Vascular question: hydralazine and AAA

[DrMetal]

questions for the Vascular types:

You know how you're not supposed to use hydralazine for BP control in AAA, per the 'shearing force' of hydralazine

a) Is that really true? does hydralazine really have a 'shearing force'? How real of a threat is this?

b) What about after repair of the AAA? say patient had it repaired 5 years ago and now just has bad HTN. ok to use hydralazine?

Thanks!

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[LucidSplash]

questions for the Vascular types:

You know how you're not supposed to use hydralazine for BP control in AAA, per the 'shearing force' of hydralazine

a) Is that really true? does hydralazine really have a 'shearing force'? How real of a threat is this?

b) What about after repair of the AAA? say patient had it repaired 5 years ago and now just has bad HTN. ok to use hydralazine?

Thanks!

This is really more important for dissection rather than AAA. Hydralazine can cause reflex tachycardia which increases shear stress. For dissection, shear stress is the entire problem; fluid dynamics, shape of the aorta, entry tears happen commonly where the aorta is tethered and where the amount of force hits hardest. Which is why the treatment algorithm is 1st to bring the HR down and then adding something like cardene if the beta blocker Isn’t sufficient to bring the BP down. Then convert to PO with combination beta blocker and calcium channel blocker ans then ACE/ARB if the 1st two aren’t enough.

People tend to conflate the treatment of dissection and AAA. In general we try to avoid shear stress in the aorta overall, but dissection and AAA are different entities. Theoretically, increased shear stress can increase size of aneurysm (especially a thoracic aneurysm) and there are studies with plenty of pretty pictures of aortas showing modeling of the effects of shear stress. But I’m going to worry about it more in the setting of a dissection that of just a known asymptomatic thoracic aneurysm.

Also hydralazine is a ****ty drug overall for a lot of reasons and there are a ton of better options. Not the least of which is that it has a rapid onset of action and then a short duration so it mostly just makes people feel good by treating the number but doesn’t have a lasting effect and doesn’t treat the problem and in a couple hours you’re dealing with the same problem again.

 

[dienekes88]

questions for the Vascular types:

You know how you're not supposed to use hydralazine for BP control in AAA, per the 'shearing force' of hydralazine

a) Is that really true? does hydralazine really have a 'shearing force'? How real of a threat is this?

b) What about after repair of the AAA? say patient had it repaired 5 years ago and now just has bad HTN. ok to use hydralazine?

Thanks!

To me, the most important element is the increase in dp/dt. Without a beta blocker... any afterload agent will increase dp/dt. The problem with hydralazine PO is that its dosed 3x per day. If you definitely want the patient to skip doses and be "noncompliant," you prescribe them a 3x daily medication.

 

[DrMetal]

This is really more important for dissection rather than AAA. Hydralazine can cause reflex tachycardia which increases shear stress. For dissection, shear stress is the entire problem; fluid dynamics, shape of the aorta, entry tears happen commonly where the aorta is tethered and where the amount of force hits hardest. Which is why the treatment algorithm is 1st to bring the HR down and then adding something like cardene if the beta blocker Isn’t sufficient to bring the BP down. Then convert to PO with combination beta blocker and calcium channel blocker ans then ACE/ARB if the 1st two aren’t enough.

People tend to conflate the treatment of dissection and AAA. In general we try to avoid shear stress in the aorta overall, but dissection and AAA are different entities. Theoretically, increased shear stress can increase size of aneurysm (especially a thoracic aneurysm) and there are studies with plenty of pretty pictures of aortas showing modeling of the effects of shear stress. But I’m going to worry about it more in the setting of a dissection that of just a known asymptomatic thoracic aneurysm.

Also hydralazine is a ****ty drug overall for a lot of reasons and there are a ton of better options. Not the least of which is that it has a rapid onset of action and then a short duration so it mostly just makes people feel good by treating the number but doesn’t have a lasting effect and doesn’t treat the problem and in a couple hours you’re dealing with the same problem again.

