelet
therapy.
OK, so starting with the statues of 300 MG followed by 75 MG for both
aspirin as well as chopedogran. So the clinical trials on aspirin and
clopidogrel are more specially on its safety and effectiveness, whereas the
newer drug like prasogil and ticular glyrol the trials are not that much and.
They are expensive. Also, aspirin is very cheap.
OK, then after that patient who received fibrinolitic, we can give them
heparin or inoxipreane any other antithrombotic agent and for their
continuous therapy or you can say secondary prevention?
We have to give them beta blocker, ACE inhibitors and statins. OK, so.
Now you can see that in the management of hypertension.
If patient has.
CAD or acute coronary syndrome, we saw beta blocker is there so
because see beta blocker indirectly also needs to be there for the
prevention of the stami and enstami. So the same drug can be used in the
treatment of hypertension as well. So beta blockers are used in
hypertension. If patient has underline coronary artery disease.
OK, so this is for the secondary prevention.
So basically, the secondary prevention of the beta, a SARB we starts in
the hospital itself, beta blocker Na S immediately, then patient continue it
at home.
OK.
So that protocol for the N STEMI and unstable angina, the initial
management is the same for the myocardial infarction.
Here the difference is we are not giving strepto kinase to the patient.
Because Fibrinolytics are not needed in partial occlusion in unstemi and
unstable angina, it is partially.
Partially blocked.
So we can use just anticoagulants.
So under anticoagulants we have 3 different options are there like
unfractionated, heparin, low molecular weight heparin for example.
For example, inoxaparin e noxa.
But in.
And then we have the factor 10 a inhibitor, Fonda, Perry, nux. So normally
in hospitals we use inoxaprine because less side effect as compared to
heparin less need for monitoring the dosing is very easy and it is cheaper
as compared to Fonda parinas. But if lets say your patient has renal
impairment.
Renal impairment. Then the Unfractionated happened can be considered.
OK, so this is the visual diagram of how we do the percutaneous coronary
intervention known as PCI.
So here you see that this is the blocked artery in that we will insert the
catheter. So this tube is the catheter.
And this is the stent. Here it is closed. Here we open up the stent and the
artery gets widened.
White.
So this is the stent. This is the balloon, which.
Inflate.
The artery.
OK so and this also we need expert surgeon to do this procedure. First we
will insert the camera, then catheter, inflate the balloon and then finally
the.
Stent will be placed.
In the artery.
So we will not go into the details of the types of the stunts, because many
types of the stunts are available in the market.
OK, next.
OK. Any questions so far?
Koh Siew Hua 2:31:24
How do we need to know the dosing for strepto kinase and other fruino
lactic?

Asst. Prof. Dr. Muhammad Junaid Farrukh 2:31:31

Other fibrinolytics no need strepto kinase initial dose can.
Because that is the initial management and the life saving drug so that 1I
will encourage you to know, but the details of inactive plays and Lt plays
no need.

Koh Siew Hua 2:31:51

OK, then you say.

