Comprehensive Guide to Drug Effects on ECG Patterns and Cardiac Safety

[Music] [Music] i welcome you all

for the session on drug effects on ecg this is one of the topics that we have

in our program on interpretation and application of ecg in clinical practice we know pretty well that ecg is one of

the crucial investigative parameters we usually take it for patients who have cardiac disease or people who complain

of chest pain or you know angina and there are few things when a patient is complaining then we will be interested

to take ecg and based on the findings in the ecg will try to you know

arrive at a diagnosis um or you know that will indicate us to guess few

you know disorders which are related to heart now in this session we are going to see

the drugs the various drugs which can cause changes in ecg so that by by

you know getting into you know the clinical spectrum of problems that the patients are having we

will arrive at a proper diagnosis and we can also you know ah treat them accordingly

now for the sake of this presentation i have actually categorized the drugs into four the reason is that

there are few drugs which affect you know heart straight away and they change the electrophysiology and they

modify the ecg pattern they are directly acting drugs we have other drugs let's say drugs

which you know do not actually act on heart but still they produce changes in the ecg through

reflex mechanisms or you know we call them as indirectly acting drugs which affect ecg

then we have non-cardiac medications you see here non-cardiac medications uh there may be

antimicrobials there may be antidepressants or antipsychotic drugs they also you know act through some

nonspecific mechanisms and they change the ecg pattern and then finally we have drugs of abuse

ah you know drugs we use for recreational purpose or non-medical purpose they also affect heart and then

we get changes in the ecg so these are you know broadly i have classified the drugs that affect ecg into four

now we are into the drugs that act directly on heart heart let us say myocardial muscle or

conducting system you know they have various you know receptors and channels um and

we have drugs which could you know um stimulate or inhibit these receptors and you know channels and thereby we get a

lot of changes in the electrophysiology and then we ultimately see changes in the ecg the crucial receptors and

channels i have listed here we have sympathetic receptors you know we have

adrenergic and you know noradrenergic and system and we have alpha and beta receptors in it and

beta 1 beta 2 beta 3 and then alpha 1 and alpha 2 in in you know myocardium we have

predominantly beta 1 receptor located we also have parasympathetic receptors cholinergic receptors basically we

classify cholinergic receptors into muscarinic and nicotinic but in heart what we see is

you know m two muscarinic two type receptor which is predominantly seen in heart both in myocardial muscle and in

in the conducting system then we have calcium channels l-type calcium channels and then sodium channels and then

potassium channels and then myocardial membrane has got sodium potassium atps which is an enzyme so these are the

potential targets for drugs and these drugs acting on various receptors and channels in the heart they you know

facilitate changes in the myocardium sometimes you know these changes may be inert we may not have significant

clinical you know outcomes of it but sometimes these changes may be dangerous and may be you know serious and which

can give you know significant cardiovascular morbidity and mortality now we are into the drugs

which could affect ecg based on you know their action somewhere else mostly let us say blood vessels

arteries and veins and you know by acting on those arteries and veins we could get changes in the ecg ah

these drugs may not straight away act on myocardium to bring in changes in the ecg okay that's why we put them as you

know indirectly acting drugs or you know drugs through reflex mechanisms they they produce changes in the ecg ganglion

stimulants i am going to the last one you know we have atomic ganglia drugs acting on those ganglia will will

release catecholamines and these catecholamines you know through reflex mechanisms act

and in heart and they bring in changes ganglionic stimulants and then we have lot of vasodilators see

here vasodilators many of them are going to act on arteries and few of them will be acting on ah you know veins and then

you know will have vasodilation may be arterial dilatation or venous dilatation and then through

reflex mechanisms you know catecholamines may be released and they may produce changes in the ecg

most importantly we have calcium channel blockers and then alpha blockers again

sympathetic we have seen sympathetic receptors alpha and beta here alpha ah one receptor

blockers um they they produce significant vasodilation reduction in the blood pressure and they may change

the ecg pattern then nitrates are veno dilators potassium channel openers and ac inhibitors angiotensin converting

