DesertMedic66
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As long as it's EMS related lol
the 100% directionless thread
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As long as it's EMS related lol
I think that's a topic for a different day :unsure:
I have a question that I've been going through for a few days now and every time I answer part of it, it opens up another question. haha
So I've found out the reasons that CPAP would cause a BP drop. So, just a question, if you have a pt that has CHF and is hypotensive (which wouldn't be too much of a reach), do you just forego the CPAP and leave the fluid? Just push some lasix and call it good...? Technically, my protocols don't say anything about hypotension, but knowing it would drop it, what would you theoretically do? For obvious reasons you don't want to put more fluid in to keep the BP, so...
I have a question that I've been going through for a few days now and every time I answer part of it, it opens up another question. haha
So I've found out the reasons that CPAP would cause a BP drop. So, just a question, if you have a pt that has CHF and is hypotensive (which wouldn't be too much of a reach), do you just forego the CPAP and leave the fluid? Just push some lasix and call it good...? Technically, my protocols don't say anything about hypotension, but knowing it would drop it, what would you theoretically do? For obvious reasons you don't want to put more fluid in to keep the BP, so...
Anjel
Forum Angel
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I'm finally embracing my night shift sleep schedule. So what if I sleep during the day, and party all night ;-p.
All the fun happens at night anyway.
All the fun happens at night anyway.
That's what I do. Great minds think alike.
NomadicMedic
I know a guy who knows a guy.
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Anyone want this? Send me a PM and I'll drop it in the mail to you.
Wasn't even thinking about Lasix causing further hypotension hypotension. So, yeah. No way around tubing them if they have bad pulmonary edema with hypotension. Good to know.
TransportJockey
Forum Chief
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bought my new DD/toy today
84 Chevy K10. Mechanically in good shape and only needs a few things (like electrical, unfortunately, in a few places)
84 Chevy K10. Mechanically in good shape and only needs a few things (like electrical, unfortunately, in a few places)
CALEMT
The Other Guy/ Paramaybe?
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Now I'm up in Merced for a interview in Mariposa tomorrow... I like all the new scenery but I'm not going to lie when I say I'm going to be glad when I'm done with all this driving.
I'm not 100% against intubating a patient like that, but positive pressure ventilation may still worsen their hypotension due to increase in intrathoracic pressure decreasing venous return. Also I imagine the patient is still awake. Attempting to intubated without sedation may cause trauma to the airway and increase heart rate worsening the pulmonary edema. If you sedate them, it may worsen their hypotension.
So sounds like to treat the pulmonary edema, we need to treat their hypotension first. I guess we'll need a pressor, I am think levophed (2-10 mcg/min, right?) instead of dopamine since I don't want to increase the heart rate. Then probably CPAP instead of intubated unless I want to sedate too. Is my thinking sound?
So sounds like to treat the pulmonary edema, we need to treat their hypotension first. I guess we'll need a pressor, I am think levophed (2-10 mcg/min, right?) instead of dopamine since I don't want to increase the heart rate. Then probably CPAP instead of intubated unless I want to sedate too. Is my thinking sound?
DrankTheKoolaid
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re
At that point it is called Cardiogenic Shock. Though it seems counter intuitive I would still be giving fluids despite the pulmonary edema (pulmonary edema in cardiogenic shock is not fluid overload so Lasix is useless) along with dopamine since we do not have dobutamine in California. Levo being a potent vasoconstrictor makes no sense to me as what they really need a B1 agonist to increase cardio strength. Also consider CA++ for its effect on increasing cardiac output via increasing the pumping action.
At that point it is called Cardiogenic Shock. Though it seems counter intuitive I would still be giving fluids despite the pulmonary edema (pulmonary edema in cardiogenic shock is not fluid overload so Lasix is useless) along with dopamine since we do not have dobutamine in California. Levo being a potent vasoconstrictor makes no sense to me as what they really need a B1 agonist to increase cardio strength. Also consider CA++ for its effect on increasing cardiac output via increasing the pumping action.
How I imagine it is that making the heart pump faster would worsen the pulmonary edema. Cause isn't the pulmonary edema from failure of the left ventricle to pump blood out (backing up into the lungs), but the right ventricle would continue to pump normally pushing more blood into the lungs.
I was thinking I want to increase system vascular resistance to increase the blood pressure, which I think levophed would do, and decrease the preload whether it's positive pressure ventilation or CPAP to reduce the amount of blood being pumped into the lung area. I don't think we can do anything to fix the left ventricle.
What's the difference between dopamine and dobutamine?
