# trauma assessment scenario



## 8jimi8

called to scene of 1 vehicle vs tree.  

Initial impression: no skid marks, moderate frontal damage, no air bag, steering wheel intact, 1 patient, driver restrained - flaccid in drivers seat, driver door won't open due to impact, no entrapment of patient beyond the damaged door.  Fire and LE on scene.

initial assessment:
no witnesses
Your partner takes c-spine
driver moans weakly to loud verbal stimuli, does not open eyes.
breathing is shallow and rapid 38/min breathe sounds are wet rales in all fields
circulation is weak and thready at 133 b/min
nrb 15l/min
high priority - rapid transport patient
medic alert bracelet: Cardiac history, allergy to HCTZ.

no sample or opqrst available
rapid trauma assessment reveals pms + (withdraws to painful) in all extremeties, eyes perrl, no signs of basilar skull fracture, no signs of dcapbtls or any obvious trauma (rapid trauma assessment is essentially negative except for a minor oozing laceration to the left cheek)
baseline vitals 90/50, hr 155, breathing 35 o2 sat 80
extricate with a KED and long backboard.

once the patient is loaded in the ambulance 2 large bore IVs
place the patient on the monitor reveals ...

multifocal pvcs and runs of paroxysmal vtach 8, 10 , 12 
Oxygen saturation reads 75, patient is breathing 28 /min

what do you do.


call out your interventions once the ambulance starts moving.  15-20 minutes until the hospital.  you can have 1 MFR/firefighter in the patient compartment with you.


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## 8jimi8

oops glucose is 136 and  4 mm st-depression in AVf


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## Melclin

Seems like LVF, or maybe a cardiac contusion (but you did say there was no obvious signs of trauma). Either way, I would think this patient is probably pretty stuffed. 

My job in this situation would be simply to call MICA. Could try some suction.

From a MICA perspective, this patient would want intubating and an adrenaline infusion with some fluid boluses I suppose.


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## 8jimi8

are you sure you want to bolus?


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## 8jimi8

oh pt is 67 years old


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## MrBrown

I would say this patient is pretty buggered myself.  

1.  Remove Firefighter from ambulance, this is not a fire truck
2.  Fluid bolus
3.  Suction and laryngeal mask airway
4.  Intensive Care Paramedic

My guess is myocardial injury.

Any sign of a haemopneumothorax, unstable pelvis or internal bleeding?


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## Melclin

I'm fairly certain the MICA deal in this kind of scenario is a fluid bolus once/if the chest clears up, with the adrenaline, yes.


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## Melclin

8jimi8 said:


> driver moans weakly to loud verbal stimuli, does not open eyes.



I'm not sure he'd take an LMA. Whats his motor response, so we can complte a GCS, 8jimi8.

Whats your rationale for fluid before inotropes? Surely that'd drown him further.


If he was really going down s**t creek, you could try some manual PEEP, I'm not personally of that persuasion, but some here are.


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## Veneficus

*are you sure this is a trauma scenario?*

It sounds like a cardiac scenario uncleverly disguised as trauma.

There are a lot of findingss here, but what does the pt. look like? I would guess cyanotic, perhaps pale. Skinny? Fat? Is his spine abnormally kyphotic? What are the angle of his femurs? Dependant Edema? internal Pacemaker/defibrilator? Surgical scars? Urinated on himself? 

For clarification there was no airbag or the airbag was not deployed?

That will make a difference on index of suspicion. Damage to the vehicle is an outdated measurement. 

Is there a "seatbelt" sign?

No eye opening: 1
Moans: 2
withdraws to pain: 4

with a GCS of 7, I have no idea why you would waste time with a KED unless you were going to not use a backboard to protect his breathing.

With the exception of a minor laceration, this seems to be a cardiac problem so far. His BP, while low and definately a concern with his EKG doesn't seem overly low if he is on an ACE inhibitor or non thiazide diuretic. It doesn't seem like there is significant beta blockade with a rate of 155 either, but still possible. Wet lung sounds also point to a cardiogenic shock type scenario from left sided failure. I think this was included specifically to rule out a fluid bolus.

Dobutamine or dopamine sounds like a good idea. I think would start with that. 

An aggressive approach would be to wait for a v-tach and cardiovert him, but I am not predisposed/condoning doing that. Just keeping options open. 

Positive pressure ventilation may help as well. 

The backboard will not help his respiratory efforts, you may have to forgo it in this case, or incline the head as much as safely possible.


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## EMTinNEPA

Any drainage or bleeding from the ears, nose, or mouth?  Any jugular venous distension?  Are the heart sounds clear and crisp or muffled?  Any pitting edema in the lower extremities?  How are the pupils?  Is the pelvis stable and firm?  Any signs of possible femur fractures?  Is the abdomen soft and nontender without masses, distension, rigidity, or guarding?  Does he have a pacemaker?  What is the baseline rhythm of his EKG?  Sinus tachycardia with multifocal PVCs and paroxysmal ventricular tachycardia, or atrial fibrillation with multifocal PVCs and paroxysmal ventricular tachycardia, or something else?

While awaiting answers to these questions...

Treatment: 15lpm NRB, extrication straight to a long back board (no KED, this patient is in too poor a condition to waste that time), IV access, 12-lead EKG, definitely a candidate for intubation.  Am I working in a system that allows paramedics to RSI?  I wouldn't worry about the hypotension too much, maybe give a small fluid bolus to get his systolic pressure above 100.  As for the PVCs and runs of V-tach, I would treat him with lidocaine once I got his pressure up, depending on the frequency of PVCs and runs.

The big question here is did he crash because he's having an MI and the PVCs and V-tach made him hypotensive and he blacked out, or are the PVCs and V-tach a symptom of cardiac contusion?

