Thursday, February 21, 2013

Extremely Subtle ECG, but Bedside Echo Shows Wall Motion Abnormality and Ischemic Pain Cannot Be Controlled Medically

A male in his 40's with no previous cardiac history had presented to a clinic recently with chest burning, had a nondiagnostic ECG, and was diagnosed with reflux. He presented to an ED with 2.5 hours of chest burning a few days later.  His BP was 152/84.  Here is the initial ECG:
Sinus rhythm,  Q-wave in III with minimal ST elevation and minimal ST depression in I and aVL.  There is a suspiciously minimally biphasic T-wave in V6.  This is a nonspecific ECG.

The ECG from the clinic was sought for comparison:
Compared to this one, the ST depression in I and aVL seen above is new and T-waves are nonspecifically different in diffuse leads. 

The patient continued to have chest pain of an ischemic quality. The clinical presentation worried the ED physicians, so they performed a bedside ultrasound (parasternal short axis view):

Cardiac Ultrasound Parasternal Short Axis from Stephen Smith on Vimeo.

The curved white line shows the wall (lateral) which has hypokinesis.  Note that the hypokinetic area is full thickness, not thinned out as in old MI.  Therefore, it is consistent with acute infarct.
The wall motion abnormality confirms that these nonspecific T-wave changes are indeed ischemic.  The chest pain is therefore ischemic.  The physicians attempted to control the pain with nitroglycerine, both sublingual and intravenous, titrating to 60 mcg/min, and BP down to 100/57.  Thus, they were trying to treat this "NonSTEMI" medically, as there was no ECG indication for immediate reperfusion therapy.

They recorded a posterior ECG:
Leads "V4" to "V6" are really V7 to V9.  Note the low voltage of posterior QRS because of more distance from the heart and because of air (lung) between heart and ECG leads.  Thus, only 0.5 mm in 1 lead is considered posterior  STEMI.  Here there is no ST elevation.  However, leads V2 and V3 are the same as the first ECG and the T-waves show are not very different.  Thus, the patient has dynamic T-waves.

The echo and dynamic T-waves confirm ACS.  Definite ischemic pain which is refractory to medical therapy is an indication for reperfusion therapy.  It is important to remember that approximately one third of NonSTEMI have an occluded infarct related artery at cath.

Heparin and Clopidogrel were given and the patient was taken to cath (after which the first troponin returned slightly elevated).  He was found to have severe LAD disease and an occluded 1st Obtuse Marginal off the circumflex.  This was opened and stented.  The troponin I (Ortho Clinical Diagnostics) peaked at 45.8 ng/ml (quite high).   Formal echo later showed anterolateral hypokinesis and an EF of 55%.

The artery was occluded and the myocardial territory at risk was very significant, yet the ECG did not have diagnostic ST elevation.  This is common.  Fantastic management led to rapid therapy and salvage of significant myocardium.

Wednesday, February 13, 2013

Acute Pulmonary Edema, Respiratory Failure, and LBBB

A man in his 70's called 911.  When medics arrived, he was in extremis with respiratory failure, able only to say he has a history of CHF.  He arrived in the ED and had pink frothy sputum, was intubated, and had the following ECG:
There is sinus tach with left bundle branch block (LBBB).  There is excessively discordant ST elevation in leads V1 and V2.  The highest ST/S ratio is in V1, with a ratio of 8/30 = 0.27, highly suggestive of LAD occlusion. 

In our study of coronary occlusion in LBBB, we excluded patients with severe hypertension, extreme tachycardia, respiratory failure and pulmonary edema for 2 reasons: 1) they often have false positive ECGs and 2) they need critical care in any case, with or without angiography.  So, although this patient has excessive discordance, it is not necessarily due to coronary occlusion.  In this case, the very high voltage suggests LVH, as does excessively discordant ST elevation confined to leads V1 and V2

The cath lab was activated.

After intubation, the BP was 120/70, there was a combined respiratory and metabolic acidosis, and further exam revealed absence of peripheral edema.  The patient was put on a nitro drip.  A bedside echo showed probable anterior, apical, and septal wall motion abnormality, but this is very difficult to interpret by the non-expert because of the dyssynchrony caused by the abnormal activation sequence in BBB.  

The patient was regaining hemodynamic stability and a repeat ECG after supportive care (cannot be found) showed much less ST elevation.

At angiogram, there was no acute culprit lesion, though there was some CAD and a chronic occlusion of the first diagonal.  The troponin I peaked at 10 ng/ml and the post cath ECG was recorded:
Now the highest ST/S ratio is still in V1, but is 4/35 = 0.11.  0.11 is the normal mean maximum ST/S ratio for leads V1-V4 in our control group.  So this discordant STE is now entirely normal.

At cath, there was a low left ventricular end diastolic pressure (LVEDP) at only 6 mmHg, indicating that whatever insult caused the pulmonary edema has rapidly resolved.  Then the pulmonary edema also rapidly resolved.  Subsequent formal echo showed concentric LVH, questionable anterolateral and inferior wall motion abnormalities, dyssynchrony from BBB, and EF of 37%. 

