Monday, June 29, 2015

A Male in his 40's with Decreasing Chest pain - what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm.
The QTc is 379 ms.
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 

The clinicians used the subtleSTEMI formula (sidebar excel applet).  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm

If we put these values into the formula, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6

Only one value is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 3.5 mm.  RAV4 = 11-12 mm.

Formula value is now slightly lower.

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).

Here is another case in which the T-wave subtly diminishes as the LAD spontaneously opens and pain diminishes (the first 4 are prehospital ECGs):

Saturday, June 20, 2015

More Evidence that Inspiratory Threshold Device Improves CPR

More evidence that inspiratory threshold device improves CPR (but only when CPR is done right!): 

Resuscitation online


To determine if the quality of CPR had a significant interaction with the primary study intervention in the NIH PRIMED trial.
The public access database from the NIH PRIMED trial was accessed to determine if there was an interaction between quality of CPR performance, intervention, and outcome (survival to hospital discharge with modified Rankin Score (mRS) ≤3).
Multi-centered prehospital care systems across North America.
Of 8719 adult patients enrolled, CPR quality was electronically recorded for compression rate, depth, and fraction in 6199 (71.1%), 3750 (43.0%) and 6204 (71.2%) subjects, respectively. “Acceptable” quality CPR was defined prospectively as simultaneous provision of a compression rate of 100/min (±20%), depth of 5 cm (±20%) and fraction of >50%. Significant interaction was considered as p < 0.05.
Standard CPR with an activated versus sham (inactivated) ITD.
Measurements and main results
Overall, 848 and 827 patients, respectively, in the active and sham-ITD groups had “acceptable” CPR quality performed (n = 1675). There was a significant interaction between the active and sham-ITD and compression rate, depth and fraction as well as their combinations. The strongest interaction was seen with all three parameters combined (unadjusted and adjusted interaction p-value, <0 .001="" 34="" acceptable="" active-itd="" all="" an="" compared="" cpr="" discharge="" for="" hospital="" i="" increased="" mrs="" of="" performed="" presenting="" quality="" respectively="" rhythms="" sham="" survival="" to="" use="" versus="" was="" when="" with="">p
= 0.006). The opposite was true for patients that did not receive “acceptable” quality of CPR. In those patients, use of an active – ITD led to significantly worse survival to hospital discharge with mRS ≤3 compared to sham (34/1012 [3.4%] versus 62/1061 [5.8%], p = 0.007).

There was a statistically significant interaction between the quality of CPR provided, intervention, and survival to hospital discharge with mRS ≤3 in the NIH PRIMED trial. Quality of CPR delivered can be an underestimated effect modifier in CPR clinical trials.

Friday, June 19, 2015

Cardiac Arrest and ST Elevation: You Should Learn to Recognize This!

The following case was incredibly interesting for other reasons, but in order to maintain confidentiality and also to allow for a subsequent case report by the physicians caring for the patient, I limit the discussion to the ECG findings and their etiology.

A man was resuscitated from an Asystolic Cardiac Arrest with Epi, bicarb, and chest compressions.  He was in shock.  

Here was the initial 12-lead:
This is nearly pathognomonic of at least one condition.  What is it?

There is sinus rhythm with a prolonged QRS, right precordial ST elevation, and very peaked T-waves in V4-V6.   This is hyperkalemia until proven otherwise.

It is possible that the ST elevation is due to STEMI, but unlikely.

Hyperkalemia often produces a Brugada-like right precordial PseudoSTEMI pattern.

The pH was 6.65, with a K of 7.5 mEq/L.

Here are 7 other examples of PseudoSTEMI due to HyperK:
5. (there are 3 in this post):

There is remarkably little literature on ECG findings in severe acidosis.
Here is a case in which one patient had 2 cardiac arrests on separate dates, both due to cocaine use, and both with severe acidosis and a bizarre Brugada-like ECG. 

He was given Calcium, bicarbonate, and Insulin

This ECG was recorded 30 minutes after the first:
Same findings, but less pronounced, and slower rate

The pH at this point was 6.80, with a K of 6.2 mEq/L.  More Calcium and Bicarb were given.

At 1 hour, with a pH of 6.95 and K of 7.2 (difficult to control), another ECG was recorded:

Wednesday, June 17, 2015

Early Repolarization, Anterior MI, or Other?

