It’s a hot summer’s day and you are working a busy shift in the Minor Care unit of a community ED when a 31 year-old man presents with a chief-complaint of shortness of breath (SOB).
He states that he has been feeling SOB on exertion for the past 3-4 weeks, having attended the walk-in two weeks prior with the same complaint. There he was diagnosed with asthma and given an albuterol MDI, a course of PO steroids, and also a course of PO azithromycin “in case it was something more.” His symptoms had not improved so he decided to attend the ED for another opinion.
From the doorway you see a moderately overweight (5’9” 200#) Caucasian male in no acute distress. He is exhibiting a normal respiratory rate with no elevated work of breathing. His skin is warm and of normal color, but upon closer inspection you’re a bit surprised to notice he is actually moderately diaphoretic. He chalks it up to the outside temperature of 90 F, but it’s a chilly 70 F in the department and he’s been seated in bed for at least 20 minutes. “Hmmm,” you say to yourself.
Vital signs at rest are as follows: HR 115 bpm, RR 20/min, BP 122/68 mmHg, Temp 37.1 C.
On auscultation he has a bit of bi-basilar rales.
After obtaining a history, you head back to your desk to enter some orders when you see that an ECG and CXR were already performed at triage.
[http://sonocloud.org/files/photos/1373606099f1a0ab_o.jpg]
The ECG shows sinus tachycardia, left-atrial abnormality, left-axis deviation, poor R-wave progression, large S-wave in the right-precordial leads, and secondary ST and T-wave changes. This picture is consistent with left-ventricular hypertrophy.
http://sonocloud.org/files/photos/13736928941892d4_o.jpg]
The CXR was read by radiology as “mild-to-moderate cardiomegaly, new from prior film (2 years ago), consider pericardial effusion.”
This Minor Care case is starting to get a bit more complicated and you’re beginning to wish you had seen the patient with chronic low-back pain instead. Not quite sure what to make of this patient’s presentation and afraid of backing up the whole department while you try to make a hard-sell on this young, otherwise healthy patient to cardiology, you instead grab your trusty ultrasound machine and head for the bedside. Here is what you see.
[http://sonocloud.org/watch_video.php?v=NAHA61SSH3B7]
In this apical 4-chamber view, you first notice that all four chambers are markedly dilated and hypokinetic. Looking specifically at the left-ventricle, it exhibits with severe hypokinesis throughout, maybe with a touch of apical akinesis. Looking closely at the apex of the LV also shows that there is an apical mural thrombus, often seen in patients with akinesis or severe hypokinesis of that region.
[http://sonocloud.org/watch_video.php?v=SG794W7MBYBG]
As evidenced by the obvious blue jet in the left-atrium, this color-Doppler image of the mitral valve demonstrates significant mitral regurgitation. At formal echocardiography it was graded as “moderate, 2+ mitral regurgitation.”
[http://sonocloud.org/files/photos/1373605496135c3c_o.jpg]
This pulsed-wave Doppler image shows monophasic flow through the mitral valve with a nearly absent A-wave. This proves that in addition to systolic dysfunction, the patient has significant diastolic dysfunction as well in a restrictive pattern.
[http://sonocloud.org/watch_video.php?v=SK85U7KAMSW1]
Here is a mid-ventricle parasternal short-axis view that further demonstrates the global hypokinesis of the left ventricle. It is also clear that the ventricle is large and dilated, but not hypertrophied. In this patient’s Cardiology echo, his ejection fraction was estimated in the range of 10-15%. I’m an inexperienced echocardiographer, but in addition to global hypokinesis I might specifically see some anterior-wall akinesis here as well.
[http://sonocloud.org/watch_video.php?v=KGUYWXGR2YG2]
This parasternal long axis view offers a final example of the patient’s global hypokinesis, along with a nice shot of the mitral valve. The aortic valve is also in view, but not clearly seen. Notably there is also no sign of pericardial effusion, often visible in this view if present.
