Friday, December 2, 2016

ST Elevation in aVL. Reciprocal ST depression in III. Is it MI?

I was reading this ECG in the queue, with no clinical info.

What do you think?


















My interpretation was LVH, no evidence of MI.   There was no previous ECG or echo for comparison.

My ECG diagnosis may surprise you, as I have long discussed "ST elevation in aVL with reciprocal ST depression in lead III" as due to high lateral MI.

This is different because:
1) There is saddleback morphology in aVL, and
2) There is also high voltage.

I have previously talked about ST elevation with saddleback morphology in lead V2 as rarely being due to anterior STEMI.  See this post (the only case I've seen in which it was STEMI): 

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)


Voltage on this ECG does meet Estes criteria for LVH: 
1) At least one R- or S-wave greater than 20 mm (lead II) = 3 points.
2) ST-T abnormalities in the absence of digoxin = 3 points
Total = 6 points
5 points is definite
4 points is probable
This scoring system comes from this original article.

However, meeting LVH criteria is not critical, as they are not sensitive.  Many cases of LVH show themselves only by the typical repolarization abnormalities.  In this case, we see somewhat typical repolarization abnormalities in leads III and aVF.

Estes criteria are only 34% sensitive for LVH as diagnosed by echo.   

In this paper that used other criteria, the sensitivity for LVH by echo was less than 10%!
At least one of, with or without ST-T abnormalities:
1) R-wave 11 mm in aVL
2) R-wave at least 25 mm in left precordial leads
3) S-wave at least 25 mm in right precordial leads
4) Sum of precordial SV1 or SV2 plus RV5 or RV6 at least 35 mm
5) Sum of lead I plus lead II at least 25 mm.

In both studies, specificity of the criteria was nearly perfect.

Case Continued

This 30-something presented with headache and chest pain.  He had a history of hypertension, apparently completely untreated.  His chest pain had lasted 40 minutes and was now gone.

Blood pressure was 170/105.


Another ECG was recorded several hours later:
No significant change



The history of HTN, the elevated BP, the high voltage, and the saddelback make it very unlikely that this ST elevation is due to STEMI.

The patient ruled out for MI by negative delta troponins.

Here is a post on True Positive ST elevation in aVL vs. False Positive ST elevation in aVL
However, I do not discuss saddleback in aVL in this post.

Wednesday, November 30, 2016

A Young Man with Recurrent Chest Pain and Dyspnea with Exertion

Case

This is a young man who has had chest pain and dyspnea with exertion for years.  He presented to the ED with these symptoms again.  On this occasion, the CP was associated with stress and accompanied by some SOB, 7/10 at it's worse and made worse with activity, with radiation up into the left side of his neck and face.

No h/o hypertension.

Here is the ECG:
Probable Diagnosis?
I was shown this ECG and gave my opinion, as below.


Here is an ED bedside echo, parasternal long axis:

Look at the small the end-systolic LV chamber size


Parasternal short axis:


Again, look at the end-systolic chamber size!

What is the Diagnosis?














The ECG shows profound LVH with secondary ST/T abnormalities.  There is deep ST depression and T-wave inversions that are discordant to (in the opposite direction of) large voltage R-waves.  These ST-T abnormalities do not represent ischemia, although they could certainly hide ischemia.  Instead, these repolarization (ST-T) abnormalities are entirely secondary to depolarization abnormalities (huge voltage).

The echo shows profound LVH.  Whether it is definitely concentric or assymetric (which is seen in HOCM with assymetric septal hypertrohy) is hard to tell for certain with these bedside echos.

Comment: In a young man with no history of hypertension, and with these typical symptoms of hypertrophic cardiomyopathy (HOCM), this is HOCM until proven otherwise.

Case continued

He refused hospital admission.  He was discharged with followup for a formal contrast ultrasound and cardiology clinic.

Comment: In someone like this who refuses to be admitted, it is wise to start a beta blocker.

Case continued

He returned about a week later with similar symptoms: Central CP and SOB that can last minutes or hours, but this time it lasted for less than an hour and was again worse with activity.  There was no nausea or diaphoresis.

Here is his ECG on this visit:
Slower sinus rate, but otherwise the same.

His serial troponin I (Abbott Architect contemporary troponin, 99% = 0.030 ng/mL):
0 hour: 0.034 ng/mL
3 hour: 0.024 ng/mL
6 hour: 0.011 ng/mL

Thus, he had symptoms compatible with myocardial infarction and a diagnostic fall of troponin with one level (the first) above the 99% cutoff.  This meets the definition of MI, but only if the troponin elevation is also thought to be due to ischemia.


A Formal stress echo was done:

Dynamic intraventricular gradient 15 mmHg at rest and increased to 26 mmHg post stress.
Normal estimated left ventricular ejection fraction at rest.
Normal estimated left ventricular ejection fraction improved with stress.
No wall motion abnormality at rest.
No wall motion abnormality with stress.
Left ventricular hypertrophy concentric .
Dynamic intraventricular gradient .
Hypertrophic cardiomyopathy .
Left ventricular hypertrophy concentric obstruction.

Comment: So he has HOCM and it is likely that stress induces some ischemia in this hypertrophic myocardium. Therefore, one would call this a type 2 myocardial infarction due to outflow obstruction in HOCM.

Case continued

He was started on metoprolol and discharged.

Comment: Explanation of outflow obstruction and use of beta blockade:  In obstructive HOCM, the end-systolic volume is very small due to the hypertrophic myocardium, and it thus obstructs aortic outflow at end systole.  This the source of the "gradient."  It is similar to mild aortic stenosis, but only at end systole.  Beta blockers: 1) diminish the contractility and thus result in a larger end-systolic volume and less outflow obstruction and 2) slow the heart rate, allowing for more time to fill, resulting in larger end-diastolic volume which also results in higher end-systolic volume.


Here are some other cases of HOCM:
Exertional Chest pain and Near Syncope in a Young Adolescent
In this case, the more typical large septal R-wave is present in V1, indicative of hypertrophy of the septum.

