Amrinone versus Milrinone

[PinchandBurn]

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Those of you that do Cardiac Cases, which one of these meds are you using ? I didnt really have much exposure to these meds in training, maybe just a few times.

Both are PDEi. Both will increase contractility and decrease SVR. Both vasodilate the pulmonary vasculture in cases of Pulm HTN.

So in patients with severe MR, coming off pump (if it were a repair) would you be more inclined to use Milrinone?

My understanding is Milrinone is 'newer' and 'better' and doesnt cause thrombocytopenia like amrinone does.....

What's your experience been with it?

 

[Gern Blansten]

I didn't think anyone was still using amrinone, for the reasons stated. It has not been used in years in our facility. Used to be a popular exam question though.

 

[Robert Loblaw]

Those of you that do Cardiac Cases, which one of these meds are you using ? I didnt really have much exposure to these meds in training, maybe just a few times.

Both are PDEi. Both will increase contractility and decrease SVR. Both vasodilate the pulmonary vasculture in cases of Pulm HTN.

So in patients with severe MR, coming off pump (if it were a repair) would you be more inclined to use Milrinone?

My understanding is Milrinone is 'newer' and 'better' and doesnt cause thrombocytopenia like amrinone does.....

What's your experience been with it?

not seen amrinone used...

 

[Noyac]

I've used both. I never really saw a difference. Both can work well.

 

[Hamhock]

I thought amrinone wasn't available in the US anymore.

Unless the poster is outside of the US, it seems I am wrong.

HH

 

[PinchandBurn]

nah..I'm in the US. Just never reallyhad to use either one.

Just wondering when you guys CLINICALLY had to use it. I've done tons of hearts in training, never had to use either.

 

[Robert Loblaw]

what kinds of hearts are we talking? i would not expect to use it on routine cases (cabg's/single valves) in a relatively healthy patient population.

milrinone is considered an inodilator, so obviously it both increases the inotropic state of the heart and vasodilates, both the pulmonary and systemic vascular beds. it is most commonly thought of as supporting right heart function more so than other inotropes.

i use it primarily in the setting of complex surgery with long pump runs in which right heart protection may be an issue, especially if there is baseline right heart dysfunction. if i think i will need it for separation, i will generally start it on bypass without a bolus, as hypotension is the major consideration. if there is acute or unanticipated right heart dysfunction on separation, i will consider bolusing 25 mcg/kg and support the blood pressure as needed. there is a long half-life and the effects will be prolonged and intensified in patients with renal failure--it is an important cause of post-operative hypotension in the ICU.

i have decided that, after watching on the sidelines for the better part of five years, i will hear noyac's call for clinical discussion on this forum. the better clinical question here is what is right heart dysfunction and how important is it clinically? which is better--a PAP of 65/33 or a PAP of 22/12?

 

[sevoflurane]

Def. not for routine hearts.

I might bolus and start an infusion if the TEE shows a crappy looking RV, especially if they have pulm. htn.

I haven't used amrinone for years... Prolly only used it a coupla times.

Milrinone is the new kid on the block, and I don't think he's going anywhere.

 

[RT2MD]

what kinds of hearts are we talking? i would not expect to use it on routine cases (cabg's/single valves) in a relatively healthy patient population.

milrinone is considered an inodilator, so obviously it both increases the inotropic state of the heart and vasodilates, both the pulmonary and systemic vascular beds. it is most commonly thought of as supporting right heart function more so than other inotropes.

i use it primarily in the setting of complex surgery with long pump runs in which right heart protection may be an issue, especially if there is baseline right heart dysfunction. if i think i will need it for separation, i will generally start it on bypass without a bolus, as hypotension is the major consideration. if there is acute or unanticipated right heart dysfunction on separation, i will consider bolusing 25 mcg/kg and support the blood pressure as needed. there is a long half-life and the effects will be prolonged and intensified in patients with renal failure--it is an important cause of post-operative hypotension in the ICU.

i have decided that, after watching on the sidelines for the better part of five years, i will hear noyac's call for clinical discussion on this forum. the better clinical question here is what is right heart dysfunction and how important is it clinically? which is better--a PAP of 65/33 or a PAP of 22/12?

Right heart dysfunction? Ok. Let's see here. Are we talking about failure of the RV to adequately pump blood forward? That seems to be the most generalized definition of right heart dysfunction that I could think of off the top of my head. My brain thinks that a PAP of 22/12 would be more beneficial. The lower the PAPs, the less resistance the RV has to pump against... I guess a better way of saying that would be RV afterload would be decreased with the lower PAPs.

How'd I do? Was that what you were looking for, or am I off base here?

 

[Robert Loblaw]

Right heart dysfunction? Ok. Let's see here. Are we talking about failure of the RV to adequately pump blood forward? That seems to be the most generalized definition of right heart dysfunction that I could think of off the top of my head. My brain thinks that a PAP of 22/12 would be more beneficial. The lower the PAPs, the less resistance the RV has to pump against... I guess a better way of saying that would be RV afterload would be decreased with the lower PAPs.

