A 50-something presented in acute hypoxic respiratory failure, alert and in respiratory distress. She required Bilevel positive pressure ventilation.
Pulse was 139 and BP 99/75. She was diaphoretic.
A bedside ultrasound was done immediately:
Notice the very large RV and very small, but well functioning, left ventricle.
What do you think?
There were also B-lines (not shown).
Here is here initial ECG:
There is sinus tach. There is a large S-wave in lead I. There is a Q-wave in III. Do these indicate acute right heart strain, typical of pulmonary embolism?
No!
First, there is no full S1Q3T3 (no T-wave inversion in lead III; for significance of S1Q3T3, see notes at the bottom).
More importantly, there is also a large R-wave in lead V1. This combined with the right axis deviation (S greater than R in lead I) is all but diagnostic of RV hypertrophy (in contrast to acute right heart strain) which is a chronic condition. Notice there are also large upright P-waves in right precordial leads (though not in lead II). These are also suggestive of right atrial hypertrophy, which often accompanies right ventricular hypertrophy.
Seeing this, the probability of PE was greatly diminished. The B-lines on lung ultrasound was also very strong evidence against PE.
She turned out to have chronic pulmonary fibrosis and acute pulmonary edema. The RV enlargement was chronic.
A previous formal echo was found:
Pulse was 139 and BP 99/75. She was diaphoretic.
A bedside ultrasound was done immediately:
Notice the very large RV and very small, but well functioning, left ventricle.
What do you think?
There were also B-lines (not shown).
Here is here initial ECG:
 |
| What do you think? |
There is sinus tach. There is a large S-wave in lead I. There is a Q-wave in III. Do these indicate acute right heart strain, typical of pulmonary embolism?
No!
First, there is no full S1Q3T3 (no T-wave inversion in lead III; for significance of S1Q3T3, see notes at the bottom).
More importantly, there is also a large R-wave in lead V1. This combined with the right axis deviation (S greater than R in lead I) is all but diagnostic of RV hypertrophy (in contrast to acute right heart strain) which is a chronic condition. Notice there are also large upright P-waves in right precordial leads (though not in lead II). These are also suggestive of right atrial hypertrophy, which often accompanies right ventricular hypertrophy.
Seeing this, the probability of PE was greatly diminished. The B-lines on lung ultrasound was also very strong evidence against PE.
She turned out to have chronic pulmonary fibrosis and acute pulmonary edema. The RV enlargement was chronic.
A previous formal echo was found:
Pulmonary hypertension. The estimated peak systolic PA pressure is 60 mmHg
plus RA pressure and diastolic pressure 13 mmHg plus RA pressure. Right ventricular enlargement with distortion of the position of the interventricular septum consistent with right ventricular pressure
overload. Decreased right ventricular systolic performance. The left ventricular is relatively small with decreased systolic performance. The estimated left ventricular ejection fraction is 39 %.
There are no convincing regional wall motion abnormalities.
After therapy for pulmonary edema, she improved.
Learning Points:
In the context of hypoxic respiratory failure and a large RV on echo, the ECG can help to differentiate acute right heart strain (which can be due to acute hypoxia, especially from pulmonary embolism) from chronic RV hypertrophy.
The presence of a large R-wave in lead V1 well differentiates acute right heart strain from chronic RV hypertrophy.
S1Q3T3
S1Q3T3
This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients who had clinical findings suspicous of PE, 354 of whom had PE. They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE.
What is an S1Q3T3? Very few studies define S1Q3T3. It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV). In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), among patients with suspicion for PE, S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.
Great post and point, Steve.
ReplyDeleteAn R/S ratio > 1 in Lead V1 is a sign of chronic right ventricular strain because it takes a long time for the RV to hypertrophy to the degree that it can be easily seen on a 12-lead ECG. Now, don't get me wrong: the right ventricle can actually hypertrophy in a matter of a week or so - but not to the extent that you will be able to detect it on an ECG. It has to hypertrophy over 3 times its normal thickness before the R/S ratio in V1 is > 1 and that takes a long time. So that is the main sign of CHRONIC RV strain. Going along with that is a rightward (inferior) mean QRS axis in the frontal plane or even frank right axis deviation.
