Antitachycardia Pacing

A 70 yo with h/o HTN, CAD and s/p AICD placement.

There are (fast) pacer spikes in the middle. Is this an AICD malfunction or just artifacts?

Image # 1

AV Nodal Reentry Tachycardia (AVNRT) for non-cardiologist

Atrial Fibrillation and Systemic Embolization

An elderly was admitted due to abdominal pain and confusion.

BP 160/90, HR irregular, not in distress, afebrile, O2sat 96%. Abdomen distended but no tenderness, no focal weakness. CBC unremarkable except for WBC 13.5, lytes - N, BUN- 15, creatinine - 1.4, INR -1, UA unremarkable except for proteinuria.

What is the rhythm and its relationship to the CT and MRI images?

Image 1 - Composite image - Long lead II, CT of the abdomen and MRI of the brain

The rhythm is atrial fibrillation. 

Image on the left and middle is the CT of the abdomen 

RED ARROW - showing embolus occluding the proximal mesenteric artery 

BLUE CIRCLE - showing embolus occluding the R renal artery with renal infarction.

Image on the right is the MRI of brain (diffusion weighted imaging - DWI) 

GREEN CIRCLE - showing an infarct on the L cerebellum

Back to the case

So, there are embolic events in the superior mesenteric artery, renal artery and the brain due to the atrial fibrillation. Thrombolysis was done on the superior mesenteric artery. Patient was also started on heparin bridge and coumadin anticoagulation. Nephrology was on-board for the renal failure (increasing creatinine). Patient was later discharged with therapeutic INR.

#224

Global T wave inversions in a Patient with CVA

A middle-aged patient with no significant past history was brought in due to decrease LOC. BP in 200's systolic. PE showed right sided-weakness.

Image 1 - Baseline 12L 

Baseline 12L showed SR, LVH with strain.

Image 2- Follow-up ecg 

Follow-up 12L (days after) showed (symmetric) global T wave inversions with slightly prolonged QTc (485 ms). 

I came up with the work of Burch et al (1954) describing marked diffuse TW abnormalities in patients (n=17) with cerebral injury. 

Global TWI is not unique to cerebral injury as mentioned in the works of Walder LA and Spodick  DH.

For the case:

Lab showed CBC - normal range, Trop - neg, Na- 135, K -  3.5, Ca - 8.5 BUN/Crea-N, CXR - NAD, CT -image.

Image 3- CT of the head

CT of the head w/o contrast showed intraparenchymal hematoma centered within the left hemithalamus with intraventricular extension.

Echo: Mild concentric LVH, EF ~ 65, LA upper limits, RA, RV normal, no WMA.

Usual stroke management was initiated and shunt was inserted due to hydrocephalus. Patient was discharged after a few days.

Reference:

Burch et al. 1954. A New ECG Pattern Observed in CVA. Circ 9:719-723

http://circ.ahajournals.org/content/9/5/719.full.pdf+html

Walder LA and Spodick DH. 1991. Global T wave inversion. JACC 17:1479-85

http://www.sciencedirect.com/science/article/pii/073510979190635M

#222

Electrical and Mechanical Components of a Code

Tracings captured during a code

The case was post-MI/ sp stenting and intra-aortic balloon pump was placed. I think the LAD was the culprit artery. 

I would just like to show in the tracings the mechanical component of VT (central venous pressure waves - CVP) and the arterial line (in a pt with AIBP - set at 1:2 AIBP support). 

Image 1 - 

Look at the mechanical effect of VT on the arterial pressure.

Image 2 -

An image showing the on-going compression (CPR) in a patient with VT and the arterial pressure it generates.

Image 3- 

CPR during VT and its generated pressure. 

Shock for VT.

Perceived organized electrical activity but absence of mechanical activity (no activity in the arterial waves).

#220

Paroxysmal AV block (Ventricular standstill)

Paroxysmal AV block (Ventricular standstill)

-characterized by an abrupt and persistent AV block in the presence of otherwise normal AV conduction.