Very good scenario!


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## Veneficus

EMTinNEPA said:


> Any drainage or bleeding from the ears, nose, or mouth?  Any jugular venous distension?  Are the heart sounds clear and crisp or muffled?  Any pitting edema in the lower extremities?  How are the pupils?  Is the pelvis stable and firm?  Any signs of possible femur fractures?  Is the abdomen soft and nontender without masses, distension, rigidity, or guarding?  Does he have a pacemaker?  What is the baseline rhythm of his EKG?  Sinus tachycardia with multifocal PVCs and paroxysmal ventricular tachycardia, or atrial fibrillation with multifocal PVCs and paroxysmal ventricular tachycardia, or something else?
> 
> While awaiting answers to these questions...
> 
> Treatment: 15lpm NRB, extrication straight to a long back board (no KED, this patient is in too poor a condition to waste that time), IV access, 12-lead EKG, definitely a candidate for intubation.  Am I working in a system that allows paramedics to RSI?  I wouldn't worry about the hypotension too much, maybe give a small fluid bolus to get his systolic pressure above 100.  As for the PVCs and runs of V-tach, I would treat him with lidocaine once I got his pressure up, depending on the frequency of PVCs and runs.
> 
> The big question here is did he crash because he's having an MI and the PVCs and V-tach made him hypotensive and he blacked out, or are the PVCs and V-tach a symptom of cardiac contusion?
> 
> Very good scenario!



I would guess with the lack of skid marks and his medical bracelet his event supposedly happened prior to.

it also mentioned the rapid trauma assessment to be negative. 

Pupils were listed as equal and reactive to light.

the underlying rhythm question is a good point though.


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## Melclin

8jimi8 said:


> + (withdraws to painful)



Oh, didn't see that. Well with a GCS of 7 and if he's truly moaning, I think we safely say he won't take an LMA.



Veneficus said:


> It sounds like a cardiac scenario uncleverly disguised as trauma.
> 
> Wet lung sounds also point to a cardiogenic shock type scenario from left sided failure. I think this was included specifically to rule out a fluid bolus.
> 
> *I sure hope there's something big we're missing. I'll be disappointed if the the big twist here is that its LVF and we were all supposed to think it was trauma, and poor saline into him. *
> 
> Dobutamine or dopamine sounds like a good idea. I think would start with that.
> 
> *Wouldn't it!..if only we carried one of them. :sad:*
> 
> An aggressive approach would be to wait for a v-tach and cardiovert him, but I am not predisposed/condoning doing that. Just keeping options open.
> 
> *I think we can agree that would be a poor idea at the moment.*
> 
> Positive pressure ventilation may help as well.
> 
> The backboard will not help his respiratory efforts, you may have to forgo it in this case, or incline the head as much as safely possible.



You don't think this pt is a candidate for intubation?


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## boingo

This is a hypoxic patient, first priority is to fix that.  The irritable rhythm is unlikely to improve without addressing oxygenation.  Skip the non rebreather and assist ventilation w/BVM.  Where does that get us?  I don't want to get too far ahead with drugs, fluids, etc...just yet.


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## EMTinNEPA

Veneficus said:


> I would guess with the lack of skid marks and his medical bracelet his event supposedly happened prior to.
> 
> it also mentioned the rapid trauma assessment to be negative.
> 
> Pupils were listed as equal and reactive to light.
> 
> the underlying rhythm question is a good point though.



I'm leaning that way too.  However, at 67 his reflexes may not be the best or he simply didn't have time to react.

The reason I ask about the underlying rhythm is because his medic alert bracelet simply says "cardiac history", which isn't very specific.  Did he have an MI in the past?  Is he being treated for atrial fibrillation?  Does he have congestive heart failure?  The answer to this question combined with assessment findings may sway me to one way or the other in terms of which treatment modalities I may use.

Also, I don't know if I would go for dopamine to increase his pressure.  In order to get the pressor dose I would have to deal with the beta 1 effects of the inotropic dose as well, which may not be the best thing since he's already showing signs of hypoperfusion and his heart-rate is in the 130s.  Correct me if I'm wrong, but increasing heart-rate would increase workload which would increase myocardial oxygen demand, and it's already obvious that there isn't enough oxygen to go around.


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## Melclin

EMTinNEPA said:


> Also, I don't know if I would go for dopamine to increase his pressure.  In order to get the pressor dose I would have to deal with the beta 1 effects of the inotropic dose as well, which may not be the best thing since he's already showing signs of hypoperfusion and his heart-rate is in the 130s.  Correct me if I'm wrong, but increasing heart-rate would increase workload which would increase myocardial oxygen demand, and it's already obvious that there isn't enough oxygen to go around.



Perhaps, I'm no expert. My thinking is that the idea with dopamine or dobutamine wouldn't be to get to a pressor dose, but used specifically because of the inotropic effects (inotrope refers to a drug that increases contractile force, not rate, although inotropes are often also chronotropes). This would increase the cardiac output which would in turn reduce the pressure behind the left ventricle that was causing the oedema, in turn fixing the problems with oxgenation. Although I'm not sure how fast that would work, if indeed it does work, so I feel directly addressing the oxygenation simultaneously is the best course of action. 

I'm thinking intubation, but vene, you are appear to be against this? Whats your thinking? How quickly do inotropes work to fix a problem like this?


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## EMTinNEPA

Melclin said:


> Perhaps, I'm no expert. My thinking is that the idea with dopamine or dobutamine wouldn't be to get to a pressor dose, but used specifically because of the inotropic effects (inotrope refers to a drug that increases contractile force, not rate, although inotropes are often also chronotropes). This would increase the cardiac output which would in turn reduce the pressure behind the left ventricle that was causing the oedema, in turn fixing the problems with oxgenation. Although I'm not sure how fast that would work, if indeed it does work, so I feel directly addressing the oxygenation simultaneously is the best course of action.
> 
> I'm thinking intubation, but vene, you are appear to be against this? Whats your thinking? How quickly do inotropes work to fix a problem like this?



