Monday, June 18, 2018

A Wide Complex Rhythm in an Intoxicated Patient

This patient presented with altered mental status and was thought to be intoxicated.  He did not have any other apparent medical issues.

I'm not certain why an ECG was recorded, but it was:
The computer and the overreading physician diagnosed "Sinus rhythm with LVH."
What is it?

This is an accelerated idioventricular rhythm (AIVR).  There is also isorhythmic dissociation (P-waves and QRS co-incidentally going the same rate, but without the P-waves consistently conducting through the AV node because frequently the ventricular rhythm usurps it (comes too early for the P-wave to conduct).

I point out the salient features on the annotated image below:
There is a wide QRS that is at regular intervals at a rate of about 65.
They are either not preceded by a P-wave, or by a P-wave that is too close to be conducting.
Black arrows points to normal P-wave that conducts to a normal QRS.
Green Arrows point to upright sinus beats that are close to the QRS and create a "fusion" beat, in which the ventricular beat and the normal beat meet up (fuse) and create a hybrid QRS that is longer than a normal one, but shorter than the idioventricular ones.
Red Arrows point to retrograde P-waves.  The idioventricular rhythm conducts up the AV node to the atrium, creating an upside down P-wave after the QRS.
Blue arrows point to upright P-waves that are within or after the QRS; they occurred too late to affect the QRS (they did not fuse).

AIVR is an automatic ventricular rhythm that is:
1.  Faster than a normal ventricular escape rhythm (which is also automatic at rates as high as 50).  AIVR is caused by enhanced automaticity (faster than normal automaticity).
2.  Slower than ventricular tachycardia (less than 100-120).  VT is a re-entrant rhythm.

It is a benign rhythm but may be seen in dangerous pathologies, particularly in the reperfusion phase of acute STEMI, digoxin toxicity, and sympathetic overload.

Clinical course

Although the overreading physician did not see the AIVR, the resident did diagnose "Idiopathic Ventricular Rhythm without Tachycardia," which does pretty well (but not exactly) describe the ECG, but does not conform to the standard terminology.  "AIVR" is much more accurate and precise.

The patient had negative troponins in the ED.   He was not on digoxin.  He did not have other evidence of sympathetic overload.

He metabolized his toxin, whatever it was, and was discharged.

It is important to know that AIVR can occur any time and does not necessarily imply significant pathology.

Since there is a great and succinct article on AIVR at Life in the Fast Lane, I do not feel the need to explain in greater detail:

Sunday, June 17, 2018

Chest Pain and Inferior ST Elevation.

A middle-aged patient with lung cancer had presented to clinic complaining of generalized malaise, cough, and chest pain.   He had an ECG in clinic which worried the providers because of possible inferior MI, and they sent him to the ED.

Here is that ECG:
What do you think?

There is sinus tachycardia.
There is ST Elevation at the J-point, relative to the PQ junction (end of PR segment) in II, III, aVF.
There is some T-wave inversion in aVL (which is a soft sign of inferior MI, but no reciprocal ST depression).

Notice, however, that there is profound PR depression.  The apparent ST elevation is mostly just relative to the depressed PR segment.

He was sent to the ED and had this ECG at t = 1 hour:

There are several issues which mitigate against acute inferior MI, and these are the Learning Points:

1. Symptoms other than chest pain (malaise, cough in a cancer patient)

2. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology.  I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies.  We showed this in a recent analysis of UTROPIA data (see abstract below).

3. PR depression, which suggests pericarditis

4. Absence of large inferior T-waves, which are very common in OMI (acute occlusion MI).

5. Absence of any ST depression in aVL.  (We showed that absence of STD i aVL rules out inferior MI, even subtle inferior MI, with 99% accuracy.  We also showed that, of 47 cases of pericarditis with ST elevation, none had ST depression in aVL.)  T-wave inversion in aVL was also very sensitive, but not as good as ST depression.