I've often wondered why we're not as concerned with the sheer stress element of hydralazine, with respect to AAA (what if it's a big one, greater than 5.5 cm, aren't you concerned about a dissecting?)

What about after repair of a AAA or a dissection? Safe to use hydralazine status post repair? If so, went after, six months one year two years? (I'm asking because I've seen patients on hydralazine after repairs. They seem to be fine on it)

 

[LucidSplash]

I've often wondered why we're not as concerned with the sheer stress element of hydralazine, with respect to AAA (what if it's a big one, greater than 5.5 cm, aren't you concerned about a dissecting?)

What about after repair of a AAA or a dissection? Safe to use hydralazine status post repair? If so, went after, six months one year two years? (I'm asking because I've seen patients on hydralazine after repairs. They seem to be fine on it)

The sheer stress is more important with regard to the fluid dynamics/physics of the thoracic aorta in the setting of an acute or subacute dissection.

Primary aneurysmal disease and thoracic dissection are different diseases - they may overlap, but their etiologies are different. You can get a primary thoracic aneurysm which is secondary to degradation of the wall of the vessel due to a combination of genetics and environmental risk factors (smoking) but aneurysmal change is also the natural history of many chronic dissections because the wall was damaged by the dissection.

When we are concerned about sheer stress it is typically in the acute/subacute setting, because we don’t want to increase/extend the dissection. Sheer stress isn’t was causes a primary aneurysm generally. So it isn’t about size, it is about the etiology of the disease.

But again, hydralazine is a ****ty drug and most cardiologists I know think it shouldn’t be used. Reflex tachycardia, short duration of action, variable effectiveness based in P450 metabolism There are other better drugs. Much the same that tramadol is a ****ty drug.

 

[Surgeon D.O.]

Thank you all for this discussion. I’m bookmarking this for my vascular elective lol.

 

[Lem0nz]

Much the same that tramadol is a ****ty drug.

What's wrong with tramadol?

 

[dienekes88]

I've often wondered why we're not as concerned with the sheer stress element of hydralazine, with respect to AAA (what if it's a big one, greater than 5.5 cm, aren't you concerned about a dissecting?)

What about after repair of a AAA or a dissection? Safe to use hydralazine status post repair? If so, went after, six months one year two years? (I'm asking because I've seen patients on hydralazine after repairs. They seem to be fine on it)

The primary issue is not necessarily hydralazine, because the evidence that hydralazine has an adveese effect other than through its vasodilatory effect is limited. For this reason putting the same patient on losartan without a beta blocker would hypothetically have a similar stress/strain on the aortic wall.

Stepping back, we have to think about 2 things, what's good for the patient and what is the patient actually going to be able to take. Labetalol is another example of a drug that may work while the patient is being administered medications routinely by the bedside nurse but has a high probability of non compliance in the outpatient setting. As such, the focus shouldn't be on "is hydralazine okay in dissection or aneurysm..." the focus should be: can I get this patient on a stable medical regimen that reduced dp/dt and is easy to take.

 

[DrMetal]

what's good for the patient and what is the patient actually going to be able to take.

Great points. Though quite frankly, if you have a large aortic aneurysm and/or a dissection---I would say to my patient, "the largest vessel in your body is about to burst and you could bleed to death in seconds!"----and you're not will to comply with medications, then perhaps we should just let evolution take its course!

 

[HighPriest]

Great points. Though quite frankly, if you have a large aortic aneurysm and/or a dissection---I would say to my patient, "the largest vessel in your body is about to burst and you could bleed to death in seconds!"----and you're not will to comply with medications, then perhaps we should just let evolution take its course!

Nah, they’ll just be non-compliant until there’s an emergency, and then they want it fixed. Immediately and without complication.

 

[LucidSplash]

What's wrong with tramadol?

Lots.

1. It is an opiod but doesn't bind directly to opiod receptors/binds super weakly. Most of its opiod action is the result of a metabolite. So basically you are depending on the patient to have a good P450 system. A good portion of the population (up to 10%) don't have the right enzyme and then there are others who are ultrametabolizers. So basically, you are not prescribing a known amount of drug - just basically throwing at a dartboard blind.