ACUTE RV strain is manifested by the RV's immediate reaction to events that greatly increase the afterload for the RV, i.e., pulmonary vascular resistance. In most cases, we are really talking about an acute PE. If the RV has not already hypertrophied, being the thinner chamber, it will react by acute dilatation. It can do that; however, the LV can't do that ACUTELY because of its muscularity. However, in dilating, the RV will stretch the right bundle branch causing a delay in conduction. This is manifested most characteristically by INCOMPLETE RBBB. Of course, complete RBBB is also a manifestation of acute RV strain, too, but the fact that iRBBB is more common suggests that in the majority of cases the stretch seldom goes quite that far.
One can see an enlarged P wave in Lead II in both cases. In chronic RV strain, the enlargement is due to right atrial hypertrophy as a result of the loss of compliance of the RV and in the case of acute RV strain, the enlargement is due to acute dilatation, just like the RV. In some cases of acute RV strain, such as a severe asthma attack, you can actually see the P waves in Lead II enlarge and then go back down once the episode has resolved.
Thanks again for a great blog. Sorry about the extra caps - I'm not shouting, I just can't bold or italicize to make a point.
Thanks for the great comments, Jerry!
DeleteHighly illustrative case (as usual) by Dr. Smith! I will add the following points:
ReplyDelete— I always like to acknowledge in my assessment when there is significant baseline artifact, because I feel this is an important limitation to interpretation that should be noted. In this case, interpretation of P wave morphology is obviously made more difficult (esp. in lead II) by all that artifact … That said, we clearly CAN interpret this ECG — and I think we can clearly identify the basic P wave appearance in the various leads.
— Even without the Echo — In a patient with acute dyspnea, this ECG strongly suggests RVH. The Echo of course totally supports that assumption.
— Although there are a number of ECG signs consistent with acute PE, no single sign is diagnostic. Instead, it is the combination of ECG findings in context with the clinical situation that may or may not suggest acute PE from ECG.
— This ECG adds a level of complexity because of the difficulty distinguishing between ECG findings suggesting chronic RVH from longstanding pulmonary disease vs acute RV “strain” that is more consistent with acute PE. Availability of a prior ECG would be invaluable in telling us which ECG findings were old (from longstanding severe pulmonary disease) vs new from possible PE …
— Findings I see consistent with RVH are: i) RAD; RAA (peaked though not overly tall P wave in lead II — but tall and pointed P wave in the anterior chest leads especially); iii) qR pattern with predominant R wave in lead V1; and iv) persistent precordial S waves (that extend to V5,V6).
— Sinus tachycardia is consistent with the presentation of acute dyspnea — but does not distinguish between longstanding pulmonary disease exacerbation vs PE.
— An S1Q3T3 pattern is not present — because there is no T wave inversion in lead 3. Clinicians often forget that all 3 components of the S1Q3T3 must be present, and they are not. Moreover, the S in lead I may simply be present as a result of the RVH and/or accompanying incomplete RBBB — so no S1Q3T3.
—The finding most remarkable for its ABSENCE is acute RV “strain”. This typically presents with T wave inversion in either anterior leads, inferior leads or both. It is absent here.
BOTTOM LINE: We have a number of findings on ECG consistent with severe pulmonary disease. While none of these absolutely distinguish between longstanding severe pulmonary disease with RVH — vs acute and/or chronic PE — vs some combination of the two — I agree that the predominant R wave in V1 AND the absence of RV strain in both anterior and inferior leads make it more likely that this ECG represents severe chronic pulmonary disease + RVH rather than acute PE ...
Thank you for another great blogpost. Can you inform me what waves I am seeing in aVF? You say this is sinus tachycardia but my eyes are tricking me into seeing 2-3 waves between every R wave in aVF.
