EMCrit Podcast 1-Sympathetic Crashing Acute Pulmonary Edema

Here it is, the 1st EMCrit podcast.

It’s on the topic of Sympathetic Crashing Acute Pulmonary Edema (SCAPE).

To boil it down to 10 seconds:

  • Start patient on Non-invasive ventilation with a PEEP of 6-8; quickly titrate to a PEEP of 10-12.
  • Start the patient on a nitroglycerin drip. Administer a loading dose of 4oo mcg/min for 2 minutes (120 ml/hour on the pump for 2 minutes with the standard nitro concentration of 200 mcg/ml.) Then drop the dose to 100 mcg/min and titrate it up from there as needed.

By 10 minutes, your patient should be out of the water.

See crashingpatient.com for the references.

 

Here is some info from a handout from a lecture I gave on the topic:

High Dose Nitroglycerin

Homeopathic nitroglycerin does not work so well
Start at 50-100 mcg/min, you can rapidly titrate to 200-400 mcg/min.

You must stand at the bedside to use these doses.
Need >120 mcg/min to get sig decreased Pulm Cap Wedge Pressure (Am J Cardio 2004;93:237)
But even this strategy is not as effective as the …
Nitro Bolus First
Can give 400-800 mcg over 1-2 minutes = 400 mcg/min for 1-2 minutes. (Annals EM 1997, 30:382)
How to do it
Standard nitro mix is 200 mcg/ml.
VERIFY YOUR HOSPITAL’S MIX BEFORE USING THESE RECS
In order to give the 400 mcg/min for 2 minutes, set the pump to
Rate: 120 cc/hr
Volume to be Infused: 4 ml (This will deliver 400 mcg/min for 2 minutes and then stop)

Or

Draw up 4 ml of the nitro and 6 ml of NS and give over 2 minutes

After the bolus, I drop the drip to 100 mcg/min and titrate up from there to effect
When the patient gets better, you need to sharply decrease this drip rate
Some folks have gone even further
High dose nitroglycerin for severe decompensated heart failure—2 mg at a time (Ann Emerg Med 2007;50:144)
Cotter gave isosorbide 3 mg q 5 minutes with good results in his study. This is equivalent to nitro 600 mcg/min. (Lancet 1998 351:9100, 389-393)

Update 6-10-12

Piyush Mallick did an amazing study on nitro-bolus to avert intubation

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Comments

  1. can you continue to keep the files under 10mb? that way you don’t need wifi to download directly to an iphone.

    thanks-
    seth

  2. Had an iatrogenic case of pulmonary edema the other day, pt with ESRD on HD; had a CTA, on the way back developed severe dyspnea, had very wet lungs and high BPs. Apparently happens commonly due to the high osmolarity of the contrast.

    Slapped the bipap on while we were getting the NTG drip set up, clinically improved and bought us time to set up the drip. Within about 2-5 minutes he felt much better. Worked great!

  3. Have you seen any cases where the BP has fallen precipitously with the use of the 400 mcg/min x 2 minutes of nitroglyerine? What is the half-life of iv nitroglycerine?

    Thanks,

    Jim Squires
    Canada

    • 1/2 life of nitro is between 1-4 minutes so even if they drop it won’t be for long
      I have never seen a precipitous drop of of their pressure at the beginning of treatment when you are giving the bolus.
      They often drop as they are resolving, which is a function of underlying dehydration.
      If they did drop at the beginning, it should respond to a small fluid bolus.

  4. Correct me if I’m wrong, but 400 mcg is the dose of a slntg. We regularly give three of those in a row, with the same BP precautions.

    • You’re correct but what is the bioavailability of sl nitro compared to IV??

      • Bioavailability is pretty near IV b/v sublingual route avoids liver metabolism on first pass. 400 mcg of SL nitro is designed to be absorbed over 5 minutes so the dose is acutally ~80 mcg/min. THis is however predicated on having spit in your mouth. Most of these bad scape patients have bone dry mouths and don’t absorb the pills well.

  5. Scott – the early management of SCAPE patients is BIPAP and NITRO – at what point do you start diuresing these patients?