Here is a fascinating case in which dehydration leads to low end-systolic volume and shock in an HOCM patient.  Esmolol works to manage the patient:

History of Hypertrophic Cardiomyopathy (HOCM), with Tachycardia and High Lactate










Monday, November 28, 2016

What are these wide complexes?

A middle-age male arrived by private car with chest pain.  He immediately became unresponsive, before an ECG could be recorded.

He was resuscitated from ventricular fibrillation and this 12-lead was recorded:
What are the wide complexes in the precordial leads?














Same ECG with annotation:
One may perceive these as wide complexes, but they are deceptive.
The arrows in V5 and V6 point to narrow complex QRS's.  What appears to be a very wide complex tachycardia is really narrow complex with massive ST elevation and huge hyperacute T-waves.

The rate is about 160.

The rhythm strip across the bottom (lead II) shows that these relatively normal duration QRS complexes are regular, but with intervening premature ventricular beats (PVC's, one of which is highlighted by the arrow, complexes 5, 6, 11, 12, 19, 22).
Thus, it is a supraventricular rhythm with PVC's.

Although no P-waves are visible in this, I suspect that it is sinus with PVC's.  PSVT should be converted by a PVC.
The cath lab was activated and the patient was intubated and received ticagrelor and heparin.  There was no treatment of the rhythm, but it gradually slowed down (as one would expect from supportive care in sinus tachycardia).


This ECG was recorded just before transportation to the cath lab:
Sinus tachycardia at a rate of about 100.
Massive ST elevation continues.



A mid LAD 100% thrombotic occlusion was opened and stented.  Door to balloon time was less than 60 minutes.  Echo next day showed 57% EF.  Peak troponin I was 250 ng/mL.  




Saturday, November 19, 2016

Diffuse Subendocardial Ischemia on the ECG. Left main? 3-vessel disease? No!

This was contributed by some folks at Wake Forest:
Jason Stopyra, Shannon Mumma, Sean O'Rourke, and Brian Hiestand.
It was edited by Smith

CASE:
A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. The paramedic’s initial impression of the patient was that he was critically ill. The patient’s mental status was altered and his skin was pale and dusky. The initial blood pressure was 80/palp with a heart rate of 104, respirations 20, oxygen saturations of 94% and a finger stick blood glucose of 268. Exam was otherwise notable for audible wheezes, sluggish cap refill, confusion, and difficulty following commands and answering questions.

An immediate 12-lead EKG was obtained:
There is ST elevation in leads aVR and V1, with marked ST depression in I, II, III, aVF, V3-V6.
What should be done?  
Should the cath lab be activated?












Smith comment:
This patient did not have a bedside ultrasound.    Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip):

This is recorded with the LV on the right.

Look at the aortic outflow tract.  What do you see?  Answer below in the still shot.









Clinical Course

The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. En route, EMS administered aspirin 325mg by mouth, but withheld nitroglycerin due to initial hypotension. In addition, the patient received 750 mL of fluid resuscitation with transient improvement of blood pressure.

The patient was brought directly to the cardiac catheterization lab for PCI, bypassing the ED. In the cath lab, the patient’s blood pressure remained low. The diagnostic coronary angiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. During the procedure, the patient had an increasing oxygen requirement and was intubated for airway protection and oxygenation. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis, severe LVH, and a small LV cavity. The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed.

Here is the still shot of the ultrasound above:
This still shot shows the area of interest:
There is a hyperechoic area at the aortic valve
This is aortic sclerosis and is highly associated with aortic stenosis.
If you see this, you should Doppler the valve.
The aortic valve in this example also had critical stenosis by Doppler

The patient continued to be hemodynamically unstable with poor cardiac output and very high LV filling pressures. Despite the use of multiple high dose vasopressors, he continued to be hypotensive. The following day, the patient underwent balloon aortic valvuloplasty for severe symptomatic aortic stenosis with hypotension and NYHA class IV symptoms. Post-valvuloplasty, the patient’s pressure gradient improved, but was still substantial. Patient was continued on maximal pressors, but remained hypotensive. Approximately seven hours after he returned from valvuloplasty he went into asystolic arrest.

DISCUSSION:
The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.  Although this is considered a "STEMI equivalent" and the ACC/AHA guidelines even approve of thrombolytics for ACS with this ECG, the usual criteria used to alert the cath lab team of an inbound Code STEMI are not met by this ECG.

Smith comment:
Remember, ST depression does not localize to the area of ischemia, so "infero-lateral" does not tell you where the ischemia is - in fact, it is diffuse subendocardial ischemia.  ST elevation in lead aVR is reciprocal to this ST depression of diffuse subendocardial ischemia; the ST depression vector is towards II and V5 and thus the ST elevation vector is towards aVR.

Author continued:
STE in aVR is often due to left main coronary artery obstruction (OR 4.72), and is associated with in-hospital cardiovascular mortality (OR 5.58).1 ST elevation of 1 millimeter or greater has been shown to be 80% sensitive and 90% specific for severe left main coronary artery and/or 3-vessel disease that may require coronary artery bypass grafting, in some series.2 The astute paramedic recognized this possibility and announced a CODE STEMI.

Smith comment:
I would change the above statement to: "In the setting of ACS, STE in aVR is often due to left main or 3-vessel obstruction...."  The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.  Diffuse subendocardial ischemia is more often due to supply/demand mismatch in the absence of ACS than it is due to ACS.  Common etiologies of supply/demand mismatch are hypoxia, tachydysrhythmias,  hypotension (from whatever cause), anemia, coronary artery stenosis without ACS, or (intraventricular) hypertension.

--Oxygen supply is determined by: 1) oxygen carrying capacity, 2) O2 saturation, and 3) Coronary flow.   Thus, in the absence of athero-thrombotic mechanism (ACS), myocardial ischemia can be brought on by:
1) Hypotension (diastolic hypotension, as all coronary flow happens during diastole because intramyocardial pressure during systole stops blood flow).  Hypotension may of course be a result of a brady- or tachydysrhythmia.
2) Hypoxia, including poisons of oxidative phosphorylation such as HS, CO, CN.
3) Anemia, or poisons of hemoglobin such as methemoglobin or CO
4) Fixed coronary stenosis that limits flow.