enzyme inhibitors and angiotensin receptor blockers um

ac inhibitors are good to heart they don't significantly change the ecg but sometimes in the peripheral vasodilation

through reflex mechanisms we may have you know changes in the ecg the third category drugs i have already told that

they are mostly non-cardiac medications maybe antibiotics maybe you know antipsychotics

maybe antifungal drugs ok or drugs acting in the gi tract they are non-cardiac drugs and most of these

drugs may increase qt interval you know and they may cause

sometimes polymorphic ventricular tachycardia now these category of drugs they they bring in changes through

non-specific mechanisms and then the fourth category we have drugs of abuse you know we use drugs

not you know sometimes people are you know getting tempted to use drugs for

recreational purposes non-medical purposes they get habituated and they started using you know

amphetamines opioids cocaine and cannabis and they may also cause you know serious

electrophysiological changes in the heart and ultimately you know the people who are using it may suffer with

significant cardiac morbidity now we are actually going ahead with

the individual drugs how they affect the ecg and what are the exact changes we will get to see in ecg

if we are using those medications and the mechanisms by which these drugs are going to cause

you know ecg changes we have beta 1 receptor and we know pretty well that beta 1 receptors are

located everywhere in heart let's say endocardium it is there and you know myocardium it is there and conducting

system everywhere it is present beta 1 receptors and it's basically a stimulatory receptor that's why we call

them as gs you know receptor and there are drugs there are

neurotransmitters that will stimulate beta 1 receptors and similarly there are drugs and

neurotransmitters that will inhibit beta 1 receptors if if something is stimulating beta 1 receptor it it

increases force of contraction it increases rate of contraction and you see increased cardiac output and

increased heart rate and similarly if if you have something which is inhibiting beta 1 receptors um you know

it causes reduction in the heart rate and reduction the force of contraction conductivity and then reduction in the

cardiac output we have drugs that stimulate beta 1 receptors like adrenaline noradrenaline isoprenaline

and dobutamine isoprenal and dobutamine they are cardiac stimulants we use them in case we have shock we have you know

cardiogenic shock and cardiogenic failure sometimes we use them nor adrenaline again in severe hypotension

cardiogenic shock we are using adrenaline we use it for anaphylaxis and then

use it again in you know cardiac arrest and cardiogenic shock they are life-saving medications

and without proper reason if you are using them they may be dangerous also because you know they are going to

stimulate heart and for no reason if you are stimulating hard with these powerful pharmacological

agents ah you know we may even have you know myocardial infarction

we have seen patients you know getting treated for allergy with adrenaline going for

ah you know acute myocardial infarction basically these drugs cause tachycardia you see the heart rate is increased more

than 100 the normal heart rate is about 60 to 100 and all these medications that are stimulating beta 1 receptor may

cause increased heart rate that we call it tachycardia and ecg will give us the heart rate of 100 and more 120 140 or

even 200 we can get the heart rate in the ecg and sometimes they also cause reduction in the t wave amplitude and

they also you know increase qt interval these are the ecg changes that we commonly encounter when we are

using drugs that stimulate beta 1 receptors and we have drugs that block

beta 1 receptors ah you know um we have non-selective blockers uh you

know you have beta 1 beta 2 and beta 3 receptors and from pharmacological action point of view

we mainly use trucks that modulate beta 1 and beta2 and we have non-selective beta blockers like they block both beta

1 and beta 2. drugs like sotalal pindalal and nadolal they block both beta 1 and beta2

and we have selective beta 1 blockers like metoprolol atenelol celiprolol esmalal and acebutolal they don't have

significant action on beta to receptor they only act on beta 1 receptors and they block beta 1 receptors

and what are the changes beta 1 inhibition brings in ecg we know

you know beta1 stimulation is stimulating heart and beta1 inhibition is inhibiting heart so the heart rate is

going to come down force of contraction is going to come down cardiac output is going to come down and hence what we see

in ecg is bradycardia and av block av node ah is located between atria and ventricle and the impulses are

