A Dozen Demos

When a transvenous pacemaker is placed in the right ventricle to manage 3rd degree AV Block, on the EKG the paced complexes have a pacemaker artifact followed by a QRS with a LBBB pattern. This is because the right ventricle is depolarized first and then the left ventricle is depolarized through non-specialized myocardial cells. When pacing the right ventricle it contracts before the left ventricle..

This can be proven by cardiac auscultation that focuses on the splitting of S2, the second heart sound (the closure of the aortic valve and the pulmonary valve), during inspiration. With normal QRS conduction or with RBBB there is physiologic splitting of S2 (A2 before P2 that splits wider with inspiration). This is because with inspiration there is greater right ventricular filling (blood returning from head and arms as well as from abdomen and lower extremities into the thorax) that prolongs right ventricular ejection time and delays P2.

With LBBB that occurs naturally or LBBB due to right ventricular pacing, there is paradoxic splitting of S2 (P2 before A2 that fuses into one un-split S2 sound with inspiration). This is because the inspiration-induced delay of P2 moves it closer to A2 which itself is delayed due to the left ventricle contracting after the right ventricle during LBBB conduction.

It is important to recognize that digitalis can account for diffuse ST segment depression in the absence of ischemia. Digitalis is a drug that was first described by William Withering in England in 1785 as a tea made from the leaves of Digitalis purpurea (foxglove) for the treatment of dropsy (edema). It was one of the most commonly-prescribed drugs for heart failure and atrial fibrillation but it has a very narrow therapeutic range and can easily reach a toxic range characterized by nausea and anorexia and dangerous arrhythmias due to increased automaticity. This is called digitalis toxicity. Today digitalis is used much less than before.

Legend for Fig. 68: This 12-lead EKG with lead II rhythm strip at standard paper speed and voltage is done on an 83 yo female who was being successfully treated with digitalis for atrial fibrillation. The rhythm is sinus as the P wave axis is ~+10⁰. There is coving upsloping ST elevation in leads aVR and V1 and coving downsloping ST depression in every other lead. Esteemed cardiologist J. Willis Hurst described this as pushing a digitalis pill into the ST segment. This is called digitalis effect.

Legend for Fig. 69:  This 12-lead EKG with lead II rhythm strip at standard paper speed and voltage is done on a 67 yo female who was taking digitalis for rate control of atrial fibrillation but was not able to resume sinus rhythm. When she presented to her doctor’s office with nausea and anorexia it was noted that her pulse was now regular. The EKG shows atrial tachycardia at 180/min with 2:1 AV conduction (best seen in lead V1). The increased atrial automaticity from digitalis toxicity provoked this, the most common arrhythmia from digitalis toxicity.  Even though she had this arrhythmia her pulse was now regular.  This must be recognized because there are effective means to treat digitalis toxicity.  Also notice the digitalis effect on the ST segments.

Legend for Fig. 72: This 12-lead EKG with 3 rhythm strips is done at 25 mm/s and 10 mm/mV on this 56 yo female with left chest pathology that compromises her respiration. The R + S in leads I, II and III add up to 14 mm. There is low voltage in the limb leads, but the R + S in lead V1 (which is on the right side of her chest) is 14 mm, so low voltage in the precordial leads does not pertain. Notice the rhythm is sinus tachycardia (111/min) and the respiratory rate is increased at 5 inspirations in 10 seconds (the frequency of the cycle of inspiratory decrease in QRS voltage seen in lead V1 rhythm strip) or 30 respirations per minute.

Drugs that are associated with QTc prolongation include:

• macrolide antibiotics
• metronidazole (with alcohol)
• antifungals
• antivirals
• antimalarials
• anesthetic halothane
• antiarrhythmics: disopyramide, procainamide, quinidine, dofetilide, sotalol, amiodarone
• antidepressants
• antipsychotics
• antihistamines

The next case is an example of drug toxicity that should be anticipated and avoided if possible.

Learning Case 3 presentation: 52 yo F cigarette smoker presents to ED 18 h after onset of chest pain

Case 3: Learning Point 1

Notice how in this tracing the R wave transition (the lead in which the R wave is taller than the S wave) is in V2 rather than the usual V3 or V4. Also note how the T wave is upright in V1. In a normal tracing the T wave in V1 is usually inverted. In leads V1-V3 the ST segments are depressed and upsloping. These are all features of an acute posterior STEMI. Of course STEMI is a misnomer here. It should be STDMI. If we want to see the EKG reflection of STEMI in an acute posterior MI look at leads V5 and V6. Here there are small Q waves and ST elevation and modest T inversion. To get a better representation of this posterior MI, record leads V7 (left posterior axillary line in the same horizontal plane as V6), V8 (left mid scapular line, just below the tip of the scapula, in the same horizontal plane as V6), and V9 (left paraspinal region in the same horizontal plane as V6). You will see Q waves and ST segment elevation in each of these leads that truly reflect the acute Posterior STEMI. Since this is a bit of a chore in a busy schedule, just take the standard 12-lead EKG paper tracing in your hands and turn it away from you, bottom-to-top and front-to-back. Then hold the paper tracing up to the light and look at the upside-down tracing through the back (blank side) of the paper. The Q waves, ST elevation and T inversion that you would have seen in V7-V9 are seen in leads V1-V3.

