Thursday, May 29, 2014

30 Year Old with Cardiac Arrest, PEA, then Cardiac Ultrasound

A 30 year old collapsed after complaining of chest pain intermittently.  He was unconscious.  First responders thought they palpated a thready pulse.

When medics arrived, there was no pulse.  Full CPR was initiated with the LUCAS device.  The  patient was intubated, an ITD (ResQPod) was used.  Other standard cardiac arrest measures were undertaken.

Here is the rhythm strip (these are two separate tracings):

The initial rhythm is regular and wide complex, with concordant ST elevation, suggesting STEMI.  The next rhythm appears to be ventricular fibrillation.

The patient could not be resuscitated, but was transported to the ED after about 30 minutes of full arrest.

Upon arrival, as is customary, a very brief ultrasound was performed to assess ventricular function.

What do you see?  See below, with arrows

White arrows outline a very large thrombus (clot) in the pericardium.  Red arrow points to a small amount of liquid blood in the pericardium.  Blue arrow points to the RV, where there is full stasis of blood flow.  Green arrow points to barely beating LV

Here is one more brief view before chest compressions resumed:

Here is a view during LUCAS chest compressions

Of course, chest compressions are not of any use when there is massive tamponade.  Even when the heart is fully beating on its own, it will arrest if there is severe tamponade because it cannot generate adequate pressures for myocardial perfusion.  So how would external compressions have any effect?

For cardiac compression to work, the clot must be evacuated.

Although there seemed little hope of recovery, a left thoracotomay was quickly performed.  A pericardiotomy was performed and this clot was evacuated:

Huge clot extracted from pericardium.  This is about 30 cm x 15 cm on the cart.

In spite of internal cardiac compressions, intracardiac epinephrine, several internal defibrillations for V fib, and other standard attempts at resuscitation, he could not be resuscitated.  The resuscitation was futile.

What caused this hemopericardium?

Possible etiologies include:
1. Hemorrhagic pericarditis, but this would be mostly effusion with some blood, not hemopericardium and certainly not clotted blood.
2. Myocardial rupture from MI.
3. Myocardial rupture from trauma (could be occult, could be due to chest compressions)
4. Ruptured coronary artery aneurysm

Here is an ED ultrasound of the aorta through the suprasternal notch:

This is annotated with arrows below:

These arrows point to a flap.  This is aortic dissection.   The aortic diameter is also excessive (greater than 4 cm is abnormal, here it is about 6 cm)

Autopsy showed a DeBakey 1 dissection ( from the arch all the way to the iliac bifurcation)

Thus, this unfortunate young man had an aortic dissection at a very young age.  It dissected back into his pericardium, resulting in hemopericardium and tamponade, which caused hemodynamic collapse.  His pulses by first responders were thready, but not enough to perfuse his brain.  Thus he was unconscious.  Shortly thereafter, the hypotension with consequent poor perfusion of his coronary arteries resulted in severe ischemia with transmural/subepicardial ischemia, and a wide complex then eventually ventricular fibrillation.

Causes of  Pulseless Electrical Activity (5 H's and 5 T's), as advertised by ACLS
Those bolded are particularly likely with a narrow QRS

Hydrogen ions (acidosis)

Tension Pneumothorax
Thrombosis (myocardial infarction)
Thromboembolism (Pulmonary embolism)

Was there any chance of resuscitation with thoracotomy? Probably not, but worth a try.

Once there is full arrest from tamponade, and it has been ongoing for this long, I believe that resuscitation is futile.  However, with a health 30 year old, one must try.

Here is a case in which the patient was alive in the ED and then arrested, had a thoracotomy (in this case subxiphoid) and survived.  The blood was not clotted.

In contrast, in this study of out of hospital cardiac arrest from non-traumatic pericardial fluid on ultrasound, only 1 of 23 patients survived.  None had dissection and none had clotted blood on hemopericardium.  The survivor had liquid blood from myocardial rupture.

Here is a case of myocardial rupture.

Here is another case of myocardial rupture.

Here is a great published case series of myocardial rupture, by my colleague Dave Plummer.  Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.  All of these patients had ECGs with ST elevation, but ultrasound showed pericardial fluid (not clot) and the patient had MI with rupture.

Monday, May 26, 2014

Acute Cardiogenic Shock: What is the Diagnosis?

Click on this link of a recently posted a similar case with great ultrasound images.  Let's see how much you learned and remember.