From 5mcg/kg/min to 10mcg/kg/min, dopamine stimulates the Beta-1 adrenergic receptors, which do cause increased contractility, but also increases automaticity, including increased sinoatrial node conduction, which means increased heart-rate.  My impression was that the dopamine would be used to remedy the hypotension as an alternative to a fluid bolus so that no more fluid would be added to an already (from the sounds of it) fluid overloaded patient.  The problem is to get the Alpha effect of vasoconstriction (and ergo blood pressure), you have to increase the dose to 10mcg/kg/min to 20mcg/kg/min, meaning you still have to deal with the Beta-1 effects.  Dobutamine is also a primarily Beta-1 agent with selective Alpha-1 effects.


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## 8jimi8

Today 05:00 AM
Veneficus	
are you sure this is a trauma scenario?

There are a lot of findingss here, but what does the pt. look like? I would guess cyanotic, perhaps pale. Skinny?Dependant Edema? internal Pacemaker/defibrilator? Surgical scars? Urinated on himself? 

For clarification there was no airbag or the airbag was not deployed?

Today 05:31 AM
EMTinNEPA	 Any drainage or bleeding from the ears, nose, or mouth? Any jugular venous distension? Are the heart sounds clear and crisp or muffled? Any pitting edema in the lower extremities?  Is the abdomen soft and nontender without masses, distension, rigidity, or guarding? Does he have a pacemaker? What is the baseline rhythm of his EKG? Sinus tachycardia with multifocal PVCs and paroxysmal ventricular tachycardia, or atrial fibrillation with multifocal PVCs and paroxysmal ventricular tachycardia, or something else?

Today 06:15 AM
boingo	 This is a hypoxic patient, first priority is to fix that. The irritable rhythm is unlikely to improve without addressing oxygenation. Skip the non rebreather and assist ventilation w/BVM. Where does that get us? I don't want to get too far ahead with drugs, fluids, etc...just yet.


Your protocol limitations are limited only by your training / con-ed ,  your medical control has personally told you that she would back you as long as you can justify your treatment plan.  (if you are a student you may intervene with any skill you have been checked off on and in that case your partner is not the firefighter/MFR, it will be your paramedic preceptor- but you are leading the call)

Car is an older model, no airbag to deploy.

Pt has circumoral cyanosis, No rhinorrhea / otorrhea, approx 5'11, 130lbs estimated,  No kyphosis, Thorax is not appreciably barrelled.  Trachea is midline, JVD is positive. Breath sounds are diminished in the bases, but still very wet bilaterally with coarse ronchi and rales in all fields.  Heart sounds are present, muffled by the loud respiratory sounds.  You think you hear an S3.  Generalized edema 1+/4 

An old scar from the angle of louis, midline descending to the epigastrium, Nothing palpable under the skin that would indicate and  ICD/Pacemaker, No seatbelt sign, abdominal palpation reveals a reducible mass in the luq - no thrill, no guarding.  Pelvis is stable, no appreciable MOI to lower extremities, except some bruising to bilateral knees.  There are 2 non-contiguous, faint, linear scars on the medial aspect of the pt's left lower extremity beginning superior to the patients knee, the second inferior and medial from the knee pt's pants / undergarments are CDI,   bilateral lower extremity pitting edema 2+/4, 


Baseline rhythm was Sinus Tach but now the runs of vtach are the predominant feature on the monitor, hr is intermittently 130-175

Pts o2 sat rises from 70 to 84 with BVM ventilations.  Pt will not accept  an oral adjunct.

You find a tattered stained medication list in the wallet... all you can make out is colace 100mg, "diltzam" (cannot read the dosage), 4 medications you cannot read except for the dosages: 5mg, 75 mg and 12.5mg and 5mg

still >15 minutes left to hospital, you can hear the driver cursing traffic.


Yah, Vene.... poorly disguised!  Rather, not disguised at all, just undiscovered in the initial assessment.


From what I understand, people are considering drugs, but have not actually administered any, correct?  

Call out your interventions and i will try to respond with tx response.  In all fairness this was (not a National Registry psychomotor exam) my final psychomotor trauma assessment scenario.  All of the initial interventions are what I did up to loading the patient in the ambulance.  If you would skip the KED or backboard, just state that you would have omitted that, as some have already.


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## EMTinNEPA

From the "Crazy Ideas" file, what about CPAP?  Perhaps if we used CPAP we could push all the fluid in the patient's lungs back into the intravascular space, simultaneously increasing oxygenation and blood pressure while eliminating the pulmonary edema.

EDIT: In light of 8jimi8's last post, CPAP might not be such a crazy idea after all.


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## Melclin

Fairly certain the idea with an inotrope like dopamine or dobutamine would be to increase cardiac output. That after all that is the problem in the first place. If the idea was solely to cause vasoconstriction then the effect would be the same as adding fluids - it would further overload an already overloaded system. You wouldn't be using a norad infusion in a patient like this.


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## 8jimi8

let me know if i skipped your intervention.