    • When they are comfortable and the blood pressure is where you want, observe intravascular status. Then consider fixing it, usually the answer is they need fluid, not diuresis

  6. Brian Hawkins says:

    What about natrecor? I know it got bad press from its mortality statistics and it was overmarketed but I felt clinically that I have had good success in the past in particular in a crashing patient

    • Brian,

      Thanks for writing.

      The data that have emerged in the past few years seems to indicate an increased risk of mortality when compared to standard care. In the reported trials, this seemed to be just a trend, but then two additional deaths seem not to have been reported in the natrecor group, which if you recalculate the p-values is actually a stat. sig. increased mortality.

      Even the original trial published in JAMA 2002 did not seem to have any clinically important effects when compared to minimal dose nitrites.

      I have found aggressive doses of nitrites to be the quickest and most effective way to go, but there are many ways to skin this cat.

      –Scott

  7. Jose D. Torres, Jr. says:

    I wonder if I only use bipap and high dose nitro, will the cxr change remarkably? I know the patients I take care get better, usually gets hits with iv nitro, not as high as you have recommended , instead at 50-100mcg/min and bipap, and lasix, double the patient’s daily use in iv form. I did once forget to give iv lasix, and more than 1.5 liter came out of the patient and he wanted to know if he could go home after 3 hrs of treatment. I know we usually diurese too much and leave them dehydrated/volume depleted.

    • Jose,

      Thanks for writing. In SCAPE patients, ALL of the chest x-ray findings are from too much afterload. X-ray will improve entirely if you vasodilate and give NIV. And, the patients will diurese as soon as you perfuse the kidneys.

      scott

  8. Medora Pashmakova (DVM) says:

    Found it very interesting that you recommended Dexdomitor for sedation as ideal in these patients – if you’re fighting afterload, won’t the peripheral vasoconstriction caused by dexdomitor be detrimental? I’m an ER veterinarian and a recent follower of the program and podcasts. Thanks!

    • Medora,

      Great to have a vet. listener! I think you are talking about the possible initial elevation of pulse and blood pressure at the very start of a dexmedetomidine infusion, yes? If so, I have not witnessed this in clinical practice in these patients, probably b/c they are already experiencing great sympathetic stimulation and I have potent vasodilators infusing. What has been you experience in 4-legged patients?

      scott

      • Medora Pashmakova (DVM) says:

        Scott,
        We see relatively profound bradycardia. Maybe due to the nature of how we use this drug (sometimes for chemical restraint, at doses of 10-15 mcg/kg IV) and also for sedation of instrumented patients (at CRI of 1-2 mcg/kg/hr) we see heart rates in the 40′s. With the higher doses the peripheral vasoconstriction is very significant (mucous membranes turn white initially) and I imagine the reflex bradycardia can only support the increased afterload and initial hypertension. I do like this drug a lot and we can perform minimal surgical procedures (i.e. laceration repairs) with this alone. My preferred recipe is Dexdomitor + a pure mu agonist + a local block. I have not measured initial blood pressure after administration – I suspect a direct arterial line would be the most accurate way to monitor hemodynamic effects. Interesting exchange of info, thanks!

        Medora

  9. I can’t tell you how many cases of SCAPE we see at my program in the Bronx. Gonna pitch the afterload reduction dose of NTG to my attendings, see how they react.

    Enjoyed the lecture this past week at Mt. Sinai. EMCrit all the way.

    • Thanks so much for your kind comments. I’m going to have to get permission from one of patients to video the change from arrival to 15 minutes later, because in this case seeing is believing.

      Scott

      • We typically slap on the bipap, get the drip going (albiet at lower dosages) and see the improvement, although I wonder how many intubations/ICU admissions we’d mitigate. BTW, where’s the data? Any upcoming studies?

        • Excellent data that high dose IV NTG prevents intubation and mortality, and the rapid turnaround clinically is the rule, not the exception. Getting people to stop giving Lasix is the challenge. As has been mentioned above, as soon as the kidney gets fed, pee appears- but if you gave Lasix, then the drug gets the credit…

  10. any place for ACE inhibitors in acute management?

  11. Salman,

    Thanks for commenting. I used to give them up front, but now I get them stabilized and see where their blood pressure winds up. Sometimes, surprisingly they are low after the acute catecholamines fade. If they are still hypertensive, I then give the ACEI.

    scott

  12. Excellent podcast.

    Why not try to get those of us in EMS to improve our care of these patients, too?

