GTN for hypertension/Stroke???

[PNWmedic767]

Hey guys, I am a QA officer at my base and I am reviewing charts and doing followups and here is the scenario.

65yo male called for headache and nausea.

Crew gets on scene patient has high BP 240/140, HR 90, GCS of 15. Patient has a noted injury to the frontal region of his skull from a fall earlier in the day, denies BT use. Crew gets IV, 4lead ->12-lead nothing exciting found. Then given GTN x2 over the course of the transport to assist in lowing BP. This is an ALS crew and have access to beta blockers but have to call OLMC prior to giving which always ends in a big NO from the ED physicians. Patient gets transported non-emergent, brain scanned is having a bleed..... In my training unless the patient is having a true hypertensive emergency, don't treat the BP. Even more so do not treat with GTN due to the possibility of stroke. Am I on the right track, I plan to call my medical director to get confirmation but its memorial weekend and he wouldn't appreciate the call.

This is my take away from what I learned and I wanted to see if you guys agree? or even more so if any of you guys have the knowledge that states different. If so please provide references.

 

[Peak]

SL nitro should not be used to treat hypertension unless the goal of therapy is directly to reduce afterload on the heart. The potential rapid rebound hypertension can result in poor outcomes. Betablockers or calcium channel blockers are generally preferred for managment of hypertensive crisis.

It is extremely risky to treat hypertension with neurological complaints without a CT. Increased ICP reduces the CPP, and the hypertension is to a large degree a compensatory mechanism.

There is risk to not controlling the hypertension, and we typically place these patients on a nicardipine in the ED, but that is after imaging and consultation with neuro. There are many studies which show that managing head BPs in the setting of ICH reduces the average increase in size of bleeds and when balanced appropriately in a specialty center results in better outcomes. Typically we will try to keep SBP below 180 and not drop below 165 through vasoactives, sometimes lower depending on the neuro team's recommendation.

I suspect there is some theroretical benifit to controlling hypertension in the field, but the risk generally far outweighs the benefit for the majority of services.

I would be extremely concerned that your medics had a more appropriate treatment modality but didn't want to call in and talk to a doc. The idea of giving a more risky and less appropriate treatment in lieu of calling in would be extremely poor patient care and poor professional ethics.

 

[PNWmedic767]

SL nitro should not be used to treat hypertension unless the goal of therapy is directly to reduce afterload on the heart. The potential rapid rebound hypertension can result in poor outcomes. Betablockers or calcium channel blockers are generally preferred for managment of hypertensive crisis.

It is extremely risky to treat hypertension with neurological complaints without a CT. Increased ICP reduces the CPP, and the hypertension is to a large degree a compensatory mechanism.

There is risk to not controlling the hypertension, and we typically place these patients on a nicardipine in the ED, but that is after imaging and consultation with neuro. There are many studies which show that managing head BPs in the setting of ICH reduces the average increase in size of bleeds and when balanced appropriately in a specialty center results in better outcomes. Typically we will try to keep SBP below 180 and not drop below 165 through vasoactives, sometimes lower depending on the neuro team's recommendation.

I suspect there is some theroretical benifit to controlling hypertension in the field, but the risk generally far outweighs the benefit for the majority of services.

I would be extremely concerned that your medics had a more appropriate treatment modality but didn't want to call in and talk to a doc. The idea of giving a more risky and less appropriate treatment in lieu of calling in would be extremely poor patient care and poor professional ethics.

My point exactly and the reason I brought it here to get more info before going further up the ladder

 

[PNWmedic767]

Could you elaborate more on the ICP reducing the CPP and how that works? I understand the abbreviations just not the way it works. Is it just due to the ICP causing lack of blood movement due to the ICP itself?

 

[GMCmedic]

There may be a more elaborate or eloquent answer but the short version is MAP-ICP=CPP. So therefore an increase in ICP will be a reduction in CPP.

We know that we need a minimum MAP of 60 to perfuse organs. So in a head injured patient if we maintained the minimum map of 60, but the ICP is 15, then our CPP is 45 and not adeqaute to perfuse the brain. Hence the recomendation of a MAP of 90 (or whatever it is now), if the MAP is 90 and ICP is 15, then we have a CPP of 70 and are perfusing the brain.