--Oxygen demand is determined by:
1)  Afterload (high resistance to LV outflow), which is increased by elevated blood pressure or by aortic stenosis
2)  Heart rate: sinus tachycardia

--This patient has both decreased supply (hypotension) and increased demand from 1) high afterload (LV pressures are very high because of the aortic stenosis outflow resistance) and 2) high heart rate.

--This demonstrates that there may be some value to heart auscultation, to listen for an aortic murmur.  In fact, bedside ultrasound might even find severe aortic stenosis.  If you can use Doppler, then you can diagnose it.


Authors' commentary: Cardiogenic shock in the setting of severe aortic stenosis.
As I met the paramedics and cath team in the lab, I was ready to see severe coronary disease (CAD), but the vessels were non-obstructive. This patient’s severe aortic stenosis (AS) and associated severe cardiogenic shock likely created the ECG pattern, resulting in a very difficult challenge for our inpatient team.

Fundamentally, cardiogenic shock is an issue of decreased cardiac output. This may be secondary to multiple factors, including decreased cardiac contractility (ie. myocardial infarction), arrhythmias, valvular pathology, shunts, or outflow obstructions.

As with other cases of shock, initial fluid resuscitation may be considered. In cardiogenic shock, fluid may worsen the pulmonary edema associated with acute heart failure, but may still be required to support the hemodynamic status of the patient.

Guidelines from the American Heart Association have been unchanged for decades with recommendations for positive inotropes, such as dobutamine and dopamine, in cases of cardiogenic shock.3 There is evidence to show that using sub-maximal doses of both dobutamine and dopamine in conjunction, rather than using a single agent, provides benefit for the patient. Benefits include improvement in the patient’s MAP and cardiac output, while minimizing the amount of myocardial oxygen used with the increased cardiac output (CO).4 This is crucial, as these patients may have already had some degree of cardiac ischemia. This was particularly important for the patient presented above, given the baseline increase in oxygen consumption seen in AS due to the outflow obstruction.

Smith comment: 
In a large randomized trial of dopamine vs. norepinephrine (11) for shock which was published after the above-mentioned recommendations, dopamine had more adverse events (especially severe dysrhythmias, and especially atrial fibrillation).  In the subgroup of patients with cardiogenic shock, dopamine had a 33% statistically significant elevated mortality over norepinephrine.   Thus, norepinephrine is a better choice in cardiogenic shock (as in this patient) than dopamine or dobutamine.  Dobutamine may be preferred in patients without severe hypotension who have high vascular resistance.
--De Backer D et al.  Comparison of Dopamine and Norepinephrine in the Treatment of Shock.  NEJM 362(9):779; March 4, 2009. 


Author continued: 
Another positive inotrope to consider would be milrinone as it decreases SVR and increases cardiac output; however, one must proceed with caution as the pharmacological mechanism of milrinone can cause vasodilation and worsen hypotension.

When pressors are not able to sustain blood pressure, balloon valvuloplasty may be considered. This is a procedure whereby a catheter is introduced through the femoral artery, and advanced to the have the tip distal to the left subclavian artery. A balloon is then threaded over the catheter, and is inflated and deflated with diastole and systole, respectively. It has been recommended as a bridge to surgery in those that are not candidates for surgery.5 Unfortunately, availability is generally limited to major medical centers.6,7 Surgical repair of AS, by either TAVR or SAVR, is the definitive treatment for this condition. It should be noted, though, that emergent surgical intervention in unstable AS patients is associated with significant mortality, with rates between 30-50%.8

Vasodilator therapy for critical AS

Although not applicable to the case above given the patient’s hypotension, nitroprusside may be appropriate for patients with pulmonary edema in the setting of acute heart failure secondary to AS. Though long thought to be contraindicated in AS due to the condition’s preload-dependent state, there has been some evidence to indicate nitroprusside is beneficial to these patients. In one important uncontrolled study, nitroprusside used in patients with critical AS and heart failure with reduced ejection fraction (mean EF of 21%, mean MAP of 81 mm Hg) had significant improvement of cardiac index, without any episodes of hypotension, ischemic EKG changes, arrhythmias, or dyspnea.9  The only criterion for exclusion from this study was hypotension, defined as either the need for intravenous inotropic or pressor agents (dobutamine, dopamine, epinephrine, milrinone, norepinephrine, or phenylephrine) or a mean systemic arterial pressure below 60 mm Hg. The mean MAP for these patients was 81 +/- 13.

Furthermore, a study compared patients with AS to patients without AS in acute pulmonary edema who received nitrates. There was no significant difference between the percentage of patients in each group who developed hypotension after starting therapy. However, there was note that once these patients did develop hypotension, patients with moderate and severe AS were more likely to have sustained hypotension despite interventions.10

The 2014 ACC/AHA guidelines for the Management of Patients with Valvular Heart Disease, referencing this article, gives this recommendation:

"CLASS IIb 1. Vasodilator therapy may be reasonable if used with invasive hemodynamic monitoring in the acute management of patients with severe decompensated AS (stage D) with NYHA class IV HF symptoms. (Level of Evidence: C) In patients who present with severe AS and NYHA class IV HF, afterload reduction may be used in an effort to stabilize the patient before urgent AVR. Invasive monitoring of LV filling pressures, cardiac output, and systemic vascular resistance is essential because of the tenuous hemodynamic status of these patients, in whom a sudden decline in systemic vascular resistance might result in an acute decline in cardiac output across the obstructed aortic valve. However, some patients do benefit with an increase in cardiac output as systemic vascular resistance is slowly adjusted downward due to the reduction in total LV afterload. AVR should be performed as soon as feasible in these patients."

CONCLUSION:
The variables that interplay in cases of severe aortic stenosis are what cause these patients to be so difficult to manage, and specific therapies targeted to fix one issue often worsen the effects of another issue. If someone is in respiratory distress, their airway and breathing needs to be secured, either through non-invasive or invasive means. Next, the patient’s blood pressure needs to be stabilized. Oftentimes the most appropriate agent will be a positive inotrope, with consideration of a vasoactive agent in persistent hypotension. Once a patient is stabilized, determining the extent of damage to their myocardium and a plan for definitive management can then be determined.

