CME INDIA Case Presentation by Prof. Dr. M. Chenniappan, MD, DM, FACC, FACP, FRCP. Consultant Cardiologist, Ramakrishna Nursing Home, National Professor of IMA – CGP. Director of Medical Education, Apollo Speciality Hospital, Thiruchirappalli (Tamil Nadu, India).

CME INDIA Case Study

ECG -1

“Block everywhere”

65y male with cardiogenic shock

ECG Findings

• This ECG with Cardiogenic Shock shows acute total occlusion of Right Coronary Artery (RCA) due to red thrombus resulting in inferior sub epicardial injury (ST elevation) which is more in LIII than LII (RCA lesion). In addition, this ECG shows ST elevation in V1, V2 with more elevation in V1 suggestive of Right Ventricular Myocardial Infarction (RVMI).
• In anteroseptal MI ST elevation progressively increases from V1-V4 whereas in RVMI ST elevation from V1 – V4 decreases. There is no discordant ST segment depression between V1 and V2, ruling out Posterior Wall Myocardial Infarction (PWMI). There is reciprocal ST depression in L1 and avL. V5, V6 do not show ST segment elevation which indicates left coronary dominance.
• The following 3 points are diagnostic of complete heart block in this ECG.
  • Bradycardia
  • Atrioventricular dissociation
  • Atrial rate faster than the ventricular rate
• In this Complete Heart Block except in inferior leads the QRS is narrow because of supra His CHB due to AV nodal disease due to RCA occlusion.
• The reason for wide QRS in LII, LIII , avF is because of intra infarction block. In Intra Infarction Block the QRS may be widened at the site of infarct because of significant delay in depolarisation through injured / infracted myocardium. Intra infarction block is a type of peri infarction block which can be focal or divisional. This QRS widening will not be typical of any Bundle Branch Block.
• There are three premature beats (2nd, 6th and 10th beat). Whenever you find a premature beat in the presence of complete AV dissociation due to block, sinus capture beat has to be excluded. Here the premature beats are preceded by a P wave which is falling in the previous ST segment and so they are unlikely to be conducted to ventricle due to absolute refractory period. So, these 3 premature beats are likely to be junctional premature beats.

Clue

This ECG shows following blocks

1. Acute total block of RCA (STE LIII>LII).
2. Acute total block of Right Ventricular Branch (STE V1>V2).
3. Acute total block of Proximal RCA (RVMI).
4. Complete Atrio Ventricular block.
5. Block of AV nodal Artery – (supra His CHB).
6. Intra infarction block (Wide QRS-inferior leads).

Because of the presence of multiple blocks in the ECG; the clue of “Block everywhere” is given.

Practical Implications

• Because the patient has Cardiogenic shock, the IWMI and RWMI due to proximal right coronary lesion, the best choice is primary PCI irrespective of FMC to PCI time. Till then, Cardiogenic shock should be treated with IV fluids which have to be adjusted according to BP and lung signs. Although this patient has multiple blocks, he may have better outcome if immediate revascularisation is done and is successful.

ECG – 2

“The Terrible Ten”

This is the ECG of 60-year-old female who has chest pain and intermittent dizziness.

ECG Changes

• The ECG shows complete RBBB, Left Anterior Fasicular Block (LAFB) with a P wave in the ST segment of all beats. Most of the leads shows deep, broad, symmetrical T inversions with prolonged QTc. The PR interval is normal and constant.
• The P wave in the ST segment can be either Atrial Premature beat or a sinus P which is not conducted to the ventricles. As the P-P intervals including non-conducted P waves are constant, it is likely that this P in ST segments is non conducted sinus P. If it is APD, conducted Sinus P to non-conducted P in the ST segment is likely to be short when compared with other P-P intervals.
• It is ideally called “non-conducted” rather than “blocked because it is falling in a period where it is not expected to be conducted. The deep broad symmetrical T inversion is unlikely due to Acute Coronary Syndrome (ACS) like “Wellens syndrome” because the QTc is prolonged, and it is diffuse.
• There is no initial r in V1 and initial q in V5 V6 indicating Antero Septal MI(ASMI). There is homophasic ST T changes with RBBB. The deep broad symmetrical T inversion with prolonged QTc is probably due to recent “Strokes Adam Attack.”

Clue

The overall 10 ECG findings are:

1. Complete RBBB
2. Left Anterior Fascicular Block
3. 2:1 AV conduction
4. Anteroseptal MI
5. Deep Broad symmetrical T inversion
6. Prolongation of QTc
7. Homophasic ST T changes in the presence of RBBB
8. Probable recent Stokes Adams attack
9. Dominant RBBB (presence of terminal r in L1 in the presence of LAFB)
10. “Pseudo” Wellen

As this ECG has “Ten” terrible changes which may be dangerous to patient’s life, the clue of “The Terrible Ten” is given.