Acute Cardiogenic Shock

A 69 yo previously healthy woman had very sudden severe dyspnea.  Her husband reported that they had been physically active that day, and that the patient had complained of some chest pain one week prior for which she did not take his advice to go to the ER.  She presented in pulmonary edema, hypoxic on high flow O2, and sats at 90% on Noninvasive Ventilation.  BP was 130/70 but she was clinically shocky.  Cardiac physical exam was unremarkable except for very coarse breath sounds. ABG was 6.99/44/201/11 on BiPAP.  Here is her first ECG:
The rate is 143.  There are P-waves, but in lead II there could be 2 p-waves for every QRS.  I have measured these with calipers, and they are exactly spaced, so it could be atrial flutter.  The second apparent P-wave comes immediately after the QRS and appears to simulate ST elevation (Atrial flutter can frequently mimic ST deviation).  There are also inferior Q-waves with T-wave inversion (in fact, there is an S1Q3T3). There is precordial ST depression which could represent subendocardial ischemia from severe tachycardia, hypoxia etc., or it could be due to inferior-posterior STEMI or old inferior-posterior MI with persistent ST elevation (infero-posterior LV aneurysm).  Maximal ST depression in V2-V4, vs. V5-V6, strongly supports STEMI/aneurysm vs. subendocardial ischemia.

What else would sway you to decide whether this is atrial flutter or sinus tachycardia?  Are the notches after the QRS in the limb leads ST segment deviation, or are they flutter waves?  Is this patient having a STEMI?

Considerations include:
1. Lead V1.  In sinus rhythm, the latter part of the p-wave in V1 is always negative, as it represents the depolorization of the left atrium, which is depolarizing away from lead V1.  In atrial flutter, the p-wave in V1 is usually upright.  Here it looks like a normal p-wave.  Furthermore, you don't see an identical wave directly between the p-waves and given that the baseline is pretty steady, it should be there.
2. If flutter, the rate should remain constant in spite of supportive care.

Therefore, sinus tachycardia is by far the most likely rhythm.

A right sided ECG was recorded 6 minutes later: 

The rate is still exactly 143.  Does this confirm atrial flutter?  There is no evidence of RV infarct.

A bedside echo showed hyperdynamic function and a large RV.  There were many B-lines of pulmonary edema and the chest X-ray confirmed pulmonary edema.  The patient's respiratory status deteriorated and she was intubated.

How do we interpret all this information?

Step backwhat caused sudden respiratory failure with pulmonary edema?
--Does acute inferior-posterior STEMI alone do this?  Not if the pump function is hyperdynamic.
--Does atrial flutter alone cause severe pulmonary edema in someone who was previously healthy and has good LV function?  No.  (However, if this is atrial flutter, it is wise to cardiovert and this can only help the situation.  This was not done.  It appears that the rhythm diagnosis of atrial flutter was not considered.  If it is sinus, cardioversion will not hurt.) 
--Does massive pulmonary embolism cause pulmonary edema?  Rarely, if ever.

A CT pulmonary angiogram was negative.

What test is now indicated?  What is the likely diagnosis?

Another ECG was recorded:

Now the rate is down to 120 and it is clearly sinus.  The p-waves are identical to those in the first ECG.  So those, too, were sinus.  Which means the waves after the QRS were indeed ST elevation and depression. There is inferior T-wave inversion and the upright right precordial T-waves are indicative of reperfusion to the posterior wall as well.  There is an infero-posterior STEMI of unknown age. 

It appears that the Q-waves were well formed at the time of presentation.  
--Do inferior Q-waves appear immediately after the onset of a STEMI?  No.  [However, anterior Q-waves (QR-waves) can be present in the first hour after onset of anterior STEMI)].  
--The inverted T-waves also argue against an acute and persistently occluded artery.

Therefore, this patient's MI was subacute.  

Now, what do you think the diagnosis is?  What was the diagnostic study?

Posterior STEMI puts patients at risk of papillary muscle infarction and rupture. (The posterior leaflet is supplied by posterior branches off the RCA and is vulnerable, whereas the anterior leaflet has its blood supply from the LAD and circumflex) An infarct in the last several days or one week is consistent with acute papillary muscle rupture.  This patient's presentation is classic for acute severe mitral regurgitation.
1. Acute pulmonary edema
2. Hyperdynamic heart (very low afterload out towards the left atrium and pulmonary veins)
3. Severe pulmonary edema without hypertension.
4. Evidence of subacute inferoposterior MI (most occur more than 24 hours from onset of MI)
5. Absence of murmur because in acute rupture, the left atrium is small and as the LV contracts, the pressure between the LV and LA rapidly equalize so that  there is no lengthy period of turbulence.

An echo with Doppler was the diagnostic study, and confirmed papillary muscle rupture with severe mitral regurgitation.  She was given immediate afterload reduction with nitroprusside, and taken for an angiogram which showed 2-vessel disease and a 90% RCA (the culprit) with flow.  Balloon pump was placed and she was taken for immediate valve replacement and CABG and did well.