The patient underwent an emergent formal echocardiogram to look for wall motion abnormality:

The estimated left ventricular ejection fraction is 63 %.
No wall motion abnormality .
Pericardial effusion very small
No evidence for pericardial tamponade.
Multiple fibrin strands in (lateral) pericardial space, c/w fibrinous pericarditis


Here is a still image from a bedside cardiac ultrasound:
See small effusion in upper right of image

The patient turned out to be septic from pneumonia, received 3 liters of fluids and antibiotics, and had the following ECG recorded:

ECG (t = 7 hours)
Fluids have resolved the sinus tachycardia.
ST elevation persists, but there is less PR depression (interesting!)
Still no reciprocal ST depression in aVL 

The Negative Predictive Value of Tachycardia for Type I MI in Hemodynamically Stable Patients with Chest Pain

Daniel H. Lee, MD – Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN
Yader Sandoval, MD - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Fred S. Apple, Ph.D. - Department of Laboratory Medicine, Hennepin County Medical Center; Professor, University of Minnesota School of Medicine
Stephen W. Smith, MD – Department of Emergency Medicine, Hennepin County Medical Center, Professor, University of Minnesota School of Medicine, Minneapolis, MN

Patients with type 1 myocardial infarction with normal left ventricular function that are hemodynamically stable do not usually manifest with sinus tachycardia. The goal of the present analysis was to examine whether the presence of tachycardia identified patients unlikely to have type 1 myocardial infarction.

This was a secondary post-hoc analysis of a prospective, observational data study of 1927 consecutive ED patients over 4 months who had at least 1 contemporary troponin I (cTnI) resulted.  

Inclusion criteria were chest pain, ≥ 2 serial cTnI, sinus rhythm, and ≥ 1 ECG. 

Exclusion criteria included age <18 b="" years="">SBP <100 b="" echocardiogram="" ejection="" fraction="" mi="" mmhg="" st-elevation="" with="">, pregnancy, and trauma. 

All cases with at least one elevated cTnI were adjudicated into specific MI type (or no MI) by two clinicians who reviewed all medical records. Patients were stratified according to presence or absence of type I MI, and of heart rate (HR) > 99 bpm, and > 120 bpm on presenting ECG. All ECGs were coded by an expert clinician as having ST-elevation, ST-depression, T-wave inversion [ST/T abnormalities, (ST/T-A)], or none of the above.

877 patients were included, of whom 135 had HR > 99 bpm (742 ≤ 99 bpm) and 23 had HR > 120 bpm (854 ≤ 120 bpm).  Of the 877, 58 (6.6%) had type I MI and 819 did not; 4 of 58 (6.9%) with type I MI, and 131 of 819 (16.0%) without, had HR > 99 (P=0.02).  The negative predictive value (NPV) of HR > 99 for type I MI was 97.04% (95%CI 92.6-98.8) and the negative likelihood ratio [(-)LR] was 0.43 (95%CI 0.17-1.12).  23 had HR > 120 bpm (854 ≤ 120 bpm); 0/23 with HR > 120 bpm had type 1 MI.  The NPV of HR > 100 bpm for type I MI among those with ST/T-A was the same as in those without, at 92.0% (95%CI 74.7.6-97.8).  Of 23 patients with HR > 120 bpm, 4 had ST/T-A.  See Table for diagnostic utility.


In hemodynamically stable patients with chest pain, sinus tachycardia aids in the identification of patients unlikely to have type I MI, especially in those with HR > 120 bpm.

Comment by KEN GRAUER, MD (6/17/2018):
Excellent case with insightful learning points explaining why these serial tracings are not indicative of acute inferior infarction. I’ll add the following 2 comments:
  • iThis patient presumably has effusive-constrictive pericarditis. ECG findings of constrictive pericarditis are generally not overly helpful clinically. Low voltage and nonspecific ST-T wave abnormalities are commonly seen but non-diagnostic. Electrical alternans is generally only seen with a large pericardial effusion. Other nonspecific findings may include P wave abnormalities, PR segment deviations, and atrial arrhythmias — though none of these findings are seen in a majority of patients. So while the ECG will often not be normal with constrictive pericarditis — nonspecificity of ECG findings offers little diagnostic assistance.
  • ii) All 3 of the ECGs in this case manifest Schamroth’s Sign! This is the presence of an almost “null vector” in standard lead I (ie, P wave, QRS complex and T wave all under 2mm in size). While sensitivity of this sign is very low — its presence is highly suggestive of longstanding and severe pulmonary disease. A small percentage of patients with effusive-constrictive pericarditis are found to have RVH — with potential explanation for this finding as a sequela of fibrous band narrowing of the RV outflow tract (Mehta A et al: Constrictive Pericarditis. Clin Cardiol 22:334-344, 1999).
The ECG diagnosis of RVH is often challenging. On occasion, I have found awareness of Schamroth’s sign to be helpful in recognizing probable severe pulmonary disease with RVH when other ECG findings were inconclusive.

Monday, June 11, 2018

"Shark Fin": A Deadly ECG Sign that you Must Know!