Asst. Prof. Dr. Muhammad Junaid Farrukh 2:31:52

OK, take a 10 minutes break and then I will see you with the remaining 2
small topics, heart failure and dysplipidemia are very small.
Students.
Let's continue to our next topic.
So next topic is heart failure. So in this, the medications are the same.
So no need to.
Go in detail on the role of the medications. So first lets see the what the
disease its about for heart failure. So what we understand from heart
failure so its a dying heart which means that when the heart is not able to
contract properly.
Or the injection of the blood not able to pump the blood properly. So that
is simply the heart failure. So lets see the theory. So abnormality of
cardiac structure or function leading to an impairment of.
Ventricular filling or ejection of the blood. So which means in the heart
failure. If we have some, you know, problem from the atrium side, then
ventricles will not be able to fill up properly. Or if the ventricles they are
not able to pump the blood to the rest of the body which we call as
ejection of the blood. So these impairment can be seen in heart failure.
So the clinic clinical syndrome in which patients have typical symptoms of
breathlessness. So why they feel breathlessness again the blood flow is
not proper there. The blood flow is impaired and oxygen is being
transported through this blood.
And other classical symptoms of heart failure includes the swelling, ankle
swelling and fatigue, and the signs include elevated jugular venous
pressure, ankle edema, pulmonary crackle and displaced apex beat.
OK, then we have here reduce ejection fraction and.
Yeah.
If.
Hmm.
Preserved ejection preference. So here P stands for preserved and the cut
off point here for us to know is less than 40% will be considered as
reduced ejection fraction and if it is 40 and above, it is considered as
preserved. OK, so in reduced ejection fraction in which the volume blood
volume is less than 40%, the cardiac output is reduced due to.
Biocardial contractility. This initiate a complex pathophysiological process
which includes hemodynamic alteration and structural changes within the
myocardium, and in that case in which it is still preserved because it is
more than 50%, the diastolic dysfunction leads to impaired left ventricle
due to decreased relaxation or reduced compliance leading to elevated
filling pressure and.
These hemodynamic changes leads to clinical symptoms of the heart
failure.
OK, so this heart failure like any other disease, it can also be acute when
the onset of symptoms are very southern, or it can be slow and silent and
progressive, and it can deteriorate the heart function.
This is the classification of the heart failure based on its ejection fraction.
So like we already discussed, when it is less than 40%, we call it reduced
ejection fraction and when it is more than 50% we call it as preserve
injection fraction.
OK, so some of the pathophysiology, its almost the same.
So it results any disordered in the endocardium myocardium, the muscles
of the.
Heart or any vessel or valve involvement, the resulting will be the reduced
ejection fraction.
Occasionally myocardial contractility may be preserved and left
ventricular ejection fraction is normal, the symptoms being due to
diastolic dysfunction, that is, heart failure with preserved ejection fraction,
and often patients with a reduced left ventricular ejection fraction have
features of diastolic dysfunctions as well. So this is further explaining on
their physiological functions.
OK, now what are the causes of heart failure? What etiology is behind
that? So first of all will be your coronary artery disease and hypertension.
These are the most common factors of heart failure. Then some less
common can include cardiomyopathy, some well disease or diabetic
cardiomyopathy. But still these are structural changes which are related
from.
The heart and some causes of shifting from chronic condition to acute like
acute myocardial infarction. So lets suppose if patient has.
Chronic heart failure, but suddenly patient get myocardial infarction
attack. This can rise to acute heart failure or patient has arrhythmia or
suddenly uncontrolled blood pressure. Any infection or patient is not
taking the medications on time. So this can again give rise to acute heart
failure or suddenly excessive fluid or solved in thake or.
Patient is having anemia.
Or development of renal failure or the drug therapy. So these are basically
you can say secondary causes of the heart failure.
OK, so for investigations, so this one, we don't need to go into detail like I
told you previously, but in general, what are the tests which can be done
to confirm the heart functioning? So of course, first we do the ECG, then
we do the chest radiographing. So with the help of a chest X ray, we can
get to see the any fluid inside the lungs because in heart failure we.
Get the you know, fluid goes into the lungs.
Or also the hypertrophy of the lungs, the cardiomegaly, the size of the
heart can gets enlarged because when your heart is in heart failure stage,
they have to pump more. They have to put extra efforts and extra
pressure. So this leads to enlargement of the heart.
So this size of the heart also we can see in the chest X ray then the blood
test, these are very common test not specific for the heart failure except
the natriuretic peptides. The hormones which are specifically for the
cardiac damage. So that one are important for that and echocardiography
will tell us or they will show us the ventricle.
And well, losing, closing and opening.
So when but this echocardiography we do only when the ECG chest act,
radiograph is telling us the problem with the heart.
OK, so similarly this is the diagnostic heart failure from the CPG guidelines
that how step by step first we see the sinus symptoms or its suggest of
the heart failure that shortness of breath and all those things. But these
sinus symptoms can be from myocardial function or angina also heart
failure sign and symptoms other than edema, the ankle edema and all
those things, yes, they are more likely for a heart failure but shortness of
breath etcetera, it can be in angina or.
In myocardial infarction as well. That's why our next step is to do the ECG
and the chest X ray and specially this nattery uretic peptide.
For thus then, if these tests are normal or abnormal, then we go for
echocardiography and finally the diagnosis of the heart failure is made.
So this is the interpretation of the.
NP.
This natriurenetic peptide is produced by the heart ventricles in response
to the increased pressure and volume overload. So these are suggestive
of the heart failure. So these levels you don't need to memorise.
OK, this is important. The classification, the clinical presentation according
and the management.
So according to the American guideline, so we classify them into 4
quadrants of heart failure, warm and wet, warm and dry, cold and wet and
cold and dry. So what warm and wet means perfurian is adequate, which
means blood is there when blood is there, it means it is warm. When
perfusion is poor, less.
Blood. It means it is cold, OK.
So similarly, when congestion is there fluid is there, we call it wet.
And it is dry, we call it not congested. Similarly here dry, not congested
and wet means congested. So based on the warm, wet, warm, dry, cold,
wet, cold, dry condition, the management is accordingly. So lets see what
is the management for worm and VET. So since the perfusion is adequate
and fluid status is congested, diuretics should be there because patient.
Is having fluid overload.
I know tropes are not needed here. Why? Because the perfusion is
adequate, which means that contractility is OK, so no need to give
inotropes in such condition. Then second condition again it is adequate
and not congested. Then no need for diuretics as well.
Cold and wet.
So since perfusion is poor, then we can give inotropes so that contractility
of the heart is improved.
And since congestion is there, diuretics can also be given. Then last one
poor and not congested. So Puffyion is poor. I know tropes are given fluid
status, not congested, so diuretics are not given. So this one very easy to
memorise. If you remember the bomb. Wet, warm, dry, cold, dry and cold.
Wet status then management will be automatically you will recall.
OK. So can we recall the choices of the inotropes? We discussed this in
previous semester in the management of shop.
What are the examples of inotropes?
Their function will be what to increase the contractility.
Basically, cardiac output heart rate increase. So what are the examples?