I'm no expert, so i can really only give you the details that were given to me.  I'll try to keep from embellishing this scenario way out of control


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## 8jimi8

EMTinNEPA said:


> From the "Crazy Ideas" file, what about CPAP?  Perhaps if we used CPAP we could push all the fluid in the patient's lungs back into the intravascular space, simultaneously increasing oxygenation and blood pressure while eliminating the pulmonary edema.



cpap initially increases oxygenation, but you notice that the patient's work of breathing is increasing, chest rise is less pronounced, bp 95/40, respir down from 25 to 14.  Breath sounds still very coarse.

monitor still showing Stach @ 140 with paroxysmal runs of vtach 20beats (@ 170)


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## EMTinNEPA

Melclin said:


> Fairly certain the idea with an inotrope like dopamine or dobutamine would be to increase cardiac output. That after all that is the problem in the first place. If the idea was solely to cause vasoconstriction then the effect would be the same as adding fluids - it would further overload an already overloaded system. You wouldn't be using a norad infusion in a patient like this.



However, dopamine and dobutamine are both positive chronotropes, so the heart rate will increase.  It's already in the 130s, and cardiac output is already in the crapper, so perhaps dopamine and dobutamine aren't in the best interest of this patient since the faster the heart rate gets, the less filling time there is between contractions and ergo less preload.


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## EMTinNEPA

8jimi8 said:


> cpap initially increases oxygenation, but you notice that the patient's work of breathing is increasing, chest rise is less pronounced, bp 95/40, respir down from 25 to 14.  Breath sounds still very coarse.
> 
> monitor still showing Stach @ 140 with paroxysmal runs of vtach 20beats (@ 170)



Ok, we've got to control that V-tach.  You said the patient weighs about 130lbs., so that's about 60kg.  So we'll give 60mg of lidocaine slow IVP and get ready to work because this guy is showing classic signs of "pre-code looking".


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## Melclin

EMTinNEPA said:


> Perhaps if we used CPAP we could push all the fluid in the patient's lungs back into the intravascular space,



Best read up on what CPAP actually does, because thats not how it works. CPAP for us is generally contraindicated in unconcious/unresponsive pts. I don't know that it would be appropriate for this pt, but others may have different approaches to it and I'm not sure exactly what constitutes unresponsive when it comes to CPAP because I'm not yet at the stage of using it.

In regards to the scenario, I'm pretty content that its not a tension pnemo or cardiac contusion. Although, I must admit, I'd be worried if I were really in charge. 

Seeing as though I'm playing MICA as the moment: For now, 100% O2 + assisted vents, with some PEEP. 

PROBLEM: Adrenaline IV 10mcg bolus + 5mcg/minute infusion and increasing the rate by 5mcg/min every minute. If his chest clears, 250 bolus NS until aduequately perfused and Amiodarone 5mg/kg over 30 mins. I don't know enough about them to know whether or no mixing the treatments is wise, or whether or not I should pick one. I feel like adrenaline is ganna make his VT problems worse. NOPE, EDIT: decision, I'd probably go with the amiodarone first on account of the fact that it seems like its getting worse fast: 





> l runs of vtach 20beats



Anyway I need to go to bed, so I'll catch the convo again in the morning.


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## Veneficus

Melclin said:


> Perhaps, I'm no expert. My thinking is that the idea with dopamine or dobutamine wouldn't be to get to a pressor dose, but used specifically because of the inotropic effects (inotrope refers to a drug that increases contractile force, not rate, although inotropes are often also chronotropes). This would increase the cardiac output which would in turn reduce the pressure behind the left ventricle that was causing the oedema, in turn fixing the problems with oxgenation. Although I'm not sure how fast that would work, if indeed it does work, so I feel directly addressing the oxygenation simultaneously is the best course of action.
> 
> I'm thinking intubation, but vene, you are appear to be against this? Whats your thinking? How quickly do inotropes work to fix a problem like this?



My thinking is his cardio problem is causing all of his other issues. From his intimate rendezvous with mother nature to his hypoxia. 

By doing something for the cardiogenic shock, which likely lead to the hypoxia and altered mental status as well, it may be getting to the root of the problem. There should be some kind of change on the EKG not long after (few minutes) starting what in all likelihood on any field unit I worked on would be dopamine, but in a perfect world there would be dobutamine and the textbook would be happy.  If things go well, the patient would grossly improve. (wake up) If not, well… then we see where we are.

The question about the underlying rhythm was a very good one, I assumed it was sinus because there was no caveat. 

I do think this patient is a candidate for intubation, but I am not too quick on it because the scenario states you are already on the way to the hospital. Intubating in the back of a moving rig is a tricky prospect. Intubating somebody in c spine precautions is a bit tricky as well. So why make an attempt when the difficulty keeps compounding? We haven’t even gotten to see the difficulty of his airway and already odds are against us. If he is being bagged and his airway controllable without the tube, I don’t see it as an immediate need and in this case the risk may outweigh the benefit.

Have to run to class, more to come.


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## mycrofft

*OK...29 minutes out ,cardiac &  low percentage concern for hidden closed injuries.*

This would be more informative for me if a few fewer acronyms were being tossed around, but that's good for my learning curve.

ZEBRA: was the car too old to have airbags? (I'm presuming this airbag datum was to let us know the impact was not the primary killer here, along with "moderate damage"; I _*"totalled"*_ a Sentra at 25 mph once). So impact is not a prime candidate. Concentrate upon cardiopulmonary, C spine as a general precaution, stick up mental post-it notes for less apparent closed insults (you wouldn't treat them, but the hospital might, such as contused lungs, slow intracranial bleed).

I would be looking for signs of elapsed time-since-crash during scene safety step; this could be informative as to whether some signs and symptoms might yet be appearing (Battle signs, contusions due to closed injury to thorax, etc.) but are not apparent yet.

Is our pt a frail little old man or a robust former bachelor farmer from Lake Woebegone?  (When given a scenario always stall for time with a useful question or two).

HCTZ (Esedrix, hydrochlorothiazide) allergy-he has been or is now under tx/rx for hypertension, maybe for a while (not a new drug). HTN plus cardiac insufficiency devolving into the current sad state of vitals can suggest the pt could be under tx with a number of meds including coumadin.

