This is a middle-aged male with h/o with a history of heart failure with severely reduced ejection fraction due to dilated ischemic cardiomyopathy (EF 5-10%), probably with some component of non-ischemic cardiomyopathy, with h/o CABG, who is status post ICD placement (and previous appropriate shocks for VT) and biventricular pacer ("cardiac resynchronization therapy"), who is on amiodarone for VT suppression, and has h/o LV thrombus and is on chronic anticoagulation with warfarin.
He presented for paroxysmal nocturnal dyspnea that didn't resolve with use of his home prn diuretics. He was hypoxic and required oxygen in the ED.
He had no chest pain.
Prior coronary angiography/revascularization: LAD 40% proximal, 80% mid and 90% distal stenosis; circumflex 70% proximal circumflex; ramus 100% occluded; RCA 90% occluded.
Here is the most recent previous ECG from 6 months prior:
This change in ST segments suggests coronary occlusion, even if it does not meet the full 25% criteria.
Is there acute coronary occlusion (Occlusion MI, or OMI)?
I performed a bedside ultrasound:
Parasternal long axis:
Parasternal short axis:
Apical 4 chamber:
When I saw this patient, my impression was one of acute decompensated heart failure, not due to acute MI. Important to this was the absence of chest pain.
Comment: Given his systolic function, it is amazing he is not in shock. Why is this? A patient with a healthy heart who has sudden large STEMI may go from EF 65% to EF 30% and be in shock, yet this patient with EF less than 10% is NOT in shock. But EF % is a percent of some end diastolic volume. Patients with terrible cardiomyopathy have very large distended hearts. If the end diastolic volume is 300 mL, then 10% of 300 results in a 30 mL stroke volume, just as with the previously healthy STEMI patient, in whom 30% of 100 mL = 30 mL stroke volume. Furthermore, patients with chronic heart failure have faster lymphatic drainage of pulmonary interstitial fluid, and so it takes even higher pulmonary pressures to result in pulmonary edema.
Looking at this case now, I must concede that an uninvolved observer (i.e., reader. i.e., you!) might think this:
"This patient with known CAD presents with SOB and hypoxia and has new excessively discordant ST Elevation and terrible myocardial contractility and you did NOT want an angiogram! I am confused!"
But I know how acutely decompensated heart failure in severe cardiomyopathy distorts the ST segments on the ECG, and I just did not think this represented acute occlusion MI (OMI).
Furosemide was given intravenously, after which the patient rather quickly improved.
His NTproBNP was 22,000 (very high).
Troponin I were slightly elevated but unchanging, consistent with chronic myocardial injury that is typical of severe cardiomyopathy.
0.054 ng/mL
0.065
0.059
0.049
Here is an ECG from 8 days later:
I have shown at least one prior case in which acute decompensated heart failure in a patient with severe cardiomyopathy and paced rhythm resulted in false positive Smith Modified Sgarbossa criteria.
He presented for paroxysmal nocturnal dyspnea that didn't resolve with use of his home prn diuretics. He was hypoxic and required oxygen in the ED.
He had no chest pain.
Prior echocardiographic study: (1/9/2017) LVEF is 10%, regional WMAs: distal septum anterior and apex, inferior and anterolateral; left ventricular enlargement and concentric hypertrophy; Severe decreased right ventricular systolic performance; no significant change compared to previous.
Upon arrival to the ED, he was hypoxic, but readily responded to oxygen.
An ECG was recorded:
 |
| Biventricular Paced Rhythm, rate 60 QRS = 265 ms, QT = 587, QTc = 610 (See two spikes approximately 40 ms apart, with large R-wave in V1 confirming LV pacing in addition to RV -- LV pacing results in RBBB configuration with large R-wave in V1) There is much discordant ST elevation, especially in I, aVL, V3-V5 V4 = 7/30, almost 25% aVL = 3-4/17, = 17-24% Is this coronary occlusion? |
Here is the most recent previous ECG from 6 months prior:
 |
| Biventricular paced rhythm, rate 75, with PVCs More proportional ST discordant ST Elevation Computer measures QRS at 209 ms The discordant ST elevation is of lower proportion. |
This change in ST segments suggests coronary occlusion, even if it does not meet the full 25% criteria.
Is there acute coronary occlusion (Occlusion MI, or OMI)?
