Pulmonary Vasodilators in PE

[turkeyjerky]

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Anyone ever throw in sildenafil or nitric oxide in a crashing PE patient? Basically just basic science and case studies or series in support (although i think theres an RCT in progress for iNO), but i'm curious if anyone's done it.

 

[Phlegm]

Inhaled prostacyclin, yes
Inhaled nitric oxide, yes

Oh, and tPA, yes

Sildenafil, wouldn't use
IV prostacyclin, wouldn't use

 

[jdh71]

Inhaled prostacyclin, yes
Inhaled nitric oxide, yes

Oh, and tPA, yes

Sildenafil, wouldn't use
IV prostacyclin, wouldn't use

Agree with this

 

[turkeyjerky]

How were the results? Who would you use it on, anyone who had to be incubated for the PE?

 

[jdh71]

How were the results? Who would you use it on, anyone who had to be incubated for the PE?

Uh. When you starting to use flolan or nitric on a patient things are bad, like really, really bad. A PE that is big enough to cause that kind of shunting and or right sided heart failure don't turn out well. It'd be a very hard thing to do a real clinical trial on.

I'd use it on someone who was hypoxic despite 1.0 FiO2 with signs of right heart strain/failure on echo and obstructive shock.

 

[Hernandez]

For the most part, I think the patient population you could or would use this on would be exceedingly small. And no, I would not use this on just anyone who ends up tubed from a PE, it would a a pt who essentially meets guidelines for tpa therapy. Who I'm buying time for the tpa to work.

If you're not treating the underlying cause, why would you do something like this?

And how many times a year are y'all even pushing tpa? Personally, with 2 months a year on nights and 2 months a year in MICU, I average 1/year.

 

[turkeyjerky]

Man, what's the deal w/ the grumpy responses.

 

[jdh71]

Man, what's the deal w/ the grumpy responses.

Wasn't grumpy brother. My bad if it seemed that way.

 

[turkeyjerky]

salright

 

[Stank811]

PE is a shunt? I am not following how either of these really would help in a massive PE. In PE, I thought hypoxia was caused by a relative decrease in V/Q in areas of the lung still be perfused. So why would increasing blood flow through the areas of already to much Q with out subsequent increasing V result in better oxygenation.

 

[jdh71]

PE is a shunt? I am not following how either of these really would help in a massive PE. In PE, I thought hypoxia was caused by a relative decrease in V/Q in areas of the lung still be perfused. So why would increasing blood flow through the areas of already to much Q with out subsequent increasing V result in better oxygenation.

Smaller PEs do tend to just be an issue of V/Q mismatch and not much else.

We are talking about massive PEs here leading to an increase in pulmonary artery pressures that can lead to many other interesting phenomena. What's one of the ways you recognize a shunt?? You apply oxygen to the hypoxemia and it doesn't help, which can be seen in patient's with massive PE. Shunts occur in massive PE by two mechanisms by 1) increasing flow through areas of the lung what are not well perfused largely dependent on where the clot landed and 2) increased pressures in the PA system back into the heart leading to an intra-cardiac shunt through a PFO, thereby passing venous blood directly into arterial. All of this is complicated by 1) dysfunctional to failing RV leading to poor CO and 2) increased oxygen extraction by the tissues leading to much lower oxygen levels in blood returning to the heart than at baseline (the cycle can get vicious at this point).

The pulmonary artery vasoldilators are being used to off load pressures from the PA into the RV. The difference that makes in decreasing intracardiac shunt and increasing CO may be the difference that the patient needs.

 

[RemyMcswain]

Smaller PEs do tend to just be an issue of V/Q mismatch and not much else.

We are talking about massive PEs here leading to an increase in pulmonary artery pressures that can lead to many other interesting phenomena. What's one of the ways you recognize a shunt?? You apply oxygen to the hypoxemia and it doesn't help, which can be seen in patient's with massive PE. Shunts occur in massive PE by two mechanisms by 1) increasing flow through areas of the lung what are not well perfused largely dependent on where the clot landed and 2) increased pressures in the PA system back into the heart leading to an intra-cardiac shunt through a PFO, thereby passing venous blood directly into arterial. All of this is complicated by 1) dysfunctional to failing RV leading to poor CO and 2) increased oxygen extraction by the tissues leading to much lower oxygen levels in blood returning to the heart than at baseline (the cycle can get vicious at this point).

The pulmonary artery vasoldilators are being used to off load pressures from the PA into the RV. The difference that makes in decreasing intracardiac shunt and increasing CO may be the difference that the patient needs.

3) PEs can impair hypoxic vasoconstriction throughout the lung. As a result, areas of the lung that are 02 poor will not have blood shunted away -> inc v/q mismatch -> Hypoxemia. This is why small PEs cause hypoxemia.

Also, regarding point 2, are you sure that SV02 is decreased in PE?

 

[jdh71]

3) PEs can impair hypoxic vasoconstriction throughout the lung. As a result, areas of the lung that are 02 poor will not have blood shunted away -> inc v/q mismatch -> Hypoxemia. This is why small PEs cause hypoxemia.