A 30 something presented with atypical chest pain.

Here is the ECG:
--There is huge ST elevation in V2 and V3, approximately 5 mm.
--There is some ST elevation in aVL with some minimal reciprocal ST depression in III
--There is a small q-wave in V4.
--There are also large S-waves in I and II, and a large R-wave in V1, suggesting right ventricular hypertrophy

It is risky to apply the early repol vs. LAD occlusion formula when there are other indications that this may be MI, such as 1) Q-wave in V4 and 2) STE in aVL with STD in III.  However, when I saw this (I did not take care of the patient), I thought this "looked" like early repol, and I did apply the formula:

STE 60 V3 = 5 mm
QTc = 411 ms
R-wave amplitude in V4 = 25 mm

Formula value = 22.079.  This is very low.  Less than 22 is about 97% sensitive for LAD occlusion.

This is very low.  Serial ECGs were recorded and they remained the same.  The patient ruled out for MI and all ECGs were stable.

Unfortunately, no echo was done to assess for RV hypertrophy.

Learning Points

1.  Early repolarization can have Scary ST elevation
2.  Pretest Probability is Critical.  Here, the low pretest probability was an important factor in this decision: in a young patient with atypical pain, scary ST elevation is much less likely to be due to ischemia.

Four Great Instructional SMACC Videos from Hennepin

These great procedural videos on online at SMACC.  All done at Hennepin County Medical Center's Emergency Department by my incredible colleagues.

All are embedded below.

3 were Winners of the SMACC instructional video contest  (Winners in September, April, and May)

Minnesota Tube by Drs. Jacoby, Helland, Simpson, and Joing (WINNER)
ILMA by Drs. Rowland-Fisher, Joing, Prekker, and Reardon (WINNER)
Williams Airway by Drs. Kornas, Rowland-Fisher, Joing, and Reardon 
Nasopharyngoscopy by Drs. Paetow, Rowland-Fisher, and Reardon (WINNER)

September Winner

Minnesota Tube from Social Media and Critical Care on Vimeo.

May Winner

Nasopharyngoscopy from Social Media and Critical Care on Vimeo.

Friday, June 12, 2015

Emergency Physicians Must Make the Tough Decisions

This recent case, which occurred within the past year, was sent to me by an unnamed 2nd year EM resident.  She says she is a believer in all things FOAM!

As this case could have been managed better, she will remain anonymous.  But rather than being critical of the management, just try to learn from it.

Case presentation:
A middle-aged woman with a history of vascular disease presented to a community Emergency Department after an episode of syncope. She complained of 24 hours of severe chest pain radiating to her back, and epigastric abdominal pain. Initial vital signs were BP 128/85, HR 122, RR 22 and O2 saturation was 98% on room air. Physical exam was significant for diaphoresis and agitation, tachycardia without murmurs, epigastric abdominal tenderness without rebound or guarding, and equal peripheral pulses.

An ECG was recorded:
This ECG is notable for narrow-complex sinus tachycardia, ST segment elevation with Qr-waves (deep Q, small r-wave) in V1-V2 and T wave inversions in V1-V4. There are no reciprocal ST segment depressions.

Is this an acute MI?
The presence of such well developed Q-waves in the anterior leads suggests that this is not an acute STEMI, but rather a subacute anterior MI.

What is your next step?

A bedside ultrasound was performed:

This is a subxyphoid cardiac view demonstrating moderate pericardial fluid.  The LV appears to have reasonable function, but is rather small, suggesting poor filling.  I do not have an image of the IVC.  The aortic root was not imaged.

Is this pericardial tamponade?

Upon close inspection of the right ventricle, you can see that there is no collapse during diastole. The RV appears to be both filling and squeezing well, which argues against pericardial tamponade.  

On the other hand, the patient has tachycardia and probable poor LV filling, so a fluid challenge would be appropriate.

Comment: What is the pericardial fluid?

In the setting of subacute MI, one must entertain the idea of myocardial free wall rupture.  Aortic dissection with leakage into the pericardial sac is certainly a possibility, but this would require 2 unusual events:
1) a delayed presentation (dissection with pericardial blood is usually so acute that the patient would present immediately after onset of symptoms).
2) Focal Anterior STEMI.  Though dissections can dissect down the left main, they are
        a) less common that the RCA
        b) more deadly (if there is Left main occlusion)
                i) when not deadly (incomplete occlusion), they present with diffuse ST depression, not anterior ST elevation (this ECG is consistent with LAD occlusion).