I performed a bedside ultrasound:
Parasternal long axis:
Extremely severely reduced ejection fraction
There are profound wall motion abnormalities, but seem to correspond to the old echo.
There are profound wall motion abnormalities, but seem to correspond to the old echo.
Parasternal short axis:
Again, extremely poor EF and regional wall motion abnormalities.
Apical 4 chamber:
Terrible systolic function
Notice that although he has a paced rhythm, there is very little "dyssynchrony" because the biventriculaer pacer paces both ventricles simultaneously.
A typical pacemaker is right ventricular, and so because RV pacing activates the RV before the LV, RV pacing results in dyssynchrony that is similar to left bundle branch block.
Notice that although he has a paced rhythm, there is very little "dyssynchrony" because the biventriculaer pacer paces both ventricles simultaneously.
A typical pacemaker is right ventricular, and so because RV pacing activates the RV before the LV, RV pacing results in dyssynchrony that is similar to left bundle branch block.
When I saw this patient, my impression was one of acute decompensated heart failure, not due to acute MI. Important to this was the absence of chest pain.
Comment: Given his systolic function, it is amazing he is not in shock. Why is this? A patient with a healthy heart who has sudden large STEMI may go from EF 65% to EF 30% and be in shock, yet this patient with EF less than 10% is NOT in shock. But EF % is a percent of some end diastolic volume. Patients with terrible cardiomyopathy have very large distended hearts. If the end diastolic volume is 300 mL, then 10% of 300 results in a 30 mL stroke volume, just as with the previously healthy STEMI patient, in whom 30% of 100 mL = 30 mL stroke volume. Furthermore, patients with chronic heart failure have faster lymphatic drainage of pulmonary interstitial fluid, and so it takes even higher pulmonary pressures to result in pulmonary edema.
Looking at this case now, I must concede that an uninvolved observer (i.e., reader. i.e., you!) might think this:
"This patient with known CAD presents with SOB and hypoxia and has new excessively discordant ST Elevation and terrible myocardial contractility and you did NOT want an angiogram! I am confused!"
But I know how acutely decompensated heart failure in severe cardiomyopathy distorts the ST segments on the ECG, and I just did not think this represented acute occlusion MI (OMI).
Furosemide was given intravenously, after which the patient rather quickly improved.
His NTproBNP was 22,000 (very high).
Troponin I were slightly elevated but unchanging, consistent with chronic myocardial injury that is typical of severe cardiomyopathy.
0.054 ng/mL
0.065
0.059
0.049
Here is an ECG from 8 days later:
 |
| Computer measures QRS at 276 ms Less ST deviation. |
I have shown at least one prior case in which acute decompensated heart failure in a patient with severe cardiomyopathy and paced rhythm resulted in false positive Smith Modified Sgarbossa criteria.
Massive Excessively Discordant Anterior ST Elevation in a Paced Rhythm
Learning Points:
1. Acute Heart Failure in patients with paced rhythm and extremely low ejection fractions can distort the ST segments.
2. Acute MI may present with only SOB, but the pretest probability of chest pain is far higher than that of SOB.
3. There are several entities that were excluded from the studies on Modified Sgarbossa Criteria: Tachycardia (because it results in higher ST segments), Respiratory Failure (also distorts the ST segments, and one does not need an ECG to know they are critically ill), Diastolic BP greater than 120, and Hyperkalemia.
1. Acute Heart Failure in patients with paced rhythm and extremely low ejection fractions can distort the ST segments.
2. Acute MI may present with only SOB, but the pretest probability of chest pain is far higher than that of SOB.
3. There are several entities that were excluded from the studies on Modified Sgarbossa Criteria: Tachycardia (because it results in higher ST segments), Respiratory Failure (also distorts the ST segments, and one does not need an ECG to know they are critically ill), Diastolic BP greater than 120, and Hyperkalemia.
interesting. and very clear presentation.
ReplyDeletedo you recall what the initial BP was, steve? just heard a Mattu lecture from 2018 EEM on recent evidence of benefit of very high dose NTG (like 2000mcg repeated for total of three doses, or IV drips of 100-400 mpg/min), with significant benefit and little downside.
i realize treatment is not the point here, but rather one can have an acutely decompensated HF patient, paced, with an ugly Sgarbossa-ish ecg, which is not an OMI, and does not require stat cath.
thank you, steve.