The initial troponin was 2.4 ng/ml (probably still elevated from the MI one week ago), but did rise to 19 ng/ml by the next morning.  After CABG, it rose to 50 ng/ml.

Friday, May 23, 2014

A Picture of Subendocardial Ischemia

This case shows a CT image of subendocardial ischemia.  The image is shown at the bottom after the case presentation.

This patient presented with a mechanical fall and had chest pain.  He had this ECG recorded:
There is slight ST elevation in lead III, with reciprocal ST depression in aVL.  However, there are also Q-waves inferiorly and the inferior T-waves are inverted, suggesting that this is an old MI with persistent ST elevation, or, alternatively, a subacute or partially reperfused, inferior STEMI.  There are somewhat large T-waves in V2 and V3 which are non-specific but could represent posterior reperfusion T-waves. There is ST depression in V4-V6. 

His previous ECG was 4 years prior and was normal.  It confirmed that the Q-waves, inferior T-wave inversion, and large T-waves in V2 and V3 were all new.

His chest pain increased and this ECG was recorded:
Now there is increasing inferior ST elevation.  There is also new ST depression in V2-V3 and increased ST depression in V4, maximal in V2 and V3.  This is all but diagnostic of inferior-posterior STEMI. However, the inferior T-waves remain inverted, and this is atypical for inferior STEMI.  

His first troponin I returned at 0.10 ng/mL (slightly elevated) and his symptoms could not be controlled with nitroglycerin, so he was taken to the cath lab and found to have:

--Severe 3 vessel Coronary artery disease involving the LM.
--Chronic Total Occlusion of the RCA filling via left to right collaterals.
--Severe Left Main disease, and chest pain with contrast injection into the LM.  This chest pain was relieved with injection of nitroglycerine, with LV end diastolic pressure (LVEDP) decreasing to 12 from 26.
--The patient was started on Heparin and NTG drips.  The pain resolved with the nitroglycerine.
--No PCI was done
--The patient went for CABG.

The post cath ECG was not recorded until the next morning:
The ischemia is almost entirely resolved.  There are inferior and posterior reperfusion T-waves.  The Q-waves appear to be smaller

Peak Troponin I was 0.106 ng/mL (not very high)

Formal Echo report, the next day:

--Regional wall motion abnormality-inferoposterior, large.
--Decreased LV systolic performance mild; ejection fraction is 47%
-- In direct comparison with the resting study from 5 years prior, the wall motion abnormality is new, as is the reduction in left ventricular systolic performance.

Summary of this case:

So the patient had transient ST elevation (transmural, not subenocardial, ischemia) of the area of the heart (inferior and posterior walls) supplied by left to right collaterals because of a chronic total occlusion of its previous supply from the RCA along with some obstruction to flow through the collateral supply from the left main.

The inferior and posterior walls are also at chronic risk of subendocardial ischemia because of this tenuous blood supply.  The remainder of the heart is also at high risk of subendocardial ischemia because of this obstructed flow in the left main and the need for the left main to supply not only its normal territory (anterior and lateral/LAD and circumflex), but also the inferior and posterior walls.

So here is the really interesting part:

The patient had had an outpatient CT scan of the abdomen done one week earlier.  It had been ordered one month prior because the patient had a complaint of abdominal pain after eating, resolved with nitroglycerine, with a "question of bowel ischemia."

There was no ECG done at the time of the scan or at the outpatient visit for abdominal pain which precipitated the CT scan.

The abdominal CT scan showed:

1. Marked atherosclerotic calcification at the origins of the celiac and superior mesenteric arteries. These arteries appear to remain patent, however a hemodynamically significant stenosis is not excluded. No
evidence for watershed ischemia.

2.  The scan also showed poor contrast enhancement of the subendocardium of the heart.  This was only seen in retrospect.
Since this is imaged with contrast, areas that are perfused should be dense (white) with contrast.  Areas that are poorly perfused will be dark (no contrast).  Notice the poor perfusion in the subendocardium of the posterior wall of the heart (dark areas pointed out by arrows below).  The inferior wall was similarly affected.

Arrows point to a poorly perfused area of subendocardial myocardium in the posterior wall (the subendocardium is the layer closest to the heart chamber).  Since this is a contrast study, well-perfused areas are bright with contrast, whereas poorly perfused areas remain dark.  The subendocardial layer is most susceptible to ischemia because it is closest to the high pressure LV chamber; that higher pressure inhibits perfusion while the subepicardial (outer) layer may still be well perfused.