Patient course

The resident wanted to do pericardiocentesis, but was not allowed by her faculty.  Labs were significant for initial mild troponin elevation (2.8 ng/mL), consistent with subacute MI. 

CT scan was performed due to suspicion for aortic dissection and was negative. Unfortunately the patient became hemodynamically unstable shortly after returning from the CT scanner.  Fluids were started. The hemoglobin returned very low and so blood was transfused.  Mental status declined and she was intubated, then went into PEA arrest (comment: "pulseless" electrical activity means that pulses cannot be felt, not that there is no perfusion and certainly not that there is no cardiac activity).  Chest compressions were begun and Cardiac surgery was called.  She did regain pulses at times and would have spontaneous movements, but would lose pulses again.


1) Chest compressions are probably not helpful.  They can improve venous return to the chest if done in conjunction with an ITD, but the problem is that the LV cannot fill, NOT that it cannot pump.  The resident recognized the futility of chest compressions.

2) In the setting of tamponade, positive pressure ventilation may be fatal.  It decreases venous return.  Poor cardiac filling is the problem.  Positive pressure ventilation makes it worse.  Ventilation will not help a patient who has no circulation.  Intubation should be a last resort.  The intrathoracic pressure regulator (CirQLator, see references far at bottom) is an FDA-approved device that sucks air out of the endotracheal tube starting at end-expiration, and this may be the solution for patients who have poor venous return but need intubation.  Unfortunately, this device is not yet commercially available even though it is FDA approved.

Case continued:

At the time of the arrival of the chest surgeon much later, the patient no longer had reactive pupils and was undergoing chest compressions.

The diagnosis of myocardial rupture was considered.  The surgeon performed a thoracotomy in the ED, which revealed blood and large clots within the pericardial sac and a small anterior wall perforation. Attempts to suture the defect failed due to friability of the surrounding tissue. Open cardiac massage and aggressive resuscitation with blood products failed to achieve ROSC and the patient was pronounced dead approximately four hours after initial presentation.

Final diagnosis: myocardial rupture

The resident presented this as an "M and M" at her institution and "the sentiment was that thoracotomy in the ED in this setting would be extreme and even frowned upon," and that the diagnosis of free wall rupture is perceived to be uniformly rapidly fatal.


Early recognition and thoracotomy, best done in the OR, or even earlier pericardiocentesis with subsequent rapid OR thoracotomy, could have been life saving in this patient who was relatively young.

This is a clear case in which one or both of pericardiocentesis or ED thoracotomy would be indicated and possibly life saving.  Emergency physicians must take the lead.  Myocardial rupture must be highest on the differential.  Treatment should be simultaneous with consultation with a cardiac surgeon, and should be fluids first, pericardiocentesis if fluids do not stabilize, and thoracotomy if the patient is in a downward spiral (or if pericardiocentesis is inhibited by pericardial thrombus).

This is a good case for demonstrating that emergency medicine must make the decisions and take the lead.  One cannot wait for cardiologists or cardiac surgeons, although of course the surgeon has to agree to take the patient to the OR.  The best way to get the surgeon to agree to take the patient to the OR is if the emergency physician successfully resuscitates FIRST; then there is no choice!

Myocardial rupture:
Mechanical complications of complete transmural myocardial infarction (untreated persistent STEMI, or treated STEMI with No-Reflow phenomenon) include ventricular free wall rupture (VFWR), inter-ventricular septum rupture, papillary muscle rupture and atrial rupture. Among these diagnoses, VFWR is the most common, occurring in 1.7% of 849 patients in the Multicenter Investigation of the Limitation of Infarct Size, published in 1989.

Ventricular free-wall rupture (VFWR, commonly referred to as cardiac rupture) typically presents either as sudden cardiac death or, less commonly, with chest pain, hypotension, syncope, cardiogenic shock or obstructive shock due to pericardial tamponade. Myocardial rupture typically occurs between 1-5 days after infarct, but has been documented weeks after AMI. Rupture can also occur early.  The “rupture” may actually be more like a slow leak developing over hours to days. Diagnosis can be made by ultrasound, which may demonstrate pericardial fluid or clot with or without tamponade and may even provide visualization of the defect in the myocardial wall. Like other mechanical complications, treatment is immediate surgical repair.