Smith comment:

Supportive care is often overlooked in the management of cardiogenic shock.  The work of breathing demands significant cardiac output and thus puts demands on the heart.  Mechanical ventilation with paralysis removes up to 50% oxygen demand and can put the heart to rest.  I would immediately intubate a patient who is this ill.

As for other invasive therapies, intra-aortic balloon counterpulsation (12, 13) appears to work well in non-randomized studies, and this would also make sense: the balloon in the aorta inflates in diastole, increasing diastolic pressure and thus coronary flow. It also deflates during systole, which normally would reduce afterload; however, in the setting of aortic stenosis, the afterload is determined mostly by the valve, not by post-valve resistance.


Smith Final Comment:It is uncertain what initiated this patient's instability.  Any alteration in physiology can change "compensated" AS to "decompensated" AS.  For instance: sepsis, bleeding, dehydration, hypoxia, and mild ACS.  This patient had a small LV cavity which is unusual for someone with AS, poor LV function, and high filling pressures, but is probably due to severe LVH.  As LV filling pressures were found to be high, this small LV cavity would not be a result of volume depletion.  In any case, once AS becomes decompensated, for whatever reason, it is extremely difficult to manage because of the low coronary perfusion pressure and high oxygen demand.
REFERENCES:

1.   Taglieri N, Marzocchi A, Saia F, et al. Short- and long-term prognostic significance of ST-segment elevation in lead aVR in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol 2011;108:21-8.
2.   Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol 2011;107:495-500.
3.      Overgaard, Christopher; Dzavik, Vladimir. Contemporary Reviews in Cardiovascular Medicine. Inotropes and Vasopressors: Review of Physiology and Clinical Use in Cardiovascular Medicine. Circulation. 2008;118:1047-1056.
4.      Richard, C; et al. Combined Hemodynamic Effects of Dopamine and Dobutamine in Cardiogenic Shock. Circulation 67, No. 3, 1983.
5.      Safian RD, Berman AD, Diver DJ, et al. Balloon aortic valvuloplasty in 170 consecutive patients. N Engl J Med 1988;319:125-30
6.      Rahimtoola SH. Catheter balloon valvuloplasty for severe calcific aortic stenosis: a limited role. J Am Coll Cardiol 1994;23:1076-1078
7.      Moreno PR, Jang IK, Newell JB, Block PC, Palacios IF. The role of percutaneous aortic balloon valvuloplasty in patients with cardiogenic shock and critical aortic stenosis. J Am Coll Cardiol 1994;23:1071-1075
8.      Hutter AM Jr, De Sanctis RW, Nathan MJ, et al. Aortic valve surgery as an emergency procedure. Circulation 1970;41:623-627
9.      Umesh N. Khot, MD; et al. Nitroprusside in Critically Ill Patients with Left Ventricular Dysfunction and Aortic Stenosis. N Engl J Med 2003; 348:1756-1763, 5/1/2013.
10.  Claveau, D; et al. Complications Associated with Nitrate Use in Patients Presenting with Acute Pulmonary Edema and Concomitant Moderate or Severe Aortic Stenosis. Annals of Emergency Medicine. 2015 Oct; 66(4):355-362.
11.  De Backer D et al.  Comparison of Dopamine and Norepinephrine in the Treatment of Shock.  NEJM 362(9):779; March 4, 2009. 
12.  Folland ED, et al.  Intraaortic Balloon Counterpulsation as a temporary support measure in decompensated critical aortic stenosis.  J Am Coll Cardiol. 1985;5(3):711-716. 
http://content.onlinejacc.org/article.aspx?articleid=1111078
13.  Olcay A. et al.  Cardiogenic shock in the setting of severe aortic stenosis: role of intra-aortic balloon pump support.  Heart 97:838-843
http://heart.bmj.com/content/97/10/838.short
14.  Nishimura RA and Otto CM, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease.  Journal of the American College of Cardiology 63(22):e57-e185; June 10, 2014.

Wednesday, November 16, 2016

Chest Pain and Cardiogenic Shock with Profound ST Depression & STE in aVR. Activate the Cath Lab?

A middle-aged woman with known severe coronary disease had onset of substernal chest pain while at dialysis.  911 was called.  A prehospital ECG was similar to the first ED ECG, which is shown below.  The patient arrived with a systolic blood pressure of 90 mm Hg, too low to administer nitroglycerine.  An initial lactate was elevated at 5.5.

She was given aspirin, heparin, and ticagrelor.

Here is her initial ED 12-lead ECG:
There is atrial fibrillation with a rate of approximately 114.
There is extreme ST depression in multiple leads and ST elevation in aVR, suggesting left main and/or 3 vessel disease ischemia.
There is some STE in V1 and aVL, further suggesting left main involvement.

Is this Acute Coronary Syndrome?
Do you want to activate the cath lab?
What else do you want to know?









It is important to note that these findings, if due to atherothrombotic acute coronary syndrome (ACS), are NOT due to occlusion of the left main, as is frequently stated in online postings and in literature.  Instead, it is far more commonly due to severe obstruction with continued flow (an open artery).  See this post:

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion


There are many causes of diffuse ST depression, with reciprocal ST elevation in aVR.  It is most commonly due to demand ischemia, not due to ACS!  So it pays to do a few minutes of research prior to making any drastic management decisions.

First, there was an ECG from 3 months prior:
This shows sinus rhythm.
This information is critical, because it shows that the patient might respond to therapy to convert her to sinus rhythm.  Chronically ill cardiac patients who are in chronic atrial fibrillation are very difficult to convert, but this patient was recently in sinus and may readily convert back to sinus.

Further review of her chart showed her to have "no revascularization potential".  Review of the previous angiogram reports showed that all native vessels were occluded and that all coronary flow depended on a single CABG Y graft from the aorta to both left anterior descending artery and to a posterior branch of the circumflex artery.  She was completely dependent on this graft.

It was known to be diseased and at extremely high risk for any intervention.

Consider this question: If this patient needs reperfusion therapy, what option(s) is (are) available?