Was the "abdominal pain" actually infero-posterior subendocardial ischemia?

CT myocardial perfusion imaging

Sestamibi myocardial perfusion imaging is well known, as is CT coronary angiography, but a new imaging modality is CT myocardial perfusion imaging.  This is essentially what we see in the image above.  However, CT myocardial perfusion imaging is rarely positive at rest.  Rather, it is a provocative test (a stress test) done with adenosine or dobutamine stress with before and after images, much like what is done with sestamibi, or even with stress echo.  It may have additive incremental value to the more traditional stress tests.

Mostly I think it just give interesting images that let us visualize the ischemic heart.

Here are some references:

Tuesday, May 20, 2014

An 8 year old with diarrhea, abdominal pain, and syncope

This case was sent by:

Maria Perez
Emergency Registrar
Monash Medical Centre

She obtained permission from the family to identify the location or origin of the case.


This previously completely healthy 8 yo girl complained of diarrhea, vomiting, and upper abdominal pain radiating to the chest, for the past 3 days.  There had been an episode of syncope 3 days prior for which she had been seen by her primary care provider, but there is no information from that visit.  

Her exam was normal except for an irregular heart rate at 78, with BP of 100/60.  Lungs were clear.

Because of the irregular heart beat and h/o syncope, an ECG was recorded: 

There is an irregular rate.  The image resolution is not ideal and it cannot be enlarged.  All beats are supraventricular.  This was my original interpretation, but was corrected (see below) by Andreas Roschl.  There appear to be P-waves in front of every QRS, at a rate of about 150 (sinus tachycardia).  The PR interval does not lengthen.  There are some P-waves that do not conduct.  Therefore, it is 2nd degree block Mobitz type II.  Even more important is the presence of right bundle branch block, and probable left posterior fascicular block, with massive ST elevation.  
Correction to rhythm interpretation: sinus rhythm with short runs of PACs (i.e. atrial tachycardia).

Besides AV block, this ECG is diagnostic of injury, which in an adult would almost always be a STEMI.  In a child, especially one who has viral symptoms, myocarditis is highest on the differential diagnosis.

Mobitz type II block has potential to evolve into complete (3rd degree) AV block.  Unlike Mobitz type I (Wenckebach), it is associated with anterior injury (injury to the septum and bundle of HIS).

Mobitz II block in STEMI and with new BBB is a class I indication for transvenous pacing, as it frequently progresses to complete AV block.

The patient had no family history of sudden death and no recent overseas travel.

3 more ECGs were recorded before the patient could be transferred:

There is continued Mobitz II block, variably blocked.  Sinus rate remains about 150.

Continued Mobitz type II block, now with a regular 2:1 AV block.  RBBB and LPFB are still present. Injury pattern continues.

Correction to rhythm interpretation by Andreas Roschl: What appear to be P-waves without conduction may, in fact, be T-waves.  This is uncertain.

Continued Mobitz type II block, still with a regular 2:1 AV block.  RBBB, LPFB, and injury continue.

The initial troponin I was 13 ng/mL

She then had further decrease in level of consciousness en route to the referral hospital, with episodes of 3rd degree heart block with ventricular escape. She underwent transvenous pacing and was started on isoprenaline (isoproterenol).  
--Immediate angiography revealed normal coronary arteries.   
--Biopsy confirmed myocarditis.  
--All viral PCR tests were negative.  
--Echocardiogram showed severely reduced biventricular function with a septal wall motion abnormality and a small effusion.

Final diagnosis: Myocarditis, likely viral, however results non conclusive for any specific viral cause.

The last ECHO before discharge: mild-moderate concentric LV hypertrophy, good biventricular contractility, globally reduced LV myocardial velocities, normal conventional diastolic function. 

She was discharged on lisinopril. 


1. Do not hesitate to obtain an ECG in children who have any chest pain or irregular heart beat
2. Myocarditis can mimic STEMI
3. Any AV block in the presence of injury or in the presence of bifascicular block is a warning of impending complete AV block.
4. Mobitz type II block is particularly worrisome

Sunday, May 18, 2014

A woman in her 50s with reproducible chest pain (seems to be chest wall pain)

This woman had recently undergone rotator cuff surgery and presented with L shoulder and chest pain.  The pain was very reproducible with palpation and with range of motion of the shoulder.  It seemed to be clearly musculoskeletal pain and my plan was to not even order an ECG (believe it or not).  I was not planning to order any tests at all.

The physician assistant, however, did obtain this one:
There are abnormal ST segments and T-waves in V2-V4, with ST segment depression in V3 and V4.