Practical Implication

• In the presence of advanced conduction disturbances such as RBBB, LAFB and 2:1 A.V. Conduction, the broad, symmetrical deep inversion represents recent stokes Adams Attacks. (Stoffweschsel syndrome).
• This T inversion in advanced A.V.Blocks or sinus node disorders, represents recent transient brain ischemia like the ECG changes which happen in CVA. Although this patient does not have typical syncope, the dizziness may represent episodes of pre syncope, and it is the definite indication for Permanent Pacemaker Implantation.
• The presence of ASMI, and homophasic ST T changes in RBBB represent occult CAD, and she also needs Coronary Angiogram to decide about further management of CAD.

ECG – 3

This is the ECG of 40 years patient who presents with chest pain and dyspnea. This is the first ECG taken for him and it is a routine ECG.

The striking feature in this ECG

• PR depression especially in leads V4, V5, V6 with no significant ST elevation and PR changes in other leads especially limb leads.
• There are 3 differential diagnosis for PR depression.
  • Normal Variant
  • Atrial Infarction
  • Acute pericarditis
• Normal variant of PR depression is less than 1mm. In this ECG it is 1 mm and above, which makes the normal variant unlikely.
• Atrial infarction almost always is accompanied by Acute Inferior Wall Infarction or lateral infarction. If PR depression happens in chest leads it should be more than 1.5mm (LIU’s criteria).
• In this ECG, there is no acute inferior or lateral infarction and PR depression is not more than 1.5mm in chest leads. In acute pericarditis, PR depression is usually accompanied by concave ST elevation in all leads except in lead avR and possibly V1 and at this stage most often clinical evidence of pericarditis in the form of pericardial rub is present.
• This patient had no pericardial rub, and the chest pain is not suggestive of acute pericarditis. Then what is the cause of PR depression in the absence of normal variant, atrial infarction, and acute pericarditis?
• A rare cause of PR depression in this ECG is asymptomatic pericardial effusion. PR depression finding alone has been noted in asymptomatic pericardial effusion with no clinical signs of pericarditis (JACC 2002).
• Our patient had mild but significant pericardial effusion which is the probable cause of PR depression. This rare sign of pericardial effusion (PR depression) has taken away our concentration from the most important but subtle sign of LA abnormality in V1 in form of deep negative force of P wave. This may be the only sign in some of the patients in mitral stenosis or LV dysfunction which is due to left atrial hypertension in the absence of classical wide and bifid p wave in L II.
• This patient had moderate to severe Mitral Stenosis of VA of 1.2cm2. He may need an intervention for this finding rather than PR depression. Sometimes, rare signs of ECG may take our attention away from a subtle but the most important sign in the ECG which is more crucial in the management of the patient. This ECG is a typical example of this phenomenon. So don’t get depressed because you may have missed LA abnormality due to your concentration on rare sign of PR depression. There is always another time!

ECG – 4

This is the ECG of 60-year-old patient with rest chest pain. Previous ECGs are not available

ECG Findings

• The main finding in this ECG is short PR with no delta wave or wide QRS. In addition, there is anterior ST depression and avR ST elevation.
• The anterior ST changes and avR ST elevation is suggestive of Left main coronary artery critical occlusion.

The Rhythm

• In the presence of short PR, with upright P in LII, L III, avF with no delta wave, we can suspect James Pathway pre-excitation which is by passing the AV node and then conducting through normal pathway, hence the narrow QRS. But only in the presence of h/o palpitation and documented episode of tachycardia it is called “Lown Ganong Levine syndrome” (LGL syndrome).
• So, this ECG you cannot interpret as LGL syndrome without history. The name given to this type of ECG is Coronary Nodal Rhythm. (CNR). That’s why the clue of “Carefully Note and Read” (CNR) is given. The flow chart explains the approach to short PR.

Practical Implications

• The immediate management in this ECG is for ST depression and avR elevation by doing immediate coronary angiogram and suitable revascularisation. The short PR interval does not need any intervention. If the patient develops tachycardia, then EP studies and Radio Frequency ablation may be planned.