A bedside ultrasound (not shown) revealed a small but hypertrophic LV chamber with reasonably good LV function.  There were no B-lines of pulmonary edema.  
(Chart review also showed previous echocardiograms had concentric hypertrophy with normal LV function.)

What do the results of bedside ultrasound tell you?  What do you want to do?







Given the new atrial fibrillation, and in consultation with the cardiologist, we decided to cardiovert her.  We gave her a small dose of etomidate (to avoid hemodynamic deterioration) and electrically cardioverted her with 150 J biphasic.   She required bag-valve mask ventilation during sedation.  She converted temporarily, then reverted again to atrial fibrillation.   We shocked her again, and she again converted to sinus rhythm. After several minutes she reverted to atrial fibrillation again.

It was now clear that to keep her in sinus rhythm, we would need an antidysrhythmic.  We chose amiodarone in spite of its possible negative inotropic effect.  She tolerated 2 150 milligram loads of amiodarone well, and was started on a drip.

This is her repeat ECG at 2 hours after arrival, on amiodarone:
There is sinus rhythm with premature beats in a bigeminal pattern.
It is difficult for me to say for certain if the premature beats are PABs with abberancy or PVCs.
The ST depression in not nearly as profound as before.

Chest pain had decreased from 10/10 to 3/10.

At this point, we were pretty convinced that her ischemia was due to atrial fibrillation with rapid ventricular response and loss of the atrial contribution to ventricular filling.  There was probably a component of volume depletion from dialysis, and we probably should have given a fluid bolus.

She was admitted to the intensive care unit in a better condition than when she arrived. Her condition continued to improve, with decreased chest pain and improving hemodynamics.  She became hypotensive at one point, with collapsing IVC on ultrasound, and improved with IV fluids.

She was admitted to the ICU on an amiodarone drip and continued to improve.

Here is her ECG at 6 hours after arrival:
There is sinus rhythm.  The ST depression in nearly entirely gone.


Troponin I peaked at 55 (very high).

She did well, was started on oral amiodarone, and was discharged after a couple days in the hospital.

What happened?

Although ACS is not out of the question, this was my assessment: the patient had a bit too much fluid removed during dialysis and, at the same time, went into atrial fib with RVR.  This resulted in decreased oxygen supply (decreased cardiac output due to decreased stroke volume, leading to poor coronary perfusion pressure in a patient with fixed coronary stenosis) as well as increased oxygen demand from a rapid rate.   This assessment is supported by the bedside ultrasound: she was in shock but had no pulmonary edema, and her LV chamber size was small with good function.

When a patient is in shock due to primary ACS without dysrhythmia, it is due to poor LV function (if not due to valvular disorder) and results in a more fully filled (even sometimes dilated) chamber and high filling pressures, and often with pulmonary edema.

When a patient is in shock due to atrial fibrillation with RVR and poor atrial contribution to ventricular filling, one may see a small, poorly LV filling, as with this patient.  [A patient may certainly get high pulmonary vascular pressures, and pulmonary edema, when atrial fibrillation is the initiating factor, but in this case such evidence of high pulmonary vascular pressure was probably absent due to volume depletion.]

It is possible that this was ACS, but that would only demonstrate how ACS with severe ischemia is not always best treated in the cath lab. Medical therapy often works (antiplatelet, antithrombtic, and -- though not in this case - nitroglycerine).

If it were ACS, what reperfusion options were available?

1) Aspirin, heparin, and a P2Y12 inhibitor.  We know that the administration of just these antiplatelet and antithrombotic agents may result in diminution of thrombus burden.

2) Very high risk percutaneous coronary intervention

3) Fibinolytic therapy!  When managing this patient, I kept this option in mind.  Fibrinolytics have long been forbidden for ST depression, but this is based on very sketchy data from the thrombolytic era.  In a nutshell, in those randomized trials, the patients enrolled had 1) few lead with ST depression, 2) very minimal ST depression and 3) were treated, depending on the study, at 6-12 hours after onset, a time at which most myocardium at risk may already be irreversibly infarcted.  Thus, the ACC/AHA 2013 STEMI guidelines now list diffuse ST depression, with ST elevation in aVR, as an indication for thrombolytic therapy.  I discuss this more at this post:

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion.



Sunday, November 13, 2016

Paper published: Terminal QRS distortion not found in any ECG of Early Repolarization

This ECG comes from a 30-something with chest pain. 

Is it early repolarization?  Or is it LAD occlusion?  The paper below helps to make this diagnosis.

See at bottom for full explanation









This paper is now published

Daniel Lee, Brooks Walsh, Stephen W. Smith.  

Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization.

Volume 34, Issue 11, November 2016, Pages 2182–2185

http://www.ajemjournal.com/article/S0735-6757(16)30545-9/abstract


Here I show it again:





So, the only plausible reasons for ST elevation are 1) LAD occlusion or 2) Early Repolarization.  One might be tempted to apply the formula that helps to differentiate the two.  However, when we studied these ECGs, we excluded patients with features that made STEMI "obvious," or at least not subtle.  These features included Q-waves and Terminal QRS distortion.  In this case, the Q-waves do not make it an obvious MI, but the QRS distortion does:
  
QRS Distortion was defined by Birnbaum as: "Emergence of the J point ≥50% of the R wave in leads with qR configuration, or disappearance of the S wave in leads with an Rs configuration)"  (from this paper by Birnbaum).    


I would add to this: if there are distinct J-waves in these leads, then early repolarization is still a likely possibility.  In this case, there are no distinct J-waves in V2 or V3 (although there is a small one in V4)

Thus, this ECG should be thought of as diagnostic of anterior STEMI.  If the formula had been used, then the value would have been [1.196 x 3.5]+[0.059 x 402]–[0.326 x 17] = 22.362 (which is less than 23.4 and thus consistent with early repolarization).  The formula would have given a false negative, because this was an LAD occlusion.  



Learning Point:

When there is Terminal QRS distortion (absence of BOTH an S-wave and a J-wave in EITHER of leads V2 or V3, it is not early repolarization).  When the differential diagnosis only includes early repol and LAD occlusion, then LAD occlusion is strongly favored.