Risk factors for myocardial rupture include first MI, single vessel disease, lack of collateral flow, transmural infarct (STEMI), female gender, advanced age, anterior MI, and delayed or no reperfusion. Patients treated with thrombolytics have higher rates of rupture than those who undergo percutaneous intervention, especially when thrombolytics are given 12- 24 hours after symptoms.

ECG in Myocardial Rupture

Myocardial rupture is preceded by post-infarct regional pericarditis (PIRP) in the majority of cases.  See this paper on myocardial rupture and this paper on postinfarction regional pericarditis, both by Oliva et al. (and both full text links).  

Full-thickness infarct causes localized inflammation of the epicardium (PIRP).  So PIRP is a sign of full thickness infarct, which is the harbinger of myocardial rupture. Persistently positive T-waves or premature (upright) reversal of previous T-wave inversions after STEMI is suspicious for PIRP and the patient may be at risk for rupture. (See a case of PIRP and interventricular septum rupture here:  

This case of rupture is unusual in that T-waves remained inverted.  

Temporizing measures may include pericardiocentesis and volume loading (for tamponade). Overall mortality is high, but not inevitable; there is also high intraoperative mortality.  Survival is higher when there is witnessed event, early medical intervention, and receipt of care at a facility with cardiac surgery.

In a large study, twenty-five (76%) of the 33 patients with subacute ventricular rapture survived the surgical procedure and 16 (48.5%) were long-term survivors.

At our institution (Hennepin County Medical Center), Dr. David Plummer reported in 1994 on 6 cases of STEMI that were diagnosed as myocardial rupture by bedside ultrasound in the ED.  2 of the 6 survived surgery.  This is not a uniformly fatal condition!

Aortic dissection was appropriately considered in the differential, but the patient should only undergo CT if stable.  This would be a great time to use ultrasound to look at the aorta.  ED Transthoracic ultrasound is pretty sensitive and specific.  

Transesophageal echo will be an important tool for the ED in the future.

Other mechanical complications of Acute STEMI

Interventricular septum rupture causes left-to-right shunting and symptoms include progressive dyspnea, heart failure, palpable thrill and a new holosystolic murmur (2). It occurs in an estimated 1-2% of all AMIs (2,3).  (I think this is overstated as well.)  Diagnosis is made by Doppler ultrasound, and treatment is surgical correction of the defect.  See this case.

Papillary muscle rupture is a result of posterior MI (inferoposterior or posterolateral or isolated posterior), and occurs in 1-3% of patients with AMI within 3-5 days. This mechanical defect leads to sudden onset dyspnea and acute pulmonary edema, and may also present with a new systolic murmur characteristic of mitral regurgitation.  However, the defective valve area is often so large that there is little turbulence and often no murmur.  Diagnosis is made by suspicion and then ultrasound with Doppler.  The ED treatment is intubation with mechanical ventilation and paralysis to decrease myocardial oxygen demand, nitroprusside to decrease afterload, intra-aortic balloon pump, and surgical repair.  See these 2 cases.

Learning points:

1. Include myocardial rupture in the differential for anyone with subacute MI AND persistent ST elevation, especially with tachycardia or hypotension.   Confirm with bedside ultrasound.  If pericardial fluid is found, aortic dissection should be pursued in a very acute situation. 

2. Findings consistent with PIRP on ECG, new murmur, pericardial fluid, hemodynamic instability, or acute pulmonary edema should make one suspicious of a mechanical compication to acute MI.

3. Perform bedside echo early if suspicious for these diagnoses and consult surgery immediately if echo shows pericardial fluid or clot.

4. Not all patients with mechanical complications of MI die suddenly; early recognition, stabilization and surgical repair can be life saving.  

