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MEDICINE OSCE - Part 2 — Transcript

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0:00Good evening dear members.
0:01We'll begin. So in the last session we
0:03discussed a few of the imaging and
0:05clinicals uh images etc. So we'll
0:08continue with that. So today we'll start
0:11with some commonly kept uh ECGs. So here
0:14is the first ECG
0:17that I'm showing you to
0:19so anyone can
0:22read and tell me what is the abnormality
0:25that you're finding and
0:35it's a young lady who is come with
0:38palpitations and this is the ECG that
0:40has been given to you. So what is your
0:43inference? How will you interpret the
0:46ECG?
0:53Anyone can volunteer and start reading.
0:55It's a 12 ECG.
0:57Okay.
0:59Normal standardization.
1:01Okay. It's normal standardization.
1:03Normal standardization.
1:05Pavs are not visible. Coming to the
1:06rhythm, the P waves are not visible.
1:09Okay.
1:09And the rhythm is irregular. Okay. So
1:12you can see
1:13R intervals
1:14rhythm strip. You can see that it is
1:16varying RR intervals that you're seeing
1:18grossly varying RR intervals you're
1:20seeing there. And then as you said the P
1:22waves are not visible. PR P waves are
1:26not visible. Yes. Proceed.
1:29Yes sir. Um
1:31the rates are approximate rate. Um
1:37so how do you calculate the rate when
1:39the rhythm is irregular? How do you
1:40calculate the rate?
1:42count for uh 6 seconds and multiply it
1:44by 10 or count for 3 seconds and
1:46multiply by 20.
1:47Okay. So, you can count for 6 seconds.
1:49So, 6 seconds would amount to
1:52um
1:5330 boxes boxes.
1:5530 30 large boxes. [clears throat]
1:5630 boxes.
1:57You can see that there and then based on
1:59that you multiply it by that.
2:01So, approximately what's the heart rate?
2:05If you could see till here possibly that
2:08would be 30.
2:11Seven
2:1470
2:15yeah around 70 75 it looks like.
2:18Okay. So irregular rhythm you always
2:20have to calculate the heart rate by that
2:22rule where you count it for uh 30 30
2:25boxes that is you count it for 6 seconds
2:27and then multiply it by 10. So that's
2:30the way to calculate for irregular
2:31rhythms. For regular rhythms, you can
2:34use the same formula or you can use your
2:36simpler formula where you divide the,500
2:39divided by the small squares or 300
2:41divid by the large space. So you have a
2:43heart rate of around 78 irregularly
2:45regular and absent P waves. Yes,
2:47proceed.
2:48What is the axis sir?
2:52Um one is positive AF is predominantly
2:55negative
2:56and lead to being bifasic. So this
2:58problem is a physiological left axis
2:59deviation.
3:01Okay. It's a left axis but it is
3:02physiological because sleep 2 is equif
3:14there's a persistent s wave in V6 also.
3:17So probably there is some component of
3:19uh right ventricle enlargement.
3:22If right ventricle should have been
3:23there what should have been the wave in
3:25V1?
3:26V1 should have been predominant positive
3:29R. Yeah. Wave one should have been
3:31predominantly positive. You wouldn't
3:33have had so prominent uh R waves in uh
3:38one and all. So you would have had a
3:40little rightward axis. So it's on the
3:42leftward axis. So doesn't look like
3:43there is a right ventricle.
3:45Poor Rwave progression.
3:46Okay.
3:46There is a poor Rway progression. That
3:48can be said. Okay. You can say that the
3:50S wave is persisting. It is may not be
3:52secondary to the chamber enlargement. It
3:54could be something else. Okay. Proceed.
3:58Um morphology is this normal or it's
4:00broad?
4:02It's normal susly
4:08enlarge.
4:09Yeah, it is quite broad. You can see
4:10that broad. Yeah.
4:12Yes sir.
4:13So it's on the upper limit of normal. So
4:15may not be a complete bundle branch
4:16block but then it could be some sort of
4:18IVCD that's there. Intraventricular
4:20conduction defects possibly. Okay. Fine.
4:25And summarizing it would be just
4:29the T waves T wave morphology is normal.
4:33Some inversions some inversions are
4:35there in JVL
4:36but not inconsistently. Okay. Fine. So
4:39what's your diagnosis?
4:41Atrial fibrillation with controlled
4:43ventricular rate.
4:43Okay. So atrial fibrillation with
4:45controlled ventricle rate uh with the
4:47Yeah. Since the heart rate is less than
4:49100 uh you can say this is a controlled
4:52ventricle rate. So what is the finding
4:54uh else what else you would have wanted
4:56to be seen in a ECG with atrial
4:58fibrillation?
5:00Uh uh one minute like you'll look for if
5:03there's any coarse uh waves in V1 that
5:06waves. So fibrillary waves you would
5:08have looked for especially in V1 you're
5:11seeing the V1. If you see the V1
5:12carefully you're seeing that there are
5:14some sort of fibrillary waves but it is
5:16not coarse. It is fine fibrillary waves
5:18that you're seeing. So you said coarse
5:21coarse means 1 mm. It should be at least
5:23one box big there. So that's not seen.
5:26So coarse fatal fibrillation would
5:27indicate what? What does coarse atrial
5:29fibrillation indicate?
5:31Uh enlargement more than
5:33coarse is very very specific for left
5:35atrial enlargement. So that is what you
5:37have to remember very clearly. So coarse
5:39means left atal enlargement. Uh but if
5:41it is not coarse it could be fine. Fine
5:43could be in various other causes. Okay
5:45fine. So this is an atrial fibrillation
5:47with the controlled ventricle array.
5:50Okay. So why is the heart rate lower?
5:53Why is the heart rate lower?
5:55Because of the AV conduction,
5:56decremental conduction along the
5:58No. Why in this atal fibrillation the
6:00heart rate is within 70?
6:02Probably patient could have been on beta
6:04blockers for
6:04possibly due to drug induced. So that's
6:06the mechanism. Possibly the heart rate
6:08is controlled. So controlled is
6:09secondary to heart rate either due to
6:11drugs or sometimes there could be a
6:14conduction blocks that could be
6:15associated. The patient can have I some
6:17conduction problems which could decrease
6:19the heart rate. So those are the two
6:20mechanisms of the heart rate is lower in
6:23a atrial fibrillation. Okay. Can someone
6:26tell me the common causes of atrial
6:27fibrillation other than vijay? Anybody
6:29else can tell me the causes of atrial
6:31fibrillation? Common ones?
6:34Alcoholism.
6:35Yes. Alcoholism. By far the most common
6:38what could be the cause?
6:40Maternal valvular.
6:42Okay. Valvvelaration in a younger
6:44patient. Valvar as you said alcohol then
6:48metalosis. Yeah, that's valvular art
6:50mital stenosis.
6:53[clears throat]
6:54Hypertension. Please remember
6:56hypertension is one of the commonest
6:57causes of atrial fibrillation. Okay. ES
7:00schemic heart disease is a very
7:02important cause. Then any other systemic
7:05diseases which can produce atrial
7:06fibrillation. Systemic disease.
7:07Thyro thyroidosis
7:10can produce thyrotoxyosis can produce
7:13chromosytoma.
7:14Yes. Pop. Yeah. Fiochromosytoma can
7:16produce COPD. Hypoxia can produce atrial
7:20fibrillation. Drugs can produce atrial
7:22fibrillation. Any drug which can cause
7:24teic cardiac can produce atrial
7:25fibrillation.
7:27Okay. What is lone atrial fibrillation?
7:30What do you mean by lone AF
7:33in elderly without cause?
7:36Yeah. When there is no structural
7:38cardiac disease. Okay. You have to do an
7:40echoc cardioraphy. You'll have to rule
7:41out that. You'll have to rule out drugs.
7:43You'll have to rule out hypothyroidism.
7:45And we do not find any cause especially
7:47in endali such an atrial fibrillation is
7:49called as lone atrial fibrillation.
7:51Okay. So these are the common causes of
7:53atrial fibrillation. So these are the
7:55things that you have to evaluate in a
7:57patient who comes with atrial
7:58fibrillation. Okay. What are the
8:00complications of atrial fibrillation?
8:03Thrombolism.
8:05Yes. Thrombolism. Correct. Then
8:08decompensated heart failure.
8:10Yes. The heart failures can
8:11decompensate. One of the commonest
8:13causes of decompensation of a stable
8:16heart failure is an arhythmia and atrial
8:18fibrillation is one of the common ones
8:20that can decompensate a heart failure.
8:22Yes. Then
8:24tic cardia associated cardiammyopathy.
8:26Okay.
8:27It can produce cardiammyopathy because
8:30of if the heart rate is higher. So
8:32embolic phenomena are the most important
8:34thing that you always have to keep in
8:37mind. Okay. So how do you manage a
8:39patient who has atrial fibrillation?
8:41What are the three main things that you
8:43have to do?
8:47Rate control, rhythm control and
8:48anti-coagulation.