Here is her previous ECG:
Normal, with some normal variant T-wave inversion in V2, but no ST depression

I could not believe that this new ST depression was due to ischemia.

What was causing the ST depression?

The differential diagnosis of ST depression in the context of a normal QRS (absence of LBBB, RBBB, LVH, RVH, WPW, hyperK, etc. etc. etc.) is very short:

1. Ischemia
2. Hypokalemia
3  Digoxin effect (associated with short QR interval)
4. Idiopathic/baseline.

Her medication list included a diuretic, so we checked the K.  It was marginally low at 3.3 mEq/L.  An hour after 40 mEq/L of oral potassium, we recorded this ECG (the pain was not resolved):
The ST depression is resolved.

Troponins were negative and the patient was discharged.


1. Remember there are etiologies of ST depression other than ischemia.
2. If you order ECGs to investigate ischemia in situations of low pretest probability, you must have the skills to differentiate true positives from false positives.
3. Hypokalemia may have pathognomonic findings, such as prominent U-waves, as seen in many of these posts, but it may have no findings or only non-diagnostic ST depression, prolonged QT interval, or T-wave flattening.

Selected Literature on the ECG in Hypokalemia


short version:

Electrocardiographic criteria of hypokalemia include various combinations of the following signs: 
(1) T/U value of 1 or less in lead II or V3
(2) U-wave amplitudes of greater than 0.5 mm. in lead II or greater than 1 mm. in V3, and 
(3) S-T depression of 0.5 mm. or more in lead II or leads V1, V2, and V3

It must be remembered that a normal electrocardiogram does not exclude hypokalemia and that an electrocardiogram which fulfills the established criteria does not necessarily indicate hypokalemia unless the factors discussed have been eliminated or minimized.

2.  ECG Diagnosis: Hypokalemia

The earliest electrocardiogram (ECG) change associated with hypokalemia is a decrease in the T-wave amplitude.1 As potassium levels decline further, ST-segment depression and T-wave inversions are seen, while the PR interval can be prolonged along with an increase in the amplitude of the P wave.1 The U wave is described as a positive deflection after the T wave, often best seen in the mid-precordial leads (eg, V2 and V3). When the U wave exceeds the T-wave amplitude, the serum potassium level is < 3 mEq/L.2 In severe hypokalemia, T- and U-wave fusion with giant U waves masking the smaller preceding T waves becomes apparent on the ECG.1,2 A pseudo-prolonged QT interval may be seen, which is actually the QU interval with an absent T wave.1Severe hypokalemia can also cause a variety of tachyarrhythmias, including ventricular tachycardia/fibrillation and rarely atrioventricular block.3 Treatment of hypokalemia involves parenteral and oral potassium supplementation, as well as identification and treatment of the underlying cause.1

3. Our Study of the ECG in Significant Hypokalemia

We found that the ECG was very sensitive and specific for K less than or equal to 2.9 mEq/L, vs. 3.5 or greater, but this sensitivity depended on a subjective aspect of interpretation as well as on findings of abnormal T-waves, prominent U-waves, ST depression, or a computerzied QTc greater than 450 ms.  

Smith, S. W., S. J. Bronner, and L. M. Hayden. Abstract 400: Derivation of a Rule for Diagnosis of Hypokalemia on the Electrocardiogram." Annals of Emergency Medicine 56.3 (2010): S129-S130.

Study Objectives: There is little data on the electrocardiographic (ECG) diagnosis
of hypokalemia (HypoK). We hypothesized the ECG to be an accurate predictor of
significant HypoK (K  2.9 mEq/L) or normoK (K  3.5 mEq/L) (NormoK).

Methods: Retrospective study. We searched the electronic medical record for
consecutive emergency department diagnoses of HypoK, then hand searched for
those in which there was an ECG recorded before administration of potassium (K),
and the K was less than or equal to 2.9 mEq/L. For controls, we searched for consecutive ECGs in
patients with K of at least 3.5 mEq/L. Abnormal QRS (bundle branch block or
intraventricular conduction delay) or extreme tachycardia (HR 130) were
excluded, as were redundant patients. One expert reader (ExR) and two resident
readers (RRs) who underwent a short tutorial interpreted the randomly sorted ECGs
while blinded to the K level and the Bazett-corrected QT interval (QTc-B). ECGs
were analyzed for computerized QTc-B, presence of U-waves [None (NUW), subtle
(SUW), or prominent (PUW)], T-Wave flattening (TF), and ST segment depression
(STD). Resident readers combined, and the expert reader, noted subjective
interpretations (SI, either ExR-SI or RR-SI) [definite HypoK (SI), or not]. Analysis
was by descriptive statistics, by Student’s t-test and by Chi-square (CS).