2. Tramadol itself also acts as an SNRI. But none of its metabolites do. So between unknown opiod activity and the SNRI activity, you have an unknown mix of pharmacology.

3. Lots of side effect. Some of which likely connected to the SNRI effects. If you get the SNRI effect from the tramadol but it gets metabolized quickly, and you use tramadol persistantly, you get a cycle of withdrawal from the SNRI effects. People who use if for awhile get opiod withdrawal symptoms but it takes awhile because of the opiod metabolites that stick around - but they also get anxiety, panic attacks, hallucinations, etc associate with SNRI withdrawal, and that happens before the opiod withdrawal symptoms.

4. People mistakenly think it is good to prescribe a "weak" opiod because it has less addiction potential. But instead, what studies have found is that people take more tramadol to get analgesic effect. If you look at the studies, for a lot of people the actual analgeisa is equal to tylenol but worse than NSAIDs. So why bother? Just given them an actual opiod that you know will have X effect.

5. BMJ published a study that showed an association between postop op tramadol use for pain control and then persistent opiod use after the postop period - higher than other short acting opiods.

6. HUGE recreational use of tramadol worldwide - significantly euphoria association, studies have said consistent with heroin.

Summary: I don't let my residents prescribe it for my patients. You don't really know what the patient will be getting because it all depends on their P450 metabolism. It doesn't work well in general, and doesn't work at all for at least 10% of the population, but still has significant side effects.

 

[HighPriest]

Lots.

1. It is an opiod but doesn't bind directly to opiod receptors/binds super weakly. Most of its opiod action is the result of a metabolite. So basically you are depending on the patient to have a good P450 system. A good portion of the population (up to 10%) don't have the right enzyme and then there are others who are ultrametabolizers. So basically, you are not prescribing a known amount of drug - just basically throwing at a dartboard blind.

2. Tramadol itself also acts as an SNRI. But none of its metabolites do. So between unknown opiod activity and the SNRI activity, you have an unknown mix of pharmacology.

3. Lots of side effect. Some of which likely connected to the SNRI effects. If you get the SNRI effect from the tramadol but it gets metabolized quickly, and you use tramadol persistantly, you get a cycle of withdrawal from the SNRI effects. People who use if for awhile get opiod withdrawal symptoms but it takes awhile because of the opiod metabolites that stick around - but they also get anxiety, panic attacks, hallucinations, etc associate with SNRI withdrawal, and that happens before the opiod withdrawal symptoms.

4. People mistakenly think it is good to prescribe a "weak" opiod because it has less addiction potential. But instead, what studies have found is that people take more tramadol to get analgesic effect. If you look at the studies, for a lot of people the actual analgeisa is equal to tylenol but worse than NSAIDs. So why bother? Just given them an actual opiod that you know will have X effect.

5. BMJ published a study that showed an association between postop op tramadol use for pain control and then persistent opiod use after the postop period - higher than other short acting opiods.

6. HUGE recreational use of tramadol worldwide - significantly euphoria association, studies have said consistent with heroin.

Summary: I don't let my residents prescribe it for my patients. You don't really know what the patient will be getting because it all depends on their P450 metabolism. It doesn't work well in general, and doesn't work at all for at least 10% of the population, but still has significant side effects.

Pretty interesting. I think I’ve Rxed tramadol about three times in 16 years, and both were by patient request as an alternative to other short acting opioids. So I’m definitely not up on the side effects as it’s largely irrelevant for my practice. But fwiw, unpredictable metabolic potential is why more or less the entire ENT community stopped prescribing codeine after tonsillectomy for kids (well, that and it turns out narcotics are generally not necessary for kids). So that alone is a good argument in my book.

 

[Lem0nz]

Huh. Today I learned.