8:49Okay, so always remember it's rate
8:51control, rhythm and anti-coagulation. So
8:54supposedly this patient has presented to
8:55the casualty with the blood pressure of
8:5880 systolic. What is the first thing
9:00that you'll do?
9:04Patient
9:05PC shock cardio version. Do you want to
9:08do cardiovasion straight in a patient
9:10who has atrial fibrillation
9:14three times? Repeat the VP.
9:16Yeah, you will have to basically rule
9:18out the embolism. That's a very
9:19important. And if you possibly have a
9:22history again if the atrial fibrillation
9:26has persisted for more than 48 hours
9:29that means the chances of embolism is
9:31definitely I mean thrombus formation is
9:33there. So if it's a new onset within 48
9:35hours you can definitely do the cardio
9:37version but before that if possible
9:39you'll have to do an echo cardiography
9:40and rule out a thrombus and if it is
9:43definitely more than 48 hours you have
9:45to first definitely anticulate the
9:49patient and then give the cardio version
9:52again very important rhythm control is
9:54not of so much importance it is the rate
9:56control that is most important rate
9:58control will decrease the symptoms and
10:01decrease the whatever heart failure
10:03So rate control can be done by using
10:05drugs. What are the common drugs that we
10:07use for rate control?
10:14Beta blockers.
10:15Yes. Amodorum doesn't control the rate.
10:18It's beta blockers or calcium channel
10:20blockers.
10:21Earlier days we used to use deoxin. Even
10:23now it's to use deoxin. If heart
10:25failures you can uh use that. So uh or
10:29the the newer other drugs can be used.
10:32Okay. For rhythm control, what's the
10:34drug that we use?
10:37Amodoron.
10:39Okay. Amiadoron is the drug which can be
10:40used for all uh you can use uh you can
10:45use other anti-arithmic agents. What are
10:46the other anti-ymic agents? You know
10:48chemical cardioverion.
10:51Uh tenide and proenamite also can be.
10:54Okay.
10:56Any other drug for which we use the word
10:58chemical cardioverion?
11:01Yes. IDEily ebitolide is where you use
11:05the word
11:07pharmacological cardiovasc.
11:11What are the complications of amiodoron?
11:14What are the side effects of amodderon?
11:19Sir cornea verticila
11:22that's a very rare. What's the commonest
11:24side effect when you give it as an
11:25infusion?
11:27thyroid from
11:28hypotensionis
11:30hypotension always remember it's
11:32hypotension the BP can crash when you're
11:35giving that that's an acute side effect
11:37then all the rest are chronic as you
11:38said thyroid what does it produce in the
11:41thyroid
11:43both hyperyroid
11:45correct so you should know the mechanism
11:47very common theory question amidon
11:49induced thyroid disease you should
11:51remember that pulmonary fibrosis as you
11:53said that can corial damage can be
11:55produced you can have pigmentation that
11:57can happen. So amadorone you have lot of
12:00side effects but it's a good old drug
12:01still used. So that is what you'll have
12:04to do and uh anticogulation very
12:06important has to be continued and any
12:10scores you are aware of whenever atrial
12:12fibrillation is asked they'll ask you
12:14certain scores
12:15char score
12:18has blood score
12:20yes charadwas score you should know the
12:22cut offs and what you'll have to do and
12:24uh if there is a elderly patient then
12:26you'll have to calculate the has blood
12:28score also and based on that you'll have
12:30to weigh whether the patient requires
12:31anticoulation or antiplatelets alone. So
12:35atal fibrillation again one of the other
12:37causes you have to always remember is a
12:38congenital heart disease which is a
12:41congenital heart disease which can come
12:42with atrial fibrillation.
12:44ASD
12:45ASD always remember ASD is one
12:47congenital heart disease where you can
12:49have atrial fibrillation. So so that's
12:52how you manage atrial fibrillation. Any
12:54other doubts with this CCG?
13:00Do you think this patient is on deoxin?
13:08Do you think this patient is on deoxin?
13:13If the patient was on deoxyin, what
13:15would you have found on the ECG?
13:18Tick sign inverted tick sign.
13:20Yeah, you would have found the
13:21depression.
13:22Yeah, this ST depressions with the
13:24T-wave inversions in most of the leads
13:26here. You're not finding it in all the
13:28leads. You would have had uh yes you
13:30would have had a short QT also. Yes. But
13:33ST segment depression and T-wave
13:35inversion that inverse salvadar mustache
13:37pattern you would have got it in all the
13:40always rule out potassium. Potassium is
13:42one more thing which can cause atrial
13:44fibrillation problem. So potassium also
13:46has to be ruled out whenever you have a
13:49atrial fibrillation like feature. Okay.
13:52So we'll go on to the next ECG that is
13:54there.
13:56Yes, anyone can start reading.
14:08Anyone can start reading the ECG.
14:11We can go on discussing with that.
14:29This is a wrong little lead lid
14:31placement. AVR is positive.
14:33So why do you say so? You're saying this
14:35is a wrong lead placement. Why do you
14:37say so?
14:38The AVR is complex or positive. And the
14:41AVR complex is positive. Yes.
14:45and uh
14:47lead one is
14:48and the lead one is P is inverted and
14:52the QRS complex also is invers is
14:55inverted in lead one and the AVR is
14:58positive. Why is it not dextroia?
15:02Why are you saying this is leading
15:03dexardia
15:06V1 the R should be more in V1 in
15:09dextrocardia
15:09you're seeing the chest leads okay so
15:11very important how do you differentiate
15:13a true dextrocardia versus a technical
15:15dextrocardia here you're saying it is
15:17technical dextro cardia that is lead
15:20has been misplaced
15:23even in true dextrocardia you will get
15:24this pattern one will be negative and
15:26AVR will be positive but then the Rwave
15:29in the chest leads will not progress
15:31here you have a normal arway
15:32progression. So this is not a
15:34dextrocardia.
15:36It is a limb lead which has been
15:39switched. So that is where you'll have
15:40to make sure that so always before you
15:43start reading the ECG make sure you see
15:45AVR. AVR should be negative normally and
15:47lead one is usually positive unless you
15:50have dextroard. Okay. So which lead will
15:54have the maximum Rwave in the chest
15:56leads?
15:59The tallest
16:01V6.
16:04Is it V6?
16:06It's not V6.
16:08V4.
16:09V5.
16:09V4.
16:10V5. V4. That's where the maximum R wave.
16:13V5 is more than V4. It is not V6 because
16:17V6 is out in the axilla there. There's
16:19no ventricle there normally. Okay. So
16:22this is otherwise called as technical
16:24dextroard. So you'll have to change the
16:26leads and or repeat the ECG after
16:28changing the leads.
16:31Okay,
16:35anyone can read this?
16:43Please read the ECG and then tell the
16:45diagnosis.
16:57Yes.
17:20It's not that difficult, I think.
17:26Standardization is not very clear.
17:29Standardization standardization is there
17:31in the end here. Class
17:33normal standardization.
17:34That's normal standardization. Correct.
17:38Um coming to the
17:40rhythm is
17:44regular rhythm. Yeah, it's a regular
17:46rhythm. You're seeing it's a regular
17:47rhythm. It's coming regularly. Yes.
17:52muscles.
17:54Heart rate is
18:02Yes. What's the heart rate?
18:08Around 50.
18:11Okay. So, it's less than 50. Heart rate
18:12is less than 50. It's around Yeah. I
18:15think 1 2 3 4 around 40. Heart rate is
18:18low. Yes.
18:21Uh every Pwave is not followed by QRS
18:25complex.
18:26Do you think there are P waves? These
18:28are P waves are flut flut waves.
18:31These are not P waves.
18:32Yeah,
18:32these are not P waves. These are flutter
18:35waves that you're seeing here. Okay.
18:37These are the flutter waves. The
18:38classical saw to pattern you're seeing.
18:41Okay. So there is an atrial flutter with
18:44uh what's the
18:47what's the ratio that you're seeing?
18:49Five 5 is to 1 conduction
18:535 is to 1. Now why do you say it's 5 is
18:55to 1? Why it's not 4 is to 1?
19:00Why are you saying it's five? Who's
19:01that? Who said five?
19:09You're saying five waves.
19:11It's four is to one. 1 2 3 4 five
19:14flutter waves means it is four is to one
19:16conduction. One less than the number of
19:18flutter waves. Okay. So it's 4 is to1
19:20conduction. So it will flutter with 4 is
19:22to1 conduction.
19:24QRS normal or wide.
19:27[clears throat]
19:30QRS is
19:32wide.
19:32Little broader. A little broader. Yes.
19:34Little broader. QRS it is. And again if
19:37you see the Rwave progression is pretty
19:40poor. Rwave is not progressing at all.
19:43ST segment looks okay. There's a little
19:46prominence of the T-wave in the
19:48precordial leaf. So the diagnosis is
19:51atrial flutter, isn't it? Atrial flutter
19:53with the uh
19:57ventricular rate is low. Ventricular
19:59rate is low. So what are the causes of
20:00atrial flutter?
