Cardiology Corner: Aortic Dissection

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Nurses Edition Commentary

Kathy Garvin, RN and Lisa Chavez, RN

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Steve D. -

Another mechanism for hypotension is retrograde dissection into the coronary arteries leading to cardiogenic shock

Joseph B. -

Agree with the above comment by Steve D. I commonly hear discussion about bedside echo to look for tamponade in dissection. The absence of tamponade should not give any assurance a type A dissection is not present.

The fixation of POCUS/TTE on effusion is an overly simplistic cognitive framework here. There are a plethora of other findings we should look for - aortic insufficiency, dilation of the aortic root, dissection flap in ascending/descending thoracic aorta or abdominal aorta, and so on. The sensitivity of TTE for type A dissection in an expert sonographers hands is >80%. Given the incredibly challenging clinical diagnosis, adding to our diagnostic toolkit is prudent. With this said, if our clinical suspicion is high enough to warrant CT-a, we should not let our bedside echo delay a scan.

To the comment that an effusion is something we can do something about - pericardiocentesis here is associated with extremely high mortality and if the patient has not arrested I would favour getting the patient to the OR stat, rather than stay/play.

I am an EP, and a cardiac surgical intensivist. I have a unique vantage point of looking at Type A presentations through the retrospectiscope. The diagnosis is no doubt extremely challenging (Yes, I have missed dissections myself). However, I do often see patients with at least one or two "classic" features that get missed. Frequently this is the sudden onset of pain (but not necessarily severe), and the presence of a new murmur. Great job Amal and Anand for emphasizing these features in the 'cast. We need to keep talking about dissection, sharing stories amongst ourselves of cases we caught and cases we missed, because patients will never read the (whole) textbook.

Justin L. -

Question about the "sub-acute" and "chronic" aortic dissection. I have looked far and wide to find the answer to this question although I fear it will be one without a satisfying resolution. I have recently had two similar patients with similar presentations and suspect there may be more with the increased prevalence of endovascular repairs. Both were patients who had been diagnosed with aortic dissection, treated medically and discharged, one with plan for endovascular repair in the future. Now patient returns and has new weakness of bilateral extremities and worsening chest/back pain. Patient is tachycardic and hypertensive despite taking his home meds this morning. Do you start him on esmolol and nicardipine (if necessary)? Can you further propagate the dissection after the acute period? Do you re-CTA the aorta? Seems like an easier answer if it's new neuro findings or signs of ascending dissection, but what if they had symmetric pulses on discharge and now they are asymmetric? What if they just have recurrence of pain? CT surgery said they don't propagate and there is no change in management. This makes no sense to me, but I can't actually find evidence to support that thought.

Anand S. -

Justin - thanks for sending the note. The idea that they can't propagate seems non-sensical to me. If you haven't repaired it, propagation is definitely possible. With new/worsening pain, new neuro symptoms, I would definitely re-CTA and would consider CTA neck/brain if you thought there were stroke like symptoms going on. If they're tachy and/or hypertensive, I would treat them just as I normally would a dissection with esmolol and nicardipine/clevidipine

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