“He looks dead,” said the other attending physician.
He did appear that way. No blood coming from the stab wound in his right upper quadrant. Just omentum and preperitoneal fat, clean and yellow. He must have been dead for some time.
Ventilated by a Combitube placed by paramedics, he had no central pulse and no spontaneous respiratory effort. But to code from a stab to the abdomen with no wound in the “box” was odd. Nurses clustered around him to place cardiac leads. “But we were talking to him on the way in,” added paramedics.
The other attending and I glance at each other; we are puzzled. That is when we heard beeping. Slow but regular. He has QRS complexes. This is pulseless electrical activity.
But what does that mean? PEA is a state without a pulse but with some form of electrical activity other than ventricular tachycardia or fibrillation. What is that electrical activity?
Just as we are not content to call all our living patients pulse-full electrical activity, we should not be content with PEA. Pulseless or pulse-full, we should specify a rhythm. Sinus tachycardia or atrial fibrillation with a pulse are two different conditions.
So too for PEA. Tachycardia with narrow QRS complexes implies a vibrant, active, and healthy His-Purkinje system delivering electrical impulses. But myocardium is contracting weakly or with a very low preload so forward flow is not palpable at the carotid or femoral artery.
Contraction may be weak in an LV that is ischemic or with little net forward flow in an LV unable to fill with volume due to external blood loss, mechanical obstruction of the pulmonary circuit, or strangulation from tamponade. All would be considered pseudoelectrical-mechanical dissociation. Electrical activity is still linked to movement of actin on myosin; it's just too feeble to be palpated. Narrow and fast QRS complexes are relatively promising.
Slow and wide implies that the Purkinje system is fatigued or nonfunctional. If the electrical tissue is too starved to transmit even a decent impulse, then myocytes must be relatively more starved: myocyte contraction requiring higher oxygen demand than simple depolarization. Slow and wide complexes are likely true electrical to mechanical dissociation: electrical activity not coupled to movement of actin on myosin. This accounts for the generally poor prognosis in PEA.
The former, pseudoelectrical-mechanical dissociation, however, may be treatable. He has QRS complexes on the monitor. They are narrow and at a rate of 60.
“It just so happens that your friend here is only MOSTLY dead. There is a big difference between mostly dead and all dead. Mostly dead is slightly alive.”
So we move, she with a right-sided chest tube and me with a left anterolateral thoracotomy incision. Optimally at a level just below the nipple line in a man, curve the incision gradually cephalad as you move posterior. Through subcutaneous tissue, breach intercostal muscle with the scalpel tip running along the superior surface of the rib. Mayo scissors can assist to take down muscle.
Once inside, no hemothorax on the left. The lung is normal. The pericardium is empty, the heart uninjured, and the LV volume feels low. The mediastinum and myocardium are not the source of PEA.
The real success with ED thoracotomy comes from the single stab wound to the anterior RV free wall. Tempered by tamponade and reparable with a horizontal mattress of prolene or silk on a tapered needle, it can be pledgeted with Teflon, or as we do in resource-poor settings, pledgeted with pericardium. I expect going in that he will not have this injury; he has no external trauma to this area. And this was not an abdominal gunshot wound in which bouncing bullets can track through myocardium.
Instead, I go with a different goal in mind.
The aorta. Clamping need not be done solely by feel, and does not require an NG tube to differentiate the esophagus. My colleague retracts the entire left lung medially, allowing clear visualization of the posterior mediastinum. The firm and rubbery aorta runs more posterior and slightly closer to me than the flimsy esophagus.
The mediastinal reflection of the pleura encases both structures, and must be opened. One can bluntly dissect anterior to the aorta using any clamp. Alternatively, pick it up with DeBakey forceps and snip it with long Metzenbaum scissors. Place a finger just anterior to the aorta bluntly to free it from the esophagus. Curve the finger around and try to re-emerge posterior to the aorta, just anterior to the vertebral bodies. Lift and snip the mediastinal reflection of the pleura here. It is more adherent posteriorly, and the hemiazygous vein runs close. Be careful, but don't worry; your patient is already mostly dead.
Once the mediastinal reflection of the pleura is opened anterior and posterior to the aorta, you have room for purchase of a vascular clamp.
He must have an IVC injury or a major laceration to multiple hepatic or renal veins to have lost pulses. We do not expect the aortic cross clamp to save his life. It cannot stop venous back bleeding from these structures, only temper arterial inflow and slow blood loss if he regains meaningful cardiac activity.
Volume pours in through a cordis; he no longer has cardiac motion, and internal compression is begun. My colleague replaces the Combitube with an ET tube, and I note better aeration of the left lung within the hemithorax.
The LV volume seems adequate. Time for epinephrine. If intracardiac, use a small gauge needle in the LV lumen. Have the internal paddles ready. The myocardium will appear as a bag of worms if he fibrillates. Vigorous cardiac activity resumes after epi. The aortic clamp bounces behind his lung: he has an aortic pulse. We feel his neck: he has a carotid pulse.
Inconceivable? Injuries to his IVC and right renal vein were addressed intraoperatively, but he lost cardiac function despite the aortic cross clamp, and did not make it out of the OR.
Aortic clamps may not make a great difference in our coding trauma patients. They mitigate arterial more than venous blood loss below the diaphragm and discourage flow down the descending thoracic aorta, persuading red blood cells to opt for coronary arteries. Unlike the more elegant intra-aortic balloon pump, the clamp cannot “deflate” during systole so afterload rises. Most penetrating arrest patients without a reparable cardiac wound will not be around long whether or not we clamp.
But for a young patient who was speaking minutes earlier and has PEA with narrow QRS complexes implying he is only mostly dead, we move.
• Just for fun: For the meaning behind this column's headline, watch this clip on YouTube: http://bit.ly/MostlyDead.
• Read all of Dr. Morchi's past columns in the EM-News.com archive.
• Comments about this article? Write to EMN at [email protected].