 

[TypeADissection]

Great points. Though quite frankly, if you have a large aortic aneurysm and/or a dissection---I would say to my patient, "the largest vessel in your body is about to burst and you could bleed to death in seconds!"----and you're not will to comply with medications, then perhaps we should just let evolution take its course!

I take 4 days of call and decide to peruse SDN only to find out that @LucidSplash has been holding down the fort with absolute solid answers.

In response to @DrMetal, when I talk to patients in clinic about their surgically indicated for repair AAA, and then they decide that they don't want surgery at all; I then bring up the point that they should then be DNR/DNI in the event of a rupture. Because if they're not willing to have it fixed electively when conditions are optimized, then they shouldn't expect us to fix it emergently when serious physiologic derangements have already begun and they arrive in extremis. I also don't force them to give me an answer in the office if they don't want to or feel overwhelmed, but rather go home and talk to their loved ones about it and give a call within a week. Probably not the most efficient thing that I do because it does leave 1-2 phone calls per week that I have to tie up, but I want my patients to be as informed and comfortable with their decisions as they can be.

Recently there was someone I with a large type 4 thoraco that I wanted to send out for 4-vessel fen and they refused. Of course, a few months later they ruptured and family is in the ED demanding that everything be done. That's always fun.

 

[LucidSplash]

I take 4 days of call and decide to peruse SDN only to find out that @LucidSplash has been holding down the fort with absolute solid answers.

Weak sauce excuse for not keeping up with SDN. 😂

I take call a week at a time, sometimes 2 if my partner is out of town. 😱💪🏻😭

 

[evilbooyaa]

Lots.

1. It is an opiod but doesn't bind directly to opiod receptors/binds super weakly. Most of its opiod action is the result of a metabolite. So basically you are depending on the patient to have a good P450 system. A good portion of the population (up to 10%) don't have the right enzyme and then there are others who are ultrametabolizers. So basically, you are not prescribing a known amount of drug - just basically throwing at a dartboard blind.

2. Tramadol itself also acts as an SNRI. But none of its metabolites do. So between unknown opiod activity and the SNRI activity, you have an unknown mix of pharmacology.

3. Lots of side effect. Some of which likely connected to the SNRI effects. If you get the SNRI effect from the tramadol but it gets metabolized quickly, and you use tramadol persistantly, you get a cycle of withdrawal from the SNRI effects. People who use if for awhile get opiod withdrawal symptoms but it takes awhile because of the opiod metabolites that stick around - but they also get anxiety, panic attacks, hallucinations, etc associate with SNRI withdrawal, and that happens before the opiod withdrawal symptoms.

4. People mistakenly think it is good to prescribe a "weak" opiod because it has less addiction potential. But instead, what studies have found is that people take more tramadol to get analgesic effect. If you look at the studies, for a lot of people the actual analgeisa is equal to tylenol but worse than NSAIDs. So why bother? Just given them an actual opiod that you know will have X effect.

5. BMJ published a study that showed an association between postop op tramadol use for pain control and then persistent opiod use after the postop period - higher than other short acting opiods.

6. HUGE recreational use of tramadol worldwide - significantly euphoria association, studies have said consistent with heroin.

Summary: I don't let my residents prescribe it for my patients. You don't really know what the patient will be getting because it all depends on their P450 metabolism. It doesn't work well in general, and doesn't work at all for at least 10% of the population, but still has significant side effects.

I Rx a fair amount of tramadol in people (Oncology) who even 5/325 of Hydrocodone/APAP is 'too strong' but APAP is too weak (and most of these folks can't take NSAIDs), but learned something today. Thanks!

 

[deleted50541]

I Rx a fair amount of tramadol in people (Oncology) who even 5/325 of Hydrocodone/APAP is 'too strong' but APAP is too weak (and most of these folks can't take NSAIDs), but learned something today. Thanks!

That's how I've used it in the past and it's worked out so-so. But LucidSplash's rundown confirms what I've always suspected about tramadol since it never seems to provide reliable analgesia.

I barely use tramadol in practice and will probably eliminate it all together after looking into it a bit more.