-may be initiated by:

conducted or blocked PAC or PVC

acceleration or slowing of sinus rhythm

**** in this case, we can see the slowing of the sinus rhythm.... went into 2:1 AVB then complete AVB with ventricular standstill.

-once the block is initiated, the block will persist until terminated by an escape, usually ventricular, with a predictable 

relationship of the escape to the following P wave

-most likely infra-His or subnodal and due to bilateral BBB (exact mechanism is unclear).

Reference: 

Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.

#215

Bradycardia due to hypothyroidism

A middle-aged person who has no known significant medical history came in due to syncope (?)/fall. A few days prior,  patient noted headache, weakness, nausea and dizziness when getting up and changing position.  + decrease vision on R eye. No palpitations, chest pain, dyspnea, seizure,tingling, focal weakness. Noted weight gain of about 6 lbs for the past month. 

VS 120/70 36.3 HR 40's RR 25. Not in distress, awake and orriented x3, no jaundice, no hyperpigmentation, normocephalic and atraumatic, wet oral mucosa, no goiter or nodules, CBS, RR and no murmur, flat abdomen and no mass or tenderness, no LE edema.

CBC in reference range, trop neg x 3, glucose 100, Na 110's, K 3.3, Cl 80, bicarb 21, BUN 6, crea 0.7, Ca 8.3, PT/PTT - N, CXR normal. ECG was captured.CT head is pending.

What is the ecg saying about the who clinical scenario? —

Image 1 - 12 Lead

The ECG showed marked sinus bradycardia. 

So, we have here someone who presented with syncope with profound hyponatremia, headache, weight gain, decrease eye vision and profound bradycardia.

Patient was placed on hypertonic saline but serum sodium remained low. CT scan and MRI revealed a large pituitary mass with suprasellar extension (impingement on the optic chiasm). So in view of these, the thought is that the patient has central adrenal insufficiency and central hypothyroidism (low TSH and free T4). Patient underwent transnasal resection and multiple subspecialties were on-board for the case and discharged a few days after.

Image 2 - CT ST/MRI head / Pituitary Hormones

"The spectrum of clinical features of pituitary insufficiency depends on several factors. In acquired pituitary insufficiency, the clinical spectrum depends on the degree of hormone deficiency, the number of hormones impaired, and the rapidity of onset"

"The order of diminished trophic hormone reserve function related to pituitary compression usually is as follows: GH > FSH > LH > TSH > ACTH. The corticotrophic cell appears to be particularly resistant to hypothalamic or pituitary destruction, and it is usually the last cell to lose function. "

So, this is case is profound bradycardia due to hyopthyroiduism.

Reference:

Melmed S, et al. 2011. Williams Textbook of Endocrinology 12ed. PA Elsevier

#210

Cardiac Electrical Events

From: Jaakko Malmivuo & Robert Plonsey: Bioelectromagnetism - Principles and Applications of Bioelectric and Biomagnetic Fields, Oxford University Press, New York, 1995.

http://www.bem.fi/book/06/06x/conducti/0607a.htm

Dual AV node conduction during sinus rhythm

This ECG is from a patient admitted due to dizziness. Work-up revealed a posterior circulation stroke. During routine monitoring this "strange" ECG strip was captured.

Image 1 - Long lead II

This is sinus rhythm. The first 2 QRS complexes were conducted with a normal PR interval of about 0.20 sec. After R3 (PVC), the PRI became prolonged at around 0.60 sec. The PRI remained prolonged up to R12. After R13 (PVC), the PRI became normal again.

This strange ECG behavior can be explained by the existence of 2 pathways in the AV node. One pathway conducts fast and creates a short or normal PRI and the other pathway conducts slow and creating a long PRI.

This is better appreciated by a ladder diagram (courtesy of a friend Jason R).