I think thats how this all works.

 

[rescue1]

No reason to give nitro for non-cardiac hypertension—it provides minimal arterial dilation and the effect is too short for it to have any real effect other than rebound HTN like Peak said. It also provides very inconsistent BP control.

Really there’s no reason to treat stroke related HTN in the field—you have no idea if it’s a bleed or not, which dramatically changes how aggressive you want to be with lowering blood pressure (ischemic strokes should be allowed a certain high level of hypertension to keep the area of infarct perfused as much as possible). Unless your transport times are exceedingly long, treating prehospital HTN is almost always purely to make the medic feel like they’re doing something but likely has no benefit or actively harms the patient (acute heart failure being a big exception).

I agree with Peak that not wanting to call the doc because you’ll get told “no” is pretty ****ty care, especially since the medics are using a considerably worse, potentially dangerous medicine to get around calling OMC.

 

[CWATT]

SL nitro should not be used to treat hypertension unless the goal of therapy is directly to reduce afterload on the heart.

I searched for a dose-response graphic for Nitro but couldn’t find one. The following article (https://link.springer.com/article/10.1007/BF00874655) suggests a 1.6mg SL dose (2-4x typical EMS protocol) primarily produce venodilation with ‘peripheral arterial resistance’ (aka Afterload) requiring further increases in plasma concentration. Assuming SL nitro spray has the same bioavailability as SL nitro tablets of 40% (https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/021134s005lbl.pdf), those are some pretty big doses (far beyond what we would expect to see in the prehospital setting) to state the “goal of therapy is directly to reduce afterload”. I would therefore like to -respectfully- suggest a correction that ‘the goal of nitro therapy is to reduce preload’.

 

[Gurby]

Interesting to me that they were worried enough to give a drug for the HTN, but transported non-emergent? What did they think was going on?

 

[CWATT]

@PNWmedic767 — Do you have the opportunity to sit-down with the medics on this call? If so, I would ask them what their goal of therapy was and why. This ‘scenario’ fringes on the cleché ‘treat the patient not the monitor’. They obviously recognized the hypertension and came to the conclusion it is typically not-good, but from what you have shared I get the feeling either one of two things happened here: either they didn’t understand what was actually going on (treated the Pt as if it were idiopathic hypertension), or they were trying to operate within the limits of the system and made decisions which were not ideal.

The questions I would ask them are — did they recognize this as a possible hemorrhagic stroke (Hx of recent head trauma is a strong indicator)? Did they perform a neurological assessment? What was the GCS? What was the the result of the Cincinatti Stroke Scale? Did they assess the 12 cranial nerves and interpret the findings? If they had enough time, what was their target BP with the nitro? Do they understand the need to balance BP against ICP to maintain appropriate CPP?

If they had a strong understanding of the mechanics, perhaps they assumed they would not get an order for adrenergic blockers (the appropriate treatment) and were trying to use what they had to achieve the same therapeutic goal. I’m empathetic to people operating within limited systems where field-actions are subject to the discretion of a doc over the phone, but a poor decision was made so I would strive to understand why.

 

[Carlos Danger]

Are there not published guidelines on how to approach HTN in a setting like this?

 

[Peak]

I searched for a dose-response graphic for Nitro but couldn’t find one. The following article (https://link.springer.com/article/10.1007/BF00874655) suggests a 1.6mg SL dose (2-4x typical EMS protocol) primarily produce venodilation with ‘peripheral arterial resistance’ (aka Afterload) requiring further increases in plasma concentration. Assuming SL nitro spray has the same bioavailability as SL nitro tablets of 40% (https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/021134s005lbl.pdf), those are some pretty big doses (far beyond what we would expect to see in the prehospital setting) to state the “goal of therapy is directly to reduce afterload”. I would therefore like to -respectfully- suggest a correction that ‘the goal of nitro therapy is to reduce preload’.

The goal of therapy with nitro will depend greatly on the indication.

For example in the setting of flash pulmonary edema when we start a very aggressive nitro drip the goal is to increase the vascular space, decrease preload, and resulting decrease pulmonary capillary pressure.

