Pumlonary Embolism and BP

[adwilcox28]

Thinking about a pulmonary embolism my guess would be that a S/S would be HYPERtension due to the blockage somewhere along the pulmonary artery. But I read the opposite that a S/S is actually hypotenstion. Why is that?

 

[foxfire]

The left ventricles are not receiving volume like they should and thus don't have much output due to the PE blocking things up.


My nut shell 2 cents worth.

 

[usalsfyre]

Thinking about a pulmonary embolism my guess would be that a S/S would be HYPERtension due to the blockage somewhere along the pulmonary artery. But I read the opposite that a S/S is actually hypotenstion. Why is that?

Think about what's needed for cardiac output. Fluid coming in (preload), approprite muscle contraction (inotropy) and a high enough rate to meet demand (heart rate or chronotropy) The LV has no preload to pump out if there is a blockage in the pulmonary artery.. What you end up with during a massive PE is PROFOUND hypotension that is unresponsive to fluids as well as profound hypoxia due to high dead space V/Q mismatch. Basically the person you cannot treat with anything other than rapid transport. This is one case where screwing around onscene=death.

 

[JPINFV]

This is one case where screwing around onscene=death.

It really depends. Not all pulmonary embolisms are emergent conditions, and depending on the circumstances (recent surgery or high risk of bleeding? Saddle emboli? Etc.), may be just monitored for a few days before getting fibrolytics or high power anticoagulants. However, they can easily turn into emergency conditions. Additionally, yes, the "EMS classic" presentation of profound hypotension, chest pain, hemoptysis, and hypoxia not fixed by supplemental oxygen are not served well by EMS waiting around on scene.

 

[usafmedic45]

To the OP, you have to remember that one of the lung's less oft described functions is as a "clot catcher". The low-pressure system that is the pulmonary vasculature is pretty well adapted to handling minor obstructions and such. It takes a pretty dramatic blockage (pretty much a saddle thrombus, blockage of one of the main PAs or a LOT of smaller vessels blocked) to rachet down the BP basically through reduction of the flood coming back to the left side of the heart. Even hypoxia is not always a finding in PEs unless you take out a significant amount of the pulmonary vasculature. It's quite common for there to be a "subclinical" PE.

The situation isn't necessarily (as JP pointed out) as dire as USALFYRE would make it sound, but then again, this isn't something you want to **** around with.

 

[usalsfyre]

It really depends. Not all pulmonary embolisms are emergent conditions, and depending on the circumstances (recent surgery or high risk of bleeding? Saddle emboli? Etc.), may be just monitored for a few days before getting fibrolytics or high power anticoagulants. However, they can easily turn into emergency conditions. Additionally, yes, the "EMS classic" presentation of profound hypotension, chest pain, hemoptysis, and hypoxia not fixed by supplemental oxygen are not served well by EMS waiting around on scene.

I agree there's probably a segment if the population that walks around with PEs, kinda like there's probably more stable, non-leaking aortic anyerusms than we know about. I should have been a little more specific, I was referring to the classic saddle embolus causing physiologic disturbance. That said, there's a good chance these patients will present to EMS in cardiac arrest.

 

[Akulahawk]

Thinking about a pulmonary embolism my guess would be that a S/S would be HYPERtension due to the blockage somewhere along the pulmonary artery. But I read the opposite that a S/S is actually hypotenstion. Why is that?

As others have stated, there's simply not enough volume being delivered to the LA of the heart from the pulmonary circuit. Remember, the flow through or out from the lungs is what's restricted, not flow into the pulmonary circuit.

You might rarely seen "profound hypotension, chest pain, hemoptysis, and hypoxia" in your PE patient... but you might also see some JVD as well.

 

[usafmedic45]

Remember, the flow through or out from the lungs is what's restricted, not flow into the pulmonary circuit.

It depends on where the embolism lodged. On echocardiograms, you will see elevated right atrial and right ventricular pressures and in severe cases a grossly dilated right side of the heart. I have a video I saved somewhere on this computer from a patient with a massive PE that lodged in the main pulmonary artery right above the pulmonic valve. The right ventricle was acutely dilated to roughly twice its normal size and you can see the tail of the embolus. I'll post it if I can locate it.

hemoptysis

Calling that a rare symptom is an understatement. I've only seen a few cases with frank hemoptysis.

 

[Akulahawk]

It depends on where the embolism lodged. On echocardiograms, you will see elevated right atrial and right ventricular pressures and in severe cases a grossly dilated right side of the heart. I have a video I saved somewhere on this computer from a patient with a massive PE that lodged in the main pulmonary artery right above the pulmonic valve. The right ventricle was acutely dilated to roughly twice its normal size and you can see the tail of the embolus. I'll post it if I can locate it.


Calling that a rare symptom is an understatement. I've only seen a few cases with frank hemoptysis.

I'd love to see that video! Would you see such a grossly dilated right heart from an acute incident or would that be more from an exacerbation of pulmonary HTN? I'm also aware that such large clots can cause an obstruction of the pulmonary artery. From another perspective though, flow into the pulmonary circuit was certainly not obstructed until it hit that embolus... which would have the effect of reducing flow through the remaining portions of the pulmonary circuit.

Did that patient survive?

 

[usafmedic45]

Would you see such a grossly dilated right heart from an acute incident or would that be more from an exacerbation of pulmonary HTN?

Well, it's acute PH due to the obstruction that causes the dilation. If you obstruct the pulmonary vasculature, you are going to wind up with PH as a general rule.

Did that patient survive?

I recall that the survived to ICU admission but I was gone for several days after his initial presentation and he was lost to my followup. I know one of the surgeons went in and removed the clot.

