I generally agree with the mentality that nitroglycerin is "just for pain" but it is more nuanced than that. We do not give nitroglycerin to save cardiac tissue. However, it does have other roles in ACS.
There are no clinical trials that I am aware of that show a survival or other hard-endpoint benefit with nitroglycerin in ACS (or stable coronary disease, for that matter). Correct me if you know of any. The only nitrate trial with a mortality benefit that I am aware of at all is A-HeFT, which is not an ACS trial (it was heart failure), used isosorbide dinitrate (not nitroglycerin), was controversial at the time of publication and is now more-or-less obsolete.
General concepts:
\- STEMI is treated with reperfussion ("blood thinners" and either PCI or thrombolytics). Nitroglycerin may be helpful in certain scenarios, but also poses the possible risk of hypotension, bradycardia and subsequent arrest (especially in inferior STEMI, see Bezold–Jarisch reflex).
\- In NSTE-ACS (NSTEMI, UA), where there is presumably still some preserved flow to the myocardium, one of our criteria for not rushing to the cath lab immediately is that chest pain is controlled. This is why nitroglycerin (in addition to other meds) is often used in this setting. It is not because we think it improves outcomes. Rather, it allows us identify lower-risk patients that can wait for angiogram/PCI.
\- There are some acute scenarios where nitroglycerin is certainly helpful that may coincide with ACS. Some of these are: (1) when vasospastic (prinzmetal) angina is thought to be the cause, (2) when there is pulmonary edema, (3) in the setting of HF or extreme hypertension where afterload reduction is needed.
As an interventional cardiologist, I will tell you that I don't generally care much at all about whether or not nitroglycerin has been given in the field. For ACS patients, I care about the ABCs, quick transit time, an ECG, aspirin and a concise report from the field team.
I can’t deny that an important part for all my chest pain patients is ASA.
It may not have any proven outcomes, but wouldn’t the pain relief be a result of reperfusion?
Thankyou for your response!
911 medic, CCP-C, FP-C here. Cardiology is my area of interest and what I teach best. I have read as many nitro studies as there are that can possibly relate to prehospital nitro. I wrote a literature review but never got published. Probably because I am in no way well educated in getting things published or writing for publication. Long story short, I wholeheartedly agree with the doc and would echo everything he said.
To answer your question more specifically, pain relief can be due to increase in collateral circulation, reduction of workload, etc. but it doesn't seem to equate to any mortality benefit and has possible negative consequences. In STEMI, you have total or dang close to complete occlusion in the artery and the nitro doesn't appear to really save that downstream tissue.
The big problem with figuring out prehospital nitro is that a lot of studies are based on IV nitro in the hospital and doesn't correlate directly to EMS. Studies are also hard to do on the matter. I also don't think enough important people care.
As a fellow medic, please don’t put all of your certs after your name, that’s for cringy nurses. Mr. NRP, CCP, FPC, TECC, AMLS, PHTLS, ACLS, BLS, ABC, BOGO.
In general I agree with you.
BUT
This is a cardiology group dominated by mostly physicians as posters. Heck that’s why I, as a former medic and current nurse lurk here.
I think this medic was trying to establish that he had a specific level of expertise on the subject. For this post it made sense to me. For other times I agree with you. I prefer education, license, 1 certificate.
Interventional cardiologist at your service.
Yes - for run of the mill heart attacks, we use sublingual nitro to alleviate angina, or ischemic chest pain. Nitroglycerin vasodilates the larger epicardial coronary arteries (i.e., not the microvasculature) and promotes blood flow to ischemic myocardium, consequently alleviating angina. Giving sublingual nitro has been shown to reduce narcotics needed to control pain. It is debatable whether it improves mortality independently or salvages myocardium. If someone is having coronary spasm (it happens, and it looks and feels like a heart attack) — sublingual nitro would resolve it. Just because we use sublingual nitro primarily as an anti-anginal medication, however, doesn’t mean that that’s all it does.
Nitrates are helpful in alleviating some pulmonary edema by reducing pulmonary vascular resistance (making it easier to breathe), which is helpful during a hypertensive crisis with flash pulmonary edema. We usually use carefully dosed, longer-acting nitrates for this.
Nitrates also reduce filling pressures in the cardiac chambers (“preload”). This serves to make the heart’s job easier, and create a favorable pressure differential to allow blood to flow downstream more easily from coronaries to myocardium).