5. Positive pressure ventilation is detrimental in tamponade.

References (CirQLator references are at the bottom):
1.   Plummer et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of Emergency Medicine. 1994 June 23;6: 1333-42.
2.     Sinikka P-S et al.  Ventiruclar septal and free wall rupture complicating acute myocardial infarction: Experience in the Multicenter Investigation of Limitation of Infarct Size.  Am Ht J 117(4):809-818; April 1989.
3.     Lopez-Sendon J et al.  Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: Sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria.  JACC 19(6):1145-1153; 1992.
4.     Sahibzada et al. Ventricular Free Wall Rupture. Journal of Ayub Medical College, Abbottabad. 2009 21;2.
5.     Moreno et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared to thrombolysis in acute MI. Journal of the American College of Cardiology. 2002 Feb 20;39 (4):598-603
6.     Smith et al. Myocardial Rupture and Postinfarction Pericarditis. In: The ECG in Acute MI. 2002 Lippincot Williams & Wilkins.
7.     Predictive factors of cardiac rupture in patients with ST-elevation myocardial infarction. Journal of Zhejiang University Science B. 2014 Dec 15;12:1048-54
8.     Wehrens et al. Cardiac rupture complicating myocardial infarction. American Journal of Cardiology. 2004 95:285-92
9.     Large transmural STEMI with myocardial “rupture” of the ventricular septum.  From: Dr. Smith’s ECG Blog.
10. Haddadin et al. Surgical treatment of postinfarction left ventricular free wall rupture. Journal of Cardiac Surgery. 2009 Nov 24;6: 624–31. 
11.   Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22:720-6.
12.   Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88:896-904.
13.     Hollander and Diercks. Acute coronary syndromes: Acute myocardial infarction and unstable angina. In: Tintinalli et al. Tintinalli’s Emergency Medicine 6th Ed. New York: McGraw-Hill.

14.     Ashfaq et al. Mechanical complications following acute myocardial infarction. Journal of Pakistan Medical Association. 2012 Aug 62;8:861-5.

CirQLator (intrathoracic pressure regulator)

This is a study I published in which we studied the use of an Impedance Threshold Device on awake, non-intubated, hypotensive patients:  

Monday, June 8, 2015

Unstable angina still exists. Beware.

A middle aged male with h/o one stent 5 years prior presented with 7 hours of continuous vague chest pressure.  During this, while he got up to walk, he had some elbow pressure bilaterally.   He took some nitro without any relief.  By the time he arrived in the ED, he stated that it was gone.

He appeared very comfortable and had a normal exam.

Here is his initial ECG:

The patient and his wife were surprised that the physicians recommended hospitalization.

An initial sensitive contemporary (not high sensitive, as these are not yet FDA-approved in the United States) troponin I drawn at 8 hours ofter onset of discomfort returned at 0.025 ng/mL (99% reference is 0.30 ng/mL; thus this level was detectable, but normal).

2.5 hours later another ECG was recorded. It is not certain whether there was any chest discomfort at this time.
What do you see?

There is now extremely subtle ST elevation in II, III, and aVF.   Even more important, there is reciprocal ST depression in aVL.  This is diagnostic of inferior MI, especially when compared with the first one.  It was read as normal.

This was not seen.

The patient was admitted for a "rule out".

At 10.5 hours after pain onset, the second troponin returned at 0.42 ng/mL. This is above the 99% reference range and indicated myocardial infarction.  At this point, another ECG was recorded:
All diagnostic findings have resolved.

These dynamic findings were not noticed.   

The patient was interviewed by the admitting physician, and stated that he had some chest pressure again.  Another ECG was recorded:
Diagnostic of inferior STEMI

The patient went for prompt and successful angiography and PCI of inferior STEMI.

Learning Points

1. This patient had angina (unstable angina) for 7 hours without developing any hint of ACS on either his ECG or his troponin.  A measurable but negative troponin is a common finding in patients without ACS, though patients with a measurable troponin do have a higher incidence of adverse outcomes than patients with undetectable levels.  See paper below.

2.  Serial ECGs are essential for patients with ACS who have persistent or recurrent symptoms, or are at high risk.

3.  The findings on the serial ECGs must be scrutinized carefully.  The change from ECG 1 to ECG 2 was real, but subtle and not noticed by very fine and well-informed emergency physicians.

4. There are those who have pronounced a requiem for unstable angina, who believe that there is no longer any such thing as unstable angina. Here are many examples to contradict this notion.

