RVI Protocols

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skyemt

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Hi there...

just wondering if systems out there have separate protocols for RVI's...

we do not, but RVI seems to be gaining quite a lot of traction as it's own subgroup of coronary syndromes.

i've read where Fentanyl could be better for pain than Morphine, due to Morhphine's vasodilating properties...

how are you handling RVI's differently?

thanks...
 
When you say "RVI" are you reffering to Right Ventricular Infarction?? If so, it is good that you enquire about subjects which are not in your scope of practice (I am not ignorent, just not 100% on top your your protocols, my bad)?? This is good to a certain extend, because it can motivate you to furthr yourself.

Yes, i know it is important to distinguish between the differefent types of Myocardial Infartions because some of them get treated differently. However id do believe that these diagnosis are best reserved for the specialist in a controlled environment. We do not carry 12 a lead ECG machine in order to look at the heart from all the angles and make such a specific diagnosis, although we should have the knowledge to diagnose when the oppertunity presents, i.e. at a primary health care cilinic or using modified chest leads, should time permit.

On a basic level your concern would be to administer a high percentage of O2, calm and reasure, don't let the patient exert themselves, and make haiste to difinative care.
 
yes, Right Ventricular Infarction...

our agencies carry 12 leads....

i am not asking for treatment options at the basic level, i am not that ignorant to think there are any, other than the obvious...

i do want to learn, and it is towards that end that i am asking...
 
Thank you for clearing that up!!

With "RVI" some text refer to it presenting as a brady & hypotension which is treatable with a N/S boulus (Small). The only difference, from other AMIs, i know about is that of using Nitrolingual Spray (as we know it), whereby it is noted as a specal precaution prior to administration or as a contra indication, depending on which text you use. The package insert notes it as a special precaution.

Hoping that answers your initial question...
 
Many EMS now have attachment protocols if right sided infarct is suspected to perform right sided ECG & posterior view, 15 lead if possible to be able to distinguish if it is truly a right sided infarct or not.

As described Morphine may be used cautiously or a substitute such as Fentanyl, and possibly a fluid bolus if hypotension and possibly TCP if bradycardia. Notification for cath lab should be emphasized as well.

Some prepare for possible "flash pulmonary edema", as right sided infarct can cause acute CHF as well.

R/r 911
 
Ridryder911 said:
Many EMS now have attachment protocols if right sided infarct is suspected to perform right sided ECG & posterior view, 15 lead if possible to be able to distinguish if it is truly a right sided infarct or not.

As described Morphine may be used cautiously or a substitute such as Fentanyl, and possibly a fluid bolus if hypotension and possibly TCP if bradycardia. Notification for cath lab should be emphasized as well.

Some prepare for possible "flash pulmonary edema", as right sided infarct can cause acute CHF as well.

R/r 911
Click to expand...


can you please tell me more about "flash pulmonary edema"...
 
Sure "flash pulmonary edema" is usually r/t an AMI so an acute (fast onset) of CHF will occur. This is not the usual symptoms one sees such as gradual onset of peripheral edema, increasing nocturnal dyspnea, weight gain, etc. Rather flash pulmonary edema is usually associated with poor ejection fraction (amount pumped out) from the left ventricle. So those that are having an AMI may present this along with rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is caused by the result of acutely elevated cardiac filling pressures (which is cardiogenic pulmonary edema). Also acute decompensated heart failure (HF) can also be present as the elevated left ventricular filling pressures and dyspnea without pulmonary edema. (sometimes called cardiac asthma).

Although more commonly seen in left sided failure, we need to remember right side occurs first causing pulmonary congestion and as well pulmonary hypertension may be present.

Basically in short they are in CHF without external signs of CHF.

I had a patient two days ago that initially had some expiratory wheezes and increasing ShOB, patient had no chest pains or peripheral edema. I initially treated the patient with nebulized medications, within 3-4 minutes the patient exhibited acute harsh rales & rhonchi and extreme ShOB. The saturation rate dropped suddenly from 94% to 86% again within 3 minutes.