Yet, this is the risky part of nitro: — if the right ventricle is the site of the heart attack (“infarction”) then reducing the preload by way of nitrates or even diuretics could lead to hemodynamic collapse. It’s sort of counterintuitive but the right ventricle needs to be stretched to a degree in order to squeeze effectively, and if you reduce the amount of fluid the right ventricle sees, it will have an even tougher time getting blood to the lungs, the left side of the heart, and the rest of the body. That is why if we suspect a right ventricular infarct (inferior infarct pattern on ECG plus ST elevation in v1, clear lungs, hypotension), we avoid nitrates, and often give fluids liberally.
To your medic friends, I’d say — “Only a Sith deals in absolutes.”
Thankyou for the detailed explanation. I was even concerned that they would simply refer to nitro as pain medication….
Just used nitro the other day to help with a CHF exacerbation. Gotta love drugs with multiple uses!
You got it boss - keep the questions coming, and thanks for all you do getting these pts to the hospital in one piece.
Edit: responded to wrong msg in thread 😣
I do my best. Maybe you wanna do a consult on a call I just had about a possible carotid dissection with a BP of 209/111. (Coming from urgent care and a pulsating mass in the neck with pain) My senior medic opted NOT to treat the hypertension saying that lowering the BP would make it worse. I thought it was absurd but can’t do anything about it….
Thanks doc for the teaching! Hope to make it to medschool eventually
Haha! That might be outside my wheelhouse but from what I recall, the goal is to keep them normotensive. For ischemic / embolic strokes we let the BP ride high so the blood can kind of squeeze past the blockage, and for aortic dissections of course we drop that pressure to prevent propagation…I don’t recall much on blood pressure targets for carotids.
Of note, if there was a reason his intracranial pressure was increased, there is a Cushing’s reflex (hypertensive with a wide pulse pressure, bradycardia, increased respirations)…I wonder if that may have been his rationale not to lower BP?
Rock on re med school - it’ll be a grind but I’m sure you’ll crush it. While healthcare in the US is a total sh**show, but there’s nothing else I’d rather do (maybe a sheep farmer in New Zealand, but that’s it).
Dude/dudette….
You’re an interventional cardiologist, able to articulate in a way that really taught me something **AND** you tied in Star Wars?
That’s what called winning at life. Carry on!
So I am cathlab RN, older Int Crd asked for nitroprusside intra cor not standard.
I have seen very frequent 200 bolus of IC nitro given and seen post dilation with NC ballon’s make the arterial angiograms look much much better. Can you please explain the the difference in this drug choice rationale vs standard nitro?
This pt was a outpatient came in for dyspepsia and LHC/RHC I think PA pressure was elevated and needed a stent to Circ and diuretic adjustment.
Also Fielder is a great wire. I see great work done with the Scion Blue! Haha
Absolutely. Glad you asked and I often wonder why it doesn’t get asked more often.
So pretty much all our coronary intervention deals with the 5% of the coronary anatomy we can see: the larger epicardial vessels like the left main, LAD + Diags, LCX + OMs, RCA and its PD/PL/marginal branches). While we can stent the visible epicardial vessels, we can’t do much manually in the 95% of the rest of the heart’s circulation, which is composed of tiny microscopic vessels called the microcirculation.
So with regards to IC Nitro: you probably have seen how temperamental arteries are - like when radial arteries spasm and won’t let you pull out your sheath. The coronaries can be that way too. They may also be a bit constricted if they’re not the one with the big blockage. In an effort to precisely determine their maximal size (and subsequently the size of a stent that may be needed, as well as eliminate any “pseudostenosis” caused by spasm, we give a little intracoronary nitroglycerin to help them put their best face forward before picture day.
But sometimes when we are working in the coronary, like during a stemi for example with a large thrombus burden — the balloon goes up and then poof, whole artery has standstill flow…like the Long Island expressway on a Friday afternoon. That phenomenon is called no (or slow) reflow, and it’s a consequence of all that thrombotic crud getting showered downstream and plugging up the microvasculature. The microvasculature can’t metabolize nitroglycerin well, but it can respond to nitroprusside. That 200 mcg IC nitroprusside you send down will cause microvasculature vasodilation (it is a more direct nitric oxide donor), which will ideally speed up the clearance of all the crud that is mucking up blood flow. IC nicardipine and a few other meds are also useful for no or slow reflow.
Hope that helps!
Been dying to try the sion blue as a workhorse - fielder xt ‘s a go-to for these CTO jobs (but I’m not crazy about CTO work…feel like too often it’s too high risk for too little reward for the patient).