DrankTheKoolaid
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Someone much more educated then myself, if this is inaccurate please jump in but i'll give it a shot.
Dopamine is dose dependent 1 - 2 mcg/kg/min renal ( no longer taught as not truly accurate ) 5 - 10 inotropic B1 ( increased cardiac strength of contraction ) and 10+ Alpha effects to increase vascular tone with the chronotropic effects being a side effect and not direct effect. Dobutamine is a B1 adrenergic which increases inotropic. Levophed/Norepinephrine is a potent Alpha adrenergic.
With someone with hypertension and pulmonary edema one has to assume the heart is no longer able to pump against the increased arterial pressure so CPAP and vasodilation (NTG/MSO4) to decrease both preload and after load is the normal path we take.
But with hypotension and pulmonary edema you have cardiogenic shock. At this point we have to increase cardiac contractility which is where the B1's come in dopamine/dobutamine. Once in hospital and after studies they can move further down the list with medications like milrinone if the patient is experiencing full washout of the Beta receptors making the dopamine/dobutamine less effective.
So your patient is already shocky and experiencing global ischemia, if you add a pressor to it you will starve even more tissue of blood and oxygenation furthering the effects of shock. So think fixing the problem.. When teaching shock I use the 3 P's. Its either the Product (Blood/Fluid) Pump (Heart) or Pipes (vascular tone). If you are able to figure out which is the main culprit attempt to fix it first instead of just shot gunning it.
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Cardiac is not my area of specialty by any means, but I'll take a shot at this.
The problem in cardiogenic shock is that the left side of the heart is not able eject blood effectively, so blood volume and pressure builds up retrograde through the cardiopulmonary circuit: LV-->LA-->PA-->RA-->RV. As volume increases in the pulmonary vasculature, pressure increases to the point that hydrostatic pressure becomes greater than the serum oncotic pressure, and serum leaks across the alveolar-capillary membrane into the alveoli, which of course impairs oxygen diffusion and causes hypoxemia.
"Drying the patient out" with fluid restriction and diuretics used to be a mainstay of treatment and from what I've seen is still used, though I know there are varying opinions on how well it works. Certainly having more vascular volume than is necessary is probably quite unhelpful, but achieving sub-normal vascular volumes causes problems of its own.
Patients in CHF/cardiogenic shock are not usually fluid depleted, so lack of preload isn't the problem, and in fact their CVP is usually high. Therefore giving IVF probably isn't going to help at all, and may worsen things as it increases volume in the vascular system but does nothing to improve heart function. Like always, you may see different protocols and practices out there. Different docs do things differently. But the basic problem is NOT lack of volume.
What we need to do here is help the ventricles pump more effectively.
Norepi actually has more beta inotropic effects than dopamine does, but they are offset by its very potent alpha vasopressor effects. The net clinical effect is often a rise in both SBP and DBP but little or no increase in CO. It causes tachycardia too, which simultaneously increases myocardial oxygen demand and decreases coronary perfusion, which is always bad for someone with a sick heart. I don't think I've ever seen or heard of it being used routinely in cardiogenic shock.
Dopamine's clinical effects are very similar to norepi, except that, as Koolaid explained, the adrenergic receptors it targets depends on the dose given. The "beta" dose range of 5-10 mcg/kg/min is probably where you want to be here, because we are just trying to make the LV pump more effectively. Unfortunately, what often happens is that people don't get the BP as high as they want it in that 5-10 range, so they keep increasing the dose until they get the BP up, but CO does not increase correspondingly because above 10, the alpha pressor effects predominate and cause a higher SVR, which impairs CO. You can see this in patients with a PA cath or other CO monitor.
Of the adrenergic agonists, dobutamine is probably the best single agent for heart failure. It has only B1 and B2 effects; no alpha effects. Because of that, it increases myocardial contractility and often cause a small decrease in SVR. You often see a significant increase in CO without a dramatic increase in BP. Unfortunately, when people use it without a CO monitor, they interpret the fact that BP doesn't improve a ton as "it isn't working well, let's switch to dopamine". Dobutamine causes less tachycardia than dopamine, which is another plus. In a patient whose SVR is already low, you can add vasopressin or phenylephrine or low-dose norepinephrine to give a little squeeze.
Milrinone is a phosphidesterase inhibitor that does not activate adrenergic receptors. It improves myocardial function by increasing intracellular Ca levels. It causes no tachycardia and, like dobutamine, causes mild decreases in SVR, which is often helpful but can be offset by other drugs if SVR is already low. It has other beneficial hormonal effects such as improving catecholamine sensitivity and reducing the vascular effects of systemic inflammation.
