Couple of questions.... (In medic school)

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DieselBolus17

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Hi all, been a long time reader of these forums, finally made an account today. I am in Paramedic school and I have a few questions for you guys. I tend to over think things a lot, so these may sound stupid, but I just need clarification.

First, the use of Epinephrine in cardiac arrest. To my understanding, vasoconstriction of vessels increases pressure, but reduces flow, and the opposite is true for vasodilation, pressure decreases and flow increases. With that said, if the flow of blood decreases when Epinephrine is administered, would it not be detrimental in Cardiac arrest since you are reducing the flow of blood? To my understanding, since Pressure is 0 while in cardiac arrest, Epinephrine is given to constrict the vessels so the blood is propelled with enough force to reach the heart, brain, ect, but going back to the reduced flow of blood in constriction it doesn't make sense. (again overthinking).

My second and last question is about Nitroglycerin. First if triple A or thoracic aneurysm is suspected, would Nitro be completely contraindicated? From what I have read in, in the hospital setting Selective Beta 1 Blockers are administered to maintain these Pt's BP between 100-120 mm/Hg and send them straight to surgery. I know Nitro is primarily a Vasodilator (mainly Venous) but with arterial effects as well, if Nitro was administered and thus dilating arteries, would the dissection get worse since you are essentially enlarging that artery and increasing the flow of blood?


Thank you all in advance, I apologize if these questions sound stupid.
 
Good questions. I'll take a stab:

Regarding epi, its alpha effects constrict peripheral vasculature, shunting more blood to the brain which is what we care about. It also might help make compressions more effective by giving you some resistance to push against. We also like epi for its beta effects, which in VFib basically increase the vigor of the fibrillation making it perhaps more likely to convert into something after we shock it. Lots of good info here: http://www.medscape.com/viewarticle/534012_2
(this is all basically conjecture and there isn't any actual evidence to suggest that epi helps patients at all in the long run... But eh, what the heck)


Regarding question 2, make sure you are careful to differentiate between aneurysm and dissection - they are not the same thing. Nitro shouldn't be contraindicated in either case, I think. But it isn't indicated under my protocols so I wouldn't give it...

You aren't "enlarging the artery" so much as you're relaxing the muscles that cause it to contract. Relaxing vascular smooth muscles should lower the pressure in the aorta and make a AAA less likely to rupture or a dissection less likely to get worse. I think. We are allowed to adjust the dose of a nitroprusside drip if the hospital starts one on an aortic dissection pt, so I assume it must not be terrible to give them nitro. If I had a high suspicion of AAA or aortic dissection, a long transport time and a hypertensive pt I might call med control and see if I could get orders for a beta blocker or something.
 
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They're doing a study in the UK looking at epi citing cerebral hypervasoconstriction causing poor outcomes, we'll see. But what JB said is correct, that's the thought at least.

2. The aorta doesn't constrict or dilate. What nitro does do is cause rapidly fluctuating blood pressures since we're blasting away with 400 mcg. Will you kill them with nitro? Probably not but it's not indicated.
 
Handsome Robb said:
They're doing a study in the UK looking at epi citing cerebral hypervasoconstriction causing poor outcomes, we'll see. But what JB said is correct, that's the thought at least.

2. The aorta doesn't constrict or dilate. What nitro does do is cause rapidly fluctuating blood pressures since we're blasting away with 400 mcg. Will you kill them with nitro? Probably not but it's not indicated.
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I see. So with the Aorta not constricting or dilating. Would it be correct to say that Epi constricts Peripheral arteries (extremities, ect) reducing their blood flow and shunting the blood to the Aorta to supply the core organs (heart, brain, kidneys, ect) in the case of cardiac arrest?
 
The idea behind epi in arrest is that it causes vasoconstriction of the peripheral vessels, which shunts blood to the brain and heart. It can also dilate or constrict coronary vessels, depending on the dose.

In an aortic aneurysm, you want to decrease shear stress (pressure) on the walls of the aorta. This is done by reducing SVR on both the aortic (after load) and venous side (preload). Nitrates are good at that. Beta blockers are used to slow heart rate, which also translates to less wall tension.
 
Was your instructor not able to assist with these questions?
 
DieselBolus17 said:
I see. So with the Aorta not constricting or dilating. Would it be correct to say that Epi constricts Peripheral arteries (extremities, ect) reducing their blood flow and shunting the blood to the Aorta to supply the core organs (heart, brain, kidneys, ect) in the case of cardiac arrest?
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That's the line of thinking however like Remi stated and I said before they think the cerebral and coronary vasoconstriction may be worsening outcomes. There's already one study out there that shows epi increases ROSC but didn't help and possibly hurt 30-day mortality. It was in Japan I'll try and find it or at least the abstract for you.

Remi, I agree that nitrates in a drip are great for reducing SVR but what are your thoughts on SL nitrates? Seems the highs and lows caused by the massive dose and potential reflex hypertension would cause excess stress on the vessel wall but I may be totally off base here.
 
Handsome Robb said:
Remi, I agree that nitrates in a drip are great for reducing SVR but what are your thoughts on SL nitrates? Seems the highs and lows caused by the massive dose and potential reflex hypertension would cause excess stress on the vessel wall but I may be totally off base here.
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Big bounces in BP are definitely a concern. I'd probly rather do the best I can with fentanyl + labetolol (or metoprolol or esmolol) rather than SL ntg.

Then again if SL ntg is all you have, slow and consistent admin should be OK in most patients. It's hard to say because responses to SL ntg seem so variable.
 
DieselBolus17 said:
My second and last question is about Nitroglycerin. First if triple A or thoracic aneurysm is suspected, would Nitro be completely contraindicated? From what I have read in, in the hospital setting Selective Beta 1 Blockers are administered to maintain these Pt's BP between 100-120 mm/Hg and send them straight to surgery. I know Nitro is primarily a Vasodilator (mainly Venous) but with arterial effects as well, if Nitro was administered and thus dilating arteries, would the dissection get worse since you are essentially enlarging that artery and increasing the flow of blood?
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NTG is not actually indicated in spray form, perhaps as a drip (although in my research on the topic for a textbook chapter it never came up). More common vasodilators for dissections are nicardipine or nitroprusside. However, nitroprusside can cause cyanide toxicity after long enough infusions. The patient's sympathetic response, typically elevated, is also blunted with short acting B-blockers such as esmolol or metoprolol.

What does this mean for 911 units? Don't touch it. Critical care providers may have some leeway, but honestly this is something you'd need good confirmation of prior to initiating this treatment.
 
These patients are often in a lot of pain and their hemodynamics can potentially benefit significantly from good analgesia. Fentanyl should probably be viewed as a first-line med for these patients, and some analgesia may be the best thing you can do in the field.
 
Remi said:
These patients are often in a lot of pain and their hemodynamics can potentially benefit significantly from good analgesia. Fentanyl should probably be viewed as a first-line med for these patients, and some analgesia may be the best thing you can do in the field.
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Agreed. I've had two patients with dissections, so a bit different but still similar. Both looked like absolute dog-poo, had crap for vitals and were coming absolutely unglued. Also...both had the "death poop" happen. I'm still trying to find a good reason behind that last one...
 
Do some reading on the difference between large/conducting/elastic arteries, medium/distributing/muscular arteries, and small/resistance/arterioles. They do different stuff and it does matter.
 
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