In the setting of fluid overload in left sided heart failure we may apply a measured amount of nitro paste to increase the peripheral vascular space to essentially store the excess fluids until we diurese the patient.

In the setting of acute MI the goal of nitro (typically given as a sublingual tap or spray in EMS) is to decrease the work of the heart therefore reducing oxygen demand and mitigating the ischemia that occurs. Nitro can also provide some benefit in dilating coronary vasculature, terminating variant coronary spasm is present (prinzmetal's angina), and increasing flow to any collaterals; such effects are modest but in the minutes before the cath lab we take every modest gain we can. Same goes for after load, we want to decrease the work the heart is performing and even a small reduction may buy us a few minutes to get into the cath lab.

In the acute MI patient the goal is to make the pump efficient and perform the least work needed. Dumping preload and reducing the benefit of normal stretch and the Frank starling law is not beneficial, in fact this is why we often are giving pretty aggressive IV fluids, to maintain the adequate preload that the patient needs.

We could talk all day about hemodynamics, but the reality is that we are not trending CVPs, RVPs, PAPs, wedge pressure, CI, arterial wave form analysis, and so on the the 911 environment.

I think that it is important to differentiate the goal of therapy from the mechanism of action, while certainly related we often use drugs for a less pronounced clinical effect especially in the emergency environment. In a less cardiac sense think of the H2 blockers we give in anaphylaxis, ranitidine is going to reduce stomach acid production more than anything else, but that isn't the therapeutic goal.

 

[Peak]

In regards to CPP, it's a bit of a simplified number that we use to gauge adequate cerebral perfusion. As touched on before CPP is your MAP less your ICP.

The reality is that our organs prefer pulsitile flow so mean pressures alone aren't the best way to gauge perfusion but is a good way for us to make a quick representation.

There is a bit of debate as to what normal CPP should be. In adults I've seen 40-70, 60-80, 60-100, and a few other variations. The assumes the patient is a otherwise healthy adult with normal physiology.

Patients who live with chronic hypertension (and subsequently chronically high CPP) have become dependent to a degree on that higher flow. Decreasing that too much can cause a perfusion injury, even if that number is now 'normal'.

Why the patient has a high ICP and/or alteration in their CPP will change based on their disease process. The pathophysiology of thrombotic stroke, dissection, all the various bleeds, infections, lesions, trauma, HACE, and so on can all differ.

 

[DrParasite]

hello, dumb fireman here.... Why are they treating the HTN with Nitro prehospitally? yes, they are reducing the sign, but not dealing with the underlying issue that was causing their pressure to spike. I'm guessing this was being done to prevent a stroke? Last I checked, doctors wanted to identify the cause of the HTN, and hopefully resolve the underlying cause, and then slowly drop their pressure over a long period of time, not just give nitro during a <1 hr transport time.

This is an ALS crew and have access to beta blockers but have to call OLMC prior to giving which always ends in a big NO from the ED physicians.

So they have a drug that they are allow to give, but their OLMC always says no? so why even carry the drug in the first place? Or are they asking to give it inappropriately, which means the field providers need a correction in education, and the docs are correct?

I would follow up with the medical director by email (this def isn't a time critical thing that requires a phone call over a 3 day weekend) for clarification, and how he expects his crews to proceed. if you have standing orders, were they followed appropriately? if deviation was needed, was a doctor consulted for approval? and what does your treatment protocol for hypertension say should have been done?

 

[GMCmedic]

hello, dumb fireman here.... Why are they treating the HTN with Nitro prehospitally? yes, they are reducing the sign, but not dealing with the underlying issue that was causing their pressure to spike. I'm guessing this was being done to prevent a stroke? Last I checked, doctors wanted to identify the cause of the HTN, and hopefully resolve the underlying cause, and then slowly drop their pressure over a long period of time, not just give nitro during a
I would follow up with the medical director by email (this def isn't a time critical thing that requires a phone call over a 3 day weekend) for clarification, and how he expects his crews to proceed. if you have standing orders, were they followed appropriately? if deviation was needed, was a doctor consulted for approval? and what does your treatment protocol for hypertension say should have been done?