transmitted from sa node through you know av node two ah the ventricles and all other zones in the myocardium so

if if we are using beta on blockers they they bring in av block and they also reduce heart rate and we

get bradycardia and sometimes they also cause prolongation of pr interval qrs widening the cause and you know

prolongation of qtc interval okay so whenever a patient is receiving beta one blockers these ecg changes may happen

okay now we are going to m2 receptor you know muscarinic two type

receptor ah you know the neurotransmitter uh endogenously present to modulate muscarinic activity is

acetylcholine which is secreted from the parasympathetic or cholinergic neurons and this receptors are located

in myocardial muscle and conducting system it is basically inhibitory in nature so it goes with gi receptor

and again we have drugs and you know mediators that stimulate m2 receptors and then that inhibits

you know m2 receptors and if we stimulate m2 receptor um you know we get a reduction in the heart rate we get

reduction in the force of contraction and conductivity and similarly if we inhibit muscarinic

receptors m2 receptors to be you know more precisely putting it here if we inhibit m2 receptors we get

increased heart rate meaning that we can have tachycardia and we may also have increased force of contraction and

conductivity now what are the drugs that stimulate m two receptors we have uh directly acting qualitics

like pylocarpine and these drugs stimulate m2 receptors straight away whereas we have other drugs which

indirectly you know stimulate empty receptors they are indirectly acting polynomics they do not act on the

receptors ah rather they you know um you know inhibit an enzyme called acetyl cholinesterase this is enzyme that

metabolizers are still choliner still colon is the cholinergic neurotransmitter and if you could

inhibit the enzyme that destroys acetylcholine what happens is that um you know

the levels of a still colon in the synapse will be more will be increased and this enhanced testile colon will

will be stimulating too much these m2 receptors and then you will have all cholinergic

activity that's why these drugs like fiso stigma neostigmine pyrudostic mean donopuzzle

stigma and galantamine these drugs they are called as indirectly acting polynomials because they are not acting

on receptors as such they only block acetylcholine stress enzyme and here if you see ah galantamine and rivastigmin

they are used in alzheimer's disease again in donopuzzle is used in alzheimer's disease you know memory loss

and old age um cinel dementia bigetna and the physostigma neostigma and pyrox treatment they've got a lot of

therapeutic potential in various conditions now what are the ecg changes we get when

we are stimulating m2 receptor like we have already discussed that it is going to be inhibitory in nature we get

bradycardia we get av nodal block most commonly first degree av nodal block and then we also get prolongation of pr

interval rr interval and qdc interval so if a patient is receiving a drugs for alzheimer's disease his ecg may go for

these changes m2 inhibition anti-cholinergics they are called we

have atropine we have hyacin eprotrophium eprotropium is an anti-cholinergic drug that we use for

bronchiolosmia and then we have tropicamate it it's used as eye drops you know for when we

check the vision refraction you know we use tropicamate to dilate the pupils and then pyronzapine is an anticholinergics

that anticholinergic that is used for peptic ulcer these anticholinergics may also affect you know heart because we

have m two receptor and these trucks may sometimes have you know minimal effect on empty receptors and they inhibit them

to receptors and what ultimately we have is that you know cardiac stimulation we have tachycardia the heart rate is

increased and we have sometimes a v nodal block and you know reduction in the ah you know duration of pr interval

and sometimes you will also have flattening of t wave then i think we have calcium channels

calcium channels are seen everywhere in muscles wherever we have contraction maybe intestinal smooth muscle may be

skeletal muscle or maybe in myocardium everywhere we have calcium channels in myocardium we have l-type calcium

channel it is present in myocardial muscle and also in conducting system we have

l-type calcium channel what it does is that it increases whenever we stimulate these calcium

channels whenever we have more entry of calcium into the muscle it causes increased muscle contraction

and we have drugs that block these calcium channels specifically in myocardium we have drugs

like varapamil and diltiacim you know it leads to inhibition of cardiac

contractility so what happens is that the heart rate is coming down um it causes bradycardia av block a widening