I said this. PE increases blood flow through areas of the lung that were previously not well perfused because of normal regulation of flow. It's not that hypoxic vasoconstriction is impaired, so much as it doesn't matter. It's not a third point. It's the same point.

Also, regarding point 2, are you sure that SV02 is decreased in PE?

If you have an obstructive shock, low cardiac output, and poor tissue oxygen delivery . . . you tell me . . . at least the SvO2 will be low until the tissue dies

 

[RemyMcswain]

With a MASSIVE PE there will be a large volume of cardiac output shunted towards a region of lung not intended to oxygenate that quantity of blood. In the setting of pre-existing lung disease or pulm edema etc that large quantity of blood will not be maximally oxygenated -> Hypoxemia. Thats my interpretation of what you said.

What I am saying is that a PE, regardless of size, is an inflammatory process. Even a small PE can cause Hypoxemia. A small PE causing hypoxemia is not explained by the above description. Rather, the small PE will cause an inflammatory process that diffusely impairs hypoxic vasoconstriction throughout the lung. Hypoxic vasoconstriction is a physiologic mechanism to minimize v/q mismatch. Therefore, when this is impaired, v/q mismatch -> Hypoxemia.

I agree that in massive PEs or any circulatory collapse condition, 02 extraction goes up (obv not sepsis, CO poisoning, etc). However, in regards to the patient in the ICU/floor who is sating 90% on RA, who improves to 100% with supplemental 02, the 90% sat is not secondary to low Sv02.

I think we are on the same page here, although you are talking big PE and im taking small PE.

 

[Hernandez]

I think we are on the same page here, although you are talking big PE and im taking small PE.

what does this thread have to do with small PEs? And the effects of acute PE are exceedingly complex, there is a substantial Vaso-constriction that is induced by PEs beyond there mechanical affect likely mediated by serotonin and Thromboxane. And a quick midline search seems to downplay the claims you're making aout the contribution of HVC to hypoxemia from a PE

And to stank811, shunt is a type of V/Q mismatch. The two primary types are shunt (ventilation w/o perfusion) and dead space (perfusion w/o ventilation). Shunts do not respond to o2, dead space does.

 

[RemyMcswain]

ha dude I re-read your post, I think we are saying the same exact thing. My bad

Carry on

 

[jdh71]

With a MASSIVE PE there will be a large volume of cardiac output shunted towards a region of lung not intended to oxygenate that quantity of blood. In the setting of pre-existing lung disease or pulm edema etc that large quantity of blood will not be maximally oxygenated -> Hypoxemia. Thats my interpretation of what you said.

What I am saying is that a PE, regardless of size, is an inflammatory process. Even a small PE can cause Hypoxemia. A small PE causing hypoxemia is not explained by the above description. Rather, the small PE will cause an inflammatory process that diffusely impairs hypoxic vasoconstriction throughout the lung. Hypoxic vasoconstriction is a physiologic mechanism to minimize v/q mismatch. Therefore, when this is impaired, v/q mismatch -> Hypoxemia.

I agree that in massive PEs or any circulatory collapse condition, 02 extraction goes up (obv not sepsis, CO poisoning, etc). However, in regards to the patient in the ICU/floor who is sating 90% on RA, who improves to 100% with supplemental 02, the 90% sat is not secondary to low Sv02.

I think we are on the same page here, although you are talking big PE and im taking small PE.

Right. We are saying the same thing the shunt is intrapulmonary going through areas of lung where gas exchange is is either poor or cannot keep up. Though, the inflammation impairing hypoxic vasoconstriction is an interesting concept, and I'm not saying you're wrong. I'm going to go check the google scholar (I like it better than pubmed, but that might make me a bad doctor) and see if there is any basic science on that because I have no clue how you'd confirm that in a human.

 

[RemyMcswain]

what does this thread have to do with small PEs? And the effects of acute PE are exceedingly complex, there is a substantial Vaso-constriction that is induced by PEs beyond there mechanical affect likely mediated by serotonin and Thromboxane. And a quick midline search seems to downplay the claims you're making aout the contribution of HVC to hypoxemia from a PE

And to stank811, shunt is a type of V/Q mismatch. The two primary types are shunt (ventilation w/o perfusion) and dead space (perfusion w/o ventilation). Shunts do not respond to o2, dead space does.

At the risk of being redundant, I was only trying to make the point that PE is a systemic process. It is not just a redistribution of blood around a clot.

 

[CriTICAL]

Hernandez, you mixed up the definitions of shunt and dead space

shunt = perfusion without ventilation
dead space = ventilation without perfusion

In PE, RV sees a high afterload 2/2 vascular obstruction by the clot, pulm vasodilators generally not really useful in decreasing PVR, better to remove the obstruction (ie; tPA) and focus on improving CO w/ ionotropes. RV failure will also impair LV function which will decrease CO further.