Its pretty common in this area for providers to have to call for orders to give antihypertensive medications.

Nobody bothers calling for orders since the docs always say no.

At my old ground service we carried metoprolol, enalapril, and labetalol. I managed to get it down to just the enalapril, but never managed to completely eliminate the hypertensive crisis protocol.

 

[DrParasite]

I get that, but if you are never allowed to give the medication, why bother even carrying it? it's just going to expire and you need to buy more, and even then, you aren't going to be permitted to use it.

I guess the crux is, if your medical director says you can (and should) use it, but your OLMC says you can't, than there seems to be a conflict between those two docs, with the paramedics in the middle. What has this not been straightened out, so there is consistency between your offline and online med control?

if the OLMC wins, then the medical director should remove it from the trucks, from the protocols, etc, so the agency doesn't need to stock a med that never gets used.

if the medical directory wins, than your OLMC should approve the drug's use, provided it meets the appropriate criteria.

it just seems wasteful to carry medications that you can't use, to treat conditions that you have protocols for but can't follow because OLMC always says no, and then the agency has to pay to replace said medications when they expire, because they aren't allowed to be used by paramedics (in general, not among this particular protocol).

 

[rescue1]

Its pretty common in this area for providers to have to call for orders to give antihypertensive medications.

Nobody bothers calling for orders since the docs always say no.

At my old ground service we carried metoprolol, enalapril, and labetalol. I managed to get it down to just the enalapril, but never managed to completely eliminate the hypertensive crisis protocol.

To be fair to the docs, hypertensive emergency is rarely a real disease process, and almost always a case of "the provider in question is uncomfortable with how high the BP is", with the notable exception of acute pulmonary edema and aortic dissection. Unless your transport times are extremely long (and I mean long, like an hour or more), I have trouble thinking of a situation where it would be appropriate. If you could somehow be 100% sure that a patient had an ICH and not an ischemic stroke, then perhaps, but without neuroimaging there's no way to be actually sure, and reducing the BP in an ischemic stroke can be dangerous.

And this is not picking on paramedics, plenty of doctors, nurses, NPs, etc all panic at high BP numbers and send them to the ED or slam them with hydralazine just to make the numbers look less scary.

For those curious as to what the actual guidelines are:

Ischemic stroke: If the patient is a TPA candidate, maintain a BP below 185 systolic/110 diastolic. If not, maintain a systolic below 220. If you do have to lower BP, it should not be by more than 15% in the first 24 hours (which for the OP's patient is 36 mmHg over 24 hours). Rapid lowering of BP beyond this can reduce cerebral perfusion around the area of infarct and worsen neurological outcome.
Obviously this changes if the patient has signs of some other hypertensive disease like (pre)eclampsia or acute CHF.

Hemorrhagic stroke: The BP should be relatively rapidly (between 1-3 hours) lowered to around 140 systolic, unless the hypertension is severe (>220 systolic), in which case it should be lowered to below 160 systolic as quickly as possible. This would be perfectly reasonable to do in an ambulance, except you can't diagnose spontaneous ICH without a CT and lowering BP in ischemic stroke is bad.

Hypertensive encephalopathy: This is what everyone is worried about when patients have a headache and a BP of 230/140. Headache, however, is not usually a sign on its own unless associated with nausea, vomiting, and potentially altered mental status and seizures. It is a diagnosis of exclusion, after stroke has been ruled out with CT. It is treated by reducing the BP (SLOWLY), with an initial goal of a 10-15% reduction in the first hour and no more than 25% reduction in the first 24 hours. In our above patient, that is reducing the BP by about 20-30 mmhg in the first hour, AFTER you've ruled out a stroke--which you are not doing in the ambulance. This is also not a disease that kills people in minutes or hours, so you are not doing them a disservice by making sure the diagnosis is correct before treatment.

Traumatic Brain Injury/hemorrhage: Almost all management is focused on lowering the ICP, not the BP. The only time this should come up in the ambulance is in the case of impending herniation, where you see hypertension, bradycardia, and irregular respirations (Cushing's triad), plus posturing, blown pupils, coma, etc. In this case, elevate the head of the bed to about 30-40 degrees, intubate if able, and hyperventilate to reduce ICP. I'm assuming no one here carries mannitol or hypertonic saline on the trucks but if you do this would be the time to bust them out. Leave the blood pressure alone, as it is trying to compensate for the increased ICP and get blood into the brain.