5. You may rule out MI only if all 3 of these variables are negative: a 6 hour undetectable troponin, a truly normal serial ECG, and a low risk patient, but if any one of these variables is positive, it is insufficient.  In this case. all 3 were positive: troponin was detectable, patient was high risk (h/o CAD), and the 2nd ECG was not truly normal. 

See this paper: 
         Here is a quote from the abstract: "The event rate in those with cTnI less then 0.006 g/L (undetectable) was significantly lower than in groups with cTnI 0.006 –0.04 g/L (detectable but in the normal range), 0.04 –0.10 g/L (slightly above normal), or 0.10 g/L (greater than 2.5 x the upper limit of normal)  (2.8% vs 11.1%, 24.1%, 55.1%, respectively; P 0.0001). Relative risks for the increasing cTnI cutoff groups were 3.9 (95% CI 1.2–13), 8.9 (2.4 – 34), and 25 (7.3–82) after adjustment for age, diabetes, history of hypertension, previous MI, and estimated glomerular filtration rate." 

Saturday, June 6, 2015

Very Wide and Very Fast, What is it? How would you treat?

This was contributed by one of our EM residents, Lauren Klein, with some editing by Smith.


An elderly male who missed dialysis presented to the emergency department complaining of 1 day of chest pain and shortness of breath at rest.  Upon arrival to the ED, he was awake and well perfused and neurologically intact, and this ECG was obtained:
What is it and how would you treat it?


This is a very wide complex tachycardia with a sine wave morphology at a rate of about 160 and a QRS duration of about 220 ms.  Hyperkalemia by itself can have exactly this morphology (sine wave), but should not be so fast.  On the other hand, ventricular tachycardia is fast but rarely has such a sine wave morphology with such a super wide QRS.  Thus, this is very likely ventricular tachycardia in the presence of hyperkalemia, especially as VT is a common complication of severe hyperkalemia. 

Hyperkalemia with extreme tachycardia may be present without VT in severely ill patients, as in this case (this is worth a look).  However, this patient is not extremely ill and it would be more common to have a heart rate like this one.

It would be appropriate to treat for both (use cardioversion and Calcium and Potassium shifting therapy).

Case continued

The ED providers went on to give the patient calcium gluconate, IV insulin and dextrose to shift the patient's (presumed) hyperkalemia. As they were doing this the potassium came back at 7.4 mEq/L.
The next ECG at 19 minutes later looked like this:
The rate remains very fast, but the QRS width is now about 180 ms.  
 Third ECG at 34 minutes looked identical.

Treatment of hyperkalemia will shorten the QRS duration of VT or of SVT with aberrancy.

As emergent dialysis was being prepared, the patient's mental status began to decline and the decision was made to intubate and cardiovert the patient. After intubation he was cardioverted (synchronized, 100J) with a single shock. This was his subsequent ECG.
There is now sinus rhythm at a rate of approximately 100 with RBBB and a QRS duration of 175 ms (long for RBBB, but typical for RBBB with hyperkalemia).  There is also a left anterior fascicular block.    This confirms that the previous fast rhythm was indeed a re-entrant shockable rhythm, VT vs. SVT with aberrancy.   

Smith Comment: It would have probably worked very well to shock earlier.  I would not use propofol for this, but would give a small dose of ketamine.  I believe that intubation could have been avoided if cardioversion with ketamine had been done early.

VT or SVT with aberrancy?  My friend from France, Pierre Taboulet, of, makes the accurate point that the QRS morphology of the fast rhythm has the same RBBB configuration as the sinus rhythm, so that the fast rhythm was probably SVT with RBBB/LAFB aberrancy, extra wide due to the hyperkalemia.  Thus, adenosine may well have worked!

Of note, the patient did have a baseline RBBB morphology, but, his QRS was not typically this wide. RBBB alone should have a QRS duration less than 170 ms (see this post) 

Later, after more decline in the potassium, this ECG was recorded: 
Now the QRS is still shorter, at 157 ms, more typical of standard RBBB.

The patient went on to emergent dialysis, was extubated later that day. He was discharged and is doing well. 

Wednesday, June 3, 2015

Wide Complex Tachycardia Refractory to Anti-dysrhythmics and Cardioversion.

This was contributed by Rebecca Kornas, MD, one of our EM Residents.  Edited and commented upon by Smith.