Here is another case:

Thursday, November 10, 2016

Biphasic T-waves in a Middle-Aged Male with Vomiting

One of our residents texted me this ECG and was worried about Wellens' waves.

A middle-aged male presented with vomiting.  Here was the initial ED ECG:

What do you think?

















Here is my response:

Wellen's waves are always Up-Down T-waves, not Down-Up T-waves as here.  Down-Up T-waves in V2 and V3 have only two causes:

1) posterior MI with some reperfusion (reciprocal to Up-Down T-waves of the posterior wall, analogous to Wellens' of the posterior wall as recorded from the anterior wall).

2) Hypokalemia (in which case the upright component is really a U-wave).  In this case, V6 is pathognomonic: you can see a clear large U-wave following the T-wave.  It must be hypokalemia.  Notice also the very long QT, which is really a long QU-wave.

What is the Potassium?

The K was 2.0 mEq/L.

Here are classic Wellens Pattern A (biphasic) waves:
Notice they are biphasic Up-Down.



Clinical Course

The patient had all serial troponins below the level of detection.  Potassium was repleted.  Here is the ECG after normalization of K at 3.5 mEq/L:




Learning Points

1. Wellens' waves (Pattern A) are biphasic Up-Down.  (Pattern B is deep symmetric inversion)
2. Down-Up waves should make you think of reperfusing posterior MI or hypokalemia.
3. A very long QT (really a QU) should make you suspect hypokalemia.
4.  Look for clear U-waves in other leads.
5.  Finally, Wellens' syndrome is a SYNDROME that requires 1) typical anginal chest pain 2) Resolution of the chest pain 3) ECG recorded after resolution.



Here is an example of a Down-Up T-wave from Reperfusing Posterior MI.
It comes from this fascinating post:

Series of Prehospital ECGs Showing Reperfusion



Monday, November 7, 2016

Respiratory Symptoms and ST Elevation with Hyperacute T-waves

An elderly woman was brought to the ED for hypoxia.  She had a history of chronic respiratory failure with a tracheostomy and had had multiple episodes over the past few days of increased respiratory effort and hypoxia (down to an SpO2 in the 70s on supplemental O2 via nasal). Associated with this has been increased secretions requiring aggressive suctioning.

On exam in the ED, the patient did not appear nearly so ill and was not hypoxic.

A routine ECG was obtained:
There is inferior and lateral ST elevation with hyperacute T-waves, and reciprocal ST depression and T-wave inversion in aVL.
This is all but diagnostic of STEMI and should be considered to be so until proven otherwise. 


The cath lab was activated.

She was given a full dose of aspirin and a heparin bolus of 4000 units. A repeat ECG demonstrated no dynamic changes.  Bedside cardiac ultrasound had grossly normal systolic function with no apparent wall motion abnormality.

Because the patient had no symptoms specific to STEMI and an ECG that was not evolving, and while waiting for the cath lab to be ready, the very astute providers sought out a previous ECG and were able to get one faxed from another hospital.

It looked exactly the same!

So they waited for the first troponin and it was below the level of detection.

They decided against an angiogram.

The patient ruled out for MI by serial troponins.

This turned out to be the patient's baseline ECG!

Learning Point

Rarely, a patient's baseline ECG looks just like a STEMI.  It never hurts to find a previous one unless it delays care.

Thursday, November 3, 2016

I saw this on the computer. Most physicians, at first glance, get this wrong. What is it?

I was reading ECGs on the system, and saw this:
I immediately recognized it like I recognize a friend's face.  (OK, I'm unusual, I'll admit it)
What is it?



















When I showed this to residents, they uniformly thought it was Left Bundle Branch Block (LBBB).  Look again.  

What QRS morphology is necessary for LBBB?
LBBB morphology requires an upright R-wave in V6.  The QRS here is all negative, depolarizing from left to right.  In LBBB, the ventricle is depolarized in the opposite direction: from right to left, not left to right.
Thus, this is very unlikely to be a supraventricular rhythm (e.g., accelerated junctional) with LBBB.

Then look again at the rhythm.  What is it? 

I always ask these questions about rhythm:
1. Is it regular, regularly irregular, or irregularly irregular?
2. Is it wide or narrow?
3. What is the rate?
4. Are there P-waves?
5. [difficult to assess on one ECG: does the rate stay always the same (re-entrant rhythm), or does it vary from minute to minute? (automatic rhythm, such as sinus or escapes)]    


Although beats 4-16 are pathognomonic once you recognize them, it is also helpful to see the first 3 beats of lead II across the bottom:
1. The 1st is narrow complex and preceded by a P-wave.
2. The 2nd and 3rd have a P-wave with a short PR interval and a wider QRS
3. 4-16 comprise a 1) regular, 2) wide complex rhythm at 3) a rate of 96 4) without P-waves.

A paced rhythm has this appearance on precordial leads, as the right ventricular pacing lead is usually in the RV apex and depolarization then proceeds from the apex to the base (from leads II and V6 towards the right shoulder).   The computer does a good job of finding pacing spikes, even when they are invisible to the human eye.  The computer did not detect pacing spikes here.  This patient's heart is NOT being paced.

Therefore, this rhythm originates in the ventricle and propagates to the "northwest."  Ventricular tachycardia looks like this, but VT is much faster, usually at least 120 beats per minute.

So what is this?

Accelerated idioventricular rhythm (AIVR).  It is an automatic rhythm originating in the ventricles.  It is frequently associated with reperfusion of STEMI.  Some studies dispute whether it is really more common in reperfusion than otherwise in acute MI.

Now, look at beats 7-15 across the bottom (lead II).  Immediately after the J-point there is a retrograde P-wave that distorts the ST segment with a slight negative deflection.  This helps to confirm AIVR, and good retrograde AV conduction.

Now that we have the rhythm and QRS (AIVR), what about the ST-T?  Is there ischemia?

I believe, due to its similarity to LBBB, that the (Smith-) modified Sgarbossa rule (SMSR) can be applied to AIVR (and also to paced rhythm), though I do not have data to support that.  Does this ECG above meet the criteria of the SMSR?  Look at lead V2: there is 1.5-2.0 mm of ST Elevation following a 6 mm S-wave, so this is consistent with anterior MI.