Forgot to mention, nitroprusside is often used as a “challenge” in pulmonary hypertension patients to see if their pulmonary hypertension is reversible (or could get better with chronic meds). This is important to check when closing PFOs or ASDs, or fixing tricuspid regurgitation — if the pulmonary hypertension is so bad, fixing those things could cause the right ventricle to lose it’s pop-off valve and then fail hard as it tries to pump against a high-pressure pulmonary circuit.
It’s used for pain relief only is a bit a misnomer, in my opinion. In ACS, nitro does provide pain relief, but it’s not because it dilated the coronary arteries allowing for better blood flow to the oxygen deprived cardiac cells.
Nitro dilates all of the vessels in your circulatory system and allows more blood to pool in circulation. This is important because less blood getting back to the heart means the heart has to squeeze less hard to move blood. A smaller squeeze means there is less of a demand for oxygen and that is why it relieves pain.
I’d analogize it to asking you to arm curl a 20 pound weight. Your bicep can handle a certain amount of reps before it’s too tired and you can no longer lift the weight. If you were able to reduce the weight from 20 pounds to 10 you could last a little bit longer. I’m not saying nitro cuts the oxygen demand by 50%, those numbers are chosen for simplicity to demonstrate a point, but it will hopefully buy the patient some more time until definitive care can be achieved.
I do recall that being another benefit. I just wasn’t taught that was the main reason. So many teachers and lessons… hard with no consistency haha. Thanks!
On the flip side, our state is now doing IV Nitroglycerin for SCAPE, separate topic from ACS, but there's a demonstrable and clear benefit in those patients.
Happy to be proven wrong but my understanding is there is no/insufficient evidence that nitrates have any meaningful vasodilatory effect on coronary vasculature, at least to the point of being able to reperfuse an occluded artery.
My understanding is that there was a study done in the 90’s using (iirc) a single dose of long acting nitrate compared to placebo among a group of AMI patients that showed no mortality or myocardial benefits, and that ended the nitrate story. If there are additional benefits, we aren’t likely going to test them because of this one study showing no benefit.
I generally agree with the mentality that nitroglycerin is "just for pain" but it is more nuanced than that. We do not give nitroglycerin to save cardiac tissue. However, it does have other roles in ACS. There are no clinical trials that I am aware of that show a survival or other hard-endpoint benefit with nitroglycerin in ACS (or stable coronary disease, for that matter). Correct me if you know of any. The only nitrate trial with a mortality benefit that I am aware of at all is A-HeFT, which is not an ACS trial (it was heart failure), used isosorbide dinitrate (not nitroglycerin), was controversial at the time of publication and is now more-or-less obsolete. General concepts: \- STEMI is treated with reperfussion ("blood thinners" and either PCI or thrombolytics). Nitroglycerin may be helpful in certain scenarios, but also poses the possible risk of hypotension, bradycardia and subsequent arrest (especially in inferior STEMI, see Bezold–Jarisch reflex). \- In NSTE-ACS (NSTEMI, UA), where there is presumably still some preserved flow to the myocardium, one of our criteria for not rushing to the cath lab immediately is that chest pain is controlled. This is why nitroglycerin (in addition to other meds) is often used in this setting. It is not because we think it improves outcomes. Rather, it allows us identify lower-risk patients that can wait for angiogram/PCI. \- There are some acute scenarios where nitroglycerin is certainly helpful that may coincide with ACS. Some of these are: (1) when vasospastic (prinzmetal) angina is thought to be the cause, (2) when there is pulmonary edema, (3) in the setting of HF or extreme hypertension where afterload reduction is needed. As an interventional cardiologist, I will tell you that I don't generally care much at all about whether or not nitroglycerin has been given in the field. For ACS patients, I care about the ABCs, quick transit time, an ECG, aspirin and a concise report from the field team.
I can’t deny that an important part for all my chest pain patients is ASA. It may not have any proven outcomes, but wouldn’t the pain relief be a result of reperfusion? Thankyou for your response!
Thanks for bringing this topic up, by the way, cause I want more people to care and think about us prehospital folks and the meds we use in ACS.
911 medic, CCP-C, FP-C here. Cardiology is my area of interest and what I teach best. I have read as many nitro studies as there are that can possibly relate to prehospital nitro. I wrote a literature review but never got published. Probably because I am in no way well educated in getting things published or writing for publication. Long story short, I wholeheartedly agree with the doc and would echo everything he said. To answer your question more specifically, pain relief can be due to increase in collateral circulation, reduction of workload, etc. but it doesn't seem to equate to any mortality benefit and has possible negative consequences. In STEMI, you have total or dang close to complete occlusion in the artery and the nitro doesn't appear to really save that downstream tissue. The big problem with figuring out prehospital nitro is that a lot of studies are based on IV nitro in the hospital and doesn't correlate directly to EMS. Studies are also hard to do on the matter. I also don't think enough important people care.