A middle-aged male with a history of CAD and two vessel CABG and ischemic cardiomyopathy (EF 20%) presented to the emergency department (ED) after an out-of-hospital cardiac arrest.  Paramedics found him in ventricular fibrillation and started mechanical CPR via the LUCAS device, five rounds of epinephrine, and delivered six unsuccessful defibrillation attempts before arriving in the ED. 

He was defibrillated into a wide complex rhythm.  There was no pulse.  Chest compressions were continued.

His initial beside echo showed moderate cardiac activity, but there were no pulses palpated initially and chest compressions were continued. 2 grams magnesium sulfate were administered, 2 50 ml ampules of 50% bicarbonate, and 3 grams of calcium gluconate were given for possible hyperkalemia. Additionally, 300 mg of amiodarone and then a single bolus of 100 mg of lidocaine were administered.

Comment on lidocaine dosing: Lidocaine, to be effective, must be loaded in several boluses.  For an 80 kg individual, give 100 mg, then give 50 mg every 5 minutes for 3 doses (total, 250 mg over 15 minutes), then start a drip at 2-4 mg/min. 
In mg/kg: 1-1.5 mg/kg, followed by 0.5 to 0.75 mg/kg to a maximum total dose of about 3mg/kg.

Clinical course continued:

His second bedside echo showed more robust activity and radial and femoral pulses were palpated. 
As femoral access was obtained to cool the patient, the first 12-lead ECG was obtained: 
What do you think?

One should err on the side of treating wide complex tachycardia as the most dangerous possible rhythm: ventricular tachycardia. Especially, in middle-aged or older patients, especially with a history of cardiomyopathy, and especially with sternotomy scars suggesting ischemic heart disease. 

The exact rhythm was not completely clear to the providers. 

However, there are several indications that the patient was in ventricular tachycardia. 

Analysis of first ECG:

There is a wide complex tachycardia at a rate of 125, with LBBB configuration (small initial r-wave in right precordial leads, deep S-wave, and upright R-wave in V6). 

Is it a true LBBB morphology?  No!  Note RS of 120 ms in V4 (black arrow below), with onset to nadir of S-wave at greater than 100 ms (all too long for normal LBBB).  Importantly, there were several fusion beats noted in lead II (see blue arrows below).  

The beats that are not fusion beats in V1 and V2 have an LBBB duration of 180 ms. Typically LBBB duration is not greater than 170 ms unless there is hyperkalemia.

Same (first) ECG Annotated with arrows:
Blue arrows point to fusion beats, which are nearly diagnostic of VT.  Black arrow points out that the QRS duration is 180 ms.

Clinical Course:

Potassium was 2.9 mEq/L, but this was not noticed.  (Comment: This may well be the etiology of the tachycardia; in refractory VT, K should be normalized to between 4.0 and 4.5 mEq/L)

The patient’s heart rate then increased to 148-152 bpm and his rhythm appeared slightly different. 

Another ECG was obtained. 
Wide complex tachycardia w/ sharp septal activation in leads V1/V2 which could suggest supra-ventricular origin. RS in V4 is still greater than 120 ms.  The entire QRS is still very wide.  From peak of r-wave in right precordial leads to nadir of S-wave is about 60 ms (equivocal).  Normal LBBB is about 50 ms.

This looks almost identical to the initial ECG, but at a different rate and with slightly narrower intervals.  Is it flutter with LBBB?  SVT with LBBB?  Or is it still VT?  Why would this VT rate be different?

Patient had BPs in 140s/90s and was perfusing. There was a discussion as to whether this was atrial flutter with LBBB, or VT. 

In an attempt to break a potential SVT, adenosine was administered via fast push: 6mg, then 12 mg, then 18 mg with no blocked p-waves or termination of tachycardia noted on rhythm strip.  Nor was flutter revealed.

Synchronized cardioversion was attempted with 150 joules —then 200 joules — then 200 joules w/ optimized placement of cardiac pads. The patient remained in this wide complex tachycardia but did have one capture beat noted transiently just after he was shocked.  

Patient was taken to the catheterization lab. 

In the cath lab, the patient was found to have patent grafts and no new lesion in his circumflex. His native RCA was 100% occluded which indicates likely scar-mediated focus of his re-entrant ventricular tachyarrhythmia. 