My interpretation before looking at the patient's chart:

AIVR (with retrograde P-waves) following reperfusion of an anterior STEMI, with ST elevation that is out of proportion due to residual ischemia.  The first beat is sinus, then the AIVR speeds up and takes over the sinus rhythm.  The second and third beats are fusion beats in which the impulse from the sinus node and the impulse from the AIVR meet so that it is wide, but not very wide.  Remaining beats activate the atrium from below, with a negative P-wave.  Thus, the ventricle is outpacing the atrium.

Let's now look at the case, the presenting ECG, and the management:





















The patient had presented with chest pain and had this ED ECG:
Obvious anterior STEMI

The cath lab had been activated and a mid LAD occlusion opened and stented.

After stenting, the patient became more hypotensive with a wide complex rhythm and the ECG we have been discussing was recorded.  He was no longer having chest pain at this point in time.

Here it is again for you:
Why was he hypotensive? 

First, in AIVR, the ventricle does not get the advantage of the filling pressure that atrial contraction normally provides (there is no "atrial kick").  In fact, the atrium is contracting during ventricular contraction and propelling blood backwards.

This patient was noted to acutely have about a ~30 mmHg drop in blood pressure while in the ventricular rhythm thought to be secondary to this loss of atrial kick and preload.

BP immediately improved after conversion to sinus rhythm. He cycled between the two rhythms fairly frequently.

How would you manage this?

One good way is to just speed up the sinus node and let it take over from the ventricle.  Atropine would help.

Antidysrhythmics should not be given.

Recommendations of the ACC/AHA, in the 2004 STEMI guidelines (there is no comment in subsequent versions):
"7.7.1.4. Accelerated Idioventricular Rhythms and Accelerated Junctional Rhythms
Class III
1. Antiarrhythmic therapy is not indicated for AIVR. (Level of Evidence: C)
2. Antiarrhythmic therapy is not indicated for accelerated junctional rhythm. (Level of Evidence: C)

"Accelerated idioventricular rhythms are characterized by a wide QRS complex, with a regular rate higher than the atrial rate and lower than 100 bpm. The appearance of an idioventricular rhythm is an inexact indicator of reperfusion.  Treatment of idioventricular rhythm is not indicated, and suppression of the rhythm may lead to hemodynamic compromise."



3 hours after the AIVR:
This shows well-developed Q-waves of anterior MI, with excellent ST resolution and shallow T-wave inversion.
This has the appearance of "LV aneurysm" morphology, though it is too early to call it this.

Next Day:
T-wave inversion, typical of reperfusion T-waves 


Outcome
The rhythm cycled between sinus and AIVR, but eventually settled on sinus
Peak Troponin I was 195 ng/mL (very high)!
However, formal echo had EF of 60%.  Good outcome.




Learning Points

1. AIVR is commonly seen in situations of reperfusion of STEMI.  Although studies do not uniformly confirm this, I can say that in my experience, I have seen this dozens of times and every one was after reperfusion.
2. AIVR is normally well tolerated and self-limited and rarely requires treatment.
3. Occasionally, patients may not tolerate AIVR due to loss of atrioventricular synchrony, as above. Atropine can be used to increase the underlying sinus rate so that it inhibits the AIVR.
4. Antidysrhythmics are not indicated and will not help: this is not a re-entrant rhythm; rather it is an automatic rhythm.
5. If it is not a situation of reperfusion, consider other causes: digoxin toxicity and other structure heart diseases. 

Monday, October 31, 2016

An apparent SVT that does not persistently correct with adenosine

A middle-aged woman presented for abdominal pain.  She was found to have a heart rate of 150.  A 12-lead was recorded:
There is a regular, narrow complex tachycardia.
What is it?















Regular narrow complex tachycardias can be sinus tach, atrial tach, atrial flutter, AV nodal reentrant tachycardia, orthodromic AV reciprocal tachycardia [using a bypass tract (accessory pathway), that is WPW], or junctional tachycardia.

Here is a one hour lecture on Supraventricular Tachycardias; everything you ever need to know.

MAT and atrial fibrillation, other causes of supraventricular tachycardia, are not possible because they are always irregular, and this rhythm is regular.

There are no definite P-waves before the QRS and there are definite retrograde P-waves (see V2 below).
Here the black arrows point out the retrograde P-waves that are clearly present in V2
Once you find this, you go up to V1 and you can see that the retrograde P-wave is all negative.


--Thus, this cannot be sinus tachycardia or atrial tachycardia, which would have upright P-waves in V2.
               Suppose the P-wave was upright in V2 and in the same location in the middle of the QRS?  Then you would have to consider that there is sinus or atrial tach with a very long PR interval.

--When there is a narrow complex tachycardia, especially at a rate of 150, you should also look for flutter waves, which are not present.

--Junctional tachycardia is possible, as it also may have retrograde P-waves.  This is much less common, so let's discard this.

--Thus, we are left with re-entrant tachycardias that use the AV node (AVNRT and orthodromic AVRT).

This can be treated with vagal maneuvers, the best of which is Modified Valsalva, which has a success rate of about 40%.  More reliable is adenosine.

Case continued

A bedside echo showed good LV function.
The patient was given adenosine 6 mg without effect.  Then she was given adenosine 12 mg and had an asystolic pause (without underlying flutter waves), followed by one sinus beat, then one early narrow beat, followed by SVT again.  

Commentary

Aside: if this were atrial flutter, you would see underlying flutter waves revealed when adenosine blocks the AV node and thus removes the QRS which obscures the flutter waves.  See this image which comes from a great article (the third of the 12 rhythms of Christmas) by Vince DiGiulio on EMS 12-lead and which Vince graciously permitted me to use:
Adenosine blocks AV conduction of flutter to ventricle, resulting in a ventricular escape rhythm and uncovering the flutter waves.

This did NOT happen in our case here.


So what happened?  Did adenosine work?