How'd I do? Was that what you were looking for, or am I off base here?

It's exactly what I was looking for in hopes of stimulating discussion. 🙂

The PAP is what it is--the pressure in the PA. Now, you have a pump on either side of the PA (RV and LV), an intrinsic PVR, a (usually) closed thoracic space, and the effects of ventilation (both positive and negative), all of which affect the PAP.

So, short answer as to which PAP is better is "it depends." So, first lets ask another question: which is better, a systemic BP of 150/85 or 95/65?

 

[RT2MD]

It's exactly what I was looking for in hopes of stimulating discussion. 🙂

The PAP is what it is--the pressure in the PA. Now, you have a pump on either side of the PA (RV and LV), an intrinsic PVR, a (usually) closed thoracic space, and the effects of ventilation (both positive and negative), all of which affect the PAP.

So, short answer as to which PAP is better is "it depends." So, first lets ask another question: which is better, a systemic BP of 150/85 or 95/65?

It depends? I mean... it depends. 😎

I suppose it depends on what pressure is needed to properly perfuse all of the end organs. If everything was getting adequately perfused, like the kidneys and brain, I suppose the 95/65 would be more beneficial to the heart. The widened pulse pressure of the 150/85 indicates that there is vascular disease, so the kidneys might actually require that higher pressure to function adequately. If that were the case, that first patient might not like a pressure of 95/65, as there would not be adequate perfusion.

 

[Robert Loblaw]

It depends? I mean... it depends. 😎

I suppose it depends on what pressure is needed to properly perfuse all of the end organs. If everything was getting adequately perfused, like the kidneys and brain, I suppose the 95/65 would be more beneficial to the heart. The widened pulse pressure of the 150/85 indicates that there is vascular disease, so the kidneys might actually require that higher pressure to function adequately. If that were the case, that first patient might not like a pressure of 95/65, as there would not be adequate perfusion.

Ok, that is not a bad answer. The best part of it realizing that oxygen delivery is dependent perfusion, and blood pressure is an imperfect surrogate for perfusion, which is why hemodynamic assessments need to incorporate multiple data points.

What is the SBP when someone is has chronic systolic HF, in general? What is usually in diastolic heart failure?

 

[sevoflurane]

The force runs strong with you padawan... I sense a new presence in the the anesthesia force... somewhere in Kansas City. 😉

Think about Blood Pressure and PA pressure and the balance between both of them in regards to forward flow out of the heart and to the rest of the body.

Well done buddy!

 

[RT2MD]

Ok, that is not a bad answer. The best part of it realizing that oxygen delivery is dependent perfusion, and blood pressure is an imperfect surrogate for perfusion, which is why hemodynamic assessments need to incorporate multiple data points.

What is the SBP when someone is has chronic systolic HF, in general? What is usually in diastolic heart failure?

"not a bad answer." I can live with that, hopefully this will fall in the same boat! 😀

Not sure if you mean systolic blood pressure or systemic blood pressure by SBP... I guess I will answer as if you meant systemic blood pressure, since that will give you systolic!

Alright. Systolic heart failure is a pump problem. The problem lies in the fact that the heart can't adequately pump blood forward, as in chronic ischemic heart disease or aortic stenosis. I would think that would result in a decreased CO, primarily by decrease SV. The patient's EF would also be lowered. This results in a lower systolic pressure, and a lower MAP. The vasculature would try to maintain the MAP and so it would constrict. The end result would be a lower systolic pressure with an increased diastolic, due to increased afterload?


Diastolic heart failure is a failure to fill, like in hypertensive heart disease. Failure to fill results in decreased SV, and decreased CO. This will still result in a "normal" ejection fraction b/c the ratio being ejected is still good... the end diastolic volume is just decreased. Again, the vasculature would sense that decreased MAP and you would end up with the same blood pressure... a lower systolic pressure with an increased diastolic pressure.

That's my attempt at an answer.

 

[RT2MD]

The force runs strong with you padawan... I sense a new presence in the the anesthesia force... somewhere in Kansas City. 😉

Think about Blood Pressure and PA pressure and the balance between both of them in regards to forward flow out of the heart and to the rest of the body.

Well done buddy!

Thanks man! I'm sure I'll royally mess this up somewhere along here! It's good for pre-board-prep board-prep. 👍

 

[Robert Loblaw]

"not a bad answer." I can live with that, hopefully this will fall in the same boat! 😀

Not sure if you mean systolic blood pressure or systemic blood pressure by SBP... I guess I will answer as if you meant systemic blood pressure, since that will give you systolic!