of cures complex and then cardiac asystole which is very dangerous the patient may even die out of it okay and

these drugs are antiarrhythmic drugs varapamil and deltyasm and many of the antiarrhythmic drugs you know they

by nature you know they are going to bring in lot of changes in the ecg because their site of action is hot and

hence naturally they are going to affect the cardiac electrophysiology and we a lot of ecg changes

sodium channel um you know these channels are present in the micro muscle and conducting

system uh what it does is that it it causes a rapid upstroke of cardiac action potential and impulse conduction

and we have drugs that block sodium channels uh

you know they are called sodium channel blockers and we actually sub categories them into three types you know sodium

channel blockers class one a one b and then one c there are basically you know anti arrhythmic drugs when when the

rhythm of the heart is already you know um uh you know affected and there is dysrhythmia or there is abnormal rhythm

of the myocardium will be using several you know antiarrhythmic drugs to set the rhythm to bring back you know

to a normal rhythm you know regularly regular whenever this regularly regular rhythm

is altered due to some reasons will be using drugs to bring the rhythm back you know ah for that purpose we may be using

sodium channel blocker some now class one a drugs they block the sodium channel in open state and they also

produce prolongation of action potential they are associated with prolongation of action potential we have class 1b

drugs you know they are sodium channel blockers they block the sodium channel in inactivated stat at the same time

they also reduce or shorten the action potential we have class 1c drugs they block the

sodium channel in open state like class 1 ear drugs but they do not have significant effect on the action

potential ok now what are the drugs we have as sodium channel blockers and what is the effect

these trucks bring in ah you know in the electrophysiology and ultimately in the ecg tracings

class one ear drugs we have drugs like quinidine um you know of course like anti malarial drug queen in

it is an isom isomer or a stereo isomer of queen in quinid and then procainamide diso pyramid you

know these drugs are used in ventricular tachyarrhythmias like ventricular tachycardia and other ventricular

arrhythmias and these trucks produce prolonged pr interval qt interval and they also widen

the qrs complex class 1b drugs lidocaine the same local anesthetic that we are using it ok and

then mexican they are used in again ventricular attack arrhythmias all sodium channel blockers are useful in

ventricular attack arrhythmias ah either class 1a or 1b or 1c and the ecg changes also are pretty similar for all the

classes of sodium channel blockers 1 a 1 b and 1 c here again they produce a prolonged pr interval widening of qrs

complex and shortening of rr interval then we have 1c drugs floccanide and proper phenom very many drugs for this

presentation purpose i am actually restricted the number of drugs that i am going to quote here

they are again used in you know ventricular attack arrhythmias and they produce bradycardia first degree heavy

block widening of qrs complex and yes is told and which is a very significant cardiac mobility in case if you are

using these drugs and we need to be aware of the fact that these drugs may also produce cardiac assist

now we are moving to potassium channels the presenting they're present in you know conducting system of the heart

mainly and these potassium channels regulate resting membrane potential and also they they try to regulate the

frequency of sa node and indirectly you know that means that it can control the heart rate

potassium channel blockers we have drugs like amiodarone protellium and dophetilide

they are again used as antiarrhythmic drugs amiodarone is one of the broadest spectrum antiarrhythmic which can be

used in any type of arrhythmia and it is used predominantly in ventricular tachycardia proximal supraventricular

tachycardia and atrial fibrillation and what these drugs produce in ecg is that they usually prolong

you know qt interval or qtc interval and this can sometimes lead to polymorphic ventricular tachycardia or which is also

known as tosidis d pointers sodium potassium atps it is present in the membrane of the myocardial muscle

and you know it is a target for a drug you know age old medication that is used

in cardiac failure digoxin and it is also present in the conducting system av node sa node everywhere it is present

what it does is that it tries to maintain low sodium and high potassium in the cell

and also it maintains a resting membrane potential and when we block this enzyme you know

sodium potassium atps digoxin does it we have lot of digoxin like drugs and many of these drugs what they do is that they