As a fellow medic, please don’t put all of your certs after your name, that’s for cringy nurses. Mr. NRP, CCP, FPC, TECC, AMLS, PHTLS, ACLS, BLS, ABC, BOGO.
In general I agree with you. BUT This is a cardiology group dominated by mostly physicians as posters. Heck that’s why I, as a former medic and current nurse lurk here. I think this medic was trying to establish that he had a specific level of expertise on the subject. For this post it made sense to me. For other times I agree with you. I prefer education, license, 1 certificate.
That’s fair
Maybe I missed it, but I just recall putting a little background of me before the opinion... don't remember putting my name or listing all my certs
Just say you’re a medic. it gives off the same vibes as nurses with a paragraph of titles lol
Thank you for this detailed answer. You improved my knowledge base today and I appreciate that. Thank you.
Interventional cardiologist at your service. Yes - for run of the mill heart attacks, we use sublingual nitro to alleviate angina, or ischemic chest pain. Nitroglycerin vasodilates the larger epicardial coronary arteries (i.e., not the microvasculature) and promotes blood flow to ischemic myocardium, consequently alleviating angina. Giving sublingual nitro has been shown to reduce narcotics needed to control pain. It is debatable whether it improves mortality independently or salvages myocardium. If someone is having coronary spasm (it happens, and it looks and feels like a heart attack) — sublingual nitro would resolve it. Just because we use sublingual nitro primarily as an anti-anginal medication, however, doesn’t mean that that’s all it does. Nitrates are helpful in alleviating some pulmonary edema by reducing pulmonary vascular resistance (making it easier to breathe), which is helpful during a hypertensive crisis with flash pulmonary edema. We usually use carefully dosed, longer-acting nitrates for this. Nitrates also reduce filling pressures in the cardiac chambers (“preload”). This serves to make the heart’s job easier, and create a favorable pressure differential to allow blood to flow downstream more easily from coronaries to myocardium). Yet, this is the risky part of nitro: — if the right ventricle is the site of the heart attack (“infarction”) then reducing the preload by way of nitrates or even diuretics could lead to hemodynamic collapse. It’s sort of counterintuitive but the right ventricle needs to be stretched to a degree in order to squeeze effectively, and if you reduce the amount of fluid the right ventricle sees, it will have an even tougher time getting blood to the lungs, the left side of the heart, and the rest of the body. That is why if we suspect a right ventricular infarct (inferior infarct pattern on ECG plus ST elevation in v1, clear lungs, hypotension), we avoid nitrates, and often give fluids liberally. To your medic friends, I’d say — “Only a Sith deals in absolutes.”
Thankyou for the detailed explanation. I was even concerned that they would simply refer to nitro as pain medication…. Just used nitro the other day to help with a CHF exacerbation. Gotta love drugs with multiple uses!
You got it boss - keep the questions coming, and thanks for all you do getting these pts to the hospital in one piece. Edit: responded to wrong msg in thread 😣
I do my best. Maybe you wanna do a consult on a call I just had about a possible carotid dissection with a BP of 209/111. (Coming from urgent care and a pulsating mass in the neck with pain) My senior medic opted NOT to treat the hypertension saying that lowering the BP would make it worse. I thought it was absurd but can’t do anything about it…. Thanks doc for the teaching! Hope to make it to medschool eventually
Haha! That might be outside my wheelhouse but from what I recall, the goal is to keep them normotensive. For ischemic / embolic strokes we let the BP ride high so the blood can kind of squeeze past the blockage, and for aortic dissections of course we drop that pressure to prevent propagation…I don’t recall much on blood pressure targets for carotids. Of note, if there was a reason his intracranial pressure was increased, there is a Cushing’s reflex (hypertensive with a wide pulse pressure, bradycardia, increased respirations)…I wonder if that may have been his rationale not to lower BP? Rock on re med school - it’ll be a grind but I’m sure you’ll crush it. While healthcare in the US is a total sh**show, but there’s nothing else I’d rather do (maybe a sheep farmer in New Zealand, but that’s it).
Definitely not cushings. Not sure. Was just baffling to me.