There are also small Q waves in leads 2, 3 and aVF. Although there are no inferior ST elevation, no T wave inversion and no reciprocal changes in leads 1 and aVL, this is not uncommon in an acute inferoposterior MI.

At coronary arteriography the LMT was disease-free as was the LAD. The Cx was proximally occluded 100% and the RCA was dominant and had a 50% stenosis in its mid-third. By echocardiography there was inferoposterior akinesis with LVEF of 50%.

Learning Case 7 presentation: 42 yo F with anxiety/panic attacks for the last year

Case 7: Learning Point 1

The rhythm is sinus with a short PR interval and a delta wave that reflects pre-excitation of the ventricle, bypassing the AV node. Notice that when the sinus rate slows the delta wave gets larger and the PR interval shortens. The slowing of the rate of the P waves is due to sinus arrhythmia. The P waves with this slower rate appear a bit different but this is due to the larger delta wave and not due to an ectopic atrial focus. Notice the repolarization changes, especially in leads I and aVL, that are characteristic of pre-excitation. Sinus arrhythmia is not usually sensed by the patient, certainly not as anxiety or a panic attack.

Case 7. Learning Point 2

This SVT is the cause (below).
The HR of her SVT is 201/min and was recorded just 1 minute prior to the sinus tracing. Notice the ST depression, especially in leads V3-V6, that is characteristic of SVT. This is orthodromic AVRT. The anterograde conduction, through the AV node, returns up the bypass tract. She was taken to the EP lab for ablation.

Case 7: Learning Point 3

There in the EP lab multiple right-sided bypass tracts were ablated. Her episodes of tachycardia did not recur. This is her EKG (below) done 3 days later, after the ablation. The PR interval now measures 140 ms and the delta wave is gone. Repolarization changes are no longer present. Her panic attacks and anxiety were cured.

Learning Case 52 presentation: 85 yo N, 12 h S/P TAVR for severe AS

Case 52: Learning Point 1

This patient had a 29 mm Edwards-Sapien S3 Aortic Valve placed via transfemoral approach to treat severe symptomatic aortic stenosis. The post-procedure AoV gradient was low and there was no aortic regurgitation. He did have a new LBBB noted directly after the procedure. Here is his EKG from the day before the TAVR:

Case 52: Learning Point 2

Features of LBBB that were not present pre-TAVR are: abnormal septal depolarization (no Q wave in leads I, aVL or V6 and poor R wave progression in V1-V3), wider QRS (≥120 ms) and repolarization abnormalities in I, aVL and V6. Compare the pre- and post-TAVR EKGs to see these features of LBBB. He went on to need a PPM 3 days post-TAVR due to 2:1 block with atrial pacing after receiving atropine. The incidence of AV block requiring a PPM following this type of TAVR is ~4%.
Incomplete LBBB (choice 50) has all of the features of complete LBBB except the QRS duration is <120 ms, usually between 100-119 ms.
It is also important to know that when LBBB is intermittent, the narrow complex QRS beats can have deep anterior T wave inversion (demonstrated in next EKG). This is known as T wave memory and can also be seen when prolonged RV pacing is terminated and intrinsic QRS conduction resumes.

Case 52: Learning Point 3

This is a 59 yo M with sinus rhythm at 61/min with no arrhythmia but there is intermittent LBBB. Notice how in rhythm lead V1 there is deep T wave inversion in all but the 2 LBBB-conducted beats. This is T-wave memory.

Case 52: Learning Point 4

This is the EKG of a 74 yo F who was 6 hours after septal myectomy to treat HOCM. Her coronary arteries were normal and her pre-op QRS duration and QTc were normal. It is common to have a new LBBB after this procedure. The learning point here is that her absolute QT interval and the QTc (HR is 60) were 582 ms. That the QRS duration is 148 ms, to correct the QTc to a QRS of 80 ms, subtract 68 ms from the 582 QTc. It comes out to 514 ms which is still significantly longer than the ULN of 450 for a QTc when the QRS duration is 80 ms. Thus this EKG should be read as NSR, LBBB and long QT interval. Any cause of QRS prolongation (IVCD, PPM, BBB) makes it necessary to also correct the QTc for QRS duration.

