Are we saving hearts and killing patients?

NYMedic828

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I think it's more an issue with how some people administer it.

The theory behind giving pressors is good. Constrict peripheral vessels to enhance blood flow to vital organ systems.

I've worked with many providers who feel its a wise idea to just pump the amps of epi into the patient.

Our protocol here in NYC is vasopressin 40units prior to epi, but vaso must be drawn up from two separate 20u vials vs the 1 amp ready to go of epi. Often we get epi first to save some time, but then people will put vaso on top of it as soon as they have it ready. Followed by another epi in 2 minutes.

There is a reason it's meant to be given q5. We don't go giving 0.3mg of epi, IM to every patient right out of the gate, why in the world do people think its a good idea to give 5mg IV in a rapid timeframe. The circulating influx of catecholimines in that high a dose of can cause more harm than good especially in the elderly.
 

Veneficus

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I remember describing the very physiologic mechanism behind this at least a year ago.

It is unfortunate there is such a lag time between academic medicine and clinical medicine. Perhaps it is why there is such a disparity between academic hospitals and community hospitals and providers?

The theory behind giving pressors is good..

Says who?

Constrict peripheral vessels to enhance blood flow to vital organ systems...

A flawed theory of amateurs.

Genrally heart, brain, and kidneys are considered vital...

But, exogenous vasopressor administration can actually shut off circulation.

Dopamine, epi and norepi can actually do so at afferent and efferent renal and cerebral arterioles. Effectively stopping blood flow in 2 of these vital organs.

But there is another important flaw in the theory.

The GI organs and their accessory organs are vital to life. You cannot live without a liver, small intestine, etc.

There is an old idea that these organs could survive a temporary insult because they had regenerative capability. It was the best idea of the time, but grossly oversimplified and lacked integrated understanding.

Without a functioning liver, you cannot clear nitrogen and other metabolic wastes. (no urea produced) Nitrogen is toxic. You cannot produce albumin, clotting factors, cell proteins etc.

You cannot replentish glycogen stores, utilize fatty acid metabolism, convert lactate to pyruvate, or other metabolic processes.

Sure the liver can regenerate, but at least part of it must survive, and what is going to perform the role of the liver in the days, weeks, and months, required for regeneration?

Without a working gut, you cannot absorb nutrients and reabsorb water.

What's worse is you create the pathological effects of systemic inflammation, which will take its toll on both the lungs and nephrons. (which can lead to ARDS, renal failure, etc.)

There is also the problem of the immunological ability to keep gut flora in check or replentish the guts' cellular integrety to stop said bacteria from infiltrating the abdomen.

You might also find it very hard to live without things like adrenal glands or a pancrease.(for both exocrine and endocrine functions of the later)

Even the spleen which was once thought of as totally optional has multiple vital functions including a physiologic cell reserve and helps removes blood born pathogens.

What is the logical outcome of every skeletal muscle in the body producing lactate and a liver that cannot convert it?

Back to renal blood flow, when you decrease it, you lose erythropoetin excretion, which helps prevent apoptosis and helps to induce mods beyond the mere loss of the kidney.

In females when the highly vascularized reproductive organs infiltrated with both fungus and bacteria lose structural stability and immune function, you have the same issue as in the gut.


Ischemic bone also loses structural and functional capacity. (like making
both RBCs and WBCs.)

Often we get epi first to save some time, but then people will put vaso on top of it as soon as they have it ready. Followed by another epi in 2 minutes..

So in a heart that cannot maintain the most minimal of cardiac output to sustain itself, the plan is to increase peripheral resistance so it must work harder to maintain the same output?

There is a reason it's meant to be given q5. We don't go giving 0.3mg of epi, IM to every patient right out of the gate, why in the world do people think its a good idea to give 5mg IV in a rapid timeframe. The circulating influx of catecholimines in that high a dose of can cause more harm than good especially in the elderly.

Why do you think there is inadequete physiologic catecholsamine reserve?

Even in a normal adult, how much is too much?

In elderly people most which in the 21 century has advanced vascular disease, how much "clamping down" does it take to completely shut off renal or cerebral blood flow? (or any other organ for that matter)

Why do we think the same dose of epi in a 50 year old SCA is right for the 70 year old with the same? How about a 10 year old?

The people in this study simply reproduced what the Australians did several years ago. Which was the same thing discovered even earlier by pathophysiologists.

No difference in 30 day survival, why not just shoot the patient and get it over with cheaper?
 

NYMedic828

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You are a god amongst mere mortals...

Always excited to see a reply from you since I know I can spend the rest of my shift decoding what you said and learn a great deal.

It never occurred to me for some reason that increasing PVR obviously increases afterload greatly.

I knew that all those pressors in the system was not so great in reality but I wasn't aware that it was powerful enough to actually constrict so far as to cause ischemia to basically everything but the heart and brain.

As the new guy, it's hard to get my partners to understand why we shouldn't just pump this stuff into people.

I had to stop my partner the other day who was about to combitube a ROSC who was breathing adequately. (he couldn't get the tube)
 

firetender

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From the boneyard

When I started out as a paramedic in the mid-1970's I worked in a small seaside town in Florida, pop. about 10,000 most of whom were retired and the rest pretty much taking care of them.

I didn't question much about the drugs I administered for cardiac arrest back then because they worked. Bicarb, Epi and ZAP! repeated again and again really did snap people back. But it wasn't until the last couple of years in reading stuff like this on this site that I realized my stock in trade was creating what we called "Cardiac Cripples."

Because I knew most of the regulars (only one ambulance in the area) and had access to all areas of the one local hospital, I got to see the aftermath of what I called back then "Clean Saves". The survivors' bodies were revived but not revitalized, making them pretty much shells tethered to oxygen and IVs (often at home) until their next arrest occured and there I'd be, bringing them back again!

Sadly, even though this article speaks of one month after discharge, I experienced more than a few of my patients lingering in such a hellish roller coaster limbo for as much as a couple of years. The suffering was spread throughout the family.

What is being spoken of is a "rebound effect" where the body is traumatized by losing heartbeat and then jump-started into life again and then experiencing the crash coming from the body's attempt to re-adjust and then re-establish homeostasis.

What isn't spoken about much is that getting the patient over the hump -- bringing him/her back from the dead -- means the administration of one drug after another in singles, tandems and God knows how many other variations, each of which carry rebound effects of their own and further complicate, if not stymie, recovery.

I honestly do not believe that today's "evidence-based medicine" is adequately addressing the interactions of the heavy-hitting drugs being used on critical patients and it's lowering the quality of life of patients who do survive.

If you think I'm off base, consider that -- as a whole -- we are proving that the agressive treatment of possibly fatal maladies by the use of pharmaceuticals brings with it more long-term problems than it solves in the short term.

Could that explain why a new trend is developing to move critically stricken patients into a suspended animation state through hypothermia and other means?

The philosophy of intervention is changing, and fast! Aggressive drug treatment, the way it is practiced today, is a juggling act, and all too often with a symptom-by-symptom approach without fully understanding how the body gets whip-sawed around by the combinations. Sure, there's lots of information on paper, but that doesn't really deal with the individual's personal, unique phisiology.

What this article addresses is a core problem in medicine today; we want to "buy time" but we haven't figured out how best to do it.
 
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