Koh Siew Hua 2:58:27

Adrenaline.

Asst. Prof. Dr. Muhammad Junaid Farrukh 2:58:29

Adrenaline.
OK, non adrenaline dobutamine.
Dopamine.
OK. So like we discussed in the last time, the choice of the iotrope
depends on what effect we want. So lets suppose if patient blood pressure
is compromised then non adrenaline and adrenaline will be used. But if
contractility is compromised then dobutamine and dopamine will be
considered as the first choice.
OK, so this is the schematic diagram of the management that in acute
heart failure. First of all, we give the oxygen.
Neuretics, then, based on the blood pressure, we will give the
management so lets say blood pressure is high.
Nitrates will be given to lower down the blood pressure and then if the
blood pressure is low nor adrenaline or dopamine can be given OK. So like
we know noradenaline is used or it target blood pressure dopamine
depends on the dose related effect.
At low doses it causes renal perfusion, moderate doses it causes cardiac
contractility and at very high doses it increases the blood pressure.
OK then after that based on the status they gave either oral medications
and then again not improved, then we continue diuretics and nitrates and
finally in continue to the oral medications.
So these are the commonly used medications with their route of
administrations. So since acute heart failure, mostly critical condition, the
these are in infusion forms. Either your diuretic, either your vasodilator or
your inotropes.
These complex dosages no need for you to memorise.
OK, so these are the examples of the diuretics which we are using in heart
failure, Lube, diuretic, thiazide, and mineralocorticoids.
These are our ACE inhibitors and their initial and target doors.
These are the beta blockers.
Ar BS.
And some other drugs. OK, so if you see that all these drugs are same
drugs which are used in the management of hypertension, a RBS ace
inhibitors, beta blockers. So you can memorise like lets say captopril one
drug, same for the management of hypertension, same management for
the heart failure. The doses may vary but overall but in fact in some cases
doses is also the same one.
Drug it can be fit for hypertension as well as heart failure.
The management of heart failure is the same. Drugs which are used for
management of hypertension.
OK, now we have some other drugs like digoxin, anticoagulants,
ivabradine. So these are case by case basis. When the patient fails the
first line therapy or if patient has some specific factors or specific
symptoms, then only we start with these drugs specifically, like these
digoxin. It is not a first line drug. Always our second line drug.
And used with caution because of its narrow therapeutics index.
And when most of the time it is considered only if the ejection fraction is
less than 40%.
Because the role of dizoxin is to increase the contractivity.
And based on the studies, the clinical trials, Digoxin has no effect on the
survival rate.
Such effect, it just helps to decrease the hospitalization of the patient.
Overall survival rate, it will have no effect.
And those patients who are at the risk of anti like coagulation.
An anticoagulants like warfarin can be given specially those patients who
have underlined atrial fibrillation atrial.
Relation.
So non pharmacological measures for the CHF. So this also very common
and general diet and nutrition, lifestyle changes, exercise, sleep disorder,
social support, education, OK, specifically in the diet and nutrition, what
we should focus on, can someone recall?
Restriction.

