There are reasons doppler ultrasound is used in the ED.
One could also check for an LVAD but hopefully that is noticed quickly.
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That extra 60 seconds.
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There are reasons doppler ultrasound is used in the ED.
One could also check for an LVAD but hopefully that is noticed quickly.
mycrofft
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As I treid to spell before, "CLINICALLY pulseless"
Sort of the opposite of EMD.
Sort of the opposite of EMD.
emtbill
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wait...what?
The dosage of atropine for symptomatic bradycardia in an alive adult patient 0.5 mg. That's what I was taught and is the dosage I give to my patients. One milligram is for an asystolic/slow PEA cardiac arrest. Can you have that much leeway when giving cardiac drugs (I'm a new ALS provider)?
FF894
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If he was CAO I would hope he would mention that part....
FF894
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No, its ok - it was 2am. If 0.5mg will work then 1mg will work better.
TJ_EMT quote
Doppler ultrasound is used on patients when pulses can not be readily palpated. On some people you just can't feel a pulse easily and that is why the AHA changes some of its quidelines for lay person CPR.
Unltrasound is also used to determine any cardiac activity during a code. Btween that and the ETCO2, we have a good prediction for resuscitation success.
At least cardiac monitors today are usually sophisticated enough to identify a problem with the electrodes...but not always.
It is not that uncommon to see a patient awake during VT and the doppler may be used to assess the pulses or BP but often it is not required. VT may perfuse very well for extended periods of time. A person can be shocked from V-fib and awaken. That usually happens best when the healthcare provider is at beside. The precordial thump can work well in the ICU.
Pt's with Sick Sinus Syndrome with have up to 20 second pauses regularly which looks frightening on a monitor screen of a just a few seconds. Some may feel asymptomatic while laying in bed. These patients usually frustrate me if I'm trying to draw arterial blood.
OP
OP
YYCmedic
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Our protocol for bradycardia is Atropine 1.0Mg IV q 3-5 mins to max of 3.0Mg or 0.04Mg/Kg. Our Asystole/PEA protocol is the same.
One way I look at it is like this:
If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.
A cardiac patient who is having an inferior MI will frequently present atypically- they will most often complain of nausea and vertigo. Such a patient who has a seizure is likely experiencing runs of VT or VF. In such a case, time is critical and preventing the patient from going over the edge is a challenge.
You did not mention what rhythm was producing the HR of 30. Was this a wide complex brady? Possibly a ventricular escape rhythm? Or was it a high degree AV block? Since this was an inferior wall, did you perform a 12 lead containing a right sided lead, such as V4R? If there was right sided involvement, that further complicates things.
Atropine given in such cases has been known to precipitate VF. Atropine increases myocardial oxygen demand, and if it fails to increase cardiac output in the process, you have just made the problem worse.
A better choice in such a case could be dopamine at 2-10 mcg/kg/min, assuming that pacing is not possible. Remember that this is a cardiogenic shock you are dealing with here.
If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.
A cardiac patient who is having an inferior MI will frequently present atypically- they will most often complain of nausea and vertigo. Such a patient who has a seizure is likely experiencing runs of VT or VF. In such a case, time is critical and preventing the patient from going over the edge is a challenge.
You did not mention what rhythm was producing the HR of 30. Was this a wide complex brady? Possibly a ventricular escape rhythm? Or was it a high degree AV block? Since this was an inferior wall, did you perform a 12 lead containing a right sided lead, such as V4R? If there was right sided involvement, that further complicates things.
Atropine given in such cases has been known to precipitate VF. Atropine increases myocardial oxygen demand, and if it fails to increase cardiac output in the process, you have just made the problem worse.
A better choice in such a case could be dopamine at 2-10 mcg/kg/min, assuming that pacing is not possible. Remember that this is a cardiogenic shock you are dealing with here.
The Doppler ultrasound is probably one of the most useful tools one could have access to. Not all of what you think to be the truth is actual reality. You can not treat PEA if one still has a pulse. There are many other effective treatments for low BP that doesn't involve running a code algorithm.
Textbook numbers are great but not always appropriate for every patient. There are, again, reasons why the AHA changed some of its guidelines.
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That would be why it is now called PEA and not EMD. PEA means PULSELESS. If it is not pulse producing, explain to me why I care? Where in any ACLS situation does it say use a doppler? Why do you think that is?
If you are not perfusing the brain with oxygen, it does not matter if you have some small amount of cardiac output. I see so many in the ER wasting time looking for a doppler pulse, when there is no blood pressure perfusing the brain.
If you are not perfusing the brain with oxygen, it does not matter if you have some small amount of cardiac output. I see so many in the ER wasting time looking for a doppler pulse, when there is no blood pressure perfusing the brain.
WuLabsWuTecH
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Sorry, a bit of a sidetrack...
Really? We were taught 60 mmHg for perfusion of the brain (palpable carotid pulse). 70 mmHg for femoral, and 80mmHg for radial. Is this not right?
WuLabsWuTecH
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I think i'm confused a bit, or just really tired today.
If you're in PEA -- Pulseless Electrical Activity -- how can you still have a pulse?
