The response I got was immediate. The double doors of my recovery room boomed
open and six OR nurses came flying through. Overhead the call for anesthesia stat to PACU rang out. My poor
coworker who had gone next door for coffee, came running behind with a shocked expression on her face. I
can only imagine what my face looked liked. They were asking what happened. I hadn't a clue. By this time
the patient's respirations began to deteriorate and her heart rate started dropping to the 40's then the
30's. The code cart had been brought to the bedside. I've been ACLS certified for a couple of decades and
asked for atropine, since anesthesia had not shown yet. We went ahead and called a hospital code Blue also.
Usually in most recovery rooms anesthesia handles our codes, but by doing this I was assured that the ER
doctor would be coming immediately also.
The anesthesiologist came in at that time and I relayed the events that had
occurred and verified the okay for atropine to be given. I thought of the Ancef that I had just given prior
to this and conveyed a concern of a reaction. The atropine was given and the heart rate had increased to
the 60's. Fluids were wide open and we were ambuing the patient with 100% oxygen. The code team then
arrived with the ER doctor. Although the patient had a pulse, it was weak and thready and almost
indictable. We were unable to get a blood pressure at this time. PEA was determined and we begin CPR. I use
the older term PEA which stands for pulseless electrical activity of the heart. The newer term is EMD,
electromechanical dissociation. This means that although the electrical activity that regulates the heart
to beat is working, the heart itself physically is not. This generates no cardiac output thus no blood
pressure. There are many causes for this to happen and we had to figure out what it was and
fast.
There must have been 20 doctors and nurses in my tiny PACU at that moment. As
the Code Team took over, I started to feel a little shocky myself. I was desperately trying to rule causes
out in my head. I was glad the ER doctor was there because he immediately started thinking hypovolemia and
hemorrhage. He called for the ultrasound machine stat from the ER. We drew labs and an ABG. About that time
in came the Podiatrists who had worked on her foot. When they saw the events that were occurring they
causally mentioned that the patient did have a history of a small 4 cm aortic aneurysm.
Ding, ding! The bells and whistles started going off in my head about that
soft statement that my patient had made to me abut her stomach hurting. The ultrasound machine arrived at
that time and confirmed a rupture in the aortic artery. Blood arrived, thanks to the ER doctors foresight,
and we began pouring it in. We then obtained a blood pressure and pulse not to long after. We stopped CPR.
Amazingly enough the patient then woke up and ask what happen. An OR room was prepared for surgery. At this
time, though in a small hospital we had no vascular surgeons or cardiac surgical units. Our general
surgeons explained this to the family and the unlikely success of them attempting it. The family agreed and
the surgeon requested a transfer to a larger facility. The patient was stabilized in the PACU then sent to
the ICU. Unfortunately, she coded and passed away before she could be transferred.
As a seasoned recovery room nurse, I questioned why this had happened at that
precise moment in my recovery room. This was just a simple foot case. The other nurses told me it was just
fate. It could have happen on the street. Had not allowing her to urinate earlier have caused it? Everyone
says no, but I always wondered. I like telling this story to other nurses, especially the younger ones.
This taught me to look outside the box and PACU for the answers. I was so grateful to our ER doctor's
observations. It reminded me how important it is to keep an open mind and rule out the causes for PEA. It
will guide you to the right conclusion and treatment.
As a reminder to all, the causes of PEA also known as EMD (electromechanical
dissociation) are as follows according to the American Heart Association ACLS standards: Hypovolemia,(which
is the most common cause), hypoxia, hypothermia, hypokalemia, cardiac tamponade, tension pnemothorax,
massive pulmonary embolism, coronary thrombosis, drug overdose (tricyclics, digoxin, Beta blockers, calcium
channel blockers), acidosis (usually preexisting), and an acute massive MI.
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