20:04What are the causes of atrial flutter?
20:13Potassium.
20:15Okay. The same the same causes which we
20:17discussed for atrial fibrillation. Yeah.
20:21The same causes could be the causes for
20:23atrial flutter.
20:25The management also will remain broadly
20:28the same. You will have to anticulate
20:30this patient. You will have to uh
20:33control the rate. Here the rate is
20:35already low. So you don't have to do
20:36anything. You will have to give
20:37antiarithmic drugs which could be used
20:39for that. Okay. So which are the
20:42patients who are more prone to develop
20:44emolism? The persons who have permanent
20:47atrial fibrillation or the patients who
20:49have peroxismal atrial fibrillation.
20:52Perox peroxisal.
20:54Peroxismal
20:55always remember peroxismal atal
20:56fibrillation are more prone to develop
20:58emolism compared to permanent. So
21:01peroximismal when the atal fibrillation
21:03settles that is where they go into uh
21:06the embolis gets dislodged and they get
21:10emolism because of that.
21:13Okay let's go on to the next one.
21:23Yes. Anybody?
21:27[clears throat]
21:34Yes. Pacemaker rhythm.
21:37Okay.
21:37Pacemaker potential.
21:38Pacemaker. Pacemaker. So where is the
21:40pacemaker put? Is it a atrial? Is it a
21:43ventricular?
21:46Both atrial and ventricle.
21:48Okay. So you're saying it is both atrial
21:49and ventricular because you're finding
21:51pacemaker artifacts before the Pwaves as
21:55well as before the QRS. You can see that
21:58the there is a pacemaker potential
22:00before the Pwave and you can see the
22:01pacemaker potential before the QRS also.
22:04Which ventricle has been paced? Right
22:06ventricle or left ventricle?
22:09Right ventricle.
22:10Why do you say so?
22:13Left bundle branch morphology. So it's
22:16an LBB morphology. That's why you're
22:18saying it is a uh uh LBB morphology.
22:22That's why you're saying it's a right
22:23ventricle that has been paste. So you
22:25have the atrium has been pasteed and the
22:27ventricle has been paste. Okay. So
22:29that's why you have a broad QRS. You
22:31have a broad QRS secondary to the
22:32pacemaker artifact. What's the axis?
22:39Whenever you have a pacemaker, the
22:40access has to be
22:44Yes. Uh
22:47one is positive, three is negative. No
22:49axis has to be
22:50extreme axis. Always remember what are
22:52the causes of extreme axis deviation?
22:551 2 3 4 5
22:59trigular ticardia
23:01VT okay correct second
23:06what's the first one you want to say
23:08before VT extreme axis
23:10toss it toss it wrongly
23:15yes dextrocardia the first cause of
23:18extreme axis is dextrocardia second as
23:20you said is v tag hypercalemia
23:23hypercalemia may not change the axis The
23:25VT like morphology it will have there.
23:28Then you have pacemaker. Whenever the
23:30pacemaker is put you get an extreme axis
23:33severe corpalmonal severe cor pulmonal
23:35you can have a extreme axis and then the
23:37technical part technical dextrocardia.
23:39So these are the causes of extreme axis
23:42deviation. Okay. So what are the common
23:44indications for permanent pacemakers?
23:47Can you tell me some indications for
23:48pacemakers?
23:50Complete hard block.
23:52Okay. Complete hard block. Fine.
23:54Symptomatic
23:56bra
23:58symptomatic bradicardia meaning u sinus
24:02nodal dysfunction if the symptomatic
24:05okay severe sinus node dysfunction or
24:07six sinus syndrome with uh if there is a
24:10symptomatic yes okay fine any other hard
24:12block which is indicated for permanent
24:14pace
24:16is causing
24:17moits type two please remember moitz
24:19type two and thirdderee heart block both
24:22are indications for permanent pacemaker
24:24Six sinus or sinus node dysfunction.
24:26Yes. Then somebody else was saying
24:32yes. Any other indications?
24:38Any other indications?
24:40Chalopathies where they prone for
24:42arythmia like
24:46there we don't be I mean that is not
24:48called a space maker. No there what do
24:51we do? We put a cardiac
24:53defibrillator.
24:54We put a ICD, isn't it? Implantable
24:56cardiac defibrillator. That's not
24:58pacemaker.
24:59Yes.
25:02Tachi brady syndrome. That's six sinus
25:04that we have already told. Any other
25:06narrative cardophythmia? Any other
25:08post uh posteptal ablation in HCM?
25:12Posteptal ablation in HOCM.
25:14Hypertropic cardiammyopathies.
25:17Okay. Again there they are
25:18defibrillators. They act as
25:19defibrillators more than pacemakers.
25:22What is
25:24if somebody has a severe heart failure?
25:27Somebody told me about dilated
25:28cardiammyopathy. What is that called as
25:31where you want to synchronize
25:33ICD crronization
25:41therapy where you have a broad QRS QRS
25:44width is really broad and the patient
25:46has a poor LV function there and you can
25:48do CRT there you want to stimulate make
25:50sure that the synchronization of the
25:51ventricles occur that is what you do for
25:54uh cardiac re-synchronization therapy so
25:56these are the again please read up about
25:58the indications. There's class one,
26:00class two indications for permanent
26:03pacemakers. Temporary pacemakers may be
26:05put for other conditions. Maybe an
26:07inferior wall MI sometimes in severe
26:09hypercalemia. Temporary pacemakers may
26:11be needed but permanent pacemaker
26:13indications are different.
26:17Okay.
26:21Okay.
26:25Yes. Somebody can tell me about this
26:27CCG.
26:45This is complete hard block.
26:47Okay. You say it's complete hard block.
26:49Why do you say it's complete hard block?
26:52There is no reason between P and QRS AV
26:55dissociation.
26:56Okay, there is AV dissociation. So
26:58what's the atrial rate? [clears throat]
26:59What's the ventricle rate?
27:02Only if the atrial rate is regular and
27:03the ventricle rate is regular, then we
27:05can call it as complete heart block.
27:08What's the atrial rate? You can see the
27:11Pwave here. That's the first Pwave.
27:13There's a second Pwave there. Third
27:15Pwave, the fourth, fifth. So P is coming
27:18regularly.
27:20The atrial rate is
27:231 2 3 4 four large squares.
27:28So atrial rate is around 60. Ventricular
27:30rate is
27:347 8 9 10
27:38ventricular rate is below 30. So you
27:40have a regular ventricle rate and you
27:42have a regular PP interval is also
27:45regular. The RR interval is also regular
27:47here. So you have a complete hard block
27:50is one of the causes of electromagnetic
27:53electromechanical dissociations. Okay.
27:55What are the other conditions where you
27:56can have a a dissociation? Other than
27:59complete hard block
28:01particip
28:04you can have it. Correct.
28:06Then any other conditions where you have
28:08an AV dissociation.
28:14Okay. What are the clinical signs?
28:16Junctional teicardius.
28:18What are the clinical signs of AV
28:20dissociation?
28:22Clinical signs of AV dissociation.
28:25Canon a waves.
28:26Okay. Canon a waves. Correct. Second.
28:32Second.
28:35Yeah. Canon a wave is correct. Any other
28:37signs which you have
28:39of a dissociation?
28:46Anybody?
28:48Clinical signs of AV dissociation.
28:55JVP will have Canon Away. What will
28:57happen to blood pressure? What will
28:58happen to first start sound?
29:01Can sound?
29:03Yeah.
29:05Can sound
29:08loud. What will happen to the blood
29:10pressure?
29:16Uh
29:17complete heart block. What will happen
29:18to the blood pressure? It'll be low.
29:20Agreed. Anything more than low? Low is
29:22okay.
29:24Anything specific?
29:31Okay. Fine. So, okay. What are the
29:33causes for complete heart block? Now
29:36this patient has complete heart block or
29:37for that matter any heart block if it is
29:39there what are the causes 1 2 3 4 5
29:42number one
29:43beta blockers
29:45number one is es is eskemia always
29:47remember it is eskemia is the most
29:49important cause
29:51IHD inferior wall mis posterior wall mis
29:55sometimes anterior wall mis wrap around
29:57LD such conditions you can cause that's
29:59the first cause second cause is drugs
30:03beta blockers calcium channel blockers
30:05is deoxin.
30:07Third is electrolyte disturbances.
30:10Always remember potassium
30:14is one important electrolyte disturbance
30:16which can cause this. That's the third
30:18cause electrolyte disturbance. Fourth is
30:21myocarditis. Myocarditis.
30:24Fifth is degenerative heart diseases.
30:26Degenerative heart diseases. So these
30:29are the causes of any heart block. Be it
30:31first degree, second degree, third
30:32degree, any of the hard blocks can be
30:34caused by these five causes. And eskemia
30:37is always the first important thing that
30:39you have to
30:41remember about. Okay. What do you think
30:42is the cause for complete heart block in
30:44this patient?