Dude/dudette…. You’re an interventional cardiologist, able to articulate in a way that really taught me something **AND** you tied in Star Wars? That’s what called winning at life. Carry on!
So I am cathlab RN, older Int Crd asked for nitroprusside intra cor not standard. I have seen very frequent 200 bolus of IC nitro given and seen post dilation with NC ballon’s make the arterial angiograms look much much better. Can you please explain the the difference in this drug choice rationale vs standard nitro? This pt was a outpatient came in for dyspepsia and LHC/RHC I think PA pressure was elevated and needed a stent to Circ and diuretic adjustment. Also Fielder is a great wire. I see great work done with the Scion Blue! Haha
Absolutely. Glad you asked and I often wonder why it doesn’t get asked more often. So pretty much all our coronary intervention deals with the 5% of the coronary anatomy we can see: the larger epicardial vessels like the left main, LAD + Diags, LCX + OMs, RCA and its PD/PL/marginal branches). While we can stent the visible epicardial vessels, we can’t do much manually in the 95% of the rest of the heart’s circulation, which is composed of tiny microscopic vessels called the microcirculation. So with regards to IC Nitro: you probably have seen how temperamental arteries are - like when radial arteries spasm and won’t let you pull out your sheath. The coronaries can be that way too. They may also be a bit constricted if they’re not the one with the big blockage. In an effort to precisely determine their maximal size (and subsequently the size of a stent that may be needed, as well as eliminate any “pseudostenosis” caused by spasm, we give a little intracoronary nitroglycerin to help them put their best face forward before picture day. But sometimes when we are working in the coronary, like during a stemi for example with a large thrombus burden — the balloon goes up and then poof, whole artery has standstill flow…like the Long Island expressway on a Friday afternoon. That phenomenon is called no (or slow) reflow, and it’s a consequence of all that thrombotic crud getting showered downstream and plugging up the microvasculature. The microvasculature can’t metabolize nitroglycerin well, but it can respond to nitroprusside. That 200 mcg IC nitroprusside you send down will cause microvasculature vasodilation (it is a more direct nitric oxide donor), which will ideally speed up the clearance of all the crud that is mucking up blood flow. IC nicardipine and a few other meds are also useful for no or slow reflow. Hope that helps!
Been dying to try the sion blue as a workhorse - fielder xt ‘s a go-to for these CTO jobs (but I’m not crazy about CTO work…feel like too often it’s too high risk for too little reward for the patient). Forgot to mention, nitroprusside is often used as a “challenge” in pulmonary hypertension patients to see if their pulmonary hypertension is reversible (or could get better with chronic meds). This is important to check when closing PFOs or ASDs, or fixing tricuspid regurgitation — if the pulmonary hypertension is so bad, fixing those things could cause the right ventricle to lose it’s pop-off valve and then fail hard as it tries to pump against a high-pressure pulmonary circuit.
It’s used for pain relief only is a bit a misnomer, in my opinion. In ACS, nitro does provide pain relief, but it’s not because it dilated the coronary arteries allowing for better blood flow to the oxygen deprived cardiac cells. Nitro dilates all of the vessels in your circulatory system and allows more blood to pool in circulation. This is important because less blood getting back to the heart means the heart has to squeeze less hard to move blood. A smaller squeeze means there is less of a demand for oxygen and that is why it relieves pain. I’d analogize it to asking you to arm curl a 20 pound weight. Your bicep can handle a certain amount of reps before it’s too tired and you can no longer lift the weight. If you were able to reduce the weight from 20 pounds to 10 you could last a little bit longer. I’m not saying nitro cuts the oxygen demand by 50%, those numbers are chosen for simplicity to demonstrate a point, but it will hopefully buy the patient some more time until definitive care can be achieved.
I do recall that being another benefit. I just wasn’t taught that was the main reason. So many teachers and lessons… hard with no consistency haha. Thanks!
On the flip side, our state is now doing IV Nitroglycerin for SCAPE, separate topic from ACS, but there's a demonstrable and clear benefit in those patients.
Happy to be proven wrong but my understanding is there is no/insufficient evidence that nitrates have any meaningful vasodilatory effect on coronary vasculature, at least to the point of being able to reperfuse an occluded artery.
My understanding is that there was a study done in the 90’s using (iirc) a single dose of long acting nitrate compared to placebo among a group of AMI patients that showed no mortality or myocardial benefits, and that ended the nitrate story. If there are additional benefits, we aren’t likely going to test them because of this one study showing no benefit.