Results: There were 100 cases of HypoK with an ECG; 13 were excluded, leaving
87. There were 58 controls. QTc-B was the single best differentiator, with accuracy
(Acc) of 74%. Expert reader Accuracy was 72%, and Resident reader was 63% accurate (p .10 by
CS). Mean QTc-B for HypoK was 475 +/- 8.2 milliseconds (ms); for NormoK is was
429 +/- 5.5 ms (p = 0.0001 by Student’s t-test). 
Prolonged QTc-B or a prominent U-wave was the best objective combination, with
Sens, Spec, and Acc of 80%, 78%, and 79%. These two criteria, if added to
subjective diagnosis by the ExR, versus none of the 3, had 86% Sens, 100% Spec and
92% Acc. If added to subjective diagnosis by the RRs, versus none of the 3, results
were 83% Sens, 98% Spec, and 89% Acc.

Conclusion: Computerized QTc is longer in HypoK than NormoK. Significant HypoK (less than or equal to 2.9) in the ED can be recognized on the ECG with high accuracy using QTc-B and presence of
prominent U-waves. HypoK can be recognized with very high Sens, Spec, and Acc,
using subjective interpretation of either the expert reader or the residents, plus QTc-B
and presence or absence of prominent U-waves.

Monday, May 12, 2014

True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

Case 1.  

A woman in her 60s with no prior history of CAD presented with 3 hours of sharp, centrally located chest pain with radiation to the anterior neck, with associated nausea. She had known HTN and DM.  She appeared to be in distress.  She was given sublingual NTG with improvement, but there was not complete resolution.

Here was here initial ECG:
There is ST elevation in I and aVL, with inferior reciprocal ST depression in all of II, III, and aVF, and a down-up T-wave in aVF (a sign that is very specific for ischemia).  There is also ST depression in V3-V6.  This ECG is diagnostic of ischemia.

It is important to compare this one with the false positive case #3 at the bottom; that one is a case which could fool you.

There was an old ECG for comparison:
One year prior with no ST segment abnormalities

A bedside cardiac ultrasound was done by the emergency physician.  Here is the parasternal short axis view:

There is an anterior and lateral wall motion abnormality.

This still helps to show the wall motion abnormality:
Arrows point to area of wall motion abnormality

The Cath Lab was activated, and here are the results:

1. LM: No significant stenosis.
2. LAD: luminal irregularities with a 40% stenosis at the take-off of a D3. D3 has a 95% tubular ostial stenosis. (Culprit, stented)
3. LCX: Luminal irregularities, no significant stenosis. Two OM branches without significant stenosis.
4. RCA: dominant. Luminal irregularities without significant stenosis.  Supplies a small RPDA and RPLA.

After cath lab activation, her initial troponin returned at 0.124 ng/mL (99% level = 0.030 ng/mL)

This was the post-cath ECG:
After reperfusion: aVL shows resolution of ST elevation and inverted (reperfusion) T-wave.  There is also some terminal T-wave inversion in anterior precordial leads

A large Diagonal artery may supply both the lateral wall and part of the anterior wall.

Case 2: Another subtle lateral MI, from this post:
A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain.  Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG.  The patient had never had pain like this before.  The pain improved from 9/10 to 3/10 after NTG.  Here is the initial ED ECG:
There is subtle ST elevation in I and aVL with subtle reciprocal ST depression in III.  Look at aVF.  There is a downsloping reciprocal ST segement followed by an upright T-wave ("down-up" T-wave).  This morphology is highly suspicious for ischemia.   There are also symmetric anterior T-waves with very poor R-wave progression.  T-waves in V4-V6 are taller than normal (compare to ECG in case 3 below)

This ECG, especially along with the very typical history, was very worrisome, but not absolutely diagnostic of, ischemia.  Several serial ECGs showed no change, even after the pain finally resolved to 0/10 after NTG.

He was given aspirin,
clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was called and notified that this patient was very high risk and needed close attention.  He readily agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063
ng/ml (upper limit of normal = 0.025 ng/ml).  Repeat ECG remained unchanged.
--He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on medical therapy with plan for angiogram in the morning.
--Just before admission to the hospital, the patient admitted to recurrent pain and appeared uncomfortable.  Therefore, the
cath lab was activated urgently.
--The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or subtotal occlusion.
cath, there was a 95% proximal LAD stenosis with TIMI-II flow, proximal to a large diagonal.  A stent was placed and the patient became pain free.

Case 3: False positive
And here is a similar one that is NOT MI.  How do we tell the difference?
There is ST elevation in I and aVL, with reciprocal ST depression in lead III.   