So what’s our final impression? Summarizing all of the specific findings listed above, this patient has a dilated cardiomyopathy. While the workup and management of this patient could encompass a week’s worth of posts, here are the main take-home points from this case:
- Beware patients who are diaphoretic or tachycardic at rest. Afebrile and in no acute distress, it became essential to find a source of this patient’s few abnormalities on physical exam.
- Don’t be afraid of ultrasound in the Minor Care department. We like to talk a lot about the utility of ultrasound during a patient’s resuscitation, but it can be equally useful in an ambulatory setting as well.
- Bedside ultrasound expedites care. Without bedside ultrasound this patient would have been waiting around hours (or days) for a formal echo, if it was going to be performed at all.
- Sell! Sell! Sell! In most circumstances cardiology would have been very reluctant to come see an otherwise healthy 31 year-old patient, but in this case the bedside images provided immediate and definitive proof that the patient needed specialty care. It also probably gained us some street-cred with the cardiologist who could look at the saved images right in the department.
- Shoot first, ask questions later. In a case like this, there is no need to perform an extensive interpretation of your images at the bedside. From the very first view it was clear the patient had a dilated cardiomyopathy, so cardiology was immediately paged and the patient was readied for admission. During that time additional views were quickly obtained for later evaluation, but that first shot told us all we needed to know to make a disposition on the patient.
As an ECG nerd, I liken it to reading the tracing of a patient with a profound wide-complex tachycardia. At the bedside there is rarely any need to get too fancy differentiating VT from SVT with aberrancy since the WCT algorithm is safe and effective for both, but once the patient is stabilized I can then go back and look for signs of AV-dissociation on the ECG to really prove it was VT.
You think I noticed the apical thrombus in this patient’s AP4 view? No-way! That’s something Mike Mallin of the Ultrasound Podcast picked up for me when I shared the case with him. I didn’t even know how to read a pulsed-wave Doppler at the time I met the patient, but I knew how to capture the image at the level of the mitral valve so that I could review and learn from it later.
Anyway, thanks to bedside US (and you!) this patient ended up having his dilated cardiomyopathy recognized and promptly treated. Without these surprising images there’s a really good chance this patient would have been symptomatically treated for his SOB in the ED and then discharged back home. If anything, being able to reference these clips gave our emergency physician a very strong card to play in getting cardiology to take the case seriously.”
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Thank you for for answers Vince.
Best
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Very interesting case. Altough is clearly evident LV size and function, RV don´t look good in size and function. It will be good to obtain a color doppler of TV to look for Tricuspid regurgitation and with CW calculate systolic pulmonary artery pressure (sure an indicator in this patients of elevated LV-LA filling pressures). One thing about doppler in echocardiography: “never use corrected angles” (in this case is 22°). 0 degrees always. Very nice restrictive pattern in transmitral flow, but is important to remember that in young people with good systolic function the pattern is very similar (“supernormal pattern”) because a great gradient exist between suction forces of a well functioning LV and LA. Not sure about thrombus.
Etiology was know? (myocarditis? idiopathic?)
Best
PB
Dear PB – thanks for your comment and I agree – both the RV and the LV do not look “healthy” – dilated cardiomyopathy was the final diagnosis and Ill allow Vince to add any additional info that he has on his case.
Thanks for the great comment! At the time of the patient’s presentation I had probably only done a couple dozen abbreviated echo’s (basic 2D views), so go so far as to attempt Doppler on the mitral valve was something I only understood as a basic concept. It was only after seeing the patient’s formal echo where they obtained similar results that I thought my own attempt might have been worth posting. Great point about the use of corrected angles as well; at the time I was yet again not entirely aware of what I was doing in that regard.
Regarding the mural thrombus: it was rather subtle and doesn’t show up great (?at all) in the above clip, but could be visualized better on a couple of other apical views.
The patient left the community hospital where he presented with a diagnosis of idiopathic CM, but I’m not sure if more extensive specialty outpatient testing and likely genetic investigation revealed a cause.