Rales and large bore IV with signs not inconsistent with cardiac failure (was pulse strong, weak, irreg or regular?) are maybe not so rational a combo unless transport time is very long, then the double big IV's could be your only avenue for pharmacologic "Hail Marys" as the pt dies enroute. If any IV is in, WATCH volume and rate and breath sounds not so much to direct care but to direct whether to continue care as aggressively as our adrenaline would goad us.

If the pt responds (albeit weakly) to loud verbal stim., how's he going to respond to an intrusive airway ? What will vagal response of airway introduction do? Might be necessary if sats not improved by O2 BVM and nasalpharyngeal airway. I know impact was probably not a factor but have the firefighter ventilate while you listen for lung sounds periodically.

Have a firefighter (they travel in packs) use fifteen seconds or less while you are busy elsewhere to toss his glove box for meds, wallet for medicalert card, pharmacy plan card, or MD/hospital card, pockets for nitro. (Ask to see if anyone already has).Quick check anterior shoulders for pacemaker scar. 

If you were going through this with newbies, try to make them consider how this info would unfold to you on a real scene, how fast, which order, how simultaneous, and how correctly? Accident scenes consist of your mental shopping list being jostled and ripped by real time urgencies and scene situation (rain, dark, traffic, fuel leak, distressed passenger, etc etc). 

ABC-spine-data-go-IV-monitor-tx-arrive-clean unit-"Miller Time".


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## mycrofft

*OK...20 minutes out , cardiac &  low percentage concern for hidden closed injuries.*

This would be more informative for me if a few fewer acronyms were being tossed around, but that's good for my learning curve.

ZEBRA: was the car too old to have airbags? (I'm presuming this airbag datum was to let us know the impact was not the primary killer here, along with "moderate damage"; I _*"totalled"*_ a Sentra at 25 mph once). So impact is not a prime candidate. Concentrate upon cardiopulmonary, C spine as a general precaution, stick up mental post-it notes for less apparent closed insults (you wouldn't treat them, but the hospital might, such as contused lungs, slow intracranial bleed).

I would be looking for signs of elapsed time-since-crash during scene safety step; this could be informative as to whether some signs and symptoms might yet be appearing (Battle signs, contusions due to closed injury to thorax, etc.) but are not apparent yet.

Is our pt a frail little old man or a robust former bachelor farmer from Lake Woebegone?  (When given a scenario always stall for time with a useful question or two).

HCTZ (Esedrix, hydrochlorothiazide) allergy-he has been or is now under tx/rx for hypertension, maybe for a while (not a new drug). HTN plus cardiac insufficiency devolving into the current sad state of vitals can suggest the pt could be under tx with a number of meds including coumadin.

Rales and large bore IV with signs not inconsistent with cardiac failure (was pulse strong, weak, irreg or regular?) are maybe not so rational a combo unless transport time is very long, then the double big IV's could be your only avenue for pharmacologic "Hail Marys" as the pt dies enroute. If any IV is in, WATCH volume and rate and breath sounds not so much to direct care but to direct whether to continue care as aggressively as our adrenaline would goad us.

If the pt responds (albeit weakly) to loud verbal stim., how's he going to respond to an intrusive airway ? What will vagal response of airway introduction do? Might be necessary if sats not improved by O2 BVM and nasalpharyngeal airway. I know impact was probably not a factor but have the firefighter ventilate while you listen for lung sounds periodically.

Have a firefighter (they travel in packs) use fifteen seconds or less while you are busy elsewhere to toss his glove box for meds, wallet for medicalert card, pharmacy plan card, or MD/hospital card, pockets for nitro. (Ask to see if anyone already has).Quick check anterior shoulders for pacemaker scar. 

If you were going through this with newbies, try to make them consider how this info would unfold to you on a real scene, how fast, which order, how simultaneous, and how correctly? Accident scenes consist of your mental shopping list being jostled and ripped by real time urgencies and scene situation (rain, dark, traffic, fuel leak, distressed passenger, etc etc). 

ABC-spine-data-go-IV-monitor-tx-arrive-clean unit-"Miller Time".


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## 8jimi8

Is everyone staying away from lasix because of the hypotension?


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## EMTinNEPA

8jimi8 said:


> Is everyone staying away from lasix because of the hypotension?



Precisely.  Same reason I'm staying away from nitrates.


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## mycrofft

*Yes. Watch your "benefit within time frame".*

After a bit you can wind up treating your drugs instead of treating the patient.

No one has said "urinary catheter".....:blush:


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## 8jimi8

amio / lido -

pt converts to stach @ 110 with frequent 6 beat bigeminal runs

bp is 98/45, respirs on cpap are 7/min o2 sat 80 

(y'all o2 sat has been low for a while)

i realize that I was emphasizing the cardiac issues, but remember A comes before C!




I think we are safe to call it here.

I was interested to see where you all would be with your cardiac interventions.  ETT or Rescue airway at this point?





From my scenario, when I was actually testing,  I asked many of the same clarifying questions that you all did.   Here was my treatment

40mg lasix IV push, NS tko to both IVs, i intervened with airway first:  RSI, handed ventilations over to my MFR and then I started freaking out about the vtach... so I went with 150mg amiodarone in 500cc over 10 minutes.  This is the intervention that my brain spat out, my mouth reacted quicker and I just had to suck it up cause the proctor said, ok, you are at the hospital.  (i know that NR would ask me if there was anything else that I would like to do) 
SO... I was left hoping that my lasix cleared his lungs and that the 500cc bolus would prevent a precipitous drop in BP from my lasix push.  It was kinda freaky for me because I haven't studied my RSI drugs yet and there seems to be a role confusion (tho the confusion is likely only mine) because the class is an EMT-I85 / Paramedic 1 course.  So he's testing me as P1 while I was only mentally prepared for intermediate interventions.