This case and discussion is written by Sam Ghali (@EM_RESUS), with a few edits by Smith  


A 75-year-old man collapses to the ground in cardiac arrest while shopping with his wife. Medically trained bystanders happen to witness the event and begin CPR right away. Paramedics rush to the scene and find the man to be in V-Fib. He is intubated and shocked 3 times prior to arrival in the ED. He comes in with CPR in progress via LUCAS device and is now in slow PEA. An intra-arrest arterial line is placed. After 3 more rounds of chest compressions there is a sudden spike in ETCO2 and the A-line shows a BP of 70/40 mmHg. Bedside Echo reveals what appears to be stunned myocardium with poor systolic function. Vasopressor infusions are started.

Here is his STAT 12-Lead ECG:

What do you think?

There are wide complexes with a regular rate at around 65 bpm. With complexes this wide one should think of toxicologic or metabolic causes of arrest. In particular one should consider profound hyperkalemia. But take a close look at the unique morphology of these particular complexes: notice how they look remarkably like Shark Fins. They are not QRS complexes but rather a combination of QRS and T-wave. What they represent is massive ST-Deviation! This is a junctional rhythm with massive ST-Elevation in leads II, III, and aVF, with massive reciprocal ST-depression in leads I & aVL. There is also ST-Depression in the precordial leads maximal in V2-V4 consistent with Posterior involvement. What you are looking at is a Massive Infero-Posterior STEMI! 

The key to seeing and understanding how these complexes represent profound ST-Deviation lies in delineating the end of the QRS . The problem is that with this unique morphology, the QRS complex and T-wave merge together as a result of extreme ST-Deviation, and the two become indistinguishable. But remember this: If you can find the end of the QRS in one lead, you can find the end of the QRS in any lead. Look in all 12 leads and find one which clearly shows the end of the QRS. Here lead V5 happens to show the beginning and end of the QRS very nicely. Now all you have to do is simply draw a line straight up from this point (J-point) in V5, and you can find the same point in any lead.

Here is the same 12-Lead ECG with vertical lines drawn at the J-points:

The profound ST-Deviations suddenly become glaringly obvious and you can now easily appreciate the classic pattern of Massive Infero-Posterior STEMI!

Case Continued:

The patient was given Aspirin and loaded with Ticagrelor via OG tube and the Cath Lab was immediately activated. Unfortunately, this was met with significant resistance. The Cardiology team was not familiar with this ECG phenomenon and there was an ongoing concern for hyperkalemia. Point-of-care laboratory testing was performed and revealed a normal K+. Despite the normal lab result there was persistent concern for hyperkalemia. (It is worth noting that it is not uncommon for labs to show falsely elevated K+ due to specimen hemolysis, but a falsely normal K+ is exceedingly rare!)

With hyperkalemia an ongoing focus, there was continued delay in catheterization. The patient was given multiple doses of calcium, insulin, glucose, and multiple ampules of sodium bicarbonate without any response or improvement of shock. He subsequently became bradycardic and a decision was made to pursue transvenous pacemaker insertion. In the process, the patient arrested once again and required an additional round of CPR to regain a perfusing circulation.

Given persistent shock the decision was eventually made to proceed with coronary angiography, which revealed a 100% thrombotic RCA occlusion. During attempts to open and stent this culprit lesion the patient arrested yet again. Unfortunately this time he was unable to be resuscitated. 

Shark Fin in the Literature:

The literature on this distinct ECG phenomenon is scant, consisting essentially of case reports--blog, book, and journal[1-11]. Therefore, its incidence is unknown. Presumably many cases go unrecognized and are mistaken for conduction abnormalities, metabolic derangements, or toxicologic insult. From the cases that have been described, Shark Fin appears to be an ominous sign with a strikingly poor prognosis. 

Here is an ECG with Shark Fin Sign from a prior post:

Here is another great Shark Fin ECG case from Steve Smith's ECG Book[6]

originally published in K. Wang's Fantastic ECG Book[7]

This is an actual rhythm strip of Lead V4 from this case:

What would you think if you saw this on the monitor before obtaining a 12-lead??You can see how easily Shark Fin ST-Elevation could be mistaken for a Wide-Complex Tachycardia!


A term that has been used in the literature to describe Shark Fin morphology is "Giant R-waves"[8-11]. This designation is suboptimal for a few reasons. Firstly, Shark Fin morphology represents extreme ST-Deviation which encapsulates both ST-Elevation as well as ST-Depression. ECG territories with Shark Fin reciprocal depression will not have R-waves, but rather S-waves. 