Learning Case 53 Presentation: 39 yo M, 1 day S/P open surgical repair of an ascending aortic aneurysm

Case 53: Learning Point 1

Acute pericarditis is characterized electrocardiographically by ST segment elevation with upright T waves in all leads but aVR and V1. In these leads the ST segments are depressed. That is different from early repolarization where the ST segments are not depressed in V1. This is also different from ischemic heart disease (especially STEMI) where the T waves are often inverted when the ST segments are still elevated. In pericarditis the T waves do not invert until the STs return to baseline. In pericarditis there is also often PR segment depression (as compared to the T-P segment), but this is absent here. The EKG of acute pericarditis changes over the course of 1 week to 1 month or more and is divided into 4 stages. The 1st stage is demonstrated here as Case 53. The 2nd stage has the ST segments return to baseline and in the 3rd stage the T waves invert (unlike ischemic heart disease). This 3rd stage of pericarditis looks like so many other EKGs with non-specific T wave inversion but it involves all of the leads and if one takes a good history and thinks of pericarditis, the diagnosis can be made. In the 4th stage the EKG returns to the pre-pericarditis pattern. In chronic pericarditis the EKG never returns to normal. The ST segments might return to baseline but the T waves remain inverted (stuck in stage 3). With a large pericardial effusion (answer choice 79) the QRS voltage becomes low (adding the R and S in limb leads I, II, and III = <15 mm), (see Learning Points (2)). While not present here, there might be electrical alternans, where every other QRS has lower voltage. By definition of Dr. David Spodick, it must be every other beat low voltage and every other beat larger voltage.
The EKG can help in auscultation of the heart of a patient with pericarditis. The patient with acute pericarditis and sinus rhythm has a 3-component rub. There is a component for atrial systole, one for ventricular systole and one for ventricular diastole. In junctional rhythm there is just a 2-component rub which is easy to be certain of, but in atrial fibrillation there is a 2-component rub that is more difficult due to the irregularity. Of course in both arrhythmias it is atrial systole that is absent.

Case 53: Learning Point 2

This 74 yo M presented with dyspnea and enlarged cardiac silhouette. There is sinus tachycardia at 101/min, generalized low QRS voltage and nonspecific T wave abnormality. More than 1 liter of pericardial effusion was removed after which the QRS voltage trebled. By pericardial biopsy the diagnosis was mesothelioma.

Case 9 Presentation: Middle-aged M with hoarseness, systolic/diastolic murmur at base of the heart and exertional chest pain (slide 41)

Slide 42: Enlarged aortic knob (arch): blue, double-headed arrow; Enlarged ascending aorta: yellow arrow

Slide 43: Dx: Luetic aortitis with ascending and arch aneurysms, mild AS/AR, CAD
Hoarseness is due to Lt recurrent laryngeal nerve compression where it wraps around aortic arch. At coronary arteriography he had ostial stenosis of both RCA and LCA; the cause of his angina pectoris.

Case 15 Presentation: Middle-aged M who is pacemaker dependent after CABG surgery but now, 2 months later, pacemaker has lost capture and he has developed postural dizziness. (slide 66)

Slides 67 and 68: Tangle of pacing wires at blue arrow; Tip of RA electrode at yellow arrow; Tip of RV electrode at red arrow

Slide 69: Dx: Twiddler’s syndrome

Slides 70 and 71: 2 months earlier when recently post-op CABG and permanent pacemaker placed

Notice there is no tangle of electrodes under the pacemaker generator (but there is a metal-laced gauze pad overlying the left infraclavicular incision).

Tip of RA electrode at yellow arrow clearly has a larger J shape.

Tip of RV electrode at red arrow was much deeper into the RV.

A Twiddler spends time rotating the pacemaker generator in the pocket “reeling-in” the electrode tips and they lose capture. Electrodes might also break or their insulation can split.

Case 16 Presentation: Young M bodybuilder complains of left upper back pain after weightlifting sessions. (slide 73)

Slides 74 and 75: Notice increased diameter of aortic knob (AK); Blue arrow points to line of calcification within the aortic arch/proximal descending aorta.

Notice the soft tissue of his muscular thorax

Slides 76 and 77: The lateral CXR blue arrow indicates line of calcification in greater curvature of the aortic arch, proximal descending aorta.

Five years earlier he was the driver in a head-on collision in which he sustained rib fractures and loss of consciousness and stayed in hospital for 2 weeks, but his passengers were even more seriously injured.

The aortic calcification represents a localized aortic dissection just distal to the left subclavian artery. It healed, but continued to enlarge, until aneurysmal and symptomatic, perhaps provoked by the dramatic increase in his BP while he lifted heavy weight.

Case 46 Presentation: Middle-aged M with chest pain and acute dyspnea (slide 218)

Slide 219: He was known to have angina pectoris, but he had never suffered like this. The EKG showed an acute STEMI and ischemic changes distant from the infarction. He went to acute coronary intervention, but in addition to an occluded LAD there were severe proximal stenoses in the other coronary aa. He was stabilized and went to CABG surgery prior to discharge.

Dx: “Bat’s wing” pulmonary edema (flash pulmonary edema) due to LV failure from acute coronary occlusion compounding severe stenoses in remaining coronary arteries

Notice air bronchograms (blue arrows) indicating alveolar edema.

Slides 220 and 221: This was the same M three months prior to flash pulmonary edema.