As far as the original question, whether or not to CPAP? I'd say definitely. PPV with pharmacologic support is they way to go.
The problem in cardiogenic shock is that the left side of the heart is not able eject blood effectively, so blood volume and pressure builds up retrograde through the cardiopulmonary circuit: LV-->LA-->PA-->RA-->RV. As volume increases in the pulmonary vasculature, pressure increases to the point that hydrostatic pressure becomes greater than the serum oncotic pressure, and serum leaks across the alveolar-capillary membrane into the alveoli, which of course impairs oxygen diffusion and causes hypoxemia.
"Drying the patient out" with fluid restriction and diuretics used to be a mainstay of treatment and from what I've seen is still used, though I know there are varying opinions on how well it works. Certainly having more vascular volume than is necessary is probably quite unhelpful, but achieving sub-normal vascular volumes causes problems of its own.
Patients in CHF/cardiogenic shock are not usually fluid depleted, so lack of preload isn't the problem, and in fact their CVP is usually high. Therefore giving IVF probably isn't going to help at all, and may worsen things as it increases volume in the vascular system but does nothing to improve heart function. Like always, you may see different protocols and practices out there. Different docs do things differently. But the basic problem is NOT lack of volume.
What we need to do here is help the ventricles pump more effectively.
Norepi actually has more beta inotropic effects than dopamine does, but they are offset by its very potent alpha vasopressor effects. The net clinical effect is often a rise in both SBP and DBP but little or no increase in CO. It causes tachycardia too, which simultaneously increases myocardial oxygen demand and decreases coronary perfusion, which is always bad for someone with a sick heart. I don't think I've ever seen or heard of it being used routinely in cardiogenic shock.
Dopamine's clinical effects are very similar to norepi, except that, as Koolaid explained, the adrenergic receptors it targets depends on the dose given. The "beta" dose range of 5-10 mcg/kg/min is probably where you want to be here, because we are just trying to make the LV pump more effectively. Unfortunately, what often happens is that people don't get the BP as high as they want it in that 5-10 range, so they keep increasing the dose until they get the BP up, but CO does not increase correspondingly because above 10, the alpha pressor effects predominate and cause a higher SVR, which impairs CO. You can see this in patients with a PA cath or other CO monitor.
Of the adrenergic agonists, dobutamine is probably the best single agent for heart failure. It has only B1 and B2 effects; no alpha effects. Because of that, it increases myocardial contractility and often cause a small decrease in SVR. You often see a significant increase in CO without a dramatic increase in BP. Unfortunately, when people use it without a CO monitor, they interpret the fact that BP doesn't improve a ton as "it isn't working well, let's switch to dopamine". Dobutamine causes less tachycardia than dopamine, which is another plus. In a patient whose SVR is already low, you can add vasopressin or phenylephrine or low-dose norepinephrine to give a little squeeze.
Milrinone is a phosphidesterase inhibitor that does not activate adrenergic receptors. It improves myocardial function by increasing intracellular Ca levels. It causes no tachycardia and, like dobutamine, causes mild decreases in SVR, which is often helpful but can be offset by other drugs if SVR is already low. It has other beneficial hormonal effects such as improving catecholamine sensitivity and reducing the vascular effects of systemic inflammation.
As far as the original question, whether or not to CPAP? I'd say definitely. PPV with pharmacologic support is they way to go.
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I don't understand why trying out for an EMS competition team made me more nervous than actual calls. Probably something to do with being filmed and having an audience of people watching and waiting for me to screw up...
VFlutter
Flight Nurse
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We rarely use Milrinone, maybe a few times a year, but it usually works well.
I am curious to see the future for Impellas in refractory cardiogenic shock. Our CV docs are still on a learning curve and I have seen some great outcomes but also some very poor attempts (massive hemolysis, migration, valvular damage).
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Anyone having any recommendations for things to sacrifice to get out of a low spot as a shift? My shift has been getting absolutely hammered since the new year. Twice as many codes in the last two months as the previous eight, pretty terrible younger patient calls, inopportune mechanical failures, the works.
One of the other shifts's captain offered us one of his roosters but we figured we'd explore all options.
One of the other shifts's captain offered us one of his roosters but we figured we'd explore all options.
mycrofft
Still crazy but elsewhere
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I'll send Herman. He makes station calls and knows all the right moves. Have a wildebeest ready.
On the other hand, print it and either rub his belly for luck, or throw darts.
Jim37F
Forum Deputy Chief
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It finally happened, the fabled no hitter, spent the entire shift without a single call. Not even a cancelation enroute/on scene, simply didn't get a single call dispatched our way.