30:52Any evidence of eskemia?
30:55Deoxin. No deoxyinox.
31:01Yeah,
31:03could be inferior wall MI. You have ST
31:06segment depression with the symmetrical
31:08T wave that you're seeing in inferior
31:09leads. So it's possibly an inferior wall
31:11MI. That's the cause for complete heart
31:14block in this patient.
31:20Yes.
31:21What is this ECG showing?
31:38the normal standardization with uh
31:41normal standardization. Correct.
31:44Negative P waves in uh uh lead 2 and
31:47positive in uh AVR with the positive QRS
31:50in AVR.
31:52Okay. Axis is
31:53the rhythm appears axis is uh one
31:56extreme sir extreme ais
31:58is extreme axis correct one and yes
32:01correct
32:04rhythm is
32:05and uh negative QRS
32:08yes rhythm is regular P waves are
32:11inverted and when you see the QRS
32:13morphology
32:15there is practically no progression of
32:17QRS
32:18no progression progression
32:20so this two of dexard
32:22so This is true dextrocardia. True
32:24droardia that you're seeing. So this is
32:26not technical dextro cardia. This is
32:28true dextrocardia that you're seeing.
32:29Okay. So which lead will you take to
32:31prove your diagnosis of true
32:32dextrocardia?
32:38Which additional lead will you take?
32:43AR is already there. Which additional
32:45lead to look?
32:46Right side preordial.
32:47Yes, right precordial. Correct. So which
32:49specific right precordial
32:51uh V14 R2
32:53V4
32:53V4R So remember V4R V4R that's the same
32:57like right leftsided you're placing on
32:59the right side so V4R V4R is the one
33:02which you're taking for the dextrocardia
33:04V4R is one for the uh posterior sorry
33:07inferior
33:09RVMI is also you're taking the V4R lead
33:12as well okay what are the associations
33:14of dextrocardia
33:16some clinical associations of
33:17dextrocardia
33:20uh situs in versus cartenus syndrome.
33:22Okay. So cartagenous syndrome bronchesis
33:26can be associated correct. Then
33:31any other conditions which could be
33:33associated with extracardia
33:37as
33:39okay asd can be.
33:42How do you clinically make out situs
33:44inverses?
33:49Clinically, how do you make out situs
33:51inverses?
33:52Abdominal organs,
33:56spleen on the right side and liver.
33:58So, how do you make out the spleen is on
33:59the right side?
34:02Unless it's enlarged, you can't palpate.
34:04No.
34:07So, how do you clinically on inspection
34:08you can make out situs inverses?
34:13You don't have to palpate also
34:15tidal perussion.
34:17Yeah. Anyways, I think in the chat they
34:19have messaged yes it is. The test is you
34:23can make out the testice. Normally the
34:25left side is lower.
34:27That's normal position in situs
34:29inverses. In males you can make out the
34:31right side will be lower. That's how you
34:33can make out the situs inverses. Yes,
34:35you can do an ultrasound and you can
34:36find out which organ is on which side.
34:39Which is dangerous dextrocardia with
34:40situs inverses. Dextrocardia without
34:42situs inverses.
34:48which is dangerous
34:52without. Yes, without is the one which
34:54is dangerous. And again remember the
34:56splenic organ they can have something
34:58called asplenia etc are the ones
35:02associated with this you have uh
35:05something called as visceral heterotaxy
35:07syndromes which are associated with
35:09aplenia and because of that they can
35:11have problems with that.
35:17Yes.
35:23What are you seeing in the CCG?
35:38Yes.
35:54Okay. Seeing that the complexes the
35:57voltages of the complex is low voltage,
35:59isn't it? You're seeing that the
36:01complexes are very low voltage
36:03complexes. So,
36:05how do you say low voltage complex?
36:07What's the criteria to say low voltage
36:08complexes?
36:14In the
36:16chest leads, in the limb leads, what's
36:18the criteria?
36:20In the limb leads, it should be less
36:22than 5 mm. In the chest leads, it should
36:24be less than 10 mm. Okay. Provided the
36:29standardization is normal. So you have
36:31to carefully look at the standardization
36:34here. The standardization I think is not
36:36seen. So the standardization should be
36:38normal. Okay, if the standardization is
36:41normal that is two large squares and the
36:43complexes are less than 5 mm in the limb
36:46leads or less than 10 mm in the chest
36:48leads we call it as low voltage
36:50complexes. So what are the causes of low
36:52voltage complexes?
36:55Paricardial eusion.
36:57Correct. Paricardial eusion correct.
36:59Hypothyroidism correct. Yes.
37:01Obesity.
37:02Obesity. Right. Then
37:04emphyma.
37:05Okay. Emphyma it will not be in all the
37:07leads. Emphyma is only in lead one. You
37:10get it in the lead one. That's the one
37:11which looks at the heart in front. All
37:13the other leads will be normal in empa.
37:16Okay sir.
37:17Any other conditions? Low voltage
37:24you can get it in hypothermia.
37:27Okay. Hypothermia you can get low
37:28voltage complexes. Sometimes with severe
37:31heart failure also you can get low
37:33voltage complexes that you can see.
37:36And the most important thing that you
37:38have to always rule out is technically
37:41where you have set the voltage at a
37:43lower half standardization. If the uh
37:46technically it has been placed in half
37:47standardization that can make all the
37:50complexes look small. So you'll always
37:52have to look at that that you can make
37:54out.
38:02Yeah. Sir in heart failure all the leads
38:04have low low voltage complex.
38:06Not in all the leads but in the
38:09especially in the chest leads you can
38:12appear they can appear in severe heart
38:14failure or sometimes in um uh usually in
38:18DCM and all you'll have a larger
38:20complexes but heart failure one of the
38:22signs is low voltage complexes that is
38:26because the Rwave does not progress so
38:28only you can see S waves only it might
38:30appear lower in complexes.
38:35Yes. What's the diagnosis of this ECG?
38:41Okay. So you have seen here it is
38:44broad complex. Isn't it broad complex,
38:47broad QRS complex, regular teicardia? So
38:51this is how you describe it as. So broad
38:53complex, regular teicardia which is
38:58looking similar or looking
39:02It's similar isn't it? So monomorphic
39:04monomorphic
39:05monomorphic broad complex teicardia. So
39:09what is the differential diagnosis?
39:14When you have a broad complex teicardia
39:16which is regular
39:19the differential diagnosis remains
39:22ventricular teicardia or
39:25with
39:27yeah supra ventricular tachicardia with
39:29either abercy or a supra ventricular
39:31teicardia with underlying
39:35underlying
39:36bundle branch
39:37bundle branch block. So underlying
39:38bundle branch block if it is there or an
39:41underlying pacemaker if it is there.
39:43Okay. So all of them will appear as
39:46broad. So SVT with abrasion, SVT with a
39:48bundle branch block, SVT on a patient
39:50who has a pacemaker or you have a
39:54ventricular teic cardia. So that's the
39:55two differential diagnosis when you have
39:57regular. If it is fast beating irregular
40:01it is AF. When it is irregular, if it is
40:05wide QRS or narrow QRS does not make a
40:07difference. It is atrial fibrillation
40:09only. Always remember atal fibrillation
40:12can never be regular. Atal fibrillation
40:14is always irregular. Now the question
40:17arises how do you differentiate this
40:20broad complex teicardia as VT or SVT
40:24with eberance. So how do you do what are
40:26the simple things that you want to look
40:27for?
40:29Absence of RS complex in A1 to V6
40:32criteria.
40:33Yes. Yeah. The classical buga criteria
40:35is what you what you have to use. Uh but
40:38simple things that you can make out
40:42AVR positive.
40:44Okay. If you have AVR positive, yes,
40:46that is one thing.
40:47Extreme axis deviation.
40:49Extreme axis deviation. Second, correct?
40:51Then
40:54a dissociation, that's the easiest one.
40:56Look for signs of AV dissociation on a
40:59ECG. So what is the sign of AV
41:01dissociation
41:04on ECG? What will you look for? like
41:06atria is beating separately, ventricle
41:07is beating,
41:08fusion, beating, capture.
41:09Ah, you can look for key waves. Key
41:11waves which are coming on their own.
41:13That's the first thing. Next is the
41:14fusion and capture beats. Fusion and
41:16capture beats. So if you're looking at
41:18it, fusion and capture beats. So that is
41:20one thing. So if you have that it is
41:24always VT always VT. Okay. Then any
41:28other ways concardance as you say if it
41:30is a positive concordance or a negative
41:32concordance on the chest leads if it is
41:34positive or negative that becomes uh VT
41:38extreme axis as you said it's always V_T
41:41or if you have a prior ECG and axis has
41:44changed okay in a whenever the rhythm is
41:48regular the axis has totally changed
41:50from a right to left that could be
41:52because and the very very simple thing
41:54is the broader the QRS So remember the
41:57QRS normal QRS width is how much
42:0280 to 120.
42:03Okay.