Wang Hanying 3:04:13

Sauce and sugar.

Asst. Prof. Dr. Muhammad Junaid Farrukh 3:04:17

OK, very good salt and water.
Do it.
Because sugar, in other words, yes can, especially because indirectly it
will be affecting BMI indirectly, it will be affecting diabetes.
Yes, good salt, sugar water. Basically its a fluid overload because if patient
is not taking control of the fluid the.
Edema problem will be there.
And also the volume overload.
Volume overload.
OK, very good then.
And then OK.
An important drug interactions with heart failure medications. Non
steroidal NS aids. These cause vasoconstriction, fluid retention. So the
same drug they had issue with hypertension also.
At the same time they have issue with the heart failure also, so easy to
memorise. Calcium channel blocker short acting, the PDP and DILTY Azim
depressed myocardial contractility. So of course in heart failure TCBS they
have to be given with very caution or discouraged.
You see a tricyclic antidepressant. They may impair cardiac contractility
and increase the vulnerability to arrhythmias. So if indicated, a selective
serotonin reuptake inhibitor may be preferred. So lets suppose if your
patient has general anxiety disorder.
Or other depression major depressive disorder. So we can give them SSRI.
Tricyclic antidepressant should be avoided in those patients, so since you
know, like if you see the latest guideline TCA are not the first line drug
anyway. So we will not see this interaction quite often unless the patient
is an, you know, old patient with 10 year history of all these things and he
is he is taking TCA for a long time. Yeah then yes but if.
Its a newly diagnosed patient. We don't really give tricycling
antidepressant and the first line is SSRI.
OK. So that's all for the heart failure. So very easy to remember. The main
things in heart failure is the cut off points for your ejection fraction. That
what is the reduced ejection fraction and what is the other 50% and above
ejection fraction. And next the the drugs are the same.
So you need to at least memorise one agent from those class, like ACE
inhibitors from the from the ACE inhibitors. And then if from the beta
blocker, which one you want to choose diuretic, which one you want to
choose and when to use the digoxin. As I told you that it is not first line
drug only used in certain conditions like ejection fraction is less than 40 or
50. The contractility is not that high and.
Patient has failed the first line drugs, then only these second line drugs.
Comes in.
OK. Next our last topic for today is dyslipidemia.
So this is also not so complex topic.
So here dyslipidemia is when in our body the cholesterol levels, the
different components of the lipid profile like your total cholesterol,
LDLHDL, triglyceride, they are impaired or they are high.
OK. And the importance of these, you have already seen in acute coronary
syndrome that what happens when your cholesterol level is high, its
straight away a risk factor or a causative factor for myocardial infarction
or angina?
So these are different causes and.
Their effect on different types of cholesterol, so no need to for you to
memorise this in detail, but in general you should know that these are the
causes which effect cholesterol dysregulation in general.
OK. Then for the CV risk assessment, there are several types of scoring
system. This is the old scoring system of the 10 year assessment of the
cardiovascular mortality. These days we follow the.
Latest scoring system which I show you. Yeah, this one. So you just follow
the a SCVD scoring system.
Latest guidelines support this scoring system, so in this based on the
LDLC values and the patient comorbidity like where the patient has
diabetes or they have no diabetes based on their age factor.
So the categorization is take place.
So this is the interpretation. So if the patient is at low risk, then we do the
lifestyle modification. If it is on the borderline risk, then again the life.
Style modification with some statin therapy is there then intermediate
risk.
Where we step, of course Staten is there and initiate statin and high risk
of course.
So this is the summary as per the CPG guidelines, again based on the.
Risk of the cardiovascular risk and the level of your LDL and non SDL.
OK. So once we identify that patient cholesterol level is high and they are
at the low level, so in the low level what we do the therapy is only lifestyle
modification.
CV risk is low for lifestyle modification will be there. So which means that.
Of course, what is the issue when the cholesterol level is high?
It will be due to, of course, patient BMI.
And then.
So other factors like social habits.
So the same thing and the diet of course.
So these will be our lifestyle modifications. So patient have to do the
regular exercise so they can control the BMI and weight.
And also diet needs to be modify if they want to reduce the weight and for
the social habits if they are cigarette smoker or alcohol smokers they
need to cut it down. So these are the lifestyle modifications.
So the drugs for the treatment options include. So we have
123456123456 yeah, 6 types of the medications are there among all of
them. The most widely used and commonly used are the statins.
And the important side effect for the statin is myopathy.
Once patients start taking the medication during our counselling points,
we can highlight this thing that patient will experience muscle pain. What
is myopathy, it is muscle pain.
And sometimes it is really quite severe.
And if patient has acute or chronic liver disease or concomitant use of
certain drugs, then the statins are.
Don't try and take it then. In such cases we will go and see other alternate
options.
OK, so according to the CPG, lipid modifying agents are necessary to
achieve the target lipid levels and only statins have been studied in the
primary prevention. So statins are your first line of drugs for moderate to
high risk of the patient.
OK, so since cholesterol is biosensed in the early morning statins with
shorter half lives.
Should be administered in the evening.
OK, because the cholesterol synthesis is at night most of the time.
And the the one with the longer half life, they can be given at any time of
the day.
So these are our examples of the statin based on their.
Potency also. So the high intensity one is atorvastatin.
Then the moderate one includes this, so see the IT is the dosing, high
dose atorva statin and roseauvo statin. They are considered as high
intensity therapy whereas the same drug with moderate doses and some
other drugs.
They are at the moderate therapy and low intensity can be simvastatin
and or low doses drugs.
OK, so these are the drug therapy and their combination based on the risk
factors of the CV risk.
So the standard one is the statins with high and very high cardiovascular
risk or even in the intermediate risk.
Then, if the LDL goal is not achieved by the statin, then only we can add
this cere.
Or if again the diabetic patient is there, then we can add this favourite
component. If fiction is not responding to statin then this can be used.
So focus, you can focus on the statins mainly.
OK, so this was the drug therapy.
So in the lifestyle modification, any supplements?
It should be used.
Any any options?

