chbare

Possibly; however, one of the concerns with beta blockade and Cocaine MI is the fact that we could precipitate unopposed alpha stimulation. As we know many vessels are stimulated via alpha receptors. Hence, the alpha effects and increased PVR when we talk about the alpha effects of medications such as norepinephrine. Remember, people with cocaine related MI can have "normal" coronary arteries without the typical evidence of CAD. The cause of the MI differs from say a plaque that ruptures triggering the clotting cascade and occlusion. If we have unopposed alpha stimulation, we can actually cause coronary vasospasm or worsen existing spasm. With that in mind, is there a beta blocker that may have more desirable effects? Obviously, this is more theoretical as people generally caution against using any kind of beta blockade. Take care, chbare.

So, just for some additional pharmacology review, which beta blocker could we consider using? Take care, chbare.

Something to consider; however, think about a class of medications we frequently give to MI patients. In fact, it is considered a core measure for MI management within the hospital. Take care, chbare.

Think about another class of medications used frequently in the management of MI. Consider what happens if we were only to block specific receptors in the setting of cocaine induced MI. Also consider the cause of the ischemia. Are we dealing with an actual occlusion or vasospasm in some cases? Take care, chbare.

I assume we are talking about a left shift? Segs, bands, or a manual differential available? Abdominal exam: tenderness, referred pain, bruising, pulsatile masses, etc. Do we have a KUB/flat plate, AAS, or any type of abdominal/pelvic radiography? Not that we would usually find perforation or bowel obstruction on a KUB. Look for air under the diaphragm and for signs of bowel obstruction or perforation. How is his neurological status? Any neck pain? Does he describe the headache. Pupils and EOM's? Is photophobia present? Is the cranial nerve exam intact? Somebody mentioned doing a LP. What do we need to rule out prior to performing a LP? Take care, chbare.

I opened the image by it's self in another window. Looks like a snopes broken penis picture. First, if anybody believes that a bony structure is used to achieve and maintain erection, they have a serious deficiency in the A&P department. Theoretically, if this was a case of a foreigh object, we could not do much. Assess the genitals, look for blood at the meatus, keep it from moving, and transport as this would be a urological emergency. Vessel and perfusion disruption, hematoma formation, and urethral injury would be serious consequences the said injury. Obviously, placing a urinary catheter would not be a priority intervention. Take care, chbare.

Exactly, any time you have a situation where hypoxia develops (hypovolemia, decreased hgb, etc) , cardiac stress is a given. I have seen young health people sustain significant myocardial insult as a result of stress conditions. Cocaine abuse, amphetamine abuse, and heat related injuries are among the top of the list. i see no problem with obtaining a XII lead provided time and situation permits. Take care, chbare.

Another concept to consider: Anytime we have a hypovolemic patient, that patient is essentially having a stress test. Depending on the situation, a XII lead would in fact be an important part of the assessment. Take care, chbare.

Shameless, I know. Take care, chbare.

The "Golden Hour," what a magnificent farce. From what I can tell, it was a really neat concept that grabbed medical providers and the public's attention, resulting in funding for somebody's pet project. Something to do with buying cool new helicopters for a hospital. :wink: Take care, chbare.

Looks like we nailed the diagnosis. As mentioned earlier, commotio cordis is the diagnosis. However, this problem is very different from say thoracic trauma that causes a myocardial contusion? What are some of the defining characteristics of commotio cordis? Does ventricular fibrillation occur because of direct myocardial insult? Take care, chbare.

I must apologize. Somebody asked about an echo and chest x-ray and rationale for the procedure. The echo is normal. Normal wall motion, normal valve motion, and normal left ventricular ejection fraction. The chest x-ray is normal. The heart is not enlarged and no pulmonary abnormalities are noted. Take care, chabre.

No known history. XII lead is unchanged from the prior post. Vital signs are stable. With the information on hand, does myocardial contusion seem likely? Take care, chbare.

