I'm not so sure about a 12 lead either, but I would hook her up to a 3 lead with the combo pads just incase she de-compensates.
Not going to help lad. Needs a surgeon.
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I'm not so sure about a 12 lead either, but I would hook her up to a 3 lead with the combo pads just incase she de-compensates.
Make sure you get a couple of large bore IVs. Your big problem is going to be hypovolemic shock. Might be a good idea to review your drip rates for dopamine.
Not going to help lad. Needs a surgeon.
I am more experienced as a Basic then a Medic (as I have only been a medic a few months), but why would you defib. a trauma pt? The H's and T's are your issue, and until they are properly addressed defibrillating will only damage the heart further, right?
Please tell me you are joking about the dopamine for hemoragic shock? Correct me if I'm wrong, and well, I know I'm not, but you don't give dopamine for hemoragic shock. You might want to recheck your medication contraindications, not to mention common sense.
The leading cause of death with regard to civilian and military traumas is hemorrhagic shock.1 Since hemorrhagic shock has a high mortality rate, research is crucial in finding the most effective treatment. The article provides a review of the 4 types of shock, the 4 classes of hemorrhagic shock, and the latest research on resuscitative fluid. The 4 types of shock are categorized into distributive, obstructive, cardiogenic, and hemorrhagic shock. Hemorrhagic shock has been categorized into 4 classes, and based on these classes, appropriate treatment can be planned. Crystalloids, colloids, dopamine, and blood products are all considered resuscitative fluid treatment options. Each individual case requires various resuscitative actions with different fluids. Healthcare professionals who are knowledgeable of the information in this review would be better prepared for patients who are admitted with hemorrhagic shock, thus providing optimal care.
In this case I would treat for shock, high flow O2, and bleeding control. I would most likely apply the three lead so I could maintain a visual on what the heart is doing, but the shock would be my main concern. I do not want her gong into shock. My job here is to prevent the patient from going into V-Tac/ V-fib. In this scenario the patient is slightly hypotensive and presents with a severe bleed, so these are my first concerns.
IN this scenerio she is conscious, has a pulse, is slightly hypotensive, RR are rapid, adn obviously has a pulse. My priority is to prevent her from getting worse, going into shock, and disrhythmias.
Again I am saying you are wrong, and I am not saying I completely disagree with you. I just think there are drugs which can do more, and taking time to set up a 12 lead would not be high on my list in this case. I could be wrong, as stated above, and the truth is you probably have more experience then I as a Paramedic, but this is simply my opinion.
I see your point. We're taught a little bit differently. In the trauma situation we were taught to treat the cause because defib. won't help until you treat the underlying cause(s). I think its a matter of protocol and state requirments. They taught we could apply it if we had time, but not to make it a prioty. Another reason could be becasue we have paddles here, and we were taught the "quick look method" where the patches are not necessary; we can use the paddles to get a picture of the rhythm.
Regardless, I do see your point. "Treat the pt. not the text book"
Ok, now who advocates the use of either "renal dose" dopamine or pressors in said uncontrolled penetrating truncal trauma? Hands up! Higher, don't be scared!.
In MA at my service that's what us basics are for We hook up the 12 leads and stuff while the medic does his interventions.. And since we r in the sticks up here.. we would draft a cop or FF to drive and we would both be in back:wacko:..i agree and think that your time would be much better spent doing a host of other services to this patient than getting a EKG
On the contrary, it shows a good appreciation of the physiology, pathophysiology and aims of treatment that we are after.
Ok, I'll just come out and say it. In the setting of uncontrolled hemorrhage in the prehospital setting there is absolutely no role for dopamine, or any other inotropes. There is a role for such agents after the damage control surgery has been carried out to maintain perfusion. You need to plug the hole first though.
There are some major issues with using either "renal dose" dopamine or higher doses:
"Renal dose" dopamine (as venficus pointed out) dilates your afferent renal arterioles. This is then thought to improve renal blood flow, which we want to maintain - if your kidneys die, you die. However, for this to be effective, you need something to flow through them in the first place. Which the hemorrhaging shocked patient doesn't have. All that is going to happen is that you are going to increase the intravascular volume that needs to be filled with the precious little red stuff that remains. Furthermore, whilst studies have shown that low does dopamine improves O2 tensions in the kidneys and liver, it decreases flow to the gut. This causes all sorts of ongoing problems assuming that the patient survives: the gut is very, very important, far more so than we usually give it credit for being.
Ultimately, despite many studies into renal dosing of dopamine in many critically ill patients of varying etiologies, there is extremely scant evidence that there is any increase in survival despite the improvement in physiological parameters.
There is also no role for higher doses of dopamine or any other vasoactive drugs in the setting of uncontrolled hemrrhage. These patients are already maximally vasoconstricted: no further benefit can be gained in attempting to vasoconstrict further, and all of these drugs (dopamine, dobutamine, epi, nor-epi) cause profound myocardial hypoxia and dysfunction and are extremely arrythmogenic in this setting.
Aggressive fluid resuscitation is also an absolute no-no in uncontrolled hemorrhage. Whilst the finer points of how/when/where/why and how much are still being worked on, I know of no reputable trauma surgeon who would advocate the old formula of 3:1 fluid resuscitation for uncontrolled hemorrhage in the prehospital setting. Heck, in my service that would get me fired!
Karim Brohl (owner of Trauma.org, surgeon and contemporary of Ken Mattox) states: ALS/ACLS algorithms DO NOT APPLY to traumatic arrest.
The primary causes of traumatic arrest are hypoxia, hypovolaemia due to haemorrhage, tension pneumothorax, and cardiac tamponade. Hypoxic arrests respond rapidly to intubation and ventilation. Hypovolaemia, tension pneumothorax and cardiac tamponade are all characterised by loss of venous return to the heart. External chest compressions can provide a maximum of 30% of cardiac output in the medical arrest situations and are dependent on venous return to the heart. Chest compressions in the trauma patient are wholly ineffective, may increase cardiac trauma by causing blunt myocardial injury and obstruct access for performing definitive manoeuvers.
The treatment of massive thoracic haemorrhage is control of haemorrhage, not intravenous fluid therapy. Fluid therapy prior to haemorrhage control worsens outcome in penetrating thoracic trauma (and perhaps all penetrating trauma patients). If there is no response to a small (500ml) fluid challenge, fluid administration should be halted until haemorrhage control is achieved.
This is obviously problematic if the patient arrests in the field with no means of controlling the bleed. Actually, maybe it isn't problematic: if this happens, the patient is dead.
VF/VT are unlikely to be your presenting rhythms in arrest following exsanguination, and it is highly unlikely that defib is going to be of any benefit in this scenario anyway.