Regarding hypoxia, as was stated throughout the thread its mainly secondary to redistribution of blood flow to poorly ventilated areas (ie; shunt). Therefore, I would argue vasodilators may actually worsen hypoxemia by impairing HPV and worsening V/Q mismatch.

Mixed Venous will most certainly be depressed because O2 delivery suffers 2/2 hypoxia and low CO

 

[Stank811]

"With a MASSIVE PE there will be a large volume of cardiac output shunted towards a region of lung not intended to oxygenate that quantity of blood. In the setting of pre-existing lung disease or pulm edema etc that large quantity of blood will not be maximally oxygenated -> Hypoxemia. Thats my interpretation of what you said.

What I am saying is that a PE, regardless of size, is an inflammatory process. Even a small PE can cause Hypoxemia. A small PE causing hypoxemia is not explained by the above description. Rather, the small PE will cause an inflammatory process that diffusely impairs hypoxic vasoconstriction throughout the lung. Hypoxic vasoconstriction is a physiologic mechanism to minimize v/q mismatch. Therefore, when this is impaired, v/q mismatch -> Hypoxemia."

Agreed....so lets get back to the main topic...how does pulmonary vasodilators help with either of these two causes. I agree if you are arguing you want to unload the RV and prevent intra-cardiac shunt pulmonary vasodilators might be beneficial but lets assume there is no intracardiac shunt. What happens when you apply these therapies to people with ARDS or COPD often times it doesn't help the oxygenation but makes it worse because you get rid of the pulmonary hypoxic vasoconstriction leading again to a low V/Q ratio leading to hypoxemia. So in the case of a large PE without intracardiac shunt giving a pulmonary vasodilator will only potentially decrease the already low V/Q by incasing perfusion to areas of lung that can't handle it. In the case of small PE that has already eliminated hypoxic pulmonary vasoconstriction to a certain extent why would getting rid of it further help any. Good discussion.

 

[jdh71]

In PE, RV sees a high afterload 2/2 vascular obstruction by the clot, pulm vasodilators generally not really useful in decreasing PVR, better to remove the obstruction (ie; tPA) and focus on improving CO w/ ionotropes. RV failure will also impair LV function which will decrease CO further.

Regarding hypoxia, as was stated throughout the thread its mainly secondary to redistribution of blood flow to poorly ventilated areas (ie; shunt). Therefore, I would argue vasodilators may actually worsen hypoxemia by impairing HPV and worsening V/Q mismatch.

The context here is the crashing (massive) PE patient, and I'm assuming intubated, refractory hypoxia, and hypotension.

You're not giving the inhaled vasodilators to improve oxygenation but to decrease decrease the load on the RV. The blood is already shunting, how much worse can/will it get? Won't know until you try. You're doing everything you can to afterload reduce the RV. You're using this in the same way you'd use nipride in LV failure. The ionotropes may or may not be a good idea, you definitely do not want to make these patients more tachycardic or drop blood pressure any further than it may already be, and then there is the arrhythmia potential.

It's one of the toughest areas to treat. The acutely failing RV in the setting of PE. You're on the wrong side of every important physiologic parameter. Patients probably survive, if they do, despite what we do.

 

[Hernandez]

Hernandez, you mixed up the definitions of shunt and dead space

editing fail.

 

[CriTICAL]

The context here is the crashing (massive) PE patient, and I'm assuming intubated, refractory hypoxia, and hypotension.

You're not giving the inhaled vasodilators to improve oxygenation but to decrease decrease the load on the RV.

I'm not saying giving inhaled pulm vasodilators is completely useless, but in a PE large enough to cause acute RV failure and shock, RV afterload is elevated 2/2 the large physical obstruction by the clot and so I don't see how vasodilators would yield much if any significant benefit in lowering RV afterload. If the pt is crashing/near code, employing inhaled vasodilators shouldn't delay attempts to do what u can to try and fix the root of the problem which is the large physical obstruction by the clot (ie; tPA, percutaneous clot removal, surgical embolectomy if fortunate enough to be at a center)

 

[jdh71]

I'm not saying giving inhaled pulm vasodilators is completely useless, but in a PE large enough to cause acute RV failure and shock, RV afterload is elevated 2/2 the large physical obstruction by the clot and so I don't see how vasodilators would yield much if any significant benefit in lowering RV afterload. If the pt is crashing/near code, employing inhaled vasodilators shouldn't delay attempts to do what u can to try and fix the root of the problem which is the large physical obstruction by the clot (ie; tPA, percutaneous clot removal, surgical embolectomy if fortunate enough to be at a center)

Right.

I thought that we were assuming that per this discussion.

I'd also say that anyone this sick, the surgeons and IR people won't go anywhere near them. Hope you made your offering to the tPA gods on a case like this.

 

[souljah1]

Massive PE:

1. TPA
2. Epi drip to whip the RV
3. Milrinone to whip it more
4. IV Flolan to offload the pressure the RV is pushing against

Normal PE:

1. Boring