I passed, so i'm assuming I didn't do anything too crazy.  I didn't even know what i wanted to use for my RSI, i just stated i'll administer a sedative, let it take effect, administer a paralytic and intubate, he said ok, you have confirmed placement.  So i knew I was left with this V TACH hanging over my head.  Very unnerving, but I appreciated my medical assessment after that because he just gave me a straight up anaphylaxis. lol

I also agree with the dobutamine!


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## 8jimi8

_Jimi, Hello, hope you made it back ok.

As for the scenario; Amiodarone would work but I would have probably used Lidocaine to suppress the irritable foci in the heart, and then focus on their origin, which is probably lack of O2, so high flow O2 by BVM to push back the fluid in the lungs would probably settle most of his problems. The scenario calls for ASA and Vasodilator (I am guessing they want NTG) but with the potential for head trauma I would not want to give ASA, and with the B/P of 90 systolic I would not give NTG we are left with an antidysrythmic and oxygen, with Oxygen being the priority.

Paramedics are taught the vagal maneuvers and CSM but he could not have complied with vagal maneuvers and most Medical Directors have shied away from CSM due to the potential for carotid artery spasm of more commonly blood clot formation in vessels leading to the brain, even with listening for bruits, they can be missed. And of course he was not in an SVT so in his case it would not have been warranted.

Your treatment was fine and as I said the big thought was did the medic notice the evidence of a medical problem in the face of a trauma event, which you caught.

Hope my answer helps, Greg_
- Hide quoted text -
-----Original Message-----
From: j c [mailto:james.marshall.clary@gmail.com] 
Sent: Monday, March 08, 2010 12:29 AM
To: 
Subject: treatment of VT

Instructor,

Hello, this is Jimi Clary again.  I wanted to get your opinion of my response to the vtach scenario.  Was my initial intervention with Amiodarone the same choice that you would have made?  I believe I called for 150mg amiodarone over 10 minutes IV.  Is there another intervention that I should have tried first?  Should I have attempted a vagal maneuver?  I understand that the patient was AMS and not really following commands.  Are paramedics taught about the carotid sinus massage?

Thank you for your time and expertise,

jimi

-- 
James M Clary, RN, EMT-B


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## Veneficus

8jimi8 said:


> Is everyone staying away from lasix because of the hypotension?



No. I would not consider lasix because of the onset time, the fact that I cannot measure the quality or quantity of urine output, and in the 20 or so minutes of this scenario, I don't see it having too profoud of an effect. As for a fluid bolus to maintain volume, a game. You have fluid, you just need it somewhere else. As well if this person has long standing cardiac or vascular disease, renal function will be an issue, though not in 20 minutes unless he is already in failure. 

On a restrained supine pt, I don't see CPAP as a viable intervention. If the bagging and an NPA isn't doing much, I don't think dropping a tube will matter much either. 

The amio and lido are good ideas, but I see it in this case as "what precipitated this event?" If the arrythmia is the result of lack of myocardial oxygenation and subsequent dysfunction, ok, sounds good. But what then if the cardiogenic shock is the primary cause and the arrythmia a result of deficent myocardium which cannot circulate blood? Seems like 6 of one or 1/2dozen of the other. 

What if the pt had a new NSTEMI or rightsided MI and your rythm prior to runs of vtach is the result of watching the last of the SA or AV node at all? 

Obviously, something has to be done in a timely manner and without a lot of advanced diagostics. But in the end, if the patient has an airway, breathing, and a pulse by the hospital, if nothing else was done then I would call it a win.


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## 8jimi8

Interesting that his intervention was less pharmacologically invasive than I was supposing, re: dobutamine.

in addition to the discussion, I did ask him if he felt that I had made the right decision to intubate him and he agreed with my decision.


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## mycrofft

*AN apology and a crystal ball*

I sincerely apologize for the double post, my computert hung and I thought I had reviewed then posted after corrections.
And the future...suprapubic cathterization?


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## MrBrown

Sounds like a wolf in sheeps clothing, good post


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## Melclin

Veneficus said:


> My thinking is his cardio problem is causing all of his other issues. From his intimate rendezvous with mother nature to his hypoxia.
> 
> By doing something for the cardiogenic shock, which likely lead to the hypoxia and altered mental status as well, it may be getting to the root of the problem. There should be some kind of change on the EKG not long after (few minutes) starting what in all likelihood on any field unit I worked on would be dopamine, but in a perfect world there would be dobutamine and the textbook would be happy.  If things go well, the patient would grossly improve. (wake up) If not, well… then we see where we are.
> 
> *What I'm getting at though is can you wait for it to work to fix the oxygenation or does the SpO2 sitting at 75 warrant more rapid and direct management via intubation. *
> 
> I do think this patient is a candidate for intubation, but I am not too quick on it because the scenario states you are already on the way to the hospital. Intubating in the back of a moving rig is a tricky prospect. Intubating somebody in c spine precautions is a bit tricky as well. So why make an attempt when the difficulty keeps compounding? We haven’t even gotten to see the difficulty of his airway and already odds are against us. If he is being bagged and his airway controllable without the tube, I don’t see it as an immediate need and in this case the risk may outweigh the benefit.
> 
> *I feel that the scenario is inherently flawed in that you begin transport before the process of working through the problem which is just silly. I am naturally assuming that the intubation would occur before transport (you guys intubate while racing along L/S?)  *
> 
> Have to run to class, more to come.





mycrofft said:


> have the firefighter ventilate while you listen for lung sounds periodically.



Nah I'm with Brown, if for some reason I'm pushed for man power, a FF may drive, but at no point are they allowed to participate in medical care (except chest compressions/holding IV bags) within a 50 metre radius of me. 