More importantly, the term "Giant R-wave" is problematic because it has also been used in the literature to refer to R-waves that are only mildly prominent and come nothing close in size or morphology to the ECG phenomenon described in this post!

This ECG is from a case report[12] referring to the R-wave in Lead V2 as a "giant R wave":

We think "Giant R-wave" is not a good term for this.


Shark Fin is an electrocardiographic sign of acute coronary occlusion. It is a unique ECG phenomenon consisting of complexes formed by the blurring together of QRS and T-wave as a result of extreme ST-Deviation. These complexes manifest in contiguous ECG leads corresponding with coronary anatomy, and represent transmural ischemia. Shark Fin Sign should be recognized based on its characteristic morphology, and confirmed by delineating the J-point using the technique described above. While there is a paucity of literature on the topic, the presence of this sign appears to be associated with a significant mortality, underscoring the critical importance of prompt recognition and emergency reperfusion.

Comment by KEN GRAUER, MD (6/12/2018):
Superb explanation by Drs. Sam Ghali and Steve Smith of this highly insightful case with tragic outcome. I’ll add Figure-1 below, in which I follow the same technique that Dr Ghali used to delineate the end of the QRS complex. Although precise determination of QRS onset is challenging due to a seemingly short isoelectric segment seen in several leads — I believe the vertical RED lines capture the beginning of the QRS.
  • This suggests that there is some QRS widening, although clearly far less than initially thought because of the shark fin phenomenon.
  • I believe there is underlying bifascicular block — which goes in concert with extensive ongoing acute infarction. While lacking amplitude, the QRS complex in lead V1, appears to be a triphasic, and associated with wide terminal S waves in all lateral leads. One could debate whether terminology is best served by calling this IVCD vs RBBB — but given the rS pattern in lead I (with steep decline and predominant negativity from the S wave in this lead) + predominant R waves in each of the inferior leads — I submit that the most logical explanation is combined RBBB/LPHB.
Our thanks again to Dr. Ghali for presenting this case!
Figure-1: Vertical RED line shows where I believe the QRS begins. BLACK lines drawn by Dr. Ghali show the end of the QRS complex in all leads.


1. Francis, R. Smith, SW. "Shark Fin" ECG in I, aVL, V4, and V5. Which artery? Hint: patient is in shock and was put on ECMO. March 26, 2016.

2. Larose D, Vadeboncoeur A, Smith, SW. VFIb Arrest, Put on ECMO, regains an organized rhythm, and a 12-lead is recorded. May 22, 2017.

3. Smith, SW. Cardiac Arrest -- Is it STEMI? April 25, 2018.

4. Walsh, B, Smith, SW. Giant R-waves. What are they? July 3, 2015.

5. Smith, SW. Wide Complex Tachycardia. It's really sinus, RBBB + LAFB, and massive ST elevation. Nov 16, 2010.

6. Smith, SW et al. The ECG in Acute MI: An Evidence-based Manual of Reperfusion Therapy. Lippincott Williams & Wilkins. 2002.

7. Wang, K. et al. Atlas of Electrocardigraphy. Jaypee Brothers Medical Publishers. 2013

8. Faillace RT et al. The giant R wave of acute myocardial infarction. Jpn Heart J. 1985. Mar;26(2):165-78.

9.  Madias JE. The "giant R waves" ECG pattern of hyperacute phase of myocardial infarction: A case report. J Electrocardiol. 1993;26(1):77-82.

10. Madias JE et al. Transient giant R waves in the early phase of acute myocardial infarction: Association with ventricular fibrillation. Clin Cariol. 1981.

11. Testa-Fernandez A et al. "Giant R wave" electrocardiogram pattern during exercise treadmill testing: A case report. J Med Case Rep. 2011 Jul 11;5:304.

12. Chugh, Y et al. Transient Giant R Wave as a Marker for Ischemia in Unstable Angina. Cureus. 2017 Apr; 9(4):e1200

Saturday, June 9, 2018

Patient with Paced Rhythm in Severe Cardiomyopathy Presents with SOB due to Acute Decompensated Heart Failure

This is a middle-aged male with h/o with a history of heart failure with severely reduced ejection fraction due to dilated ischemic cardiomyopathy (EF 5-10%), probably with some component of non-ischemic cardiomyopathy, with h/o CABG, who is status post ICD placement (and previous appropriate shocks for VT) and biventricular pacer ("cardiac resynchronization therapy"), who is on amiodarone for VT suppression, and has h/o LV thrombus and is on chronic anticoagulation with warfarin.