Alright. Systolic heart failure is a pump problem. The problem lies in the fact that the heart can't adequately pump blood forward, as in chronic ischemic heart disease or aortic stenosis. I would think that would result in a decreased CO, primarily by decrease SV. The patient's EF would also be lowered. This results in a lower systolic pressure, and a lower MAP. The vasculature would try to maintain the MAP and so it would constrict. The end result would be a lower systolic pressure with an increased diastolic, due to increased afterload?


Diastolic heart failure is a failure to fill, like in hypertensive heart disease. Failure to fill results in decreased SV, and decreased CO. This will still result in a "normal" ejection fraction b/c the ratio being ejected is still good... the end diastolic volume is just decreased. Again, the vasculature would sense that decreased MAP and you would end up with the same blood pressure... a lower systolic pressure with an increased diastolic pressure.

That's my attempt at an answer.

You're doing very well...and brave, too.

Generally, patients in diastolic heart failure have impaired relaxation and blood pressure is often normal or even high, compared to systolic failure in which it is almost always low. Elevated blood pressures increase wall stress which can cause sub-endocardial ischemia and worsen relaxation, which is an ATP dependent process, further worsening the problem. The end result is pulmonary edema in either setting.

So a few more questions: (1)what types of diseases cause diastolic heart failure? (2) in general, what is the morphology of a LV that is failing in systole? how does it differ from an LV that fails in diastole? (3) what are the PAPs in either case?

 

[RT2MD]

You're doing very well...and brave, too.

Generally, patients in diastolic heart failure have impaired relaxation and blood pressure is often normal or even high, compared to systolic failure in which it is almost always low. Elevated blood pressures increase wall stress which can cause sub-endocardial ischemia and worsen relaxation, which is an ATP dependent process, further worsening the problem. The end result is pulmonary edema in either setting.

So a few more questions: (1)what types of diseases cause diastolic heart failure? (2) in general, what is the morphology of a LV that is failing in systole? how does it differ from an LV that fails in diastole? (3) what are the PAPs in either case?

(This is way more fun than the small group assignment I should be working on...)

I'm a little confused on why the diastolic failure would result in normal systemic BP. I guess if I think about it, MAP = CO x SVR and CO = SV x HR, so the only real options for MAP to be maintained in the face of decreased SV is to either increase HR, increase SVR, or both. Do patients in diastolic heart failure generally become tachycardic? If so, wouldn't that further decrease preload by shortening filling times? Do they just undergo peripheral vasoconstriction, increasing afterload? I think I'm talking myself in circles and making myself more confused!

My attempted answers:

1) Hypertensive heart disease, mitral stenosis, restrictive cardiomyopathy, and hypertrophic cardiomyopathy are the ones that come to mind... and I put them in order of what I think is the likelihood

2) The LV will be more dilated in systolic failure, and hypertrophied in diastolic failure (except in the case of restrictive cardiomyopathy).

3) I think you kind of helped me out on this one... you said that pulm edema would occur in both cases, so I'm going to say that PAPs are elevated. In systolic failure it's due to the inability to properly pump forward - blood backs up, in diastolic failure it's because the blood can't get into the ventricle (a very awkward way of saying that... can't figure out a better way to put it). Preload would be increased in systolic failure, but decreased in diastolic, correct?

 

[Robert Loblaw]

(This is way more fun than the small group assignment I should be working on...)

I'm a little confused on why the diastolic failure would result in normal systemic BP. I guess if I think about it, MAP = CO x SVR and CO = SV x HR, so the only real options for MAP to be maintained in the face of decreased SV is to either increase HR, increase SVR, or both. Do patients in diastolic heart failure generally become tachycardic? If so, wouldn't that further decrease preload by shortening filling times? Do they just undergo peripheral vasoconstriction, increasing afterload? I think I'm talking myself in circles and making myself more confused!

My attempted answers:

1) Hypertensive heart disease, mitral stenosis, restrictive cardiomyopathy, and hypertrophic cardiomyopathy are the ones that come to mind... and I put them in order of what I think is the likelihood

2) The LV will be more dilated in systolic failure, and hypertrophied in diastolic failure (except in the case of restrictive cardiomyopathy).

3) I think you kind of helped me out on this one... you said that pulm edema would occur in both cases, so I'm going to say that PAPs are elevated. In systolic failure it's due to the inability to properly pump forward - blood backs up, in diastolic failure it's because the blood can't get into the ventricle (a very awkward way of saying that... can't figure out a better way to put it). Preload would be increased in systolic failure, but decreased in diastolic, correct?

you can conceptualize diastolic failure as not a problem with forward flow so much as a bottle neck, as you describe in your third response. it can be a problem with forward flow if you are simultaneously hypovolemic or vasodilated.

so great, you are absolutely correct in your answers. so the "it depends" on the left side--right side--depends on the morphology of the ventricle, which generally reflects the time course over which the pathophysiology has occurred and the adaptations that are in place.