The patient did very well and was extubated the next day.

So what happened?

Was the excessive discordance on the ECG due to physiological stress of respiratory failure, pulmonary edema, tachycardia, and hypoxia (severe demand ischemia), or was there another inciting factor?

It might be better to ask: what initiated the pulmonary edema? 

1) Was it fluid overload leading to pulmonary edema, then a worsening cycle of fluid retention, catecholamines, and vasoconstriction?  Unlikely because of the absence of edema and the low LVEDP.  LVEDP caused by fluid overload does not resolve rapidly.

2) Was it transient ACS with transient ischemia, resulting in poor LV function, then temporarily high LVEDP, then pulmonary edema., then spontaneous lysis of thrombus with resolution and negative cath due to lysis of thrombus?  --Possibly.

3) Or was there a transient dysrhythmia (never recorded) that resulted in poor stroke volume, temporarily high LVEDP, onset of pulmonary edema, then resolution of dysrhythmia, then resolution of pulmonary edema?

The answer is uncertain.  However, the fact that the ECG shows acute current of injury in this case does not necessarily mean coronary occlusion, though transient occlusion or obstruction remains a possibility.  Severe demand ischemia can also cause ST elevation.  See this case.

Tuesday, February 5, 2013

Regular Wide Complex Tachycardia. What is the Diagnosis?

A male in his 40's with no previous heart history presented with palpitations.  There were no symptoms or evidence of hypoperfusion.  A 12-lead was recorded during the tachycardia:

There is a regular, wide complex tachycardia at rate of 170 bpm, with QRS duration of 124 ms.  There are no p-waves, no AV dissociation, no concordance (QRS in precordial leads are not all in the same direction).  There is inferior axis (all positive in II, III, aVF, and all negative in lead aVR.  There is an initial wide septal r-wave in V1 and V2 (greater than 40 ms).  There is a left bundle branch block morphology, except that the initial r-wave is wider than 40 ms.
What is the diagnosis?

The tachycardia resolved on its own with no therapy.  The post conversion ECG is below. 
There is lead reversal, making it appear as if there are Q-waves in leads I and aVL.  Otherwise it is normal.

Had it not spontaneously converted, what therapy would be appropriate?

Answer: this is RVOT, right ventricular outflow tract ventricular tachycardia, and it is usually sensitive to adenosine.  (I have been waiting for a case of this for years, and here it is!)  This is one of the "idiopathic" (though no longer actually idiopathic) VT types that occur in the absence of structural heart disease.  They generally have a relatively narrow QRS, less than 140 ms, whereas most VT has a QRS greater than 140 ms.  Here is a fine article discussing these and other types of VT in the absence of structural heart disease.

Adenosine would be appropriate here, as it generally is for regular, monomorphic, wide complex tachycardia, as long as you recognize that not all wide complex tachycardia that converts with adenosine is SVT with aberrancy.  This is the exception to that rule. In other words, conversion with adenosine does not prove SVT.  

The 12-lead ECG in RVOT VT has

1. LBBB pattern
2. wide septal r-wave
3. Inferior axis. 
4. The transition from S-wave to R-wave in the precordial leads depends on how far anterior (RV outflow tract vs. LV outflow tract) the origin of the VT is.

Here is a short quote from the article:

"Patients may be asymptomatic but often present with palpitations, chest pain, dyspnea, presyncope, and even syncope. In general, Outflow Tract Arrhythmia occur more frequently with exertion or emotional stress, and may have a diurnal variation. Women may have an increase in symptoms related to changes in hormonal status. In general, the prognosis of truly idiopathic OTA is benign.  Long-term follow-up studies have provided evidence that the vast majority of patients do not develop structural heart disease or SCD. However, as already noted, a small percentage of patients with very frequent VAs may have LV dysfunction over time, and rare reports have documented cardiac arrest and Polymorphic VT in patients who were initially thought to have “benign” Outflow Tract Arrhythmia."

Here are 2 more relevant posts, which include the approach to wide complex tachycardia: 1)  SVT with aberrancy  2) verapamil-sensitive posterior fascicular VT

Saturday, February 2, 2013

Right Bundle Branch Block with ST Elevation in V1?

There is a wide QRS with a tall R-wave in aVR and V1 and wide S-wave in lateral leads, leading one to believe this is RBBB.  There is ST elevation in V1, and ST depression in V4-V6, suggestive of ischemia/MI.   What is the Diagnosis? --see Below

This is a classic pseudoinfarction pattern -- hyperkalemia, with K of 6.9 due to DKA (pH 7.12, bicarb 6).  In this case the diagnosis was easy because the patient presented very ill with known Type I diabetes and with vomiting, not chest pain.

However, here are two from my files that presented with chest pain:

The peaked T-waves give it away, but the ST elevation in V1 and V2 is a little known pseudoinfarction pattern.  There was no MI here.

Thanks to K. Wang for this EKG.  Again, there was no MI, only hyperkalemia.

In all 3 of these cases, the findings disappeared with treatment of hyperkalemia, and the ECG normalized.