Koh Siew Hua 3:15:50

Fish.

Asst. Prof. Dr. Muhammad Junaid Farrukh 3:15:50

What are the OK fish oil?
Anything else?
4Q 10.
Then we have red.
Rice.
And many more. Actually, there are so many complimentary and
alternative medicines which are used among them. These 3 are most
commonly studied as well as shown to be effective.
And fish oil. Keep in mind high dose.
By dose, fish oil and Co, Q, 10, Coenzyme Q 10 and the red cheese rice.
So when we see a patient who has dyslipidemia but they do not have any
cardiovascular risk factors and we classify them in the low category. So
along with the lifestyle modification, because we know that if someones
BMI is high, they cannot reduce 10 KG in one month. So we have to put
them on some supplements also.
On its anti oxidant effect cholesterol lowering effect like that, so
supplements plus lifestyle modification can be a good start.
And also some of the studies have shown that because we just studied
that statins, the side effect is this muscle pain and myopathy. So some
studies says that if we give Co Q 10 along with the statins, it can reduce
this side effect as well. So there are multiple benefits of using this Co Q
10:00 in the dyslipidemia patients.
K students. So that's all for today. Later you can go and read the notes
again. Mark the points which you do not understand and we can discuss in
our next session as well. OK.
OK, have a good night and eat good dinner. Bye bye.

Koh Siew Hua 3:18:28

Nice. Thank you, Sir. Bye bye.

Wang Hanying 3:18:30

Nice girl. Thank you, Sir.

Li Chengying 3:18:32
Bye.

Asst. Prof. Dr. Muhammad Junaid Farrukh 已停止听录