So, what does everybody think? Lidocaine or amiodarone following successful defibrillation? We need to consider the risks and benefits of giving these agents. One of the goals following ROSC is to try to stabilize cardiac activity. Did the patient's cardiac activity stabilize without the use of agents rather quickly? While I will not say you are incorrect in giving agents, do we need to give every V-fib arrest these agents? Can we actually monitor and provide supportive care? A little "benign neglect" perhaps? Tox screen is negative. Blood Glucose is : 116 mg/dl. He remembers taking an elbow to the chest prior to "passing out." No history of caffeine intake or energy drinks. At this point can we assume it may be related to the blow? If that is the case, what problems can we rule out? Myocardial contusion vs tamponade vs commotio cordis vs congenital problem? Can we rule any of these in our out? What criteria can we use to identify the problem and rule out other problems? Take care, chbare.

XII Lead Heart tones: S1 S2 no murmur, gallop, rub, etc. What are you looking for with the ABG? What are you looking for with the Chemistry? Cardiac enzymes are negative. What imaging do you want and what are you looking for? Healthy kid, no medical history, normal if not a bit on the athletic side regarding build. Neuro exam is unremarkable. Take care, chbare.

No problem considering the DDX. Just challenging everybody to think and research hopefully. All the considerations thus far should be ruled out. Now that we are in the ER, how will we further investigate and treat this patient? Most of you have a pretty strong working diagnosis, how will you go about proving or disproving your suspicions. As far as the bicarb issue: No problems, just challenging you to research and learn. With acidosis, it is very easy to get ourselves trapped into the give bicarb mentality. However, consider the following. Acidotic hearts do not like to respond to therapy. This patient had rather quick ROSC following one defibrillation attempt. The down time was three minutes, with a witnessed arrest (bystanders at least), and immediate CPR. This is a situation where we may not see significant acidosis. In addition, what are some of the complications associated with bicarb therapy? Could these complications in fact prove to hamper our resuscitation efforts? The precordial thump has fallen out of favor these days. No definitive evidence saying it is a helpful procedure. Some reports of it both helping and causing harm. Take care, chbare.

Possibly; however, can we definitively say that is the problem laying out on the soccer field? Please explain the reasoning for giving bicarb? His heart rate begins to increase slowly without intervention and you note spontaneous respirations. En-route to the ER, he regains consciousness and his vital signs remain stable. His neurological status is grossly intact without any noted deficits. Upon arrival, you transition into the receiving team. How will you manage and assess this patient? Take care, chbare.

You identify coarse ventricular fibrillation and defibrillate. Following defibrillation, you note a slow weak carotid pulse. You note the following on the monitor: Take care, chbare.

History per prior post. Noting different or unusual in game play, behavior, or attitude. No known history of substance abuse and or use. He collapsed immediately following the collision. You place two nasal airways and an oral airway and begin bag valve mask ventilations. Good chest compliance, rise and fall, and symmetry is noted with ventilations. No carotid pulse is noted. CPR is continued while your partner places the fast patches. You note the following via quick look through the patches: Approximate down time is three minutes. Take care, chbare.

He is unresponsive and two adults are performing CPR. No history, healthy kid per the parents." Just collapsed after running into a fellow team mate." Take care, chbare.

You are called to a local soccer field for a 14 year old male who collapsed. Take it away. Take care, chbare.

Cannot argue with you on that point. Take care, chbare.

Hehe, thought so. Not everybody was supporting leaving people on the board. Take care, chbare.

Agreed, the incidence of PRIS appears to be on the increase. I also suspect this is related to the fact that we are starting to use diprivan quite frequently outside of the OR and specialty units. I even see patients frequently go on Diprivan following intubation in the ER. I hope everybody enjoyed this scenario. Hopefully, we can use this to realize that pharmacology is a dynamic field and we should strive to understand the problems associated with the medications that we give to our patients. In addition, new problems associated with medications we are accustom to using can occur. Additionally, things do not always fit into the nice box we are so often taught. Hence the title of this thread. We should also strive to stay on top of the newest literature. Firemedic, looks like you nailed the diagnosis. Take care, chbare.

Let us take the diprivan consideration a step further. Does this patients condition fit with any of the complications associated with diprivan use? A syndrome perhaps? I know a few members already know the problem, thanks for allowing additional conversation that will hopefully benefit people who have never herd of this problem. Take care, chbare.