42:03So you can say it's 110. So anything
42:06more than 150. Okay. Normally 110 or
42:10less. Anything more than 150 if it is
42:12there it's always a sign of VT. Always a
42:16sign of WT more of that. So very
42:19importantly you have to see there are
42:21various algorithms. There are more than
42:2323 algorithms that are there for
42:25differentiating BT and SVT. The Bugardas
42:29is a traditional algorithm but the
42:31sensitivity and specificity of Bugard's
42:33algorithm is around 88 and 92%. So it's
42:37not a very very sensitive and not a very
42:38specific one. What uh the most specific
42:41criteria and the most latest criteria
42:43which uh has been defined is by looking
42:47at one lead. You have something called
42:49as a pavas criteria. Anyone can tell me
42:51what is power.
42:53Yeah.
42:54What are you looking at? What are you
42:56looking at
42:58in Pav's criteria?
43:00It is
43:02Rwave peak time, isn't it?
43:05Anyone can tell me what is Rwave peak
43:07time?
43:13Anyone
43:16that has a sensitivity and specificity
43:18both more than
43:2090 bas criteria has a sensitivity and
43:24specificity more than 90. So you see the
43:27uh starting of the Rwave to the peak of
43:30the Rwave. You're seeing the how much
43:31time it is taking.
43:36What is the cutff? Anyone's
43:39criteria?
43:3945.
43:40Okay. Anything more than 45? Anything
43:42more than 45 is suggestive of a
43:45ventricle teicardia. So it means that
43:46the uh what do you say the uh the
43:50initial part of the QRS itself is going
43:52very far. It's going much wider. that
43:54means it's originating from the
43:56ventricle. So uh in the exams I think in
44:00theory they can ask you about these
44:02criterias bugata's criteria but I think
44:04in your v separately they will ask you
44:06about this uh bugard algorithm is simple
44:11you can remember the a dissociation then
44:13you can see the absence of rs complex
44:16and then the
44:18duration
44:19width of the QRS you can make on based
44:21on that you can easily differentiate the
44:24ordency
44:26when in doubt VT or SV necency treat it
44:29as VT that is the rule. Patient history
44:32is very important. If suppos supposedly
44:34somebody has an age of more than 50
44:37years definitely VT is more likely. If
44:41somebody has had recurrent episodes of
44:43broad QRS teicardia and has walked into
44:46the casualty a walking patient into the
44:49casualty with multiple episodes of broad
44:51complex teicardia in the past. What is
44:54it? SPT or VT
44:56walking patient
45:03walking patient who is multiple episodes
45:05in the past it is always SMT patient had
45:08MI in the past and had broad complex
45:10teicardia
45:11VT
45:13patient has been brought with broad
45:15complex teicardia and is collapsed BP is
45:18not recordable it is VT
45:20it's always VT so patient history is
45:21also very important you can Based on
45:24that you can diagnose it and uh okay so
45:27how do you approach this patient when
45:29the patient has appeared with a casualty
45:31with a VT
45:32hemodynamical
45:35stable or not if the patient is
45:37hemodynamically unstable
45:39cardio version electrical
45:41cardio version
45:42how much jewels will you start with
45:45200
45:46200
45:46you can start with 200 again remember
45:48that time we discussed about atrial
45:50fibrillation when we uh shock an Atrial
45:53fibrillation what is the jewels you
45:54start with
45:5650.
45:57Yeah you always start it with the lower
45:58you have to start with 50 and then go
46:00above. Whereas ventricular you can
46:02straight start with 200 and go. So you
46:05do the cardio version. So if supposedly
46:07the patient is stable
46:09if the patient's blood pressure is fine
46:11and you diagnosed ventricle teicardia
46:14what's the drug that we use?
46:18Yes.
46:26Is the most important drug that is to be
46:28given. What is the side effect of
46:30ividocine?
46:34Side effect of ividocaine.
46:37Yes.
46:40Convulance.
46:41Convulsions. Convulsions. It can
46:42precipitate convulsions. So that's what
46:44you have to be careful about. Okay. So
46:46always rule out electrolyte
46:48disturbances. Whenever a VT [snorts]
46:50potassium has to be sent, magnesium has
46:52to be sent and oxygenation has to be
46:54ruled out. Many a times hypoxia just
46:57start the patient on oxygen the VT will
46:59revert back. So oxygen and potassium and
47:03magnesium. And one more important thing
47:05you'll have to use is a drugs. Drugs
47:08which is a common drug which can be
47:11producing something like this.
47:15You can have a broad QRS.
47:21Any of the anti-ythmics can produce
47:24tricyclic anti-depressants. Always
47:26remember TCAs. Tricyclic anti-depressant
47:30poisoning can produce broad QRS
47:32ticardia. Uh but again remember the TCA
47:36and hypercalemia will produce broad QRS
47:39but the heart rate will be within 100.
47:42Always remember slow VT. We call it a
47:44slow WT. It looks like WT but the heart
47:46rate is less than 100. Two diagnosis
47:49hypercalemia and triccyclic
47:51anti-depressants.
48:05Yes.
48:08What is the CCG showing?
48:21She shows a normal sinus rhythm with
48:24normal Pwave axis.
48:27Okay.
48:28Rhythm is regular.
48:30Okay.
48:30Heart rate of about uh 80 beats per
48:33minute with
48:35normal axis. Normal QRS axis.
48:38Okay.
48:40Um the chamber enlargement sir there is
48:43uh
48:45the normal arway progression with uh no
48:49okay evidence of any
48:51no evidence of hypertrophy. Yes
48:54no evidence of enlargements.
48:55Okay [clears throat] the st changes
48:57there are uh um
49:01you should calculate the QT sir but QT
49:03grossly appears to be a little
49:04prolonged.
49:06Okay. So QT is appearing prolonged.
49:09How do you say the QT is prolonged?
49:12Like we draw a midway between the two R
49:16interval and if the T wave is uh T
49:19should end before the the line imaginary
49:21line that
49:22calculate the QT here. Here here if you
49:24see here this is the starting of the Q
49:27and going at the end of the T. It is
49:29just crossing more than two large
49:30squares. So anything which crosses more
49:32than two large squares so it appears to
49:35be prolonged. So actually you'll have to
49:37measure it. Again remember to measure
49:39the QT you have or to draw a tangent to
49:41the down slope of the T-wave. You'll
49:43have to draw a tangent like this and
49:45that where it cuts the baseline. From
49:46there you'll have to calculate and then
49:48you'll have to correct it for the heart
49:50rate. You'll have to correct it for the
49:52heart rate. How do you correct it for
49:53the heart rate?
49:58Basit's correction. Bad correction is QT
50:04by root of R
50:05by root of RR by root of RR. So this
50:08looks like a prolonged QT is there in
50:09this patient. So but you'll have to
50:11calculate the actual number and seat.
50:12Okay. What are the causes of prolonged
50:14QT?
50:16Hypocalcemia.
50:17Hypocalcemia. Correct. Then
50:20electrolytes hypocalcemia
50:24hypomagnesmia hypocalemia
50:26all the things can cause it. And drugs
50:28very important lot of drugs simple drugs
50:31like aithroycin simple uh
50:34antihistaminics all of them
50:36antiarithmics can prolong the what is
50:38the problem with QT prolongation
50:41[clears throat]
50:43yeah this pro this the repolarization
50:47yeah you can the patient can go into
50:53that can happen ventricular teic cardiac
50:55can happen yes congenital longcut
50:56syndromes are also known You have some
50:58named syndromes of congenital long
51:00cutie. We have something called as a
51:02Romanov syndrome or the Jerange Lange
51:06Neielson syndrome. So those syndromes
51:08are also known.
51:16Yes, someone can tell me the diagnosis.
51:32What do you think is the
51:33extensive anti?
51:34Okay. If see it is an extensive anterior
51:37wall MI
51:40it's crossing from V1 up to V6.
51:43You're finding that there is segment
51:45elevations. You can see that there is
51:47gross ST segment elevations in V_sub_1
51:49to V6. that's there also you're seeing
51:51it in one and AVL also. So you're seeing
51:54findings both in anterior as well as
51:56lateral leads. So it's a very much
51:59prominent ST segment elevation. So it's
52:01a this pattern is called as anything
52:04tombstone
52:06or grave
52:06tombstone tombstone. Yeah tombstone
52:08pattern. You can see there that's an
52:11extensive anterior as well as lateral.
52:14So where is the block? Which vessel is
52:16blocked?
52:18Left interior LED left
52:19ant left ant descending where proximally
52:22or
52:23proximal branch
52:24it's very proximal it's a very proximal
52:26always look at the AVR I think AVR is
52:29not very clear here AVR is fing you'll
52:32always have to look at AVR so AVR will
52:34give you the clue for proximal LED
52:36occlusions okay proximal LED occlusions
52:38you should always look at AVR there okay
52:41what are the causes of noniskeemic ST
52:45segment elevations
52:49Correct.
52:50Correct.
52:51Ventricular aneurysm.
52:53Ventricular aneurysm. Good. Yes.