so, if you have primarily diastolic LV dysfunction, you generally have a concentrically hypertrophied ventricle which has changed shape to deal with the pressure load on the heart, and it is subsequently closer to its ischemic threshold for a number of reasons--it's much larger so requires increased vascularity, the wall stress is much higher in both systole and diastole which increases myocardial oxygen consumption throughout the cardiac cycle. the walls are 'stiff,' and elevated PAPs (like 65/33) are usually an adaptive response in order to maintain adequate LVEDV. if the PAP is 23/13 in this type of patient, it probably means that the patient is hypovolemic and hypotensive and the heart is empty with an EF of ~100%. this is very common post-bypass after an AVR, for example. in this setting, one can think of the PAP as a 'filling pressure,' other things (like intrinsic pulmonary vascular resistance and intrathoracic pressure) being equal. generally, the right ventricle will have adapted similarly in order to generate the necessary PAPs to fill the LV, and it, too, will be hypertrophied. in this setting, the PAPs are not so much the afterload but the pressure generated by the RV.

if you have primarily left sided systolic dysfunction, you generally have an eccentrically dilated LV which has changed shape in response to a volume load. here you have a forward flow problem and the PAPs are more generally reflective of RV afterload. The RV can be either hypertrophied or dilated. here it gets even more tricky because if you see a PAP of 65/33 and a CVP of 12, you can generally be reassured that the RV functioning well enough, but i like the tee to help in this assessment. if the PAP is 65/33 and the CVP is 22 or 25 with a waveform that looks like there is significant TR, then i would be very concerned that the RV is significantly dilated and failing.

 

[Robert Loblaw]

so when you are done digesting all of this, another question--this relates to the question as to whether a PAP of 23/13 is good or not:

whose RV is better equipped to handle a massive pulmonary embolism--yours or mine, which are presumably young and healthy, or someone who has long standing stage ii hypertension with associated adaptive changes in heart morphology, but otherwise is healthy (no cad, etc.)?

 

[RT2MD]

you can conceptualize diastolic failure as not a problem with forward flow so much as a bottle neck, as you describe in your third response. it can be a problem with forward flow if you are simultaneously hypovolemic or vasodilated.

so great, you are absolutely correct in your answers. so the "it depends" on the left side--right side--depends on the morphology of the ventricle, which generally reflects the time course over which the pathophysiology has occurred and the adaptations that are in place.

so, if you have primarily diastolic LV dysfunction, you generally have a concentrically hypertrophied ventricle which has changed shape to deal with the pressure load on the heart, and it is subsequently closer to its ischemic threshold for a number of reasons--it's much larger so requires increased vascularity, the wall stress is much higher in both systole and diastole which increases myocardial oxygen consumption throughout the cardiac cycle. the walls are 'stiff,' and elevated PAPs (like 65/33) are usually an adaptive response in order to maintain adequate LVEDV. if the PAP is 23/13 in this type of patient, it probably means that the patient is hypovolemic and hypotensive and the heart is empty with an EF of ~100%. this is very common post-bypass after an AVR, for example. in this setting, one can think of the PAP as a 'filling pressure,' other things (like intrinsic pulmonary vascular resistance and intrathoracic pressure) being equal. generally, the right ventricle will have adapted similarly in order to generate the necessary PAPs to fill the LV, and it, too, will be hypertrophied. in this setting, the PAPs are not so much the afterload but the pressure generated by the RV.

if you have primarily left sided systolic dysfunction, you generally have an eccentrically dilated LV which has changed shape in response to a volume load. here you have a forward flow problem and the PAPs are more generally reflective of RV afterload. The RV can be either hypertrophied or dilated. here it gets even more tricky because if you see a PAP of 65/33 and a CVP of 12, you can generally be reassured that the RV functioning well enough, but i like the tee to help in this assessment. if the PAP is 65/33 and the CVP is 22 or 25 with a waveform that looks like there is significant TR, then i would be very concerned that the RV is significantly dilated and failing.

For some reason I was trying to make myself think that the "bottle neck" that occurs with diastolic dysfunction would result in lowered CO. I guess it doesn't, does it? I don't know why I was trying to talk myself into that. Thanks for straightening me out on that one.

Everything else you said makes perfect sense to me. Thank you so much for taking the time to allow this teaching moment. I appreciate it. 👍

 

[Robert Loblaw]

For some reason I was trying to make myself think that the "bottle neck" that occurs with diastolic dysfunction would result in lowered CO. I guess it doesn't, does it? I don't know why I was trying to talk myself into that. Thanks for straightening me out on that one.

Everything else you said makes perfect sense to me. Thank you so much for taking the time to allow this teaching moment. I appreciate it. 👍

it's sort of a pet-peeve of mine when a colleague sees a PAP of 55 and automatically thinks it needs to be lowered or the patient is too sick for surgery. you have to know what a ventricle looks like in order to make some interpretations of numbers.