Long story short, there are basically no neurological emergencies where you should be lowering BP in the ambulance. Not only is it rarely time sensitive, it can worsen outcomes in certain conditions. Perhaps the one exception would be extremely long (several hours) transport times where OLMC and the paramedic are willing to gamble on lowering the BP of a suspected ICH.


Preferred agents for all of these are calcium channel blockers (nicardipine), nitroprusside, and labetolol. Enalapril has pretty unpredictable effects because it depends on the level of renin activity and is not as recommended. If I had to pick one I'd keep labetolol, since it's probably the best for aortic dissection, one of the only hypertensive diseases you should be treating in the ambulance. However, dissection is both very rare and very sneaky, and so you probably won't ever get a chance to use it.


I also agree with @DrParasite, that if you have an agent on the truck that no one can use it seems like a waste of money.

 

[GMCmedic]

To be fair to the docs, hypertensive emergency is rarely a real disease process, and almost always a case of "the provider in question is uncomfortable with how high the BP is", with the notable exception of acute pulmonary edema and aortic dissection. Unless your transport times are extremely long (and I mean long, like an hour or more), I have trouble thinking of a situation where it would be appropriate. If you could somehow be 100% sure that a patient had an ICH and not an ischemic stroke, then perhaps, but without neuroimaging there's no way to be actually sure, and reducing the BP in an ischemic stroke can be dangerous.

And this is not picking on paramedics, plenty of doctors, nurses, NPs, etc all panic at high BP numbers and send them to the ED or slam them with hydralazine just to make the numbers look less scary.

For those curious as to what the actual guidelines are:

Ischemic stroke: If the patient is a TPA candidate, maintain a BP below 185 systolic/110 diastolic. If not, maintain a systolic below 220. If you do have to lower BP, it should not be by more than 15% in the first 24 hours (which for the OP's patient is 36 mmHg over 24 hours). Rapid lowering of BP beyond this can reduce cerebral perfusion around the area of infarct and worsen neurological outcome.
Obviously this changes if the patient has signs of some other hypertensive disease like (pre)eclampsia or acute CHF.

Hemorrhagic stroke: The BP should be relatively rapidly (between 1-3 hours) lowered to around 140 systolic, unless the hypertension is severe (>220 systolic), in which case it should be lowered to below 160 systolic as quickly as possible. This would be perfectly reasonable to do in an ambulance, except you can't diagnose spontaneous ICH without a CT and lowering BP in ischemic stroke is bad.

Hypertensive encephalopathy: This is what everyone is worried about when patients have a headache and a BP of 230/140. Headache, however, is not usually a sign on its own unless associated with nausea, vomiting, and potentially altered mental status and seizures. It is a diagnosis of exclusion, after stroke has been ruled out with CT. It is treated by reducing the BP (SLOWLY), with an initial goal of a 10-15% reduction in the first hour and no more than 25% reduction in the first 24 hours. In our above patient, that is reducing the BP by about 20-30 mmhg in the first hour, AFTER you've ruled out a stroke--which you are not doing in the ambulance. This is also not a disease that kills people in minutes or hours, so you are not doing them a disservice by making sure the diagnosis is correct before treatment.

Traumatic Brain Injury/hemorrhage: Almost all management is focused on lowering the ICP, not the BP. The only time this should come up in the ambulance is in the case of impending herniation, where you see hypertension, bradycardia, and irregular respirations (Cushing's triad), plus posturing, blown pupils, coma, etc. In this case, elevate the head of the bed to about 30-40 degrees, intubate if able, and hyperventilate to reduce ICP. I'm assuming no one here carries mannitol or hypertonic saline on the trucks but if you do this would be the time to bust them out. Leave the blood pressure alone, as it is trying to compensate for the increased ICP and get blood into the brain.