ReplyDeleteJust a lot of artifact!
DeleteNice case! She was hypotensive at arrival. Was she treated with inotropy given the hypotension? Dobutamin?
ReplyDeleteNo. We just gave positive pressure ventilation and furosemide. Your comment prompted me to look at her outcome. She had a positive viral resp panel and was though to have viral pneumonia, not heart failure, and she did well with continued positive pressure ventilation and time.
DeleteDobutamine might be a good choice, but I would go with a pressor if I had to. Hypotension can be very deleterious to RV failure and dobutamine does not elevated BP very much if at all.
Steve Smith
Very istructive case which has refreshed my knowledge on RVH.
ReplyDeleteLet me add that there could be another ecochardiographic sign for the differential: I refer to systolic pulmonary pressure. It is much more frequent to see much higher systolic PA pressure in chronic overload than in acute situations such PE (in the latter case the RV, unless hypertrofied, is not able to produce such high pressure). Isn’t it. Many thanks.
Mario
ReplyDeleteInteresting case! I always like to start by acknowledging when significant artifact is present — because I feel this is an important limitation to interpretation that should be noted. In this case, interpretation of P wave morphology is made more difficult (esp. in lead II) by all that artifact … That said, we clearly CAN interpret this ECG — and I think we can clearly identify the basic P wave appearance in the various leads. While I essentially agree with your interpretation that the ECG favors chronic pulmonary disease — I don’t think this ECG is definitive …
Even without the Echo — In a patient with acute dyspnea, this ECG strongly suggests RVH. The Echo of course totally supports that assumption.
Although in general there are a series of ECG signs that may be consistent with acute PE, no single ECG finding is diagnostic. Instead, it is the combination of ECG findings in context with the clinical situation that may or may not suggest acute PE from ECG.
This ECG adds a level of complexity because of the difficulty distinguishing between ECG findings suggesting chronic RVH from longstanding pulmonary disease vs acute RV “strain” that is more consistent with acute PE. Availability of a prior ECG would be invaluable in telling us which ECG findings were old (from longstanding severe pulmonary disease) vs new from possible PE …
Findings I see on this ECG that are consistent with RVH are: i) RAD; ii) RAA (peaked though not overly tall P wave in lead II — but tall and pointed P wave in the anterior chest leads especially); iii) QRS appearance in lead V1 (hard to tell if we are seeing a qR pattern in V1 with a predominant R wave — or an rsR’ from incomplete RBBB given suggestion of a tiny initial positive deflection in V1 with those terminal s waves in leads I,V6); and iv) persistent precordial S waves (that extend to V5,V6).
Sinus tachycardia is consistent with the presentation of acute dyspnea — but does not distinguish between longstanding pulmonary disease exacerbation vs PE.
An S1Q3T3 pattern is not present — because there is no T wave inversion in lead 3. Clinicians often forget that all 3 components of the S1Q3T3 must be present, and they are not in this case. Moreover, the S in lead I may simply be there due to RVH and/or accompanying incomplete RBBB — so no S1Q3T3.
The finding most remarkable for its ABSENCE is acute RV “strain”. This typically presents with T wave inversion in either anterior leads, inferior leads or both. It is absent here.
BOTTOM LINE: We have a number of findings on ECG consistent with severe pulmonary disease. While none of these absolutely distinguish between longstanding severe pulmonary disease with RVH — vs acute and/or chronic PE — vs some combination of the two — I agree that the predominant R in V1 AND the absence of RV strain in both anterior and inferior leads make it more likely that this ECG represents severe chronic pulmonary disease + RVH rather than acute PE ...
How much Q wave do we need for S1Q3T3?
ReplyDeleteThe Qs in III seem really minimal in depth and width, and I would not have considered it.
The S1, of course, is quite prominent!
Brooks,
DeleteAs originally described, only 1.5 mm. This ECG has 1.5 mm!
Steve