Image 2 - Ladder diagram

The PVC's made one pathway refractory and allowed preference of conduction to the other pathway. This is just one of many manifestations of dual AV node conduction during sinus rhythm.

The existence of 2 pathways in the AV node is also called dual AV node physiology. Some individuals have this. This particular strip manifested dual AV node conduction during sinus rhythm. Another instance where we can see dual AV node physiology is during AV nodal reentry tachycardia (AVNRT).

#204.1

Tall T waves due to hyperkalemia

An elderly hypertensive was admitted due to generalized weakness and nausea for a month and 2 weeks watery diarrhea.

This is the ECG. What do you expect to see in the lab of this patient?

This is sinus rhythm with tented T (tall and narrow) waves from V3 to V6.

Labs came back: WBC and PC - N, Hb 7.6 (L), Trop - 0.09, BG - 120, Na 135 (N), K 8.5 (H), CO2 9 (L), BUN 150's (H), Creatinine 19, UA showed pyuria and proteinuria. USD showed bilateal hydronephrosis.

So there was severe hyperkalemia due to renal failure (acute on chronic) prob obstructive uropathy with hypertensive nephrosclerosis. 

#216

Prolonged QTc due to hypocalcemia

A middle-aged pt non-compliant DM II, CKD, hypertensive is being managed as  hyperosmolar hyperglycemic state (formerly called HONK) with glucose in the 800's, Na 113, K 3.5, BUN 65, creatinine 6.1.

What is the ECG telling us and probable cause of the ECG finding/s?

The 12L is sinus rhythm with prolonged QTc (> 500 ms). Additional labs revealed phosphorus 5.2 (high), calcium 5.8 (corrected - 6.2)(low), albumin 3.4, troponin negative, magnesium 1.9. (normal). So, the cause of the prolonged QT/QTc was hypocalcemia due to renal failure.

The blood sugar was eventually controlled and the calcium was corrected. Pt was eventually discharged a few days and advised for close ff-up.

#211

The effect of a spontaneous PVC in a supraventricular tachycardia: It's significance

Image 1

A 65yo pt c/o of shortness of breath.

As most will call it, this is a supraventricular tachycardia (SVT). A SVT is a narrow complex  (unless there is aberrant conduction) tachycardia that requires the atrial tissue or the atrioventricular (AV) node as an integral part of the arrhythmia.

SVT is classified as short RP' or long RP' tachycardia depending on the RP or PR interval. If the interval from the R wave to the next P wave exceeds the  interval from that same P wave to the next R wave, then the SVT is called long RP' tachycardia. If the interval form the R wave to next P wave is shorter than the interval from the same P wave to the next R wave, then the SVT is called short RP tachycardia.

Image 2 - Short RP' and long RP' tachycardia

Image 2A is a short RP' tachycardia and image 2B is a long RP tachycardia. 

These are the SVT's based on this classification

Image 3 - Short RP' and long RP' tachycardia

About 90% of AV nodal reentry tachycardia (AVNRT) and 87% of AV reentry tachycardia (AVRT) are short RP' tachycardia. Only 11% of atrial tachycardias (AT) are short RP' tachycardia. 

AVNRT is the the most common form of paroxysmal SVT.

Image 4  - ECG case highlighted

The ECG case  is a regular short RP narrow complex tachycardia (~190 bpm) . There is a pseudo-R' in V1 (red arrows) and pseudo-S in II, III and aVF (blue arrows).  There is lengthening of the RR interval before the termination of the tachycardia. The arrhythmia is terminated with a P wave (black arrow). A PVC can be seen that did not disturb the rate of the tachycardia. All this points to AVNRT.

The presence of a pseudo-S, a pseudo-R', or both is 90-100% specific for typical AVNRT and has an 81% positive predictive value for typical AVNRT. AVNRT terminates with a P wave. The change in the cycle length or the change in the RR interval prior to the termination is not diagnostic for AVNRT because it can also occur during AVRT.

The tachycardia RATE CANNOT BE USED TO DIFFERENTIATE BETWEEN SVT's. AVNRT can vary between 100-280 bpm (200-250). AVRT and AT can also have similar heart rates.

A short review on what creates the pseudo-S and pseudo-R and the concept of RP/PR classification

In some individuals, there are 2 atrionodal connections (dual AV node physiology). One connection (pathway) conducts fast but recovers slow (longer refractory period) and the other pathway has a slower conduction but recovers fast (shorter refractory period). 

Image 5 - Dual AV node physiology

In a short RP tachycardia, the retrograde conduction is via the FAST PATHWAY. This creates a short RP interval. The anterograde conduction is via the SLOW PATHWAY. This creates the long PR interval. The retrograde impulse also reaches the atria and creates an inverted P wave in II, III and aVF  (pseudo-S) and a small R wave in V1 (pseudo-R). 

In long RP tachycardia, retrograde conduction is via the SLOW PATHWAY and the antegrade conduction is via the FAST PATHWAY. Thus, on the surface ECG, there is a a long RP and shorter PR interval.

Effect of spontaneous PVC during a short RP tachycardia

Image 6 - PVC during AVNRT when HIS is refractory

During AVNRT, the retrograde conduction after a spontaneous PVC cannot reach the atrium because there is no alternated pathway. So, the AVNRT cycle is not changed and the PP interval is not change after the PVC. This means that the ventricles are not part of the circuit.

Image 7 - PVC during AVRT when HIS is refractory

During AVRT,retrograde conduction after a PVC cannot reach the atium (via the AV node) when the His bundle is refractory but can reach the atrium via the AP. So, the subsequent the atrial depolarization will occur earlier or the P wave on the surface ECG will occur earlier. This means the an AP is present. 

Image 8 - PP interval and the PVC

In this ECG case, the PP interval (red arrows) did not change as revealed in the simultaneous comparison of leads.

This termination of the tachycardia was due to adenosine.

Reference:

Bonnow et al. 2011. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th Edition. PA.Saunders 

Das and Zipes. 2012. Electrocardiography of arrhythmias : a comprehensive review. Elsevier PA

Kumar UN et al. 2006. The 12L Electrocardiogram in Supraventricular Tachycardia. Cardiology Clinics ;24: 427-437

#618

Dynamic changes in lead III in a patient with low O2 saturation

An elderly c/o SOB for 2 days. Sat at ~ 80's at room air and increased to 93% at 4LPM. VS 200/100, HR 120 RR 26 afebrile. + Wheezing.

Image 1 - 12 L

Image 2 - Full disclosure on telemetry

Trop was negative, K and Ca was in the normal range, pro-BNP ~ 3000, D-dimer ~ 700. CT showed bilateral pulmonary embolism (PE). 

Image 3 - Composite images of CXR, CTA of the chest and lead I/III

In the real world, the classic changes we expect to see are not there all the time but I think they are there somewhere. The 12L only captures the 10 sec event. During telemetry, the ECG showed dynamic QRST changes: S in I and Q in III and T wave inversion or S1Q3T3 pattern seen in patients with PE.

The patient was started on enoxaparin (bridge) and coumadin. Patient was discharged after a few days.

#206

The "skipping" P waves

ECG case

Vignette: 70yo with h/o HTN, s/p valve replacement c/o one-sided facial numbness and dizziness. Work-up for stroke was negative. CBC - N, chemistry and troponin - N, CXR negative for acute disease.

What is the rhythm?

Image 1 - Long lead II

Long lead II can be interpreted as atrial fibrillation (AF). However, it is very odd for AF to be regular unless there is a complete heart block, AF with a pacemaker and AF with entrance block and junctional rhythm with an exit block. The machine read this rhythm as AF.

