Written by Pendell Meyers, edits by Smith and Grauer
One of my fantastic residents brought me an ECG on shift and asked for my interpretation without any context:
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| What do you think? |
I responded that it looks like chronic right ventricular hypertrophy. This is due to the QRS morphology and axis including incomplete RBBB pattern in V1, precordial R wave progression reversal, matching deep S waves in leftward leads I and aVL, very rightward limb lead axis including R wave in aVR. See Ken Grauer's comments below where he points out that the tall P-wave in lead II is diagnostic of right atrial enlargement, which supports RVH as well.
The patient was in her 80s with history of atrial flutter, congestive heart failure, ESRD on hemodialysis, who was brought by ambulance to the ED for 2-3 days of worsening dyspnea, nausea, vomiting, diarrhea, and missed dialysis due to symptoms. EMS found her in respiratory distress, hypotensive to 70/50 mm Hg, and hypoxemic to 87% on room air. No prior history of right heart dysfunction, and an echo from 4 years ago showed normal right heart function.
A bedside echo was performed and showed severe right heart strain, severely dilated right atrium and ventricle, with very poor RV EF.
CT angio of the chest showed no pulmonary embolism.
She required vasopressors and respiratory support, and was admitted to the ICU.
A formal echo the next day showed:
mild concentric LV hypertrophy
hyperdynamic LV function, EF 70%
no segmental WMAs
Right ventricle is severely dilated, systolic function severely reduced
Right atrium severely dilated, moderate TR
Pulmonary artery estimated peak systolic pressure: 67 mm Hg
Compared to the prior study 4 years ago, the right heart failure is new
Here are her ECGs from prior years, in order of time, to show her progression from normal to RVH:
4 years ago:
Please compare these examples of chronic right ventricular hypertrophy with acute R heart strain! Here they are without labels, look at each one and decide whether it is acute or chronic:
Acute right heart strain (both due to acute PE):
Learning Points:
ECG findings of RVH can include large R waves in the right precordial leads (V1-V3), deep S wave in lead I, rightward axis, incomplete right bundle branch block morphology, and a large R/S ratio in V1.
Often, the abnormal QRS of RVH will cause appropriately discordant ST deviations and T wave inversions, such as STD or TWI in V1-V3 which is explained by the RVH (rather than posterior OMI for example!).
Acute R heart strain is very different from chronic R ventricular hypertrophy.
Chronic RV hypertrophy is associated with very high pulmonary artery pressures and has extreme physiologic consequences.
Chronic RV hypertrophy with pulmonary hypertension is frequently missed by emergency physicians and, if not recognized, medical interventions (such as intravenous fluids or intubation with positive pressure ventilation) may lead to death!
The ECG is often the key to recognizing RVH, and is very helpful for differentiating acute RV strain from chronic RVH. This is important because the management differs.
See these other posts discussing RVH, mimics, etc.:
21 year old woman with CP, SOB, then syncope, and with ST depression with T-wave inversion in V1-V3
ST Depression and T-wave inversion in V2 and V3.
Young Woman with history of repaired Tetralogy of Fallot presents with chest pain
ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma
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MY Comment, by KEN GRAUER, MD (3/6/2022):
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- There is significant baseline and movement artifact. This appears to be most prominent in leads I, III and aVL — which suggests the main "culprit extremity" is the Left Arm (For review of how to quickly determine the extremity responsible for artifact — Please see My Comment at the bottom of the page in the September 27, 2019 post of Dr. Smith's ECG Blog).
- As astutely determined by Dr. Meyers — this initial ECG suggests RVH (Right Ventricular Hypertrophy).
- There are atypical features that complicate diagnosis.
My THOUGHTS on the ECG in Figure-1:
The rhythm is sinus at ~85/minute — with a PAC ( = beat #12). The PR interval is normal. Although the QRS looks to be wide in leads V2, V3 — to my measurement, the QRS is not prolonged (ie, not more than 0.10 second). The QTc is probably upper normal.
- There is marked RAD (Right Axis Deviation) — as determined by predominant negativity in lead I.
- There is a qR pattern in lead V1 — which is distinctly abnormal. Criteria for IRBBB (Incomplete Right Bundle Branch Block) are satisfied — because in addition to the qR pattern in lead V1 — there are terminal S waves in lateral leads I and V6.
- Normally, when the QRS is narrow — there should be predominant negativity in lead V1. Predominant positivity (as seen in Figure-1) — suggests the possibility of RVH, especially given the marked RAD in this tracing.
- As per Dr. Meyers — additional features in favor of RVH include the lack of chest lead R waves, with persistent S waves through to lead V6.
- Another feature in favor of RVH — is the presence of RAA (Right Atrial Abnormality). This is because the only condition in medicine that produces right atrial enlargement without also producing RVH is tricuspid stenosis. Normally, RAA is diagnosed as diagnosed by the finding of tall, peaked and pointed P waves in each of the inferior leads (at least 2.5 mm tall in ≥1 of the inferior leads). Although P waves do not strictly satisfy this criteria in ECG #1 — the P wave in lead II clearly is more peaked than is usually seen — and — pointed positive P waves are seen in leads V2 and V3, which in the context of the other suggestive findings of RVH above, is further supportive evidence of this diagnosis!
- Finally — the presence of a qR pattern in lead V1 in a patient with RVH is a marker of significant pulmonary hypertension, often with increased risk of mortality (Waligóra et al: J Electrocardiol — 50(4): 476-483, 2017).
- In my experience — this type of "fragmentation" in inferior leads is highly correlated with inferior infarction at some point in time. It certainly is not an expected finding with RVH.
- Technically — the ECG in Figure-1 shows an S1Q3T3 pattern. And, there is T wave inversion in both leads III and aVF. That said — I have no idea if this finding in the context of this ECG represents RV "strain" — pulmonary emboli at some point in time — ischemia related to inferior infarction at some point in time — or — some combination thereof.
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Below in Figures-2-thru-5 — "My Take" on the ECG diagnosis of RVH (from Grauer K: ECG-2014-ePub).
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| Figure-2: ECG Criteria for RVH. |
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| Figure-3: ECG Criteria for RVH (Continued). |
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| Figure-4: ECG diagnosis of pulmonary disease and RVH in children. |
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| Figure-5: Example tracings of RVH. |
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