Just so you don't think I'm cheating by using a retrospectoscope, this was sent to me without any outcome, and I read it as "no MI" with a high degree of certainty.  This is because:
1. The remainder of the ECG is normal.  No poor R-wave progression, no other ST depression, no symmetrical T-waves, no large T-waves, no down-up T-waves, typical early repol in anterior leads
2. The reciprocal ST depression is in lead III only.  Not in leads II and aVF.
3. There are distinct J-waves in the two leads with ST elevation.  This is highly suggestive of early repolarization in these leads.
4. The T-waves in I and aVL are not large (this was also true with the MI case 1 at the top, but that case had many other suspicious findings (many leads with ST depression and no J-waves)

When there is ST elevation in aVL, with reciprocal ST depression in III:
1. Look for:
    a. J-waves
    b. Other ST depression
    c. Large T-waves
    d. Symmetric T-waves
    e. Down-Up T-waves
2. Compare with an old ECG
3. Use ED Echo if available 
4. Use formal Echo 
5. A positive troponin is helpful (a negative one is not)

Saturday, May 10, 2014

Inferior and Posterior STEMI. What else?

A male in his late 30's to early 40's presented with 24 hours of intermittent typical chest pain.  The following ECG was recorded:
There is an obvious acute inferior STEMI.  The inferior Q-waves suggest that there is an old inferior MI or that this one is subacute, but an old ECG was available and also had similar Q-waves..  There is also ST depression in V2 and V3, also minimal in V4-V6.  This is posterior injury, which frequently is simultaneous with inferior injury. There are also large R-waves in V2 and V3, which could represent infarction of the posterior wall.                                                                                                                     There is one other interesting finding.

There is some STE in lead V1.  There should be some ST depression in V1 corresponding to the posterior injury.  Whenever there is inferior STEMI, one should think about Right Ventricular STEMI (RVMI).  RV MI can only occur with RCA occlusion, as the RV marginal branches off the RCA.  As 85% of inferior STEMI are due to RCA occlusion [the rest due to occlusion of a "dominant" circumflex (i.e., it supplies the inferior wall)], one must frequently consider RV MI.  RCA occlusion usually has reciprocal ST depression in lead I (all inferior STEMI have reciprocal ST depression in aVL!) and STE in lead III > STE in lead II.

When there is RV MI, there is almost always some ST elevation in lead V1.  And if there is ST elevation in lead V1, one must consider RV MI.  This STE in V1 prompted recording of a right sided ECG:

Leads V1 and V2 were not reversed as they should be in a right side recording, so V1=V1 (not V1R) and V2 = V2 (not V2R):
V1 now has much more ST elevation (the STEMI has progressed, which one can also see in the inferior leads).  V2 has less ST depression than before, probably because right ventricular injury is "pulling the ST segment up".  There is profound STE in V3R to V6R

Right ventricular infarct is associated with right sided failure, hypotension, and higher mortality, and also with particular sensitivity to the hypotensive effects of nitroglycerine because the ischemic RV needs higher filling pressures.  Fluids are often necessary to maintain BP.  The best leads for diagnosis are leads V3R and V4R, with an ST elevation cutoff of 0.5 mm at the J-point, except for males under age 30, for whom a cutoff of 1 mm is more accurate.  As always, ST elevation should be interpreted in the context of the QRS amplitude: if QRS amplitude is particlarly high, then more ST elevation is requirred; if particularly low, then less STE is required.

Interestingly, this patient had a BP of 190/120 and required IV and oral metoprolol, as well as nitroglycerine, to control his BP.

Initial troponin I was 3.8 ng/mL.

The patient went to the cath lab and had a proximal RCA occlusion that was opened.  

Highest troponin I was 16 ng/mL

The next day, he had a formal echo.  In order to get good visualization of the RV, Intravenous Definity (brand name echo contrast material) was required.  Here is the cardiac ultrasound:

The orange colored area is the Definity contrast in the chambers of the heart.  The RV is on the left (circled below).  This shows very poor RV function except at the apex (arrow below).

This is known as McConnell's sign, and is described for Pulmonary Embolism; here we see it in right ventricular MI.

Here is the formal echo report, which is remarkable for no left ventricular wall motion abnormality (all resolved!)
The estimated left ventricular ejection fraction is 69 %
The estimated pulmonary artery systolic pressure is 20 mmHg + RA pressure.
Based on the appearance of the IVC, the RA pressure is low.
Normal estimated left ventricular ejection fraction  and Normal left ventricular size.
No wall motion abnormality of the Left ventricle

Decreased right ventricular systolic performance severe .
Regional wall motion abnormality-right ventricle .