Yes!  Adenosine's only job is to stop the AV nodal re-entrant circuit.  Its effect is of extremely short duration, so it will be gone immediately and be unable to terminate a subsequently initiated episode of Paroxysmal SVT.  So one may have to prevent initiation of PSVT.

How does PSVT start?  PSVT requires 2 pathways.  In AVRT, one of them is the accessory pathway.   In AVNRT, there are 2 pathways in the AV node, a fast pathway with a long refractory period, and slow pathway with a short refractory period.  PSVT starts with a premature atrial beat (PAB) that reaches the AV node when the fast pathway is still refractory, and the slow one is not.  Then it travels down the slow pathway to the inferior part of the node where it then finds the fast pathway is no longer refractory and ascends that fast limb.  When it gets to the top it goes to BOTH the atrium and back down the slow pathway. Then around and around. For a more detailed explanation with an image, watch this lecture from minute 3:18 to 4:54.

PSVT is stopped by stopping the circuit.  If it recurs, further recurrence can be prevented by either 1) having a continuous AV blockade, as with a longer acting medication such as a calcium channel blocker or 2) preventing PABs.  PABs can be prevented by beta blockers or amiodarone.

Beta blockers may be detrimental in patients with poor LV function because of their negative inotropic effect.  In such cases, I have tried esmolol, as it has a short half-life and can be turned off.  I did not have success.   See this case:

Paroxysmal SVT (PSVT) that repeatedly recurs in spite of successful conversion with adenosine.

In that case in which esmolol did not work, I then gave amiodarone bolus of 150 mg, followed by an infusion, after which intervention the patient stayed in sinus rhythm.

In this case today, the adenosine worked, but within one beat, there was another PAB that initiated the PSVT again.

What to do?  Amiodarone?  Calcium channel blocker?  Something else?  As this patient has good LV function, a calcium channel blocker is an excellent and safe choice.  Before adenosine, verapamil was the standard way to terminate PSVT.

Verapamil IV dosage: the recommend IV dose of verapamil is 5 mg over 2 minutes, followed in 5 to 10 minutes (if no success) by a second 5 to 7.5 mg dose.
Diltiazem IV dosage: The recommended IV dose of diltiazem is 20 mg followed, if necessary, by a second dose of 25 to 35 mg.
An oral dose may be given for ongoing maintenance.

Case continued:

In this case, 2 g of Mg (8 mmoles, 16 mEq) was given by one of my excellent partners, Laura Shrag, and the patient converted!

Here is the post conversion ECG:
What is this? Sinus rhythm?


This was read as sinus rhythm, but it looks more like an ectopic atrial rhythm.  The P-wave in V1 is upright, whereas it should be biphasic.  This means that lead V1 is to the left of the source of the P-wave.  Either the heart is far to the right, or V1 was placed too far left, or there is a left-sided atrial source.  In any case, it is a stable rhythm at a good rate and we shouldn't worry about it any more than that.

--There are no delta waves, so this is less likely to be WPW, though absence of delta waves does not rule out WPW.
See explanation of this at these two posts:

--A large R-wave in lead V1. And why is the PR interval not short?


Also of concern: this patient had tachycardia and was completely unaware of it. She presented only for abdominal pain.  This implies that she is not aware of her PSVT and may live with it for long periods of time.  Long duration tachycardia may lead to cardiomyopathy, so it is particularly important for her to be on long term medications, or have an ablation, so that this does not recur.

Magnesium in PSVT:

Magnesium may be loosely thought of as a nonspecific Calcium channel blocker.  I was unaware of its effect on PSVT until this case.  There is data to show that Magnesium, in a dose of approximately 0.15-0.30 mEq/kg (10.5- 21 mEq per 70 kg, or 1.3-2.6 grams per 70 kg) is often effective for termination of PSVT with a low incidence of mild side effects (transient sensation of warmth, flushing, and diaphoresis).
10 mmoles = 2.5 g = 20 mEq

In the electrophysiologic (EP) literature below, it had variable effects on termination, but consistently prolonged antegrade AV node conduction, which is a necessary component to termination. 
1. In an EP study, after a bolus of 0.3 mEq/kg, followed by a 0.2 mEq (0.025 gm)/ kg/hr maintenance infusion, Mg was shown to increase the tachycardia cycle length by about 10% by slowing the antegrade conduction in the AV node of the re-entrant circuit.  However, it did not appear to convert any of the 4 AVNRT studied or any of the AVRT.  It did not prevent inducibility of SVT or affect the refractory period: http://www.sciencedirect.com/science/article/pii/S0002870305800213

2.  In this EP study, 8 of 10 episodes of SVT that involved the AV node (4 AVRT and 6 AVNRT) were terminated with 2 grams of MgSO4 by rapid bolus, flushed with saline.  http://www.sciencedirect.com/science/article/pii/0002914989900921

3.  In this dose-finding EP study, prolongation of the atrial-His interval was no more pronounced at doses higher than 5 mmols (=1.25 g) than at 5 mmoles:  http://europace.oxfordjournals.org/content/2/4/320.short

4.  In this EP study, Mg was effective in termination of 5 of 15 with dual AV node physiology and 0 of 8 cases without dual AV nodal pathways: 

See this post for an explanation of dual AV nodal pathways: 

Wide Complex Tachycardia in a 20 something.


5.  Here is a case report of termination of SVT in the ED, from Annals of EM in the 1990s: http://www.sciencedirect.com/science/article/pii/S0196064496702755

Outcome

The patient was started on Diltiazem CD 120 mg daily.

Learning Points:

1. SVT that is converted by adenosine to sinus may revert back to SVT.
2. SVT is initiated by PABs.  Prevention of PABs helps to prevent recurrence.
3. Calcium channel blockers are very effective in conversion to, and maintenance of, sinus rhythm.
4. Especially in patients who cannot tolerate calcium channel blockers, it is reasonable to attempt an IV bolus of Mg at 1.25 to 2.5 g.
5. In patients who do not respond to Mg and cannot tolerate calcium channel blockers, amiodarone 150 mg followed by an infusion, may be effective in preventing further episodes of PSVT.  One may have to additionally convert the patient to sinus with adenosine.
6. Chronic tachycardia may lead to cardiomyopathy

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