increase the force of contraction at the same time they produce every nodal block and they reduce the heart

rate so digoxin like drugs are you know so unique you know they increase the

heart i mean they increase the cardiac output they increase the force of contraction at the same time they reduce

heart rate they they reduce you know uh the conductivity of the impulses and they produce bradycardia okay which is

very unusual for a drug ok increased cardiac output at the same time bradycardia they

they also produce significant ecg changes for example you take digoxin-like drugs practically they can

they can cause any any change in the ecg they can cause atrial premature beats

you know functional premature beats atrial tachycardia av block premature ventricular beats and ventricular by

germany now i think we are moving towards indirectly acting drugs what we have seen so far is you know the drugs

that were acting directly on heart on various receptors and channels and bringing in changes in the ecg now we

are going to talk about drugs that act in the periphery vasodilators at the same time producing

changes in the ecg if you see here calcium channel blockers we are taking first

they act um you know in the arteries smooth muscles they are l-type calcium channel blockers

drugs like nephidupin amlodipine nicardipine and phallodipin they are used in hypertension

very popular in the treatment of hypertension calcium channel blockers they do not have significant direct

cardiac activity they only have very minimal cardiac activity as such these calcium

channel blockers ah but what they do is that because of the peripheral vasodilation that will be

reflects you know secretion of catecholamines from the autonomic

ganglia and these catecholamines act on myocardium and they cause reflux tachycardia and occasionally minimal

bradycardia you know is associated with nephidupin-like drugs and they also produce av block non-specific st and t

wave changes calcium channel blockers they are vasodilators

and then we have alpha blockers alpha one blockers because we know that there are receptors alpha one and alpha two

and alpha one a receptor is present in the arterial smooth muscle ah drugs like prazos in terrazzos and

doxazosin and tampsilocin they are used in benin prostate hypertrophy also especially thamsilozin and oxazosine

whereas brazosin is mainly used in systemic hypertension when there is a you know very severe elevation of blood

pressure and you know when we find it difficult to handle

systemic hypertension with routinely used drugs we go for these alpha 1 blockers they are very significant

you know in reducing the blood pressure and what they do in the ecg is that they produce ventricular brady and

tachyarrhythmia first degree av block then we have nitrates unlike you know calcium channel blockers and

you know alpha one blockers nitrates they predominantly are venodilators they dilate the veins larger veins also

smaller veins and they act by releasing nitric oxide and they are used in angina bacterias

um see when patients have cardiac chest pain and we want to relieve the chest pain immediately you know we give

nitrate sublingually and then you know it releases nitric oxide produces veno dilatation and reducing you know venous

return they reduce the cardiac workload and they reduce anginal chest pain and what nitrates produce here in ecg is

that you know they cause tachycardia and otherwise i mean they are pretty safe there is no significant

you know electrophysiological changes that we encounter with nitrates potassium

channel openers we have drugs like nicorandal and minoxidil minoxidil is a potassium channel opener

you know rarely used in hypertension nowadays but it is found to be associated with

increased hair growth and hence minoxidil um as a lotion or you know as a liquid preparation it is used in

alopecia you know baldness we are using minoxidil but then it is a you know vascular smooth muscle ah relaxant ok

and you know it it causes increased intracellular potassium and muscle relaxation and what it does is that it

causes a t wave changes and also shortening of qt interval potassium channel openers

then we have isodilators ac inhibitors angiotensin converting enzyme inhibitors drugs like kept april

anal april and lysine opera and then arbs angiotensin receptor blockers like valsartan tell me saturn urban saturn

you know there are very many drugs that are used and now this is the class of drugs both ac inhibitors and arbs are

very commonly used in hypertension their antihypertensives they also have cardiac protective activity okay but

then they do not have much or significant electrophysiological changes though rarely they produce qt

prolongation av nodal block and then st depression they are considered to be pretty safe as

far as heart is concerned ac inhibitors and angiotensin receptor blockers

now we have the last category of drugs in the indirectly acting are the drugs that act