 

[RT2MD]

so when you are done digesting all of this, another question--this relates to the question as to whether a PAP of 23/13 is good or not:

whose RV is better equipped to handle a massive pulmonary embolism--yours or mine, which are presumably young and healthy, or someone who has long standing stage ii hypertension with associated adaptive changes in heart morphology, but otherwise is healthy (no cad, etc.)?

I would think the HTN patient. The hypertrophied RV, which stems from increased PAP to get adequate LVEDV, has more contractile force and therefore could handle a sudden increase in PVR better than a "normal" heart... it's already used to generating high pressures.

 

[Robert Loblaw]

I would think the HTN patient. The hypertrophied RV, which stems from increased PAP to get adequate LVEDV, has more contractile force and therefore could handle a sudden increase in PVR better than a "normal" heart... it's already used to generating high pressures.

Perfect. So our piddling rv's would be hosed and our PAs would be 20/10 (normal) but we'd be screwed. This is directly analogous to systolic left heart failure in which pressures are usually low normal. So if you see a PAP of 23/13 on an echo, you might be more worried than if you saw 65/33, depending on what the RV looks like.

This is typically the scenario in a freshly transplanted heart by the way, especially if the donor was young and healthy. The RV usually needs both milrinone and an inhaled pulmonary vasodilator. We use prostacyclin...

 

[RT2MD]

Perfect. So our piddling rv's would be hosed and our PAs would be 20/10 (normal) but we'd be screwed. This is directly analogous to systolic left heart failure in which pressures are usually low normal. So if you see a PAP of 23/13 on an echo, you might be more worried than if you saw 65/33, depending on what the RV looks like.

This is typically the scenario in a freshly transplanted heart by the way, especially if the donor was young and healthy. The RV usually needs both milrinone and an inhaled pulmonary vasodilator. We use prostacyclin...

I worked in the Cardiovascular ICU quite a bit as an RT. We also used nebulized epoprostenol on many of these people... I was unsure of how widely it was used in this delivery format. It's nice to hear others doing it as well!

Thanks again for taking the time to have these discussions.

 

[TrojanGopher]

Wow guys, great thread. As a PGY1 having today just finished reading the "Special Anesthetic Considerations: Cardiovascular Disease" chapter in Baby Miller, this thread really helped reinforce some of the concepts.

Thanks Robert Loblaw for the tutelage!

 

[crossfitisfun]

As a student I love reading these types of threads. I'm just tryihng to tie this together and straighten things out in my head...please correct me.

Diastolic Dysfxn ....(stiff ventricle)
- LV needs adequate filling pressures so: RV acheives this by pushing harder --> and this may be reflected in high PA pressures?
- low PA pressures would make you worried that the Right side is not functioning well (ischemic insult, valvular dysfxn) or the patient is hypovolemic with not enough fluid on the right side to push forward and generate high PA pressures?
- PA pressures have the top and bottom numbers...are both indicative of how hard the RV is pushing? or does the systolic tell you one piece of the puzzle and the diastolic tell you another?
- this thread really made me think because I've always just though of the PA pressures as a function of intrinsic pulmonary vasculature + backwards reflection of pressure on the left side....obviously I am a bit mixed up.

 

[crossfitisfun]

Again tyring to put this in my own words to make sure I'm not confused....

Systolic Dysfunction...

detecting RV dysfnx in the setting systolic heart disease requires not just the high PA pressure but also the CVP...

CVP high as well= right heart crappy and is not able to pump out the venous blood that it is receiving? What is the result of the high PA pressure in this case?

I think I need a refresher on variables that contribute to the PA pressure. I'll read, but I'd appreciate any response. Thanks!

 

[RT2MD]

As a student I love reading these types of threads. I'm just tryihng to tie this together and straighten things out in my head...please correct me.

Alright, let's see how much I learned... 😀 I fully expect somebody to correct me if I am wrong...

Diastolic Dysfxn ....(stiff ventricle)
- LV needs adequate filling pressures so: RV acheives this by pushing harder --> and this may be reflected in high PA pressures?

Yes. The fact that the LV is having a filling issue (either compliance issue, or valve issue) means that the filling pressures need to be higher. Since those pressures need to be higher, the pressures "down stream" also need to be higher. This is accomplished by RV hypertrophy.

- low PA pressures would make you worried that the Right side is not functioning well (ischemic insult, valvular dysfxn) or the patient is hypovolemic with not enough fluid on the right side to push forward and generate high PA pressures?

That is correct, in the setting of a patient with LV diastolic heart failure you would expect PAPs to be elevated... BUT, I think the point he was trying to make is this: Just looking at a set of numbers, a PAP in this case, is pretty much worthless when done in isolation. If you are able to look at the RV via TEE, and you see nice thick walls to go with that PAP of 20/10... well... that's not a good thing. I imagine you would then be able to use the TEE to see how full the ventricles are vs. wall motion vs. valve issues to be able to differentiate as to why your PAs are so "normal" in the presence of an "abnormal" RV.