52:57Some more.
52:58Early deolarization.
52:59Early repolarization.
53:01Syndrome.
53:01Okay. Again remember earlier it was
53:03called as benign early repolarization.
53:05Now we don't call it as benign because
53:07it has a relevance. Early repolarization
53:10is associated with very many things. So
53:12we don't call it as benign early. Now
53:13it's called as early repolarization.
53:15Correct? Then
53:17buggada syndrome.
53:18Bada syndrome. Very good. Yes. Proatada.
53:20Which leads will you find it in?
53:22V_sub1 to V3.
53:24V_sub1, V_sub_2, V_sub1, V_sub2,
53:27maybe V3 also. You have three patterns
53:29there. Saddle backing pattern you can
53:31get. Yes. So these are the common causes
53:34of ST segment elevations that could be
53:36there. And uh so you will have to know
53:39about it and how do you evaluate? I
53:41think this is a very common thing all of
53:43you should know. And how do you manage
53:45these patients? And what are the
53:47complications of MI? Always remember
53:49whenever they ask you classify it into
53:51electrical complications, mechanical
53:54complications and based on that you can
53:56tell the complications of that.
54:15Yes.
54:16Normal sinus rhythm with normal uh P.
54:21Okay. Well standardized normal sinus
54:23rhythm with a heart rate of
54:27around 100 sir.
54:29Okay. Heart rate is Yeah. Three boxes.
54:30So it's 100. Yes.
54:31100. Um
54:33with the axis
54:39normal axis sir
54:41is it normal
54:45one is equacic
54:51mild right axis
54:53towards right okay towards right okay
54:56what can you tell me what is right axis
54:58how much is right axis from from where
54:59to where is right axis Anyone?
55:06How much is right access?
55:10Plus plus 90 sir
55:14plus
55:18is from how much to how much? No this
55:20patient I'm not talking about this
55:21patient. I'm asking how much is the
55:23range of normal right axis plus
55:2690 uh 60
55:30what is the range of the right
55:3390 to0
55:35plus 110 to plus or - 180
55:38plus or - 180 plus 110 to plus or - 180
55:41is uh right axis always remember that
55:44and true left axis is -30 to - 90
55:48physiological left is 0 to -30 that is
55:51Physiological.
55:53Okay. So here it looks like rightward
55:56axis. Okay. It's okay. No just coming at
55:5890. It's not right. Okay. Fine. Yes.
56:01What else?
56:04Anything else you're finding?
56:06Acute RV strain is there. There is
56:09you're finding that there is T-wave
56:10inversions in the right sided leads.
56:12Isn't it in V12
56:14V4 up to V4 with T-wave inversions also
56:17in the inferior leads. Inferior leads
56:20also is showing T-wave inversions.
56:21Correct. The
56:22S1 in lead one with the Q wave in three
56:27with the T wave inversion in lead three.
56:28Finding there is an S1 which is if you
56:31find a S1 what does it indicate in V1?
56:34Sorry in lead one S. Save indicates
56:37RV pressures are high.
56:39Okay. RV pressures is more. It could
56:40mean right bundle branch block also.
56:42Okay. You have Q in the lead three and
56:45T-wave inversions in the lead three.
56:47That is what you said. S1 Q3 and T3 is
56:50there. Okay. Fine. [clears throat]
56:53So what is your diagnosis?
56:56RV strains probably pulmonary emolism
56:58based on.
56:59So you think so this could be a sinus
57:01teicardia is there with a rightward axis
57:04and a right ventricular stain and S1
57:07QT3. So this could be a pulmonary
57:09pulmonary thrombololism. So this could
57:11be the possibility that you could have
57:13in this patient. So you will have to
57:15evaluate.
57:17You will have to evaluate what is
57:18investigation of choice.
57:21CD pulmonary
57:22CTD pulmonary angio
57:23pulmonary angiogram can be done. You can
57:25do the
57:27dimer etc. And then you'll have to
57:29manage these patients. Okay. What are
57:31the causes of T-wave inversions? Tell me
57:33some causes of T-wave inversions.
57:37Esteemia.
57:39So eskeeia is the main thing. Correct.
57:40Okay.
57:41Other than that.
57:43Okay. Hypocalemia.
57:46Yes.
57:48More causes. You have 100 causes of
57:50T-wave inversions.
57:52Cerebral
57:53increased intracraanial pressure.
57:55Increase
57:55in intracraial pressure.
57:59I said 100 causes. So anything you say
58:01is correct.
58:03They say there is anything under the sun
58:06including the sun can cause T-wave
58:08inversions. Even a cup of coffee can
58:11cause T-wave inversions. So drugs can
58:13produce myocarditis, pericarditis,
58:16anything can produce electrolyte
58:18disturbances all those things can
58:19produce T-wave inversions. So T-wave
58:21inversions is schemic T-wave inversions
58:23always remember is symmetrical. All the
58:25rest are asymmetrical. Tway chamber
58:27enlargement can produce T-wave
58:30inversions as you see here. The RV
58:32strain can produce conveyism can
58:33produce. Okay.
58:37Okay. This one.
58:42[snorts]
58:48What's your diagnosis?
58:51Can see the rhythm strip. Based on the
58:53rhythm strip, you can make the
58:54diagnosis.
58:59Wave back. This progressive
59:01prolongation.
59:01So you can see that there's a PR PR is
59:04prolonging. PR is further prolonging.
59:06PRS further prolonging and then the P is
59:08not followed by the QRS. So this is the
59:11type two
59:13hard blocky back phenomenon or type one.
59:16So again we have discussed about the
59:18causes of this isn't it? We have
59:20discussed all the causes of that. So the
59:21management also would depend upon
59:33Yes. What's the diagnosis?
59:39It's a teicardia. Yes. Regular
59:42teicardia.
59:43Narrow complex teicardia which is
59:45regular. So when you have a narrow
59:46complex the first thing you should
59:48always look is whether it is regular or
59:49not. Please remember irregular. We have
59:51already discussed AF in the beginning.
59:53So this is a regular narrow complex
59:55teicardia. So what are the differential
59:58diagnosis? 1 2 3 4
1:00:00SVT supra
1:00:02SVT SVT is the first one
1:00:03teicardia
1:00:04sinus teicardia correct then
1:00:08atal teicardia the various types of SVTs
1:00:11isn't it the most common cause 90% of
1:00:14the narco complex teicardas are
1:00:19junctional
1:00:20which one
1:00:24a
1:00:26sir
1:00:2690% of them are AVNRT some small
1:00:30percentage is AVRTS then you can have
1:00:32the atrial teicardias etc. So how do you
1:00:35manage this patient
1:00:38when the patient comes hemodynamically
1:00:40stable?
1:00:41IV adinosin
1:00:42IV adinosin is the drug of choice in a
1:00:44patient who is hemodynamically stable.
1:00:46What are the two prerequisites that you
1:00:48have to do when you have to give
1:00:50adinosin? Before you give adinosin you
1:00:52can do something
1:00:54last month.
1:00:56You can do the veagal maneuvers like a
1:00:57caroted sinus massage etc can be done.
1:01:00Okay.
1:01:00Yeah. What is that you said before
1:01:02giving adinosin two things that you have
1:01:03to do is
1:01:05rule out
1:01:06rule out ama. Very good. Second
1:01:11this select will take time before
1:01:13adinosin. You have to give it rapidly.
1:01:16You will have to give adinosin through a
1:01:21large
1:01:23preferably a central line. Okay.
1:01:24Preferably a central line otherwise you
1:01:27will have to flush it immediately
1:01:28because adinosin gets metabolized really
1:01:30rapid. 6 mgs you give by the time it
1:01:33reaches the heart it is metabolized. So
1:01:35you no use of giving it and you rule out
1:01:38ama that's the two important thing that
1:01:40you have to do. Okay. If the patient is
1:01:43hemodynamically unstable, you will have
1:01:45to straight give the cardio version
1:01:48provided the patient has uh yeah it's
1:01:51regular. Yes.
1:01:55What's the diagnosis?
1:02:07Hypercalemia.
1:02:08Hypercalemia.
1:02:09Hypercalemia. Why do you say so?