Image 2 - Long lead II and V1

Adding long lead V1 revealed a different story. Organized atrial activity can be seen in V1. The PP rate is about 88 bpm. Some of the P waves are distorting the initial and terminal portion of the QRS. 

Image 3 - Ladder diagram 

Image 3 marked in red arrows some hidden P waves. The complexes with red arrows highlight the typical morphology of a QRS with no P wave distortion.

The laddergram also illustrates an interesting pattern. The P waves depolarizing the the QRS is "skipping" the nearest QRS. The initial QRS complexes are conducted with 1:1 pattern and the latter part is conducted with a 2:1 pattern (rate ~ 40 bpm). There is a very long PRI of about 0.56 sec and a left bundle branch block.

Interpretation: Sinus rhythm, first degree AV block, second degree AV block type I (Wenckebach/Mobitz I), LBBB.

This patient eventually got a pacemaker.

#617

Sudden prolonged PRI due to concealed conduction by Dr. Tính Nguyễn Chí

Image 1 : The ECG of the middle-age man who was diagnosed as myocarditis.

Image 2 - ladder diagram

As we can see, beats # 1, 2 are normally conducted complexes. Beat #3 is an interpolated PVC. Beat # 4 is sinus rhythm but with the prolonged PRI and beat 5 is also a PVC with retrograde atrial capture and then the cycle repeats. Notice that beats # 3,8,13 are interpolated PVCs and beats # 4,9,14 have the prolonged PRI. The possible interpretation for the prolonged PRI of beat 4,9,14 is the  concealed retrograde conduction of the premature ventricular complex. The sinus P waves after the interpolated PVCs reach the AV node during its relative refractory period ( caused by the concealed retrograde conduction of the interpolated PVCs), so they take much more time  to penetrate the AV node. That phenomenon created the long PRI (beats #4, 9 and 14).

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Wide QRS Tachycardia (WQRST) in a Patient with a Pacemaker - Is this VT?

Image 1

Is this Ventricular Tachycardia?

The WQRST tachycardia is initiated by ventricular couplet. On the second wide QRS complex, distinct atrial activity can be seen. After that the PM delivers a stimulus to the ventricles and the tachycardia is initiated.

Image 2 -PMT (Pacemaker-Mediated Tachycardia) Initiation

This is an attempt to simplify initiation of a classic form PMT (ELT - endless loop tachycardia).

Pacemaker-Mediated Tachycardia

Pacemaker-mediated tachycardia is any undesired pacing rate caused by the pulse generator or by the interaction of the pacing system with the patient.

The following are well documented causes of PMT:

• Runaway pacemaker
• Sensor-driven tachycardia
• Exposure to MRI scanners
• Mypotential tracking
• Atrial arrhythmias
• Endless-loop tachycardia

Reference:

Ellenbogen e al. 2011Clincal Cardiac Pacing, Defibrillation, and Resynchronization Therapy (4th Ed). Saunders PA

# 203

Pericarditis

A pt in the 60's with hx of DM and HTN is complaining of chest pain. 

What do you think of the 12L?

The 12L showed sinus rhythm with what looked like ST elevations in limb leads and precordial leads.

Heat cath showed mild, non-obstructive CAD.

Going back to the 12L, the  PR depressions  in I, II, aVF and lateral leads created what it looked like an STE. There is also PR elevation in aVR. 

Those ECG changes were due to pericarditis.

#202

A case of trifascicular Block by Dr. Tính Nguyễn Chí

This ECG case was posted in the FB ECG Rhythms page on10.31.15. 

The ECG shows sinus rhythm with 1^st degree AV Block and RBBB and LAFB. So, this is trifascicular block. ECG Holter monitoring showed intermittent 3^rd AV block. A permanent pacemaker was implanted.

AF cardioversion

This was new onset  atrial fibrillation (AF) and was cardioverted (of course after checking there is no thrombus is the LAA by TEE).

# 91

Polymorphic Ventricular Tachycardia or Torsades de Pointes?