Long story short, there are basically no neurological emergencies where you should be lowering BP in the ambulance. Not only is it rarely time sensitive, it can worsen outcomes in certain conditions. Perhaps the one exception would be extremely long (several hours) transport times where OLMC and the paramedic are willing to gamble on lowering the BP of a suspected ICH.


Preferred agents for all of these are calcium channel blockers (nicardipine), nitroprusside, and labetolol. Enalapril has pretty unpredictable effects because it depends on the level of renin activity and is not as recommended. If I had to pick one I'd keep labetolol, since it's probably the best for aortic dissection, one of the only hypertensive diseases you should be treating in the ambulance. However, dissection is both very rare and very sneaky, and so you probably won't ever get a chance to use it.


I also agree with @DrParasite, that if you have an agent on the truck that no one can use it seems like a waste of money.

I understand it now, there was a time when like most I didnt, my understansing now is why Ive actively tried to stop carrying them. I now work in an environment where our guidelines are essentially exactly what you posted but with OLMC, the caveat is that if OLMC is unavailable, we use our discretion. Its rare that we will treat pressure without a docs approval.

 

[medic2EMSdoc]

@rescue1 gave a great summary of general guidelines for blood pressure management in the varied emergent hypertension scenarios. Although there is alot of debate on how low is too low for ICH. Many trials have mixed data that <140 has more bad outcomes than good outcomes. Key point summary

65yo male called for headache and nausea.

Crew gets on scene patient has high BP 240/140, HR 90, GCS of 15. Patient has a noted injury to the frontal region of his skull from a fall earlier in the day,

Since there is reported signs of trauma I would definitely be wanting to know if the headache and nausea came before or after the fall. With the information provide, the top of my differential would definitely be ICH vs TBI. As was discussed above, if this is a TBI the pressure should be left alone because this could be a compensatory mechanism for increased ICP and get blood into the brain.

I think without a CT Scan there are a few scenario's where I would want the blood pressure lowered in the pre-hospital setting - i.e. extremely long transports.

Labetolol, baring any direct contraindications, is my initial go to medication for blood pressure control. I find it to be the most predictable, fairly quick in onset, and doesn't affect ICP. It is a fairly cheap drug and I would think it would be nice for it to be available for OLMC directed administration. If a patient had convincing story for an Ischemic Stroke and blood pressure was way beyond the pressure needed to give TPA (185/110) I would want to give a dose to start getting it closer to that goal. If it turns out to be hemorrhagic after the CT then we will just be lowering more.

 

[MackTheKnife]

The goal of therapy with nitro will depend greatly on the indication.

For example in the setting of flash pulmonary edema when we start a very aggressive nitro drip the goal is to increase the vascular space, decrease preload, and resulting decrease pulmonary capillary pressure.

In the setting of fluid overload in left sided heart failure we may apply a measured amount of nitro paste to increase the peripheral vascular space to essentially store the excess fluids until we diurese the patient.

In the setting of acute MI the goal of nitro (typically given as a sublingual tap or spray in EMS) is to decrease the work of the heart therefore reducing oxygen demand and mitigating the ischemia that occurs. Nitro can also provide some benefit in dilating coronary vasculature, terminating variant coronary spasm is present (prinzmetal's angina), and increasing flow to any collaterals; such effects are modest but in the minutes before the cath lab we take every modest gain we can. Same goes for after load, we want to decrease the work the heart is performing and even a small reduction may buy us a few minutes to get into the cath lab.

In the acute MI patient the goal is to make the pump efficient and perform the least work needed. Dumping preload and reducing the benefit of normal stretch and the Frank starling law is not beneficial, in fact this is why we often are giving pretty aggressive IV fluids, to maintain the adequate preload that the patient needs.

We could talk all day about hemodynamics, but the reality is that we are not trending CVPs, RVPs, PAPs, wedge pressure, CI, arterial wave form analysis, and so on the the 911 environment.

I think that it is important to differentiate the goal of therapy from the mechanism of action, while certainly related we often use drugs for a less pronounced clinical effect especially in the emergency environment. In a less cardiac sense think of the H2 blockers we give in anaphylaxis, ranitidine is going to reduce stomach acid production more than anything else, but that isn't the therapeutic goal.

You're the first person to mention nitro reduces preload!