through reflex mechanisms producing ecg changes we have ganglionic stimulants autonomic ganglia you know they have

parasympathetic nerve supply and they act by releasing a still choline and this acetylcholine will stimulate

nicotinic receptor here basically nicotinic receptors there are two classes

n n type they act on neurons and then n m type they act on skeletal muscles and here we are talking about

you know nicotinic receptors present in the neurons in the autonomic ganglia and stimulation of these ganglia will cause

release of catecholamines adrenaline and noradrenaline and they will stimulate myocardium to cause you know increased

force of contraction and rate of contraction drugs like nicotine and labylin you know they cause sometimes ah

release of catecholamines and they produce ecg changes like sinus tachycardia and ventricular tachycardia

we have now you know non-specific mechanisms non-cardiac medications you know we use

like i i was saying you know drugs for other purposes like you know antibacterial antiviral antifungal

antipsychotics antidepressants antihistamines are prokinetic drugs all these drugs sometimes you know they are

associated with cardiac issues ah they they cause prolongation of qt intervals and they may produce

ventricular arrhythmias how they produce the mechanisms are not very clear but still

they mediate through multiple receptors they they produce interactions among various receptors and they may also be

associated with electrolyte abnormalities and other unknown mechanisms they cause this electrolyte i

mean electrophysiological changes in the heart and they produce changes in the ecg and there are drugs which were

banned for their cardiovascular effects you know they were approved for some other indications they were in the

market but later they have realized that they are associated with electrophysiological changes and

significant cardiovascular morbidity and mortality and these trucks were banned drugs like terrafonadine

it was used for itching for running nose okay ostema's all again for allergy and hypersensitivity reaction

sysaprad a prokinetic drug for gastrointestinal problems they were all approved for their indications but then

later you know the scientists have realized that they were associated with

significant cardiovascular problems and they were all banned from the market and these are the drugs which are

already available in the market but still they are associated with you know

cardiac issues antibacterials levofloxacin even azithromycin has it clarifies in erythromycin many of the

macrolide antibiotics have got this problem and antifungals like intraconozol or ketoconazole antivirals

nelfina where they increase the qt interval they are associated with significant cardio

cardiovascular problems in case if the patient is already having a cardiac problem then we need to be very careful

when you are using these medications antidepressants like amitriptyline imipramine and doxapin they cast qt

prolongation and antipsychotics like haloperidol respiration and kutiapin they cause you

know this problem polymorphic ventricular tachycardia and susceptible patients

antioxidants supposed to be a very safe drug has got this issue on dom peridot you know they they may cause qt

prolongation and polymorphic ventricular tachycardia now the point is that why we need to

know these things is that when when we are using these medications in any other individual you know who is normal whose

cardia function is fine he does not have any morbidity then the the issue that these drugs are you know predisposing

the patients may be very very minimal but if the patients after 50 years knowingly or knowingly they may be

having cardiovascular problems and if you are using these medications and you know we may predispose the patients to

get into this you know arrhythmias and you know we may unknowingly you know predispose them to

get into this cardiovascular morbidity and mortality ok now what ah finally we have is drugs of

abuse illicit drugs you know opioids

for unapproved indications we are using and people who are mixing these medications

and liquor and they are drinking it and without knowing that these drugs have got significant cardiovascular

you know interactions opioids they may produce bradycardia

and heroin is an opioid which can cause cardiac conduction abnormality and many of these drugs are associated with

you know lung utc syndrome widening of the qrs complex hallucinogens like lysergic acid diethylamide they may

produce tachycardia cocaine it can cause sinus bradycardia complete heart block we have seen patients who have abused

cocaine you know getting into complete hard block then marijuana cannabis ganja you know

tachycardia non-specific st t wave changes and amphetamines ecstasy like drugs sinus

tachycardia supraventricular attack arrhythmia also without you know understanding the

implications of you know interaction of these drugs in the cardiovascular system people are

abusing it i mean we need to strongly you know disagree with the practice of using these medications okay for that it

also makes them to get into lot of psychological issues central nervous system issues and also cardiovascular