I noted that the patient appeared to have a possible old inferior wall infarct, and who knows maybe another one? My treatment of course changed to CPAP, in which the patient described ShOB decreased. Again, the patient never exhibited HTN, edema, or even chest pain. Due to the possible inferior wall or right sided involvement I witheld NTG, and due to the increase pulmonary congestion, I was cautious with fluids. Patient was normotensive.

The problem is many may not catch the cause and only attempt to treat the initial symptoms.

R/r 911
 
Last edited by a moderator:
Ridryder911 said:
Sure "flash pulmonary edema" is usually r/t an AMI so an acute (fast onset) of CHF will occur. This is not the usual symptoms one sees such as gradual onset of peripheral edema, increasing nocturnal dyspnea, weight gain, etc. Rather flash pulmonary edema is usually associated with poor ejection fraction (amount pumped out) from the left ventricle. So those that are having an AMI may present this along with rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is caused by the result of acutely elevated cardiac filling pressures (which is cardiogenic pulmonary edema). Also acute decompensated heart failure (HF) can also be present as the elevated left ventricular filling pressures and dyspnea without pulmonary edema. (sometimes called cardiac asthma).

Although more commonly seen in left sided failure, we need to remember right side occurs first causing pulmonary congestion and as well pulmonary hypertension may be present.

Basically in short they are in CHF without external signs of CHF.

I had a patient two days ago that initially had some expiratory wheezes and increasing ShOB, patient had no chest pains or peripheral edema. I initially treated the patient with nebulized medications, within 3-4 minutes the patient exhibited acute harsh rales & rhonchi and extreme ShOB. The saturation rate dropped suddenly from 94% to 86% again within 3 minutes.

I noted that the patient appeared to have a possible old inferior wall infarct, and who knows maybe another one? My treatment of course changed to CPAP, in which the patient described ShOB decreased. Again, the patient never exhibited HTN, edema, or even chest pain. Due to the possible inferior wall or right sided involvement I witheld NTG, and due to the increase pulmonary congestion, I was cautious with fluids. Patient was normotensive.

The problem is many may not catch the cause and only attempt to treat the initial symptoms.

R/r 911
Click to expand...

this is very interesting... we picked up a 72 y/o female a few weeks back, presented with expiratory wheezes, dypsnea... symptoms were sudden onset in the early am, which woke her out of her sleep... she was in obvious respiratory distress, could not complete sentences, but still denied she was in distress... she denied any chest pain or discomfort... there was some pedal edema, which patient said was normal for her... also of note, was a syncopal episode the previous evening, which was new for her. she exhibited some s/s of what you would have thought could be CHF, but there was no history there...

Med control was contacted, and advised us to give a combi treatment for the respiratory distress... the patient did not improve...

tests done at the hospital confirmed an MI... CHF-like symptoms were secondary to the MI.

this sounds exactly like what you are talking about, although even after discussion about this case, i had not heard the term "flash pulmonary edema"...

Rid, is this what you were referring to?
 
Sky to me what you describe is typical of CHF related pulmonary edema.

Wheezes, dyspnea, pedal edema, onset at night, probably has nocturia to go with the orthopnea, maybe JVD, HTN, HJ reflux, S3, SOBOE, all fits.

Flash pulmonary edema happens FAST, no gradual onset. The ones I have seen come on in under 3 hours, sometimes 20 minutes. Often they will have coarse rales, productive red sputum which if tubed turns into a geyser.

I try to listen for heartsounds on these pt's to rule out valvular causes, which if identified indicate intubation and rapid transport.

As with an inferior IF you can ID a R MI, NTG/beta blockade/morphine avoid.

I do V4R often if I am seeing inferior involvement.

High JVP, low BP, clear lungs = R infarct
 
Bone Dog is correct describing they will usually have "pink frothy sputum". These patients are on the teeter totter of going down the drain. CPAP does make a difference, but sometimes the event is so drastic intubation (elective or have to situation).