    High-dose NTG and CPAP are also treatments that can be given by EMS. In some places, these are given by EMS.

    With sublingual NTG we probably cannot give these patients too much to these patients.

    We should be using NTG by IV in EMS. In Pennsylvania, NTG is an optional drug for 911 services.

    • thanks so much for writing. I am a big fan of starting these protocols in the field as well. Just CPAP alone would do enormous things for these patients. High dose nitro may be tough, but SL nitro and SL or IV ACEI coupled with NIV would do incredible things for these patients by the time they hit the ED.

  13. What is the difference between “SCAPE” and “CHF exacerbation”? They sound identical with sudden onset pulmonary edema and respiratory distress with crackles and hypertension on exam that is treated with large doses of nitroglycerin and BiPAP to rescue and prevent intubation.

    Also in the recording it is mentioned that treatment is to reduce afterload, which I believe is backward (or perhaps I misheard). Since nitroglycerin is primarily a venodilator and BiPAP increases intrathoracic pressure both serve primarily to decrease pre-load. By decreasing preload you prevent pulmonary edema without decreasing cardiac output because the patient has “fallen off” the Starling curse and is not preload dependent.

    Thanks for the podcasts, we need more medical podcasts like this for learning on the go.

    • Hi Cameron,

      CHF exac encompasses a wide variety of presentations including:
      severe hypertension and acute pulmonary edema
      peripheral edema with volume overload
      low BP and pulmonary edema
      and many mixed presentations

      sympathetic-surge hypertensive APE is a situation of sharply increased afterload leading to LV failure and pulm edema. If the patient is going to get tubed in the next minutes without turnaround, then they are crashing. SCAPE is this patient

      afterload reduction is all these patients need
      they are not volume overloaded
      they do not need preload reduction or diuresis.

      sorry about the late reply, you message got lost in the ether.

      scott

  14. John Holst says:

    New emcrit listener, excellent podcasts! Scott, in your very severe flash pulmonary edema patients with BPs of 300/150 (MAPs 200ish) do you follow strict 25% BP reduction with the Non-invasive ventilation/Nitro protocol or follow more of a clinical response or a combination?

    • Hey John,

      flash APE is by definition an acute condition, so you can take these pts all the way back to their normal BP almost immeditately. You’ll know they are there b/c they go from looking like death to sitting comfortably. So answer is I don’t worry about 25%.

      scott

  15. Lance C. Peeples says:

    As a 30+ year veteran of pre-hospital EMS, there is no doubt that CPAP in the ambulance prevents many of these patients from proceeding to respiratory arrest. However, intravenous NTG is not routinely used (probably because few if any ambulances carry IV pumps). It strikes me as unacceptable in 2012 that few medical control physicians seem concerned that vasoactive medications such as dopamine are administered via guesstimating the number of microdrops/min via gravity infusion. Perhaps pre-hospital NTG IV would prove beneficial if “smart” IV pumps were available on ambulances. I’d be interested in hearing others views on the need for pre-hospital IV NTG in SCAPE patients.

    • Lance C. Peeples,

      Does EMS need pumps for IV NTG?

      No.

      Bolus dosing can be better, but it requires aggressive oversight (not the silly magic phone call that some people claim is oversight) and continual reassessment.

      It isn’t as if giving NTG to CHF patients is in any way new –

      Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis.
      Levy P, Compton S, Welch R, Delgado G, Jennett A, Penugonda N, Dunne R, Zalenski R.
      Ann Emerg Med. 2007 Aug;50(2):144-52. Epub 2007 May 23.
      PMID: 17509731 [PubMed - indexed for MEDLINE]

      Free Full Text PDF Download from Ferne.org

      -

      [1] Intravenous nitrates in the prehospital management of acute pulmonary edema.
      Bertini G, Giglioli C, Biggeri A, Margheri M, Simonetti I, Sica ML, Russo L, Gensini G.
      Ann Emerg Med. 1997 Oct;30(4):493-9.
      PMID: 9326864 [PubMed - indexed for MEDLINE]

      A Protocol of Bolus-Dose Nitroglycerin and Non-Invasive Ventilation to Avert Intubation in Emergency Department Acute Pulmonary Edema
      Piyush Mallick, Surjya Upadhyay, TS Senthilnathan, El Matit Waleed , Al Jahra Hospital, Scott Weingart, Mount Sinai School of Medicine
      Prepublication abstract
      PDF Download of page at EMCrit

