A 60-year-old male with a history of a bicuspid aortic valve presented to the ED as a transfer from an outside hospital (OSH) with a Type A aortic dissection. He had been getting ready for bed when he had acute onset severe substernal chest pain. A CT scan obtained at the OSH revealed the dissection. At the OSH, a central line and an arterial line were placed, and the patient was packaged for transport, as there was no cardiovascular surgeon available at the OSH. BP was reported to be normal before transport. En route to the ED, he developed bradycardia, hypotension, nausea, and vomiting.

Initial VS: BP 65/34, HR 50, T 36.4 °C (97.5 °F), RR 14, SpO2 91% on RA

Blood pressure measurements from the right radial arterial line correlated with BPs taken by the cuff on the contralateral arm. He was alert and oriented with a GCS of 15.


What could be the cause of the new hypotension in this gentleman with a Type A aortic dissection?


The ED team taking care of the patient was concerned about a few complications of thoracic aortic dissections in particular. They wanted to assess for severe aortic valve insufficiency, a pericardial effusion from rupture of the aorta into the pericardium, or evidence of a large wall motion abnormality causing systolic dysfunction from the dissection cutting off blood flow to one of the coronary arteries.


The ED team did not have access to the CT images yet, and they wanted to rapidly figure out the cause of the hypotension using bedside cardiac ultrasound.

Here is the parasternal long view:


You can see that the aortic root is dilated. The ascending aorta is normally <4.0 cm. You can also see the proximal intimal dissection flap. There was no large pericardial effusion appreciated in this view.


Color Doppler was placed over the aortic valve.

You can see that there is forward flow during systole. You can also see that there was some amount of aortic valve regurgitation present.


Next, a parasternal short view was obtained with strain. Strain is a measurement of the deformation of myocardial tissue from systole to diastole. In this clip circumferential strain is measured. The myocardial tissue is shorter in systole with circumferential strain, so the change in myocardium from end systole to end diastole creates a negative strain value. Why does this matter? Well, strain has been shown to be better at detecting ischemic myocardial tissue than visual wall motion abnormality scores in multiple studies.

In this clip, you can see the strain values on the right. These are all normal values, i.e., non-ischemic. You can also see that the strain rate curve is very similar for all the walls, which is reassuring.


Here is an apical-4-chamber view.

You can see there is no pericardial effusion. You can also see that the cardiac systolic function seems to be normal.


They also looked at his IVC to see if he was volume depleted or not.

His IVC appears large without respiratory variation. This correlated with his CVP readings from his central line, which were 18-20.
Here is a still of his abdominal aorta.

dissection abdomen

You can see the celiac trunk and the SMA in this view. You can also see an intimal flap.


Color flow was placed over the aorta to see if the bowel was being perfused.

You can see that there is flow through the celiac and SMA.


The patient’s labs began to come back, and his hemoglobin was stable. His lactate was only 1.5. This information was confusing to the team as these values and ultrasound images did not seem to correlate with his hypotension.


Next, the team placed a BP cuff on the patient’s leg and measured his BP there. His BP reading was in the 120’s systolic.


The CT images were then available and here is a picture of what was seen:

Screen Shot 2015-06-01 at 1.12.29 PM

There was an aortic dissection beginning at the aortic valve and extending to the level of the renal arteries. There was extension into the right brachiocephalic and the left subclavian artery that seemed to explain the hypotension in his upper extremities.


On the day of admission, he underwent surgery and had a mechanical aortic valve replacement as well as an aortic root and ascending aorta  replacement with re-implantation of the left coronary artery. He did well post-operatively.



  1. Eek C, Greene B, Brunvand H, Aakhus S, Endresen K, Smiseth OA, Edvardsen T, Skulstad H. Strain echocardiography predicts acute coronary occlusion in patients with non-ST-segment elevation acute coronary syndrome. European Journal of Echocardiography. July 2010; 11:501-508
  2. Greene B, Eek C, Sjoli B, Dahlslett T, Uchto M, Hol PK, Skulstad H, Smiseth OA, Edvardsen T, Brunvand H. Actue coronary occlusion in non-ST-elevation acute coronary syndrome: outcome and early identification by strain echocardiography. Heart. 2010; 96:1550-1556
  3. Sjoli B, et al. Diagnostic Capability and Reproducibility of Strain by Doppler and by Speckle Tracking in Patients With Acute Myocardial Infarction. Journal of the American College of Cardiology: Cardiovascular Imaging. 2009;2(1):24-33
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