no capture......

[OVeractiveBrain]

The gentleman was placed on a crapload of LR. His potassium level was probably through the roof. Potassium controls the inward hyperpolarizing current in cardiac as well as skeletal muscle. This means, at high levels of K, the inward hyperpolarizing current dominates the open potassium channels. This manifests itself in profound bradycardia, increased irritability (especially after 5 hrs of administration and an already apparent MI). Hyper K can also be noticed by a flat P wave and Heightened T waves.

If it were not HyperK the fact that he had potassium administered at all with crushing chest pain was a mistake. By the time you found him he was probably so badly infarcted it as too late. Remember that the heart will respond to infarct first by increasing heart rate to compensate for the lack of 02, then wear itself out faster. If you caught this guy in the latest stages of an evolving MI, the tissue was so badly necrossed that no matter how much electricity you put across him, there would not be enough live tissue to contract. Atropine and TCP are the recommended therapies, but if the prison put a CP pain on ringers and told to wait it out, they sentenced him to death right then and there. Even with an increaed fluid challenge and all the medications you have, again, the heart was so badly damaged that it was too late.

IN response to above comment about atropine use: If the patient is bradycardia as a RESULT of an MI, hes dead. Hes in the final stages of the MI and you can watch him die. If the MI is the result of bradycardia, you an save that person with atropine and TCP. Without an excellent history, the only way to tell the two apart is to give them the atropine. Should it make the MI worse, then you havent lost much, PCI or fibrinolytics are still indicated, and hes still circling the drain (just as he was before). If you make teh MI better, you save him. Most protocols are pretty straight forward when it comes to hypotensive bradycardia = Atropine and TCP, unless a high degree block is noted, in which case TCP is the best choice. Note that Atropine can cause rapid atrial rate, while the AV conduction system may overload and fail to conduct (or conduct less frequently than at the atrially bradycardic pacer).

Other electrolyte imbalances or sugar can be ruled out. His sugar was in the 100s, hypocalcemia results in often spastic muscle contractions prior to electrical conduction problems. Hyper K can be seen on the ECG as above. Hyponatremia should not be expected unless their was profound weight loss, diarhea or vomitting. If he were on any meds that slowed the heart, you probably should have known about them and treated them accordingly (Glucagon for B-blocker, Calcium Gluconate / Chloride for Ca++ channel blockers)

That being said, pad placement or user error is most often the problem when it comes to electricity and monitors. However, given this patient, I would be confident in saying that you more than likely did everything right, this guy was a gonner before you even got there.

-OveractiveBrain