Approach To Short PR

ECG – 5

ECG of 60 y female; Guess her complaints apart from ECG interpretation

ECG Changes

• ECG shows basic bradycardia with right bundle branch block (RBBB) with qR pattern and Left Anterior Fascicular Block (LAFB). PR interval is normal and fixed. There is Atrio Ventricular association. There seems to be ‘P’ in the ST segment of all beats. There is horizontal ST with splayed deep T inversion, the QTc is prolonged. The presence of S wave in V1 indicates RBBB is dominant. The absence of initial r in V1 and initial q in V5, V6 suggest probable old septal MI.

Similar But Not the Same Findings

• The regular P wave in ST segment in all beats looks similar to 2:1 AV Block. So, in the presence of bifascicular block (RBBB+LAFB) it looks similar to Trifascicular block. But P wave in ST segment(P’) looks different from sinus P especially in V2 (Fig). In addition to this, sinus P to P’ interval is shorter than P’ to sinus P interval indicating the P in ST segment (P’) is premature. As the p wave in ST segment (P’) has different configuration and prematurity, it is likely to be Atrial Premature Depolarisation (APD) in bigeminy rather than blocked sinus P. So, this P-P’ sequence is similar to 2:1 AVB but not the same.

Fig-The P in ST segment (P’) is different from the previous P and P-P’ interval is short in this expanded V2

• The deep T inversion is similar to ischemic deep inversion (Flat ST, symmetrical T inversion). But here T wave inversion broad and splayed with prolonged QTc. In the presence of conduction disturbance (Bifascicular block), there deep broad T inversion indicates recent Stokes Adam Attack which is called “Stoffweschsel syndrome.”
• So here T inversion is similar to CAD but not same. The qR in V1 is similar to RVH and RAE. But here the QRS is wide and it is accompanied by loss of initial q in V5V6. There is no right axis deviation. So qR pattern in RBBB is due to loss of initial septal q due to old ASMI. The qR in V1 is similar to RVH, RAE but not the same. In the presence of bi or trifascicular block, the broad splayed T inversion with prolonged QTc indicates recent SA attack. So, this patient needs early permanent pacemaker implantation with this ECG itself without undergoing any costly investigation such as EP studies. So, this ECG has saved the spending of the patient. The complaint is likely to be syncopal attack because of these typical T changes.

Practical Implication

• The immediate Permanent Pacemaker Implantation is needed in this patient, from this ECG itself. If the APD is misdiagnosed as 2:1 AV Block, administration of cardiac stimulants will further aggravate atrial arrhythmias. If the T wave inversion is misdiagnosed as CAD, the investigations and management will be diverted to a completely wrong direction.

ECG – 6

ECG Changes

• ECG shows normal sinus rhythm with chronic stabilized phase of inferior wall myocardial infarction (IWMI). There are anterolateral and high lateral minor T wave inversions. The inferior wall infarction is likely to be due to right coronary occlusion because of the deepest Q is seen in LIII.
• In addition, there is a ventricular premature depolarization (VPD) in V4, V5, V6 and rhythm strip of LII. This VPD shows negative QRS complex in V6 suggestive of LV origin and negative QRS in LII is suggestive of inferior origin. So, this VPD is likely to come from left posterior fascicular distribution area which is infarcted.
• In addition, VPDs in V4, V5 show pathological Q wave with small qR complex in V4, QRS complex in V5. This pattern is suggestive of chronic MI or scar in this region, although the basic sinus beats are not showing the infarct pattern. Infarction was diagnosed from the morphology of a VPD when it has a QR or QRS pattern with Q wave greater than or equal to 0.04 second.
• Morphologic analysis of VPDs had a low sensitivity but high specificity and high predictive value for the diagnosis of MI. In some ECGs, angiographic MI had no MI according to standard electrocardiographic criteria but did have an MI manifested by VPB morphologic analysis. Despite low sensitivity, analysis of the morphology of VPBs may be useful for the diagnosis of MI when the morphology of sinus beats is not diagnostic. Therefore, VPD analysis is complementary to the standard electrocardiographic diagnosis of MI.

Information Given By VPD

• The ventricular premature beat gives so much of information.
  • 1. The site of origin; left posterior fascicular area.
  • 2. VPDs are arising from infarct area itself.
  • 3. VPDs are unmasking the chronic MI or scar in low septal and anterolateral areas even though the sinus beats are not showing the infarct pattern.

Practical Implications

• In addition to IWMI, the VPD has unmasked additional MI in low septal and lateral areas which may need detailed investigations such as ECHO for LV function, Holter to decide about the malignancy of VPDs and coronary angiography to decide about revascularisation and the management of VPD.

See Part 1:

See Part 2:

(This series is brought in collaboration of USV/Scan the QR code to watch video by the author.)

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