ok....whats your take...

[piranah]

I was working a code the other day in the ER status witnessed arrest immediate CPR, EMS within 5 min..pt arrives in ER I cont. CPR...pt asystolic upon arrival (checked in 2nd lead)-pulse/-cardiac activity w/ ultrasound..line unable by EMS..upon arrival line started in L hand...1 mg epi/1mg Atropine admin...cpr cont pt converted to V-fib...shocked @ 200j biphasic.---pt converted to agonal rhythm w/ as the nurse said a palpable @ femoral a approx. 10 BPM....


so hers my question...would you immediately pace this rhythm...since it it technically symptomatic bradycardia.or since it was a re-perfusion rhythm..or would you do something else..I will reveal what we did after a few posts....CALLING RID>>>I WOULD LIKE YOUR INPUT...

 

[MSDeltaFlt]

What were the VS? HR? BP? Do you have a copy of the rhythm? Without that all I can go on is just what you wrote. So, yes. I would pace a wide complex brady at 10.

 

[Ridryder911]

Technically one would not be wrong attempting but in practicality such a slow rate is usually considered aystole.

Even though the nurse felt a pulse I doubt that it was sustainable for very long. Usually patients in aystole; there has been severe damage to the myocardium and most will not respond to pacing; hence why it is no longer recommended in this rhythm.

R/r 911

 

[piranah]

ahh i see.. ok... well we started a dopamine drip at 10 mcg/kg/min but lost cardiac functuion in about 15 seconds after the shock at 200 j......thanks rid/delta it maked sense why he didnt now....

 

[emtbill]

why would you give dopamine to this pt? Seems like a better treatment would be to increase the rate and pace. If you're not going to pace, seems like atropine would be a better drug. My understanding of dopamine is that it has minimal chromotropic effects, and has more inotropic and vasoconstrictove properties, making it better suited for cardiogenic shock. I bet this pt will need dopamine at some point, but I would try to increase the rate first to increase cardiac output.

Just my thoughts...am I wrong?

 

[Veneficus]

why would you give dopamine to this pt? Seems like a better treatment would be to increase the rate and pace. If you're not going to pace, seems like atropine would be a better drug. My understanding of dopamine is that it has minimal chromotropic effects, and has more inotropic and vasoconstrictove properties, making it better suited for cardiogenic shock. I bet this pt will need dopamine at some point, but I would try to increase the rate first to increase cardiac output.

Just my thoughts...am I wrong?

Despite the simplified version of picking up the pace, increasing the rate of an already hypoxic myocardium will just kill what remains due to the increased o2 demand/lactic acid production. In addition, the heart gets most of its energy from metabolism of fatty acids, if the cellular machinery to do this is already impaired (as probable by Asystole) it is pretty much a done deal.

TCP also can cause some direct damage.

There is also the possibility that so much of the heart is already gone, pacing will have little if any effect even if it could capture as all the cells that could fire probably were. It is also very likely the cytochrome C apoptotic cascade already started and in a few minutes nothing would be salvageable anyway. (as witnessed by loss of cardiac function in 15 seconds)

This could be considered cardiogenic shock. Dopamine was probably the best choice to try and increase the effectiveness of contractility by increasing vascular tone. Epi would increase vascular resistance and contractility but also increase 02 demand (providing there were any mitochondria working at all and the carnitine shuttle was operational) so a drip probably wouldn’t work. If you wanted dramatic effect, levofed might have gotten some, but just until you removed it. I also doubt atropine would have any measurable effect as parasympathetic stimulus was probably already suppressed. Depending on the length/severity of hypoxia, it is also possible that the vagus nerve was already impaired or even dead. No telling how good the bystander cpr was either.

I would call the rhythm agonal and terminate efforts, but I think all that could have reasonably been done was done.

 

[emtbill]

Fair enough, but let's assume that the patient is still viable. We could also assume that the patient is bradycardic with a rate of 30 or so rather than agonal. I don't have the luxury of pronouncing patients in the field. So, what's the least of the evils in increasing the heart rate?

The myocardium is already ischemic, and I agree that whatever interventions you do are going to increase oxygen demand even more, but the patient is going to die with a rate of 10 anyway so you (or at least I) would have to do something. Since this is a cardiac arrest patient I assume they are intubated and receiving 100% oxygen. This is all we can do to try to get the pyruvate that is causing the lactic acid production to be converted to acetyl CoA and enter the citric acid cycle and oxidative phosphorylation, right? I can't think of any other way to get those two pathways going, but my biochem is a little rusty. Also, if they're that acidotic, we can also think about bicarb.