8jimi8 said:


> Is everyone staying away from lasix because of the hypotension?



I'm staying away from it because I don't think its a good way to treat APO. First of all, it won't clear his lungs in anything like the time frame mentioned; two, too much fluid is not really his problem, its just not being pumped correctly; three, lasix causes more trouble than its worth, electrolyte imbalances, hypovolaemia - all of which is going to be a problem when this pt gets intubated. 



Veneficus said:


> On a restrained supine pt, I don't see CPAP as a viable intervention. If the bagging and an NPA isn't doing much, I don't think dropping a tube will matter much either.
> 
> The amio and lido are good ideas, but I see it in this case as "what precipitated this event?" If the arrythmia is the result of lack of myocardial oxygenation and subsequent dysfunction, ok, sounds good. But what then if the cardiogenic shock is the primary cause and the arrythmia a result of deficent myocardium which cannot circulate blood? Seems like 6 of one or 1/2dozen of the other.
> 
> *I agree about the CPAP, if we're still worried about airway control (which at least I am), then CPAP is not the way to go. I'm all for addressing the the route cause of the problem as I mentioned earlier, but the dramatic increase in VT altered my thinking. Is it appropriate to be pushing catecholamines into a person who has a quickly worsening problem with VT? Its not rhetorical, I'm actually asking, whats the relationship there?*





8jimi8 said:


> _
> As for the scenario; Amiodarone would work but I would have probably used Lidocaine to suppress the irritable foci in the heart, and then focus on their origin, which is probably lack of O2, so high flow O2 by BVM to push back the fluid in the lungs would probably settle most of his problems. The scenario calls for ASA and Vasodilator (I am guessing they want NTG) but with the potential for head trauma I would not want to give ASA, and with the B/P of 90 systolic I would not give NTG we are left with an antidysrythmic and oxygen, with Oxygen being the priority.
> _


_

It worries me that even your instructor still seems to think that CPAP or even manual ventilations will "push back the fluid in the lungs". How would you be giving ASA or NTG to an unresponsive pt if their pressure were higher?_


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## 8jimi8

I read his statements as a contraindication for Asa and ntg


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## Veneficus

*What I'm getting at though is can you wait for it to work to fix the oxygenation or does the SpO2 sitting at 75 warrant more rapid and direct management via intubation.*

In my anecdotal experience, unless there is major airway destruction or obstruction, a patient can be ventilated without a tube. As one of my anesthesia preceptors repeats ad nauseam, “Nobody ever died from not having a piece of plastic in their throat.” I also like to be psotioned for success, I would rather "know" I can ventilate than "think" I could get the tube. But certainly I would assess that before moving and if I liked how it looked I would intubate prior to transport.

_
*I feel that the scenario is inherently flawed in that you begin transport before the process of working through the problem which is just silly.*_

You said it perfectly.

_* I am naturally assuming that the intubation would occur before transport (you guys intubate while racing along L/S?)*_

Tubing before transport is most certainly best practice. Especially when there are more hands than just your MFR to help. On occasion during longer transports I have had to tube medical patients in moving truck. (Tilting the stretcher head to 30 degrees helps a lot.) While moving, by yourself, and the real problem of lack of space, it is quite challenging. I wouldn’t make a habit of it.

*I agree about the CPAP, if we're still worried about airway control (which at least I am), then CPAP is not the way to go. I'm all for addressing the the route cause of the problem as I mentioned earlier, but the dramatic increase in VT altered my thinking. Is it appropriate to be pushing catecholamines into a person who has a quickly worsening problem with VT? Its not rhetorical, I'm actually asking, whats the relationship there?*

With 2 hands, an NPA, and a bag I can control almost any anyway.
 Dobutamine is indicated in cardiogenic shock. Outside the hospital I have never had it. But along the same lines, dopamine will work almost as good. If you look at my earlier statement, it depends on the nature of the heart failure. If you are looking at a condition caused by something such as unstable angina, you first have hypoxia that causes arrhythmia. If you have mechanical failure which causes arrhythmia, you have arrhythmia with hypoxia secondary to it. 

A 67 y/o male (almost certain to have hypertension) subsequent left heart failure, possibly right as well, depending on the time of onset, with most likely a CABG from his scar in this scenario, and despite the med list, most likely on Beta blockade and/or ace inhibitors, his ability to compensate is reduced if not taken away completely, It is my thinking his “faint” s3 sound was caused by myocardial failure. As well, if you became short of breath while driving, I would think most people would try to brake before crashing into a tree as a natural reaction. His condition had to be nearly instantly incapacitating for the events to unfold as they did. Even with unstable angina, people generally are aware they are worsening. I have noticed it is in late stage heart failure people suddenly lose consciousness. They can be talking to you then out, without finishing the sentence as a baseline. In such a case you need the increased contractility. Other than epi or norepi, (which might be too potent for this and not to mention I would have to mix an epi drip.) I couldn’t think of anything else I had on a truck that would do that. The Dopamine receptors in central circulation cause vasodilatation so that would also increase myocardial blood supply in diastole. The effects would be fast enough to be practical, as it is a drip you can simply shut if off if it is not working and do something else in a few minutes as the catecholamine has significantly lower half life than amiodarone. That way if you have to switch from one to the other you have less what I call “mad scientist effect” of having multiple active drugs in the mix. As well there is a Beta blockade effect of Ami on the SA and AV nodes, but I can’t tell you how significant it is.

I also opted out of using Ami as it is indicated for a stable VT. Which this patient is ceetainly not stable by mental status or BP. I am not one of those “you’re going to kill the person” if you don’t follow the exact cookbook types, so I can see where starting with ami might help also.


