Two hearts.

[paramedicmike]

There is much more to this story than what is being reported. I haven't had time to look it up yet, though.

Sounds interesting.

[Eydawn]

Awesome! That's really cool. Heterotropic transplant is what they're hoping to do for my brother (hopefully I match!) for his renal failure.

Is there a journal article available on this case, by chance?

Wendy

CO EMT-B

[systemet]

Citation here:

http://www.ncbi.nlm.nih.gov/pubmed?term=mugnai%20heterotopic%20heart

Full text here / .pdf here, but I think you might need a university proxy.

http://www.sciencedirect.com/science/article/pii/S0196064411018804

A little bit about heart transplantation here:

http://www.heart-transplant.org/guide/

And here:

http://emedicine.medscape.com/article/429816-overview

[systemet]

Just had time to quickly read the original article. For those who are interested:

* The patient has had a second heart placed in the chest, on the right side, oriented 180 degrees to the normal position around the vertical axis. So the front of the donor heart faces the back, and the posterior wall faces towards the sternum. The heart is normal with respect to the horizontal axis, i.e. the apex is inferior, the base is superior (the pointy bit still points down).

* The right atria of both hearts have been opened, and sewed together, so that the IVC / SVC feed the right atria of both hearts.

* The PA from the donor heart has been sutured into the pulmonary trunk.

* The left atria are also anastomosed, so blood enters both hearts upon returning from the lungs, and the aorta from the donor heart is joined to the aortic arch, so both eject into the aorta from the LV.

In effect, there's two hearts in parallel. This patient had a AICD with biventricular pacing on the native heart.

So the guy presents to the ER, complaining of dyspnea. He's tachycardic @ 130 bpm, got some signs of failure (B/L rales, SpO2 = 86%. His ABG is ok considering -- pO2 49, pCO2 31 mmHg, bicarb = 20 mmol/L, pH = 7.42. The CXR looks pretty awesome, because there's this enormous pair of hearts in the mediastinium.

And they do a 12-lead, and it looks like a.flutter with a narrow response in the rightward leads (and arguably in lead I), and looks like coarse VF in most of the precordial leads, especially as you move leftwards.

The authors say that they didn't perform a right-sided ECG in their patient as they initially suspected a.flutter with RVR, and didn't consider fibrillation of the native heart. As the patient was fairly healthy they gave amiodarone, and even dopamine and crystalloid (dopamine seems a strange choice in light of a suspected a.flutter? But perhaps they assumed that the hypotension was from another cause, as the rate was so slow? They're not clear about this in the paper).

After an ICU admit both hearts end up fibrillating (they don't 12-lead this!) So they defibrillate, and a post-defib ECG (evidentally the electrical activity from the donor heart is preventing the AICD in the native heart from defibrillating) is obtained. Now you see a nice wide paced rhythm in the native heart, and a narrow sinus rhythm from the donor heart, that becomes more clear as you move rightward across the ECG. It appears that the pacemaker in the native heart is sensing off the sinus rhythm in the donor heart, and firing shortly (~ 200 ms) afterwards.

They also copy an image from a previous paper showing VT in a native heart. Here the entire 12-lead looks pretty much like VT. But with rightward leads, you can see hints of a sinus rhythm in the donor heart in V4R-V6R.

So the patient survives, and I guess he must have had an old pacemaker, as they state they "upgraded" his pacemaker to an implantable cardioverter, then discharged him. They make this interesting point at the end:

"Pharmacologic cardioversion is usually ineffective because of loss of intrinsic inotropy caused by end-stage heart failure; hence, the only adequate therapy is a “synchronized defibrillation” by means of a high-powered direct current shock on the left side of the chest.

In conclusion, whenever ventricular tachycardia/fibrillation of the native heart is diagnosed by ECG, immediate defibrillation is indicated, regardless of hemodynamics and clinical background."

They also note in the discussion that:

* This sort of transplant is good if the patient has severe pulmonary hypertension, and it's suspected that a normal donor heart won't have a strong enough RV to perfuse the lungs.

* It's good if the available hearts don't match the donors body size well, because you can use a smaller heart here, that wouldn't be large enough for the patient normally.

* It's becoming less common as better LVAD /BiVAD solutions are being developed.

[i would assume that this might be a mixed bag in a patient with serious pulmonary problems as well? I think it might require removing some lung tissue to make space for the extra heart, or at least will result in a loss of TLC. I haven't check this though.]