1:02:13T-wave more than 50% of the positive R
1:02:16have the tall T waves okay always
1:02:19remember tall T- waves more than 23 of
1:02:21the neighboring QRS and uh you find it
1:02:24in almost all the leads the P waves are
1:02:26absent please remember absent P waves
1:02:29okay P waves are absent here the QRS is
1:02:31widened and in the later how much would
1:02:33be thinking the potassium is in this
1:02:35patient how much would the potassium be
1:02:38based on this ECG
1:02:40around 6.5 5
1:02:42more than seven
1:02:43more than 6.8 around seven around seven
1:02:45it would be okay if the sine wave comes
1:02:48then it is more than eight sine wave is
1:02:50more than eight potassium that you would
1:02:52see okay so you should know about the
1:02:56causes of tall t waves one is eskemia
1:02:58and one is MI sorry one is MI and one is
1:03:01hypercalemia how do you differentiate MI
1:03:04will be in specific leads whereas
1:03:05hypercalemia will be in all the leads
1:03:08and uh MI you'll have a broad base and
1:03:12going tall whereas As in hypercalemia
1:03:15you get the classical tented T- waves
1:03:17stented T- waves tall tented T- waves
1:03:20again you'll have to uh remember that
1:03:24the management how do you do what are
1:03:26the drugs and how do they act everything
1:03:27you should remember
1:03:30okay I think with that we finished the
1:03:31ECGs
1:03:33I think we'll continue for some more
1:03:35time then I'll stop maybe another 10
1:03:37minutes and then we'll wind up so here
1:03:40is the next set of case scenarios that
1:03:44are given to you in your OSKIS. So here
1:03:48we have a young lady who has presented
1:03:50for pre-employment
1:03:52and you find that she is mildly anemic
1:03:54and there is mild etc. there's a small
1:03:56spleen that is there. Rest of her
1:03:58examination is normal
1:04:04and this is the peripheral smear that
1:04:05you're seeing. So this is the peripheral
1:04:07smear finding that they have given. The
1:04:10image is showing what and what do you
1:04:12think is the diagnosis?
1:04:18Peripheral smear showing teardrops and
1:04:21target cells.
1:04:22Okay, teardrop cells are there. Target
1:04:24cells. What about the RBCS? How is the
1:04:26RBCS?
1:04:27NO hypocchromic anop.
1:04:31So there is hypochromia. You can see
1:04:32that there is hypocchromia there.
1:04:36Prominent
1:04:36central por is very prominent. Look a
1:04:39little we don't have a lymphosy to
1:04:41compare but uh whether it is microitic
1:04:44we can only compare based on the
1:04:45lymphosy we're not able okay but there
1:04:47is hypocchromia and the classical target
1:04:50cells isn't it you can see the target
1:04:51cell that you're seeing so what is your
1:04:53diagnosis
1:05:00so whatmia is this
1:05:03this ismia trait
1:05:05trait
1:05:08minor
1:05:09Minor or
1:05:09minor?
1:05:11It's not major definitely because the
1:05:13patient does not have significant anemia
1:05:15there.
1:05:15Minor
1:05:16minor talismia.
1:05:17So it's minor minor talismia minor that
1:05:19could be there. Okay. What are the
1:05:21differential diagnosis for microitic
1:05:22hypochromic anemia? So there
1:05:28anemia.
1:05:28Yes.
1:05:30Chronic.
1:05:31Anemia of anemia of chronic disease.
1:05:33Chronic disease.
1:05:34Okay. Rarely anemia of chronic disease.
1:05:36Lead poisoning is one thing you'll have
1:05:38to
1:05:38rule out. Yes.
1:05:40So what is the differential diagnosis by
1:05:43the peripheral smear is already asked.
1:05:45Okay. The fourth question I think you
1:05:46can say what are the laboratory
1:05:48investigations that you want to do it in
1:05:50this patient. What investigations can
1:05:51confirm your diagnosis?
1:05:53HP electrophorosis.
1:05:54You'll do the HB electrophysis.
1:05:57You want to do the studies.
1:06:01Iron studies.
1:06:03You need to do the study in this
1:06:04patient.
1:06:05Yes sir. Yes, because you don't want to
1:06:08overload the patient with giving iron.
1:06:10Okay, you want to not give iron too much
1:06:12in this. So, what do you find in the HB
1:06:14electrophorosis? What do you
1:06:16specifically look for?
1:06:20What will you look for in the HB
1:06:22electrophorosis?
1:06:22A2 levels.
1:06:24Yes, HBA2 levels. Based on that, you'll
1:06:26be able to determine the patient whether
1:06:28it's a uh
1:06:32rate or not. So you can see the
1:06:33hemoglobin is around 8.3 in this
1:06:35patient. So there is anemia. So it
1:06:37cannot be trait. It is minor. He met is
1:06:40also low. MCV is very low here. RDW is
1:06:4322.9. What's your inference?
1:06:46It is increased.
1:06:49So what does that mean?
1:06:50It means
1:06:53anopic
1:06:55microitic microitic.
1:06:58So it means there is an isop. So what
1:07:00does it indicate? Is it seen in talismia
1:07:02RDW
1:07:04visually there is deficiency there is
1:07:07iron deficiency that that is very
1:07:09important it indicates iron deficiency
1:07:11that is there you can see the reticular
1:07:13count is elevated and the absolute
1:07:15reticular site is also increased there
1:07:18that you can see that so how do you
1:07:21differentiate between iron deficiency
1:07:23and talisman
1:07:27what is that index
1:07:29yes what is that mcv by RBC in RBC in
1:07:32mill.
1:07:34Yes. MCV by RBC. So what is the cutff?
1:07:37More than 13
1:07:39induction.
1:07:40More than 13 would indicate
1:07:42induction.
1:07:43Iron deficiency. Okay. More than 13
1:07:44would indicate iron deficiency. So this
1:07:46patient can have coexisting iron
1:07:48deficiency also. Okay. So you can see
1:07:50that the bilerubin is elevated 4.5 that
1:07:53is elevated there. The feritin is very
1:07:55much elevated, 104. So possibly there is
1:07:59no iron deficiency state as such. Okay.
1:08:01And this is the HB electrophorosis that
1:08:04you're seeing here.
1:08:05You're finding that there is a HBA2
1:08:07which is this much percentage and the
1:08:08hemoglobin F. So what's your diagnosis?
1:08:15Final diagnosis.
1:08:20Yes.
1:08:23Minor only sir.
1:08:24It's minor only. Okay. Okay. Fine. So
1:08:27that's the
1:08:29so then they may ask you certain
1:08:31complications of thalismia and how do
1:08:33you manage and uh what is genetic
1:08:35counseling all those things can be asked
1:08:37and what is the counseling you want to
1:08:38do this for this an asymptomatic patient
1:08:41so you'll have to know about that so
1:08:43that would be the questions that would
1:08:44be asked
1:08:47okay
1:08:51yes somebody can tell me about this
1:08:54image
1:08:59This is from Kansky I've taken. So what
1:09:02are these images showing
1:09:04the first image?
1:09:05After image first image showing
1:09:07bilaterally unequal pupil.
1:09:10Yes. Bilaterallyis right side.
1:09:13Right sidetosis.
1:09:16No.
1:09:17Yeah. Right sidetosis.
1:09:19Right sidetosis. The first image. No.
1:09:22There's no tois. Not.
1:09:24What is What are you finding which is
1:09:26abnormal?
1:09:28Right. Left side.
1:09:30Left side. What are you finding?
1:09:31Lag of
1:09:34lag of themalus. What about the pupilary
1:09:36size?
1:09:39Left side is uh more than right.
1:09:41So left side you're finding there is a
1:09:43dilated pupil. You're finding it's there
1:09:45is a dilated pupil on the left side.
1:09:48Okay. What are you finding in the image
1:09:50below?
1:09:52tois leftid
1:09:53finding there is leftsidedtosis.
1:09:56So this is related to your third fourth
1:09:58six cranial nerve that is there. So what
1:10:00are the causes of a dilated pupil?
1:10:02Common causes for dilated pupil.
1:10:06Drugs.
1:10:07Drugs. Okay. What are the drugs?
1:10:11Atropen. Atropen is one drug is
1:10:14What are the other causes of dilated
1:10:15pupil?
1:10:17Third paly. Third paly. Correct.
1:10:20Correct. What sort of third known paly
1:10:22produces dilated pupil?
1:10:27Compressive causes or vascular.
1:10:32What is pupil sparing of theopoplegia?
1:10:35Diabetes always remember compressive.
1:10:38Yes, compressive lesions always produce
1:10:40the pupilary damage whereas vascular
1:10:42lesions like diabetes does not produce
1:10:44the pupillary damage. What's the
1:10:46commonest cause producing compression of
1:10:48the third? Huh?
1:10:51Anorism.
1:10:52Yeah. PCOM aneurysm is the commonest
1:10:54cause for third nerve compression which
1:10:56you can encounter. Okay. So you can have
1:10:58third pales. Yes. Other than that what
1:11:00are the causes of pupilary dilotation?
1:11:07Yes.
1:11:10Any other causes? Third nerve dilation.
1:11:15Can it occur due to coning? Third nerve
1:11:16can get compressed somewhere else.
1:11:21Cerebral Masa.
1:11:24So what is that? Where where does it
1:11:25come get compressed
1:11:27between the two artists?
1:11:32PC.
1:11:35Have you heard of something called as a
1:11:36kernahans
1:11:38phenomena?
1:11:39Yes sir.