- PA pressures have the top and bottom numbers...are both indicative of how hard the RV is pushing? or does the systolic tell you one piece of the puzzle and the diastolic tell you another?

PA pressures to the right heart are like systemic BP is to the left heart... which is why you have a systolic and a diastolic pressure. Remember that diastolic pressure is influenced by 3 main things:
1) how fast the blood flows from the arterial system to the venous system
2) the amount of time blood has to flow to the venous system
3) the starting point (systolic pressure)

And systolic pressure is influenced by:
1) How fast the blood is pumped from the ventricle
2) the amount of blood pumped from the ventricle (stroke volume)
3) the compliance of the arterial system
4) the starting point (diastolic pressure)

- this thread really made me think because I've always just though of the PA pressures as a function of intrinsic pulmonary vasculature + backwards reflection of pressure on the left side....obviously I am a bit mixed up.

I try to think of it in a purely plumbing sense. 2 pumps, 2 sets of pipes. Pump R pumps into pipe P, which drain into pump L, which pumps into pipe S, which drain into pump R... etc. Your pulm vasculature will affect your preload on the LV and afterload on the RV... just like the systemic vasculature will affect preload on the RV and afterload on the LV.

Another thing is don't forget you have intrathoracic pressure that is also affecting your pressures. During negative pressure breathing, as you inhale your intrathoracic pressure drops negative with respect to atmospheric pressure. This pressure change also affects preload. During inspiration, you are increasing venous return to the right side of the heart while decreasing it to the left.

I hope that is all correct, and I hope that it makes sense...

 

[RT2MD]

Again tyring to put this in my own words to make sure I'm not confused....

Systolic Dysfunction...

detecting RV dysfnx in the setting systolic heart disease requires not just the high PA pressure but also the CVP...

CVP high as well= right heart crappy and is not able to pump out the venous blood that it is receiving? What is the result of the high PA pressure in this case?

I think I need a refresher on variables that contribute to the PA pressure. I'll read, but I'd appreciate any response. Thanks!

Just as clarification, you are asking about detecting RV dysfunction in the setting of LV systolic heart failure, right?

Again... let's see how much I learned... same disclaimer as above, I'm not swearing this is correct.

Systolic heart failure. That means a problem with the pump. The LV is not able to adequately pump blood out, so it ends up backing up... first to the LA, then to the PA, eventually to the RV. The RV hypertrophies, because it is essentially going into diastolic heart failure (Just like the LV during systemic HTN). The issue that he was talking about above is that as long as the RV is compensating adequately, the CVP should stay somewhat normal --> slightly elevated... But if the RV diastolic failure ends up switching over to more of a systolic failure, and your RV becomes more dilated, your CVP will rise due to blood continuing to back up.

That's my take.

 

[Robert Loblaw]

i would agree with this, for the most part. if a thick RV was generating a PAP of 20/10, if the change was acute, i would be worried about hypovolemia (CVP low, left heart hyperdynamic, ef high-normal) or RV failure (CVP = PAD, left heart either hyperdynamic [for example, pure right heart failure], normal'ish [for example new or worsened MR], or dilated with low EF [left heart failure leading to secondary right heart failure]). the most important thing to understand is that you cannot interpret a PA catheter in isolation (some may argue that you should not try to interpret it at all, and should even stop looking--there may be some merit to this).

in my practice, i'm not really that interested in what the numbers are unless i also have some idea about the ventricular morphology and function. it doesn't have to be concurrent (i.e. with a TEE probe in the patient), although that is certainly helpful.

just to finish the whole discussion, a thick hypertrophied right ventricle can easily fail and dilate, but this is usually due to ISCHEMIA and not due to volume overload. a normal RV is being perfused in systole and diastole because the CPP is greater than the RVESP. when the ventricle hypertrophies, it is closer to its ischemic threshold. this is why hypotension is bad in these patients--if the CPP falls, a cycle very similar to that seen with aortic stenosis ensues: decreased BP leads to decreased CPP which leads to subendocardial ischemia which leads to further fall in BP which leads to more ischemia which leads to further falls in BP...eventually the ischemia leads to either frank failure or ischemic arrhythmias. for this reason, i think it is useful to lower PAPs by altering the PVR directly (with milrinone, which is also an inotrope or inhaled pulmonary vasodilators) in someone with chronically elevated PAPs--to decrease wall stress and hopefully improve perfusion to the RV and give you a little more room before bad things happen.

 

[Robert Loblaw]

Just as clarification, you are asking about detecting RV dysfunction in the setting of LV systolic heart failure, right?

Again... let's see how much I learned... same disclaimer as above, I'm not swearing this is correct.