 

[usalsfyre]

Not having seen but one or two significant PEs myself, how often do you get the peaked P waves on EKG that are described in the "classic" presentation?

 

[usafmedic45]

Not having seen but one or two significant PEs myself, how often do you get the peaked P waves on EKG that are described in the "classic" presentation?

I've never heard that described as the "classic" presentation. The classic EKG presentation for PE described in the literature is what's called the "right ventricular strain pattern" or "S1Q3T3". It's the presence of an S wave in Lead I, a Q wave in Lead 3 and T wave inversion in Lead 3. That said, like most "classic presentations", it's something you see only on occasion. My guess would be about 1 in 4 cases have this finding. I would also like to point out that it's not specific to PE. If you have a person with chronic cor pulmonale, PH and some other pulmonary conditions, you will often see it as a chronic feature.

I can't say that I have ever seen "peaked" T waves in a PE patient. I assume you mean increased amplitude (indicating more 'voltage')? Most commonly you'll see sinus tachycardia, right bundle branch block and axis deviation to the right.

 

[Aidey]

I have a video I saved somewhere on this computer from a patient with a massive PE that lodged in the main pulmonary artery right above the pulmonic valve. The right ventricle was acutely dilated to roughly twice its normal size and you can see the tail of the embolus. I'll post it if I can locate it.

I had one of those on a transfer recently. I'm glad I didn't see the CT before the transfer or I likely would have said "F--- That". The clot started in the R ventricle, extended down both the left and right branches of the pulmonary artery and had multiple termination points at the distal alveoli. It was honestly an amazing view of pulmonary circulation. No chest pain, just SOB, needing 8lpm or so to maintain his SpO2 in the mid 90s. EtCo2 in the low teens.

When we were back at that hospital later on in the shift I asked the charge RN to show me the CT. He was like "Ehhh, PEs really aren't all that interest....Holy :censored::censored::censored::censored:!" I have no idea if the guy lived or not.

 

[Akulahawk]

Well, it's acute PH due to the obstruction that causes the dilation. If you obstruct the pulmonary vasculature, you are going to wind up with PH as a general rule.


I recall that the survived to ICU admission but I was gone for several days after his initial presentation and he was lost to my followup. I know one of the surgeons went in and removed the clot.

Good to know that right sided dilation that's significant in size can happen acutely. In any event, I hope the patient survived to discharge and is leading a normal, healthy life.

My question was more related to the acute dilation issue than pulmonary vasculature obstruction leading to pulmonary HTN. I'm pretty familiar with that end of it... Thankfully it's not me.

 

[usalsfyre]

I've never heard that described as the "classic" presentation. The classic EKG presentation for PE described in the literature is what's called the "right ventricular strain pattern" or "S1Q3T3". It's the presence of an S wave in Lead I, a Q wave in Lead 3 and T wave inversion in Lead 3. That said, like most "classic presentations", it's something you see only on occasion. My guess would be about 1 in 4 cases have this finding. I would also like to point out that it's not specific to PE. If you have a person with chronic cor pulmonale, PH and some other pulmonary conditions, you will often see it as a chronic feature.

I can't say that I have ever seen "peaked" T waves in a PE patient. I assume you mean increased amplitude (indicating more 'voltage')? Most commonly you'll see sinus tachycardia, right bundle branch block and axis deviation to the right.

Hmmm, somewhere along the way I picked up "P for pulmonale" referring to peaked P waves of increased amplitude from right heart strain, both acute and chronic. Guess that's one of the ones that shouldn't have stuck.

 

[usafmedic45]

Well, you're right that it can be, but I've never heard or seen it as reliable in acute cases.

 

[Melclin]

It really depends. Not all pulmonary embolisms are emergent conditions, and depending on the circumstances (recent surgery or high risk of bleeding? Saddle emboli? Etc.), may be just monitored for a few days before getting fibrolytics or high power anticoagulants. However, they can easily turn into emergency conditions. Additionally, yes, the "EMS classic" presentation of profound hypotension, chest pain, hemoptysis, and hypoxia not fixed by supplemental oxygen are not served well by EMS waiting around on scene.

And even if it is emergent, they still sit in resus with their ABCs being tinkered with until they're stable enough to go to CT.

But its not a bad rule of thumb from an EMS point of view to think PE = big sick = much quick.


To the OP, think about your types of shock (depends how you divide them I suppose). A significant clot in the lungs can obstruct the return of blood to the heart right? Shock caused by an obstruction...obstructive shock.

http://en.wikipedia.org/wiki/Shock_(circulatory)#Obstructive_shock

 

[Melclin]

Hmmm, somewhere along the way I picked up "P for pulmonale" referring to peaked P waves of increased amplitude from right heart strain, both acute and chronic. Guess that's one of the ones that shouldn't have stuck.

"The classic findings of right heart strain and acute cor pulmonale are tall, peaked P waves in lead II (P pulmonale), right axis deviation, right bundle-branch block, an S 1 Q 3 T 3 pattern, or atrial fibrillation. Unfortunately, only 20% of patients with proven PE have any of these classic ECG abnormalities."

http://emedicine.medscape.com/article/759765-diagnosis

As I understand it, P pulmonale is a sign of cor pulmonale.

 

[MediMike]

Hmmm, somewhere along the way I picked up "P for pulmonale" referring to peaked P waves of increased amplitude from right heart strain, both acute and chronic. Guess that's one of the ones that shouldn't have stuck.

P Pulmonale can be clinically indicative of Right Atrial Enlargement, along with a biphasic P in V1 in which the first 1/2 is longer than the first 1/2 of the P wave in V6. Haven't heard of it in regards to an acute presentation of a PE though!