problems okay now ah we have almost come to the end of this session what we have seen is that

um you know the drugs we have categorized into four types directly acting drugs indirectly acting drugs and

then drugs through non-specific mechanisms non-cardiac medications affecting ecg and then drugs of abuse

producing ecg changes why we need to know this is that number one

which is very important you will have a drug which doesn't have this you know

you know changes in the ecgs so you can always go back and then use an antibiotic in case if you are treating a

cardiac patient who has got a respiratory infection instead of choosing azithromycin and levofluxin we

can use amoxicillin because amoxicillin is an antibiotic which is useful in respiratory infection but doesn't have

significant ecg changes so the idea of giving this session is that we can we can choose drugs which are not having

significant you know interaction with uh you know cardiac receptors they they don't have you know

significant you know interaction with alpha beta or

muscarinic receptors so they can be safely prescribed in a condition in which you can also you know prescribe a

drug which has got significant ecg changes that's the point we would like to impress here that always try to

choose a drug which does not have cardiovascular you know interactions in that way giving you an overview of drugs

which have got changes you know in the ecg is to guide you in choosing a drug which will not hit the

ecg this is point number one point number two if at all you want to use the same medicines which have got

significant ecg changes you can be you know preparing the patient and also the physician can prepare himself in in

handling an eventuality ok azithromycin can lead to increased or prolongation of qt interval and if

you are knowing the fact then you can prepare the patient and the physician also will prepare himself in handling

the cardiovascular problems so these are the two points i think as as a medical student or as a treating

physician we need to know one is that choose a drug which doesn't affect ecg number one number two if at all we are

choosing a medication which can cause ecg changes be prepared uh yourself in handling the eventuality that's the idea

of having this session in this you know program interpretation and application of ecg in clinical practice

now before concluding i thought i will make a small remark on regulatory requirement of developing a drug

if we develop a drug for a non-cardiac purpose non-arythmic purpose okay maybe an antibiotic may be an

analgesic may be an antihistamine maybe an antihypertensive medication which is not indicated for arrhythmia if

you have the idea of developing a drug now there is a guideline which which talks about every drug has to be

evaluated for its action on qt interval because you know we have seen many of the non-cardiac medications are

affecting qt interval okay and hence this ic hick is the agency like international conference on

harmonization this agency is giving guidelines on development of drug products okay they have given this

guideline on efficacy 14 e 14 guideline which is titled like you know clinical evaluation of qt interval prolongation

and pro arithmic potential for non antiarrhythmic medications like any other medication which is not

meant for arrhythmia if you are developing it is not just enough we are we are evaluating the efficacy and

safety in that particular indication it is also very important that we need to test the drug for its potential to

increase qt interval so we have to do a thorough qt study and also we need to have end

points in the clinical trials so that whatever drug that we are getting for the market is not having significant

cardiovascular action significant effect on the qt interval ok why we are concerned about the

cardiovascular effects because many of the non-cardiac drugs may also be associated with you

know significant morbidity like you know polymorphic ventricular tachycardia or toss seriously point is a sudden cardiac

death can happen in case if you are using those medications if they are associated with significant

you know interaction in the ecg or you know qt interval cardiac electrophysiology and they may you know

produce or they may predispose patients to get into ventricular tachycardia ventricular fibrillation and flutter

they may produce syncopal attacks or sometimes she's us in order to avoid all these complications whenever we develop

a drug i think we need to make sure that the drugs are not having their actions on you know qt interval and also in the

myocardial muscle and conducting system okay i think with this we have come to the

end of the presentation ah this session was about drugs drug effects on ecg ok i

hope the session was useful to the beginners especially the medical students and practicing physicians um

you know in in giving you know thought whenever they are choosing a medication like i have

already highlighted try to choose a medication which is not having ah you know any cardiovascular interaction or

if at all we are forced to choose a medication which is having all these changes in the ecg's or interactions in

the myocardial muscle and you know conducting system please be ready to handle any eventuality ok

thank you very much for patient listening