I also found it interesting that you say that the myocardium gets most of its energy through fatty acid metabolism. I haven't had any physiology, so I don't doubt you, but that seems inefficient. Although fatty acid metabolism produces about twice as much ATP as glycolysis, it takes longer depending on the length of the aliphatic chain, and this energy would also have to be transported to the heart since it is (or...should be) deficient in fat. The heart will need ATP at a rate much faster than fatty acid metabolism could provide it whereas glycolysis is speedy and there is always glucose available in the blood. Oh well, such is life.

Anyway, back to how to increase heart rate: Although there is a risk for electrical damage, wouldn't TCP cause the smallest increase in oxygen demand since although the rate is increasing, which will increase demand, there are no drugs introduced that themselves cause an inherent increase in oxygen demand like the catecholamines epinephrine and dopamine. Also, I don't know what you mean by pacing being ineffective since all the myocardial cells that could fire were. I thought we used TCP as an external pacemaker to force the cells to fire faster when we don't have time for drugs to work, rather than using it to force some "inactive" cells to fire when they previously were not, or is it some of both?

Lastly, say you succeed in increasing vascular tone and force of contractility using a dopamine drip...is a heart rate of 10 really going to sustain them long enough for the rate to increase on its own? Also, dopamine itself is going to increase oxygen demand which you stated above would kill what remains of the hypoxic myocardium?

 

[Ridryder911]

It all goes back to basic hemodynamics:
Total peripheral Resistance X Stroke Volume = Cardiac Output X Heart Rate = perfusion.

If one has a no cardiac output due to damaged or diseased myocardium, pacing is not going to increase automaticity. One has to have myocardial cells to respond to the stimulus and if the damage is too great it just doesn't matter. Basically a dead heart. Verily rarely heart with so damage can recuperate and cessation of the code should be considered.

Even administering Epinephrine and similar catecholamines, even Atropine will only cause more oxygen demand and realistically only have a short effect until aystole returns. Experienced providers have witnessed numerous times that med.'s have been administered to only see the response to be short lived and then suddenly stop. Death is imminent, and most agree only so much efforts should be attempted as resuscitation is futile.

R/r 911

 

[bonedog]

A trial of pacing early won't hurt if justifiable...all the drugs increase effect MVO2, this never changes in any code.

Anerobic vs aerobic.

As of late the best intervention is continuous compressions, keep the perfusion up, you may reverse some of the ischemic effects.

 

[Veneficus]

ACLS = BLS + some toys

You have to determine what your end game is with a patient like this. Something caused this person to go into cardiac arrest. The underlying condition has to be fixed. (or as close as possible)

Increasing the HR and BP does not mean the body will suddenly return to working order. The purpose of these interventions is to allow certain cells (tissues, organs, etc) to suffer an insult while you keep metabolism in cells etc that cannot absorb or compensate. This artificial compensation buys time for the actual problem to be addressed.

Sometimes the initial insult is self righting, not always and not usually. It is not a set of numbers that determines if a patient is doing well or not. The numbers give you a way to figure out what the patient is doing. I can make a corpse have a bp of 120/80.

What would make this patient viable is not a HR of 30 or any specific blood pressure. What makes a patient viable is the ability to return to physiological function. Without any history you have to consider that epidemiologically this person probably suffered a massive MI. What is the benefit of increasing the workload and demands of a heart that cannot support itself as it is? Are there even enough cells alive to function? The second question we answer clinically, if you cannot achieve ROSC you probably don’t have anything to work with. If you do, and it is not adequate, if you want a save you must consider how to make it work better without damaging anymore. Otherwise your efforts are self defeating.

The short term goal in this patient (and indeed others in the same condition)is to compensate for specific organs.(specifically heart and brain) It will probably take several tests and some epidemiology without a good history or obvious clinical finding to determine what is wrong which will lead to other treatments not available Prehospital or in the ED. Even then it is likely to take days or weeks before there is a good prognosis.

Pacing is useful when other body functions (like disorganized conduction) are impeding the heart from meeting the body’s demand, it is harmful when it is the heart cells that are damaged. (sort of like beating an injured animal) In such case it is best to maintain what you have and let cardio/thoracic surgery or other specialist for the specific pathology take care of the problem. But you can kill viable patients by pacing them to make the numbers you want to see.

There is no hard fast rule; it is a judgment call you have to make on a case by case basis. Welcome to medicine. :wacko: