A middle-aged, obese, non English speaking man presented as a walk-in with SOB and leg swelling. His O2 saturations were 59% on room air. Systolic BP was in the 170's. He appeared to be mildly dyspneic, in no great distress, and was speaking in almost full sentences. Breath sounds were slightly distant but seemed to be clear. Pulses were full and extremities warm, but with bilateral leg edema. The patient was put on Bilevel Positive Airway Pressure [BiPAP (R)] and an immediate ED cardiac ultrasound was performed (there are 2 clips here; the RV is on the left and LV on the right of the screen):
These ultrasounds were interpreted to show a very large right ventricle (RV) and also left ventricular hypertrophy. The differential included acute right heart strain (such as pulmonary embolism) and chronic right ventricular hypertrophy (RVH). A high quality ultrasound could tell the difference between these two, but in the ED at that moment, only a bedside ultrasound without Definity contrast was available.
However, an ECG was immediately recorded:
Now the suspicion was that this patient has chronic hypoxia, such that he is not in great distress from a saturation of 59%. He likely has any one of a number of problems that cause chronic hypoxia, pulmonary hypertension, and RV hypertrophy. The possibility of a septal defect, or other defect, with right to left shunting (Eisenmenger's syndrome) was entertained.
On BiPAP with 100% O2, the O2 saturation came up to 97%, suggesting that if a right to left shunt were present, it could not be very large. Obstructive sleep apnea, with chronic hypoventilation, with hypoxia and hypercarbia and resulting RV hypertrophy, was also high on the differential diagnosis.
Finally a BP of 170/100 was obtained by manual blood pressure. The hemoglobin returned at 20g/dl, confirming chronic hypoxia. The total CO2 returned at 33, suggesting chronic hypercapnia. A venous blood gas returned with pCO2 of 66, confirming present hypercapnia.
Further history thru an interpreter was obtained: the patient had been SOB for months, worse recently, and much worse in the last day. He had no medical history and was on no medications.
Bedside ED Ultrasound of the lower legs was done and confirmed no DVT.
The patient was much better after the nitroglycerine dose reached 200 mcg/min and the BP was down to 130 systolic. Furosemide was also given.
A rapid d dimer was obtained which was only minimally elevated, effectively ruling out pulmonary embolism.
Subsequent testing revealed a previously undiagnosed congenital heart defect, with right to left shunting and Eisenmenger's syndrome, complicated by acute heart failure.
The ECG was instrumental in differentiating chronic RV hypertrophy from acute right heart strain, and helped guide therapy towards left heart failure (nitroglycerine) which could be dangerous in pulmonary embolism.
These ultrasounds were interpreted to show a very large right ventricle (RV) and also left ventricular hypertrophy. The differential included acute right heart strain (such as pulmonary embolism) and chronic right ventricular hypertrophy (RVH). A high quality ultrasound could tell the difference between these two, but in the ED at that moment, only a bedside ultrasound without Definity contrast was available.
However, an ECG was immediately recorded:
 |
| There is a large S-wave in lead I and a very large R-wave in V1. This is diagnostic of RV hypertrophy, not of acute right heart strain. |
Now the suspicion was that this patient has chronic hypoxia, such that he is not in great distress from a saturation of 59%. He likely has any one of a number of problems that cause chronic hypoxia, pulmonary hypertension, and RV hypertrophy. The possibility of a septal defect, or other defect, with right to left shunting (Eisenmenger's syndrome) was entertained.
On BiPAP with 100% O2, the O2 saturation came up to 97%, suggesting that if a right to left shunt were present, it could not be very large. Obstructive sleep apnea, with chronic hypoventilation, with hypoxia and hypercarbia and resulting RV hypertrophy, was also high on the differential diagnosis.
Finally a BP of 170/100 was obtained by manual blood pressure. The hemoglobin returned at 20g/dl, confirming chronic hypoxia. The total CO2 returned at 33, suggesting chronic hypercapnia. A venous blood gas returned with pCO2 of 66, confirming present hypercapnia.
Further history thru an interpreter was obtained: the patient had been SOB for months, worse recently, and much worse in the last day. He had no medical history and was on no medications.
Bedside ED Ultrasound of the lower legs was done and confirmed no DVT.
The patient was much better after the nitroglycerine dose reached 200 mcg/min and the BP was down to 130 systolic. Furosemide was also given.
A rapid d dimer was obtained which was only minimally elevated, effectively ruling out pulmonary embolism.
Subsequent testing revealed a previously undiagnosed congenital heart defect, with right to left shunting and Eisenmenger's syndrome, complicated by acute heart failure.
The ECG was instrumental in differentiating chronic RV hypertrophy from acute right heart strain, and helped guide therapy towards left heart failure (nitroglycerine) which could be dangerous in pulmonary embolism.
Great case and very informative.
ReplyDeleteInitially looking at the ECG, I immediately thought PE based on the right ventricular strain patterns including RAD, RVH, Incomplete RBBB, S1Q3T3, and most importantly inverted T waves in inferior/anterior leads.
I have trouble distinguishing RVH and incomplete RBBB in cases like this. It is my understanding that incomplete RBBB can be consistent with an acute PE by causing RV strain, so when I saw this EKG I though it could be consistent with PE because of incomplete RBBB, S1q3T3 (very small Q), and tachycardia.
ReplyDeleteLooking back at your other cases of acute right heart strain, I can definitely see that this is different, but I am still having trouble saying this is RVH and not incomplete RBBB.
So my questions are:
1) How do you tell between RVH and incomplete RBBB?
2) Is incomplete RBBB consistent with PE?
Pendell,
DeleteThe QRS duration in RBBB should be greater than 120 ms. Here it is much shorter (I did not report that the computer, which measures this pretty accurately, gave it a QRS duration of 103 ms). So it is not even an incomplete RBBB.
Any ECG is consistent with PE, but RBBB or incomplete RBBB is slightly more specific than other findings.
See this post for more on PE EKG findings:
http://hqmeded-ecg.blogspot.com/2012/04/cardiac-ultrasound-may-be-surprisingly.html
Steve Smith
Great case!
ReplyDeleteWhich comes back to a question which has been hunting me for a long time; how many PEs have their origin in lower extremity DVTs?
Ultraound is 99% sensitive and 100% specific so a DVT cannot be missed. But how good is that as a negative predictive value for PE?
Anybody know the golden answer?
I do not have the answer, but I doubt it is a very high percent. However, in patients who are not ill and who may have PE, absence of DVT is a very good predictor of good outcome (no further thrombus to cause trouble). There was an analysis from the 1990's of the original PIOPED study that showed that if patients had an intermediate risk VQ scan (30% of these have PE), are stable, and have no DVT, then only 0.1% died without therapy (as I recall, though that sounds impossibly low and I can't find the study now)
DeleteThanks Steve, that's very applicable then in stable patients with minimal symptoms. Still a dilemma for those coming in acutely sick or in arrest. This one I found from 2011, don't know about the reliability of the source but it's an scholar article:
ReplyDelete"A contributing factor to the failure to diagnose the disease is that the identification of the source of emboli is often elusive [2]. Clinical and autopsy studies have demonstrated the source of thromboemboli in 50–70% of cases [1]. The majority of emboli have been shown to originate in the veins of the legs, frequently at the level of the femoral and iliac veins [1]. Upper extremity venous thrombosis and thrombi in the superior vena cava, attributed to invasive procedures, may be associated with PE [1, 3, 4]. Cardiac origin of PE as from right atrial or ventricular thrombi plays only a minor role in the overall incidence of the disease [4, 5]. Demonstration of pelvic vein thrombosis as the source of pulmonary thromboemboli is rare. We have been unable to find reports of this site of origin in the recent literature and have found only one abstract of a case which reports the potential of the periprostatic plexus "
http://www.hindawi.com/crim/vasmed/2011/108215/
I would love to hear someone confirm pelvic thrombi to be benign as these are the ones I fear the most, them being relatively common especially in pregnant women who relatively often die of PE.
Dr. Smith,
ReplyDeleteAlways enjoy reading your blog, have learned a lot! I'm a second year medical student and feel like I have learned more from your blog than I have from my EKG classes.
I thoroughly enjoyed this case as we just went over cardiac imaging... and I thought that Eisenmenger's Syndrome was something that would only turn up on an embryo exam, let alone discovering it an adult pt!
Thanks for all your work and all of these interesting cases, it's greatly appreciated and I've learned a lot!
Chris
Chris, Thanks for the feedback. I appreciate it!
DeleteSteve Smith
Hi is there a way to differentiate right ventricuar strain from right ventricle nstemi on ecg]
ReplyDelete