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## MrBrown

Our guideline for APO/CPE says to particulary look for, and exclude, VT and yet I did not, whoops 

My primary concern is to fix his oxygenation problem.  If he will not take an LMA and we cannot get his O2 up with a bag mask then all I can do is call for an Intensive Care Paramedic able to perform rapid sequence intubation.

As for CPAP hmm .... not sure to be honest.  I know the M&M goes up in patients if you intubate them but I think it may be prudent to intubate this patient before he gets any worse which he may do with or w/o CPAP.  

Now my bet from physiology 101 is that the VT is causing his circulatory and oxygenation problem.  Could try amiodarone or we could cardiovert, I would be more inclined to cardiovert first then and hang up some amiodarone.

I'm going to stay away from lasix.


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## Veneficus

I missed where the patient went from having runs of vtach to just vtach?


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## MrBrown

Apparently I did too.


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## 8jimi8

I don't ever think i said just vtach,

I believe we went from stach with runs of vtach @ 8, 10 , 12 beats to

stach with runs of vtach 20 beats.

after intervention we went to

stach with bigeminal runs.

The reason that I increased the intensity of the vtach is because no one was moving beyond bagging in the airway portion of the exercise, my instructor kept making his O2 sat get worse (refractory to bagging with npa and 100 o2), until I intubated him.  At that point his focus shifted to the runs of vtach.

I understand that everyone is frustrated with the timeline of moving the truck before intubating.

I apologize, that is my fault, I gave you the scenario "half way into" the scenario, if that makes sense.  My bad y'all,  like i said i was going to try and keep it from spiraling into infinite silliness!


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## Veneficus

*I thought you were implying*

because of the Vtach you were going to cardiovert them?



MrBrown said:


> Our guideline for APO/CPE says to particulary look for, and exclude, VT and yet I did not, whoops
> 
> My primary concern is to fix his oxygenation problem.  If he will not take an LMA and we cannot get his O2 up with a bag mask then all I can do is call for an Intensive Care Paramedic able to perform rapid sequence intubation.
> 
> As for CPAP hmm .... not sure to be honest.  I know the M&M goes up in patients if you intubate them but I think it may be prudent to intubate this patient before he gets any worse which he may do with or w/o CPAP.



my primary concern about intubating was the scenario starting in a moving vehicle with a patient in c-spine precautions. That is not conducive to intubation. I agree it would be better to intubate the pt before wheels start turning. 

controlling the airway should not be the difficult part of this scenario.



MrBrown said:


> Now my bet from physiology 101 is that the VT is causing his circulatory and oxygenation problem.  Could try amiodarone or we could cardiovert, I would be more inclined to cardiovert first then and hang up some amiodarone.
> 
> I'm going to stay away from lasix.



I was trying to get to the cause of the VT.


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## 8jimi8

according to my instructor hypoxia was the primary culprit; however in the scenario, taking control of the airway did not lesson the degree of arrythmia.  I guess he was going to see how far I would go.

That is the scary thing about scenarios... lots of slack to tie a noose and then put it on....


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## mycrofft

*I wonder what the ER take on this would be?*

Are there interventions they would rather were not field started (like inadequate IV's) because it muddles the diagnostic, or buggers theirn Rx regimens?


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## Veneficus

mycrofft said:


> Are there interventions they would rather were not field started (like inadequate IV's) because it muddles the diagnostic, or buggers theirn Rx regimens?



In my ieal world, there is no seperation of care. If you do not posess the ability to definitively care for a pt. the goal should be to best prepare them for the next step.

Sometimes that means a treatment to make sure they live that long.
Sometimes it is a happy medium.
Sometimes it means doing nothing at all. 

In a scenario (especially incomplete or unrealistic ones) we can really only say what we would do and why or what the current practices are. 

I try to answer from a personal perspective as I think (and desperately want to believe) everyone who posts a scenario has at least an idea of what the standards of care are.


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## rhan101277

8jimi8 said:


> called to scene of 1 vehicle vs tree.
> 
> Initial impression: no skid marks, moderate frontal damage, no air bag, steering wheel intact, 1 patient, driver restrained - flaccid in drivers seat, driver door won't open due to impact, no entrapment of patient beyond the damaged door.  Fire and LE on scene.
> 
> initial assessment:
> no witnesses
> Your partner takes c-spine
> driver moans weakly to loud verbal stimuli, does not open eyes.
> breathing is shallow and rapid 38/min breathe sounds are wet rales in all fields
> circulation is weak and thready at 133 b/min
> nrb 15l/min
> high priority - rapid transport patient
> medic alert bracelet: Cardiac history, allergy to HCTZ.
> 
> no sample or opqrst available
> rapid trauma assessment reveals pms + (withdraws to painful) in all extremeties, eyes perrl, no signs of basilar skull fracture, no signs of dcapbtls or any obvious trauma (rapid trauma assessment is essentially negative except for a minor oozing laceration to the left cheek)
> baseline vitals 90/50, hr 155, breathing 35 o2 sat 80
> extricate with a KED and long backboard.
> 
> once the patient is loaded in the ambulance 2 large bore IVs
> place the patient on the monitor reveals ...
> 
> multifocal pvcs and runs of paroxysmal vtach 8, 10 , 12
> Oxygen saturation reads 75, patient is breathing 28 /min
> 
> what do you do.
> 
> 
> call out your interventions once the ambulance starts moving.  15-20 minutes until the hospital.  you can have 1 MFR/firefighter in the patient compartment with you.



Continue NRB at 15L

Lidocaine 1mg/kg - tach still present? shock 200J

1000cc fluid bolus re-assess B/P and bolus again

12 lead assessment, treat what you can

ETC02

Take o2 sat with a grain of salt BP low.

Continuous monitor in route


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