I have seen so much frothy sputum that it will go into the BVM, and suctioning seems like a consistent thing.

As I described many of these patients do not make it.

R/r 911
 
Do you guys need to do anything to your 12-lead monitors other than move the electrodes and label?

On my monitor I'm suppose to just move the V3 to V6 electrodes to stick on the right side, then label the print out with V3R, V4R, V5R, V6R. I'm just curious if your monitors need you to push another button to relabel them.
 
bonedog said:
Sky to me what you describe is typical of CHF related pulmonary edema.

Wheezes, dyspnea, pedal edema, onset at night, probably has nocturia to go with the orthopnea, maybe JVD, HTN, HJ reflux, S3, SOBOE, all fits.

Flash pulmonary edema happens FAST, no gradual onset. The ones I have seen come on in under 3 hours, sometimes 20 minutes. Often they will have coarse rales, productive red sputum which if tubed turns into a geyser.

I try to listen for heartsounds on these pt's to rule out valvular causes, which if identified indicate intubation and rapid transport.

As with an inferior IF you can ID a R MI, NTG/beta blockade/morphine avoid.

I do V4R often if I am seeing inferior involvement.

High JVP, low BP, clear lungs = R infarct
Click to expand...

well, her CHF symptoms started suddenly in the middle of the night, woke her up... she never had any type of CHF or related symptoms before...

isn't that what you are referring to with "sudden onset"?
 
Sky, unless she had woken' up and then developed the symptoms the onset time may have been over the amount of time since she went to bed, then awoke. eg to bed at 2100 wake at 0330 with dyspnea. This is typical of the CHF pt who has a stressor ( forgot med, excessive salt intake, recent emotional stress, infection,etc) and develops from chronic compensated CHF to decompensated pulmonary edema. As your pt had no symptoms prior to this she was most likely a new onset MI, which with pulmonary edema makes for a bad prognosis.

Sudden onset I have seen is the patient suddenly feels short of breath, calls us and sits down and we find them in the pink frothy state, catecholamine overdrive, maybe obtunded.

IF it is a ruptured papillary muscle our tx is severely limited, transport is also of utmost importance, same as if it is a new onset MI. That being said ABC's as usual are paramount.(assist vents or tube, what ever will get you by)

Markhk, I would do the V4R and put 3/5 posterior, just below the left scapula. Then mark it as either R or P on the print out.

IF only they would do another study on cardiac pain in females, as the indicators emperically accepted all relate to middle aged males.

Personally females often present with burning or indigestion, big flags for me, unless they are over 65 ish, then many times they are just "weak" or exercise intolerant = MI.
 
I used to use PPV long time ago. It is difficult, but with some coaching I have seen it work. We now use CPAP quite a bit. I do not remember the last elective intubation I performed on a CHF'er. Even in the small service I work at I would state I use CPAP at least twice a week. Our physicians love it and are now switching it to Bi-pap after the danger period. (I'll let Vent discuss this more)

When I do have to intubate, I am cautious about the vent settings and personally like using PEEP, which I find most medics do not understand.
(Again, I will allow Vent to give her view).

The main emphasis alike all medical cases is a thorough history as much as possible, and a good and thorough assessment. Alike bonedog discussed even listening to heart tones to detect possible regurgitation or a floppy valve is a good indicator to add such as S3, S4 gallop.

R/r 911
 
we do not yet have CPAP in our protocols... however it is coming...

but the plan will be to use CPAP pre-hospital, and the switch over to Bi-PAP at the receiving hospital...

does this make sense to you, as opposed to just using BI-PAP pre hospital?
 
Most modules of prehospital CPAP devices cannot perform Bi-Pap. It is a totally different mode.

I do believe the new EMT curriculum will allow Basics to administer CPAP in the future. We are going through our finalization to allow Basics to perform such in my state.

R/r 911
 
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