While in the cath lab he was given additional lidocaine and Potassium was optimized. It was around this time that overdrive pacing in the 240s was delivered, at which time the patient converted to normal sinus rhythm.  The patient was maintained on lidocaine drip in the MICU and transitioned to digoxin, carvedilol and mexiletine.

ECG after conversion to sinus rhythm. 
This is clearly sinus rhythm, and has nearly the same morphology as the 2nd tachycardia.  This suggests that the 2nd tachycardia was also supraventricular.  It is not entirely clear, but the electrophysiologist was quite certain that the tachycardias were VT.  He was not certain whether it was terminated by the lidocaine or by overdrive pacing.

The patient had an ICD placed.  He did well.

Sasaki's Rule for Diagnosing VT: 
This case does not meet all of the criteria, however, this is an interesting rule (not yet validated) to review.

1. Initial R in aVR?  If so, then VT, if not, go to 2.
2. Longest RS in precordial leads greater than 100 ms?  
                     If so (as it is in this case), then VT.  If not, go to 3.
3. Initial r- or q- in any lead greater than 40 ms?  If yes, then VT.  If no, then SVT with aberrancy.

This rule is probably too simple, and not yet validated. But it's simplicity is a virtue, too.

Learning points
1. If RS is greater than 100 ms in any lead, think VT 
2. Appreciate fusion beats. Among wide complex tachycardia, they almost exclusively (with exceptions) occur in VT.  
3. LBBB duration is typically between 120-170 ms. Longer than that should increase suspicion for possible VT or hyperkalemia.
4. Lidocaine must be given with serial boluses
5. VT that is refractory to all other treatments may be converted with overdrive pacing, which is listed in the ACC/AHA guidelines as class IIb for incessant VT.  
6.  I cannot find reports of overdrive pacing by a transcutaneous pacer, but I do not see why that would not work as well.

Other interesting VT cases: 

Wide complex tachycardia in a 36 year old

Wide Complex tachycardia: VT or SVT with aberrancy?

VT vs. SVT with aberrany: here is the sequence of analysis I (Smith) use:

Consider in the context of clinical scenario.  
(None of this applies to fascicular VT or RV outflow VT, which are associated with normal heart structure and originate in or near conducting fibers.  However, these are rare exceptions):

a. VT is more common than SVT among WCT
b. Older patients are more likely still to have VT
c. Any history of cardiomyopathy, MI, structural heart disease, or coronary disease makes VT much more likely

And then consider the ECG.  

The unifying principle of most VT (not "idiopathic" fascicular VT) is that the first part of the QRS is initiated in myocardium, NOT in conducting fibers, and thus it conducts slowly.  Therefore, the initial part of the QRS changes its voltage SLOWLY (wide).  This is what I look for to diagnose VT:

1. The longer the QRS, the more likely it is VT.  A QRS duration greater than 140 ms is likely VT, though it is not a terribly reliable differentiator.  However, a QRS duration of 200 ms is almost always VT or aberrancy with hyperkalemia.  This case is thus very likely to be VT.
2. Obvious AV dissociation?  Then VT, if not:
3. Obvious fusion beats?  If so (as in this case), then VT, if not:
4. Leads V1-V6 unidirectional (no RS or SR) and "concordant" (in the same direction)?  Then VT
5. If there are RS complexes in precordial leads (i.e., they are not concordant): is there any precordial RS that has a duration from onset of R- to nadir of S- that is greater than 100 ms?  Then VT (as in this case).
6. Abnormal LBBB or RBBB pattern (see this link for a figure from the Brugada paper):
----a normal RBBB or LBBB pattern makes SVT very likely: both have a rapid initial deflection, the r-wave in LBBB and the rS in RBBB, followed by a slowly conducting latter part of the QRS.
     a.  If there is LBBB pattern, is the initial r-wave greater than 50 ms?  Or is the onset of the QRS to nadir of the S-wave in V1-V3 greater than 60-70 ms?  If so, this is not true LBBB.  VT.  In this case, it is 100 ms.
     b. If there is RBBB pattern, is there a monophasic R-wave?  Or is the first R of the Rsr' larger than the second one?  Then VT.
7. Initial R-wave in aVR (not an r-wave, not preceded by q-wave)?  Then VT
8.  If the initial deflection in aVR is an r-wave or q-wave, is it greater than 40 ms?  If so, then VT

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