This is a 60 yo patient admitted due SOB.

Figure 1

It started with a (sinus) narrow QRS rhythm with a Qtc of 485 ms. Then it converted to a wide QRS rhythm with  varying amplitude (height). 

So, someone checked  and found the patient to be unconscious and with no pulse. CPR was initiated and a code was called.

Figure  2

With very good CPR, 1 shock and 1 dose epinephrine the rhythm came back in 10 minutes (perfusing SR).

Is this Torsades de pointes (TdP)? 

Tdp refers to a VT characterized by QRS complexes of changing amplitude that appear to twist around the isolelecttic line and occur at rates of 200-250 bpm. It is characterized by prolonged QT intervals (generally exceeding 500 ms).

There is a less common form of TdP (short-couple variant). This is initiated with a close-coupled PVC and usually does not involve preceding pauses or bradycardia. This is a malignant disease with high mortality and had several characteristics with idiopathic VF.

VT that is similar in morphology to TdP that occurs in patients WITHOUT QT prolongation should generally be classified  as polymorphic VT and not as TdP.

Why make a distinction between TdP and polymorphic VT (similar in morphology to TdP wtihout QT prolongation)? 

This is due to therapeutic implications. In patients with TdP, giving drugs like amiodarone/dofetlide or sotalol can increase the already abnormal QT interval creating more problems. For TdP from acquired causes, magnesium is the initial treatment of choice followed by temporary pacing.

When QT is normal (polynmorphic VT resembling TdP) then standard antiarrhtyhmics can be given. 

So this one was polymorphic VT, the case entered the pulseless VT algorithm and interventions (and the team) did well.

All the electrolytes are in the normal range but the ejection fraction (EF) is about 25%.

Reference:

Bonnow et al. 2011. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th Edition. PA.Saunders 

#96

There is no abrupt change in rate in sinus tachycardia

No clinical history.

Image 1

What is the rhythm? What are your differential?

This is a narrow complex tachycardia at a rate of about 150 bpm. There is an ABRUPT/SUDDEN change in the rate towards the end of the strip which is from about 150 bpm to 83 bpm. This abrupt change is not seen in sinus tachycardia. Sinus tachycardia will show a gradual decrease in rate.

The differential diagnoses are: 

1. Inappropriate sinus tachycardia (IST)

2. Atrial reentry tachycardia (ART)near the sinus node

3. Sinoatrial reentry tachycardia (SART/SNRT)

IST is non-paroxysmal, elevated resting rate and gradual (excessive 

acceleration as reaction to mild exercise.However, as we  see in the strip, this is paroxysmal. Thus, IST is ruled-out.

ART - paroxysmal and difficult to differentiate from SART.

Sinus node reentry tachycardia is defined as a reentrant tachycardia involving the sinus node and perinodal tissue.  It is possible that SNRT may represent a high cristal atrial tachycardia (AT) originating near the sinus node . The features of SART/SNRT are:

The features of SART/SNRT are:

1. Abrupt onset/termination (may have gradual slowing)

2. Similar p-wave morphology compared to regular sinus beats (or may 

differ slightly)/ upright in leads II, III and aVF

3. Rate may vary from 80-140 bpm (ave apprx 100-110)

Thus, this is ART vs SART/SNRT.

References:

Das and Zipes. 2012. Electrocardiography of arrhythmias : a comprehensive review. Elsevier PA

Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical  Arrhythmias. Futura Pub NY

Mohammad-Reza et al.1985 Sinus Node Reentry: Case Report and  Review of Electrocardiographic and Electrophysiologic Features. Texas Heart Institute 12(3) 249-252 

Sanders et al. 1994. Catheter Ablation of Sinus Node Reentry Tachycardia. JACC 23 (4) 926-934 

Simmers TA and Seeram N. 2003. Sinoatrial Reentry Teacycardia: A  Review. Indian Pacing and Electrophsiology 3(3):109-116 

#174