Systolic heart failure. That means a problem with the pump. The LV is not able to adequately pump blood out, so it ends up backing up... first to the LA, then to the PA, eventually to the RV. The RV hypertrophies, because it is essentially going into diastolic heart failure (Just like the LV during systemic HTN). The issue that he was talking about above is that as long as the RV is compensating adequately, the CVP should stay somewhat normal --> slightly elevated... But if the RV diastolic failure ends up switching over to more of a systolic failure, and your RV becomes more dilated, your CVP will rise due to blood continuing to back up.

That's my take.

i would just differentiate between 'rv diastolic failure'--which one of my mentors thinks is an actual clinical entity that is under-recognized--and adaptive RV hypertrophy. but the idea you have is correct. the adaptive response of hypertrophy is protective for the RV with respect to volume, so it will be relatively harder to flood the RV and dilate it out--for example, post-cpb in complex surgery, when large volumes of clotting agents might be needed after a long pump run.

we refer to the difference between the PA diastolic pressure and CVP as the 'delta', which is kind of an indicator of how much pressure the RV is adding to the closed circuit. if the PAD and the CVP are equal, you can sort of infer that the RV is not adding any pressure to the system. if the PAD is 33 and the cvp is 15, you can presume that the RV is contracting well enough to add pressure to the circuit. if i don't have an echo and a patient is going sour, i will place a lot of stock in this measurement, even if the numbers are relatively normal (PAP 23/13 and CVP after zeroing, etc, is 13).

 

[proman]

Great thread. The right heart is really never taught in med school or residency. I do want to clarify something about left ventricular diastolic dysfunction:

When the LV starts to develop impaired relaxation (which is an active process), it's the left atrium, not the right ventricle that feels the effects. In Grade I diastolic dysfunction (impaired relaxation), there is a shift in when most of the LV filling happens. In normal, young adults, over 80% of filling happens early, due to a suction effect of the LV relaxing. As impaired relaxation occurs, there's less early filling and the atrial contraction contributes more. This is seen on echo as E/A wave reversal which may be abnormal or normal based on age of the patients.

As diastolic dysfunction progresses, the left atrium compensates by increasing filling pressures. The result is that the normal gradient between the LA and LV during diastole is restored. This is grade II or "pseudonormal" dysfunction. Things are fine, except at higher pressure. Higher pressure aren't good for any part of the heart. The increase in LA pressure decreases the amount of LA filling from the pulmonary veins during systole and increases pulmonary vein pressures.

As diastolic dysfunction progresses to LV restriction, the LA is no longer able to generate a high enough pressure to fill and most of the LV filling happens in early diastole. But the total amount of blood is less, resulting in decreased LV preload and less efficient contraction. The LA dilates, atrial arrhythmias happen and pulmonary pressures go up.

As the pulmonary pressures go up, the RV has more work to do, and either dilates and/or hypertrophies. All the bad things mentioned then happen.

 

[RT2MD]

Thank you both for the added clarification. Very helpful. 👍

 

[Robert Loblaw]

Great thread. The right heart is really never taught in med school or residency. I do want to clarify something about left ventricular diastolic dysfunction:

When the LV starts to develop impaired relaxation (which is an active process), it's the left atrium, not the right ventricle that feels the effects. In Grade I diastolic dysfunction (impaired relaxation), there is a shift in when most of the LV filling happens. In normal, young adults, over 80% of filling happens early, due to a suction effect of the LV relaxing. As impaired relaxation occurs, there's less early filling and the atrial contraction contributes more. This is seen on echo as E/A wave reversal which may be abnormal or normal based on age of the patients.

As diastolic dysfunction progresses, the left atrium compensates by increasing filling pressures. The result is that the normal gradient between the LA and LV during diastole is restored. This is grade II or "pseudonormal" dysfunction. Things are fine, except at higher pressure. Higher pressure aren't good for any part of the heart. The increase in LA pressure decreases the amount of LA filling from the pulmonary veins during systole and increases pulmonary vein pressures.

As diastolic dysfunction progresses to LV restriction, the LA is no longer able to generate a high enough pressure to fill and most of the LV filling happens in early diastole. But the total amount of blood is less, resulting in decreased LV preload and less efficient contraction. The LA dilates, atrial arrhythmias happen and pulmonary pressures go up.

As the pulmonary pressures go up, the RV has more work to do, and either dilates and/or hypertrophies. All the bad things mentioned then happen.

Great point, thanks for adding. I think diastolic left heart dysfunction and right heart dysfunction will be active areas of research and progress in cardiovascular medicine over the next decade. I agree that there is an under-appreciation of right heart physiology. I was taught in medical school that when the right heart fails (classic RCA infarct) you are supposed to give volume to push blood through the akinetic RV 😱

 

[urge]

Great point, thanks for adding. I think diastolic left heart dysfunction and right heart dysfunction will be active areas of research and progress in cardiovascular medicine over the next decade. I agree that there is an under-appreciation of right heart physiology. I was taught in medical school that when the right heart fails (classic RCA infarct) you are supposed to give volume to push blood through the akinetic RV 😱

That's not true anymore?