He presented for paroxysmal nocturnal dyspnea that didn't resolve with use of his home prn diuretics.   He was hypoxic and required oxygen in the ED.

He had no chest pain.

Prior coronary angiography/revascularization: LAD 40% proximal, 80% mid and 90% distal stenosis; circumflex 70% proximal circumflex; ramus 100% occluded; RCA 90% occluded.

Prior echocardiographic study: (1/9/2017) LVEF is 10%, regional WMAs: distal septum anterior and apex, inferior and anterolateral; left ventricular enlargement and concentric hypertrophy; Severe decreased right ventricular systolic performance; no significant change compared to previous.

Upon arrival to the ED, he was hypoxic, but readily responded to oxygen.   

An ECG was recorded:
Biventricular Paced Rhythm, rate 60
QRS = 265 ms, QT = 587, QTc = 610
(See two spikes approximately 40 ms apart, with large R-wave in V1 confirming LV pacing in addition to RV -- LV pacing results in RBBB configuration with large R-wave in V1)
There is much discordant ST elevation, especially in I, aVL, V3-V5
V4 = 7/30, almost 25%
aVL = 3-4/17, = 17-24%
Is this coronary occlusion?

Here is the most recent previous ECG from 6 months prior:
Biventricular paced rhythm, rate 75, with PVCs
More proportional ST discordant ST Elevation
Computer measures QRS at 209 ms

The discordant ST elevation is of lower proportion.

This change in ST segments suggests coronary occlusion, even if it does not meet the full 25% criteria.

Is there acute coronary occlusion (Occlusion MI, or OMI)?

I performed a bedside ultrasound:

Parasternal long axis:

Extremely severely reduced ejection fraction
There are profound wall motion abnormalities, but seem to correspond to the old echo.

Parasternal short axis:

Again, extremely poor EF and regional wall motion abnormalities.

Apical 4 chamber:

Terrible systolic function
Notice that although he has a paced rhythm, there is very little "dyssynchrony" because the biventriculaer pacer paces both ventricles simultaneously.

A typical pacemaker is right ventricular, and so because RV pacing activates the RV before the LV, RV pacing results in dyssynchrony that is similar to left bundle branch block.

When I saw this patient, my impression was one of acute decompensated heart failure, not due to acute MI.  Important to this was the absence of chest pain.

Comment:  Given his systolic function, it is amazing he is not in shock.  Why is this?  A patient with a healthy heart who has sudden large STEMI may go from EF 65% to EF 30% and be in shock, yet this patient with EF less than 10% is NOT in shock.  But EF % is a percent of some end diastolic volume. Patients with terrible cardiomyopathy have very large distended hearts.  If the end diastolic volume is 300 mL, then 10% of 300 results in a 30 mL stroke volume, just as with the previously healthy STEMI patient, in whom 30% of 100 mL = 30 mL stroke volume. Furthermore, patients with chronic heart failure have faster lymphatic drainage of pulmonary interstitial fluid, and so it takes even higher pulmonary pressures to result in pulmonary edema.

Looking at this case now, I must concede that an uninvolved observer (i.e., reader.  i.e., you!) might think this:

"This patient with known CAD presents with SOB and hypoxia and has new excessively discordant ST Elevation and terrible myocardial contractility and you did NOT want an angiogram!  I am confused!"

But I know how acutely decompensated heart failure in severe cardiomyopathy distorts the ST segments on the ECG, and I just did not think this represented acute occlusion MI (OMI).

Furosemide was given intravenously, after which the patient rather quickly improved.

His NTproBNP was 22,000 (very high).

Troponin I were slightly elevated but unchanging, consistent with chronic myocardial injury that is typical of severe cardiomyopathy.

0.054 ng/mL

Here is an ECG from 8 days later:
Computer measures QRS at 276 ms
Less ST deviation.

I have shown at least one prior case in which acute decompensated heart failure in a patient with severe cardiomyopathy and paced rhythm resulted in false positive Smith Modified Sgarbossa criteria.

Massive Excessively Discordant Anterior ST Elevation in a Paced Rhythm

Learning Points:

1.  Acute Heart Failure in patients with paced rhythm and extremely low ejection fractions can distort the ST segments.

2.  Acute MI may present with only SOB, but the pretest probability of chest pain is far higher than that of SOB.

3. There are several entities that were excluded from the studies on Modified Sgarbossa Criteria: Tachycardia (because it results in higher ST segments), Respiratory Failure (also distorts the ST segments, and one does not need an ECG to know they are critically ill), Diastolic BP greater than 120, and Hyperkalemia.

Recommended Resources