In inferior STEMI, V1 should be scrutinized for any ST elevation and RVMI should be highly suspected if there is STE, especially if there is posterior injury.  It is recommended to record a right sided ECG, as leads V3R and V4R have the best sensitivity and specificity for RV MI.  

Thursday, May 8, 2014

Agitation and Tachycardia

A young male with unknown past medical history presents with AMS and tachycardia. EMS was called by a roommate after the patient was noticed to be nonverbal and lethargic. He reportedly took meth and had a recent drinking binge, but has not had alcohol for the last 2 days. His HR was 160 on arrival of EMS, and they gave him adenosine 6 mg and 12 mg and 500 cc NS, but with no response.  The preshospital ECG and strips are not available.  The patient was restless, agitated, and nonverbal on arrival to ED, with elevated HR at 150.  Here is the first ED ECG:
What is the likely diagnosis?

There is sinus tachycardia, a prolonged QRS (computer read it as 114 ms, previous ECG with 102 ms).  There is a large R-wave in lead aVR.  These findings are nearly pathognomonic of, or at least highly suspicious for, tricyclic antidepressant (TCA) overdose.

One can read about management of TCA overdose in many places, and I have put some links to lifeinthefastlane below.

A few important points:

1. An R-wave in lead aVR  greater than 3 mm, or an R/S ratio greater than 0.7, is highly suspicious for sodium channel blockade, which is the most important of the many toxicities of TCA overdose.

2. In 49 patients with known TCA overdose, a maximum limb lead QRS duration greater than 100 ms was 100% sensitive for detecting patients who will seize, and seizure is a harbinger of cardiovascular collapse.  At this cutoff of 100 ms, however, the specificity was not perfect.  Of 11 patients with an initial QRS duration of 100-119 ms, 2 (18%) had seizures, and of 22 with an initial QRS duration of 100-139 ms, 4 (18%) had seizures.  Of 14 with initial QRS of 140 ms or longer, 8 (56%) had seizures.  No patient with a QRS of less than 160 ms had ventricular dysrhythmias.

2a.  In an unselected population with suspicion of overdose, a minimally wide QRS (less than 110 ms) will be much less specific; furthermore, it is likely that frequent serial ECGs, by detecting an increasing QRS duration, will detect those at risk of toxicity.  On the other hand, administration of bicarbonate, the antidote, is relatively safe compared with a seizure.  If the diagnosis is unclear, narrowing of a widened QRS on ECG following sodium bicarbonate administration (1-2meq/kg) adds further support that pharmacologic sodium blockade is present.

3. There are multiple mechanisms of toxicity of TCAs:
a.   Blockade of cardiac fast sodium channels (leads to wide QRS, R-wave in aVR, R' wave in V1, Brugada pattern ECG, ventricular dysrhythmias.)  Sodium channel blockade in the CNS leads to seizures.
b.   Blockade of potassium channels (leads to long QT and torsade)
c.   Antagonism of central and peripheral muscarinic acetylcholine receptors (leads to delirium)
d.   Antagonism of peripheral alpha-1 adrenergic receptors (causes hypotension)
e.  Antagonism of histamine (H1) receptors (may contribute to sedation)
f.  Antagonism of CNS gamma-aminobutyric acid (GABA) A receptors (increase risk of seizures)
g.  Exaggeration of therapeutic effect of inhibiting central serotonin re-uptake. (may cause/contribute to serotonin syndrome)
h.  Exaggeration of therapeutic effect of inhibiting central norepinephrine re-uptake (increase risk of seizures)


When it became clear that the patient had sinus tach and not PSVT, his presentation was recognized as an overdose or drug toxicitiy.  But because the physicians were so focused on his tachycardia, meth use, and rhythm, they did not look for or appreciate the findings of TCA overdose.  We in emergency medicine obtain ECGs in overdoses mostly to look for TCA findings.  So when you get an ECG in this situation, look for them!

Much later, the roommate called and reported that 20 amitryptiline (unknown mg per dose) were missing.  Fortunately, the patient had not had any adverse outcome by that time.
He was given multiple amps of bicarb and a bicarbonate drip.  He remained delirious and was given 3 mg of physostigmine (after pretreatment with 2 mg of lorazepam to prophylax against seizures).  His delirium greatly improved and he was then able to follow commands.

He had a prolonged stay in the ICU requiring days of bicarbonate.  The tox screen only showed amitryptiline.

Articles on TCA

More TCA ECGs from Dr. Smith's ECG Blog

More on TCA overdose, with ECGs, from life in the fast lane.

More still on TCA overdose, from lifeinthefastlane.

Recommended Resources