If people don't immediately feel a pulse they assume it is PEA. If the doppler picks up blood flow or a pulse, it is NOT PEA and should not be treated as such.
Arkymedic
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People assume that because that is correct. PEA is defined as:
A form of cardiac arrest in which the continuation of organized electrical activity in the heart is not accompanied by a palpable pulse or effective circulation.
PEA is composed of a group of rhythms that include:
EMD
pseudo-EMD
idioventricular rhythms
ventricular escape rhythms
post-defibrillation idioventricular rhythms
bradyasystolic rhythms
The only thing a doppler tells you is that you are not dealing with EMD. The rhythm is still PEA. In this case, we KNOW that this is not hypovolemia or EMD. This is obviously a cardiogenic shock. What good does a doppler do here?
Have you seen a doppler ultrasound in action?
True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity.
Pseudo-PEA is what you have described. The doppler ultrasound may assist with identifying the presence of cardiac contractions. Patients with pseudo-PEA may have a rapidly reversible cause such as auto-PEEP and hypovolemia. Auto-PEEP is a condition of over ventilation either mechanically by a ventilator or manually with a BVM. It can be easily remedied.
Compressions and initiating the PEA protocol maybe needed but a different plan of care may be taken according to the heart's contraction quality and tamponades as well as other cardiac structure problems can also be readily identified.
You may be limited to only the capabilities within your service but don't knock those that are in progressive EMS systems or the EDs that routinely utilize this technology. It is another tool to provide a more patient defined treatment. The doppler ultrasound is also now listed in almost every service capable of doing doppler ultrasound or ED ACLS protocols. Combine that with the ETCO2 and one can see if their resuscitation efforts are going in the right direction.
Granted, the ultrasound is not cost effective for every EMS service and the training might be even more farfetched to consider for some services where Paramedic insist on just getting trained by the slim contents of the new ACLS book of guidelines. In many EMS systems the doppler ultrasound would probably not change the care given because of limitations in their practice. But, that doesn't make the use of the doppler ultrasound wrong in the hands of trained and educated providers.
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EMD, Electrical Mechanical Dissassociation is coordinated electrical activity with an absence of myocardial contractions. That is exactly what the name means, the electrical system is active, but is disassociated from the myocardium. If you were to open the chest, you would see that the heart is not contracting at all.
Pseudo EMD is electrical activity with coordinated muscle contractions that produce cardiac output that is not palpable- this is what a doppler detects. That is, you are moving blood, but not at a palpable pressure. The most common cause for this is hypovolemia.
There is no such thing as pseudo PEA. You are confusing PEA and EMD.
Don't take my word for it, read a cardiology journal:
http://www.chestjournal.org/cgi/reprint/101/1/123.pdf
We measured aortic pressure during clinically apparent
cardiac electromechanical dissociation (EMD). Patients
with pulse pressures were designated as having pseudo-
EMD; those without, as having true EMD.
Don't patronize me about being progressive or about experience. This is not about who is the biggest kid on the block. Simply put, in a code situation it is in appropriate to play with toys when your patient is not perfusing. I know it isn't sexy, but the fact is, we treat patients, not technology.
Pseudo EMD is electrical activity with coordinated muscle contractions that produce cardiac output that is not palpable- this is what a doppler detects. That is, you are moving blood, but not at a palpable pressure. The most common cause for this is hypovolemia.
There is no such thing as pseudo PEA. You are confusing PEA and EMD.
Don't take my word for it, read a cardiology journal:
http://www.chestjournal.org/cgi/reprint/101/1/123.pdf
We measured aortic pressure during clinically apparent
cardiac electromechanical dissociation (EMD). Patients
with pulse pressures were designated as having pseudo-
EMD; those without, as having true EMD.
Don't patronize me about being progressive or about experience. This is not about who is the biggest kid on the block. Simply put, in a code situation it is in appropriate to play with toys when your patient is not perfusing. I know it isn't sexy, but the fact is, we treat patients, not technology.
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When did you last take an ACLS class?
That article is from 1992.
You no longer have to crack the chest to see heart movement. We now have ultrasound in the year 2008.
Please refer to page 52 of the current ACLS book.
PEA is one of those different situations where you may have to search for a cause. If you don't find a cause quickly that can be corrected, the code will probably be futile and the patient will be dead.
If I have access to ultrasound or a Point-of-Care machine to assist me in finding one of the Hs and Ts, I will use it.
You have to know what the advantages and capabilities are for each piece of technology. Don't be afraid of technology but do understand it.
That being said, am I going to trust an SpO2 reading on a patient we are doing chest compressions on? No.
However, when it comes to the ETCO2 monitor, many just use it to "see a wave if the tube is in" with little or no idea of all the information the machine can provide if correlated to the patient.
I was making a point. I TEACH ACLS as an EP instructor, and have for quite a few years. I understand and use doppler. I also stand by my statements. Go play with your toys, I will continue to save actual patients.
I repeat my original question:
What would a doppler have done to help this patient? Nothing. This was a cardiogenic event. Doppler will solve nothing here.
I am out of this pointless conversation.