 

[Robert Loblaw]

right heart failure = inodilator (milrinone), diuresis, inhaled pulmonary vasodilators...then ecmo. much more difficult to manage than lv failure,where you have all sorts of neat toys like impellas and balloon pumps.

 

[anes121508]

How is the PA pressure determined from an echo? I usually see one number displayed.

If I see an echo report with moderately concentric lv hypertrophy and a PA pressure (from the echo report, which i think is mean?) of 41....Would a moderately concentric hyperophied LV correlate to a pa pressure of 41, or is something else the pulm htn? is that elevated because she has had long standing lv hypertrophy and now the right side is pumping hard? I remember having been assigned to a patient like this. I was confused because there were also Bilateral PEs (if these were chronic, they could cause pulm HTN?). Also had OSA.

 

[Robert Loblaw]

How is the PA pressure determined from an echo? I usually see one number displayed.

If I see an echo report with moderately concentric lv hypertrophy and a PA pressure (from the echo report, which i think is mean?) of 41....Would a moderately concentric hyperophied LV correlate to a pa pressure of 41, or is something else the pulm htn? is that elevated because she has had long standing lv hypertrophy and now the right side is pumping hard? I remember having been assigned to a patient like this. I was confused because there were also Bilateral PEs (if these were chronic, they could cause pulm HTN?). Also had OSA.

the pap is calculated on the echo only if there is a TR jet. basically, the velocity of the tr jet is used to calculate the pressure difference between the two chambers (ra and rv). the cvp is estimated by ivc collapse (or known if being transduced) and the the pressure difference is added to the cvp to give you the PASP.

as to your second question--all of the above are possible correct answers. the multiple points you raise highlight why i make the statement that the PAC numbers cannot be interpreted in isolation. it also is why the utility of PACs is constantly questioned...

 

[proman]

Just one point: the pressure from the TR jet is really the RVSP. Since most people don't have subpulmonic stenosis, the RVSP reflects the PASP. You can also calculate the PAD if a PI jet is present.

 

[periopdoc]

But last weekend at the two-day CRNA echo cert course they said the TR jet was the PASP. Who do I believe?


Great discussion BTW.

- pod

 

[anes121508]

Does everybody have a tr jet, or only patients with pathological tricuspid regurge?

Also, if i were to have a pac in the patient, how close would the pac pulm pressure be to the number reported on the echo? If the numbers were to come out vastly different, what would be the reason?

 

[Bertelman]

Does everybody have a tr jet, or only patients with pathological tricuspid regurge?

Also, if i were to have a pac in the patient, how close would the pac pulm pressure be to the number reported on the echo? If the numbers were to come out vastly different, what would be the reason?

If you don't have a significant TR jet, chances are your RVSP is pretty normal.

We very often get an echo report of "elevated RVSP of 55 with TR jet", only to drop in a PAC and get 24/10. This differential is not necessarily from hemodynamic changes under anesthesia. I can do the same calc with a TEE simultaneously measuring PAP, and get vastly different numbers. So as a lesson, an RVSP suggestive of elevated PA pressures on preop TTE as measured by a TR jet does not mean the patient necessarily has elevated PA pressures.

 

[periopdoc]

A TR jet is a pretty common finding that in and of itself does not indicate significant valvular pathology or elevated right ventricular pressures. It would be exceedingly rare to have significantly elevated right ventricular pressures without some jet.

Typically the numbers correspond very closely. Errors in echo measurements typically are from misalignment resulting in an underestimation of the pressure. If you are frequently getting different numbers, I would suggest that there is something wrong with your technique. Occasionally, a patient will present with a jet that is just not possible to line up well, but they should be fairly rare.

- pod

 

[Bertelman]

What would you suggest the problem is if I get a jet suggesting an RVSP of 45, and the PA says 25?

My alignment is dead-on balls accurate in this scenario.

 

[RT2MD]

What would you suggest the problem is if I get a jet suggesting an RVSP of 45, and the PA says 25?

My alignment is dead-on balls accurate in this scenario.

Could pulmonary stenosis cause this?

 

[proman]

What would you suggest the problem is if I get a jet suggesting an RVSP of 45, and the PA says 25?

My alignment is dead-on balls accurate in this scenario.

Gold standard is a pressure transducer in the chamber in question. Assuming the lines are appropriately zeroed, I'd go with the measured PA pressure.

Echo derived values are only useful if there isn't an invasive monitor. They are still calculated from velocity, and have all the problems of continuous wave Doppler.

 

[Bertelman]

Could pulmonary stenosis cause this?

Yes. But not if you can simultaneously see good excursion of pulmonic leaflets on your exam.

RVOT obstruction can, as well