1:11:41Karnahans phenomena. kernahans notch
1:11:43that is there between the supra and the
1:11:45infractoral that uh that's where it gets
1:11:48affected so it can get compressed there
1:11:50also so that's called as a kern
1:11:53phenomena that could be there okay so
1:11:55third nerve can get compressed in
1:11:56various causes okay what are the of
1:11:58themas where the pupils are spared
1:12:01examples
1:12:04myastinia gra is good
1:12:08second
1:12:10medical causes no so Mythenia and
1:12:13diabetes pupil sparing
1:12:14diabetes diabetes diabetes myastthenia
1:12:17vasculitis. Those are the pupil sparing
1:12:19of the pitch. Okay. Okay. Tell me some
1:12:21causes of tossis.
1:12:26This patient has tossis the below.
1:12:29Yeah.
1:12:33Cos oftosis. Okay. Horners. Okay.
1:12:36Secondia
1:12:39gravis. Correct. Then
1:12:42third no
1:12:43snake bite.
1:12:44Okay. Snake bite. Correct. Neurotoxic
1:12:46snake bite. Correct. Then
1:12:48third nopulsey.
1:12:50Third no paly. Third nopaly produces
1:12:53stosis.
1:12:55Okay. Unless there is a horner syndrome
1:12:58associated you don't get there but kind
1:13:00of local causes. Mechanicaltosis can be
1:13:02there. There could be tumors that could
1:13:05be
1:13:06seniletosis can be there. All those toes
1:13:08can be there. Okay. So what are the
1:13:11features of Hner syndrome?
1:13:18Loss of celos
1:13:19loss of celio reflex. So these are the
1:13:22various causes that could be there
1:13:24ortosis that could be there. Okay.
1:13:27So what are you seeing in this image?
1:13:41Bellh
1:13:43sign is there. Uh wringling of forehead
1:13:46is absent on right side.
1:13:47So wrinkling of forehead is not there on
1:13:49the right side. Correct. And he's not
1:13:52able to close his eyes, isn't it?
1:13:53Eyes on right side. Bells.
1:13:55Bell's phenomena. What is bell's
1:13:56phenomena?
1:13:59While uprolling of
1:14:01While uprolling of the aisles.
1:14:03Well trying to close sight there is
1:14:05uping of the eyeballs.
1:14:07Okay. Uprolling of the eyeballs. Okay.
1:14:09Okay. And the visibility of the lower
1:14:10sclera. You're able to see the
1:14:12visibility of the lower sca that you are
1:14:14seeing there. So it indicates what? So
1:14:17what is it? What is the diagnosis?
1:14:22L facial pulsy.
1:14:24LM facial
1:14:25seventh ln
1:14:27seventh facial paly. That's there. Okay.
1:14:29Why is it not a facial paly?
1:14:33You'll spare the upper part.
1:14:35Okay. So the upper part is spared. So
1:14:37the oricular oculi closure will be fine.
1:14:40So the uh this won't happen in a um
1:14:43facial paly. Okay. Tell me some causes
1:14:45of LM facial paly.
1:14:52Yes.
1:14:58I can't
1:15:01communist first. Commonest cause
1:15:03elemental
1:15:05idiopathic
1:15:07idiopathic is commonist.
1:15:09Okay. So commonest is bells followed by
1:15:11middle ear problems. It could be
1:15:14infections in the middle ear tumor in
1:15:15the middle ears it could be there. Then
1:15:17problems in the anywhere in the tract of
1:15:19the facial nerve be it in the parotid be
1:15:22around the styomtoid parame it in the
1:15:24petus part of the temporal bone be at
1:15:26the CP angle. Okay. uh you could get it
1:15:30bilateral facial nopaly what are the
1:15:32conditions where you get bilateral
1:15:33facial
1:15:33GBS
1:15:34GB syndrome always remember GB syndrome
1:15:37is one of the commonest ones it could
1:15:39due to
1:15:40sarcoidosis it can yeah it can occurs
1:15:43due to limes disease it could occur due
1:15:45to diabetes leprosy leprosy can produce
1:15:48so those are the other conditions where
1:15:50you could get bilateral facial ny okay
1:15:54how do you differentiate bilateral
1:15:57lower motor versus bilateral upper motor
1:16:00emotional fibers will be preserved in
1:16:03bilateral.
1:16:05What about bell's phenomena?
1:16:09Bell's phenomena.
1:16:12If bilateral upper motor is there, will
1:16:14you have bells phenomena or no?
1:16:20You said bell's phenomena is seen in
1:16:22unilateral element. Correct? So
1:16:24bilateral element anywhere anyhow will
1:16:27have bells phenomena. Both eyes you can
1:16:28see. What about bilateral um upper part
1:16:32is gone but will the bell phenomena be
1:16:34there or no
1:16:39anyone? Yes or no bilateral?
1:16:41No sir.
1:16:42No
1:16:43always remember bell's phenomena is only
1:16:45element only seen in element. Even if
1:16:48the orbicul your frontalis is involved
1:16:52in bilateral um bell's phenomena will
1:16:55not occur. The center is different. You
1:16:56should have an intact center. Only then
1:16:59the bell's phenomena will happen. That
1:17:00is only in peripheral you will get that.
1:17:02Okay. And as you said the emotional
1:17:05fibers. So emotional fibers are spared
1:17:07in bilateral whereas it is lost in
1:17:10bilateral element. How do you test for
1:17:12these emotional fibers?
1:17:16How do you know the emotional fibers are
1:17:18intact?
1:17:22Who answered that? Emotional fibers.
1:17:30So how do you check for emotion of a
1:17:32patient?
1:17:35Okay, I think in the chat they have said
1:17:37okay this patient has to spontaneously
1:17:39emote. So you have to tell him a joke.
1:17:41So you ask the patient to move his face,
1:17:43you ask him to smile, he won't be able
1:17:45to smile. But on spontaneously on a joke
1:17:48he'll be able to smile. So that is how
1:17:50you know that the emotional fibers are
1:17:52intact. So always remember in a um
1:17:54facial paly the emotional fibers will be
1:17:57intact whereas LMN facial paly the
1:18:00emotional fibers will be lost. Emotional
1:18:03fibers also will be lost. And the other
1:18:06important thing when you have bilateral
1:18:07um facial palsy what condition you get
1:18:11that bilateral facial paly
1:18:16what disease you get that? M&D motor
1:18:19it could be motor neuron disease or it's
1:18:21stroke it is a pseudo bulbar paly bulbar
1:18:24pseudo bulbar paly so they will have
1:18:26other features of pseudobelvar falsy
1:18:28what is that
1:18:30tongue exaggerated jger
1:18:31correct exaggerated jarger bilaterally
1:18:34the lower yeah the bilaterally the lower
1:18:36limb reflex upper limb reflex will be
1:18:38exaggerated bilateral plantar will be
1:18:40extensor so these would be the
1:18:42differences between bilateral um women
1:18:43and bilateral element disease very very
1:18:46common question asked for you in your
1:18:48vivas as well as in your exams when a
1:18:50case is kept between facial palsy be it
1:18:54any case bell's paly or any cranial
1:18:56nerve examination they will ask you
1:18:58about facial nerve you have to know
1:18:59facial nerve thoroughly
1:19:03you should know the complete pathway of
1:19:04the facial nerve also
1:19:07okay I think we'll stop with that for
1:19:09today we'll continue the rest on
1:19:12Thursday
1:19:14hopefully we'll finish all the rest by
1:19:15Thursday I think we finished majority
1:19:17ity of that what is remaining I think is
1:19:20uh some more clinical images and some
1:19:22instruments and uh
1:19:26ABGs I think that we'll try to cover on
1:19:28question
1:19:31okay
1:19:33fine any other clarifications regarding
1:19:35today's session you can ask otherwise
1:19:37you can wind
1:19:47How to keep bilateral element facial
1:19:50posal
1:19:58element facial poly correct
1:20:02bilateral element facial paly all
1:20:03expressions are lost the patients will
1:20:05have bell phenomena all the expressions
1:20:08I mean upper part is gone both sides
1:20:11like in GB syndrome very commonly
1:20:15but bell's phenomena will be there they
1:20:17will not have uh any other long track
1:20:19sign
1:20:21will be normal maybe
1:20:26whereas inn you'll have uh juk
1:20:29exaggerated and emotional fibers will be
1:20:32spared in lmmen both emotional as well
1:20:34as voluntary fibers both will be lost so
1:20:37they won't be able to smile on a joke
1:20:39also they will have actual mask Okay.
1:20:51Okay.
1:20:54Thank you.
1:20:55Thank you, sir.
1:20:56Thank Thank you, sir.
1:20:59Thank you, sir.
1:21:00Thank you, sir.

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This page contains the full transcript of MEDICINE OSCE - Part 2 by THE WHITE ARMY, generated from the public captions YouTube serves with the video. The transcript has 10,406 words across 1,914 segments, with the original timestamps preserved so you can click any line to jump to that moment in the embedded player.

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Use the transcript to take notes, quote the speaker, build a study guide, generate a summary with ChatGPT or Claude via the YouTube Summary tool, or export it as a timed subtitle file with YouTube to SRT. You can also re-open it in the transcriber to choose a caption track available on the video.

Free YouTube transcript tool

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