      -

      EMCrit Podcast 1-Sympathetic Crashing Acute Pulmonary Edema
      by EMCRIT on APRIL 25, 2009
      Link to Podcast page

      Link to page with other evidence supporting this treatment

      -

      Preclinical intravenous nitroglycerin therapy.
      Roeggla G, Hauser I, Wagner A, Roeggla M.
      Ann Emerg Med. 1998 Mar;31(3):416. No abstract available.
      PMID: 9506507 [PubMed - indexed for MEDLINE]

      -

      Bolus i.v. nitroglycerin treatment of ischemic chest pain in the ED.
      Nashed AH, Allegra JR, Larsen S, Horowitz M.
      Am J Emerg Med. 1994 May;12(3):288-91.
      PMID: 8179732 [PubMed - indexed for MEDLINE]

      -

      Intravenous nitroglycerin boluses in treating patients with cardiogenic pulmonary edema.
      Nashed AH, Allegra JR.
      Am J Emerg Med. 1995 Sep;13(5):612-3. No abstract available.
      PMID: 7662071 [PubMed - indexed for MEDLINE]

      -

    • Robert McCusker says:

      Our department has been administering IV NTG via pumps for 2 years now. Originally used the Alaris Minimed (3 channels) but now use the Braun Infusomat. Single channel so each medic unit has 2 pumps. Protocol is 0.4mg SL, 0.8mg SL, and 0.8mg SL while the patient has CPAP applied and then once in rig IV NTG initiated. Generally, I will coordinate initial care of patient in house with engine company and send my partner out to the medic unit to set up the drip, that way it is ready to use as soon as we are in the back of the unit.

      Our engines do not have IV pumps so they are unable to hang IV NTG but we still follow same SL dosing regimen and CPAP.

      All of our infusions are required to be on IV pumps when on a transport unit. The only exception to this is if I am on an engine and I mix any of the ACLS/Mag Sulfate infusions prior to one of our department’s medic units arriving. The only meds carried on our medic units that the engine doesn’t carry is ketamine, diltiazem, and IV NTG.

  16. Matt Wong says:

    After a couple of difficult cases I was hashing out ideas with a co-resident about the crashing pt with critical aortic stenosis. What parts of this approach do you think are applicable to the pt with critical AS with pulmonary edema with a normal/high blood pressure? With a low blood pressure? NIV makes sense, but anything else? And heaven forbid if you have to intubate someone with critical AS, but would your strategy be?

  17. Terry Ross says:

    Great Lecture — One question I have is on MAP. I have been very aggressive on these patients for years. When I trained 14 years ago I had one of our cardiologists tell me that he felt taking them down to a systolic pressure of 90 was perfectly acceptable. Is there a minimum MAP you will take them too and try to hold them at i.e. 65 or do you base the decision purely on clinical response?

    The second part of my question is do you have a general guideline on how long you leave them on BIPAP/CPAP after you have them looking “pink” again.

    Thanks

    • Two great questions: Without any data, I try to take them down to what I view as their norm. Since many of these patients have baseline hypertension, that is usually SBP of 140-160 for me. See no reason to take them beyond that. When the patient clinically looks great we’ll give them a CPAP break and just see how they do, if they start raising their pressure again, we just put them back on CPAP.

  18. Juan Carlos says:

    Great podcast!! What about sodium nitroprussiate? Do you have any experience with that? Or boluses of urapidil? Thanks!!

  19. Great podcast, thanks. Sorry for being so late to the party on this topic but I have a question regarding what can be done in the pre-hospital setting. I am an Emergency Care Practitioner in South Africa and unfortunately we are governed by a scope of practice that precludes us from administering IV nitroglycerin. What you said about these types of patients being volume depleted makes a lot of sense and therefore steering clear of diuretics is correct. From your lecture the only plausible management option left to us is then non-invasive ventilation stratagy with increased PEEP. So back to my question… What else could an advanced life support paramedic do for such a patient as you described?

    Regards,
    Nicholas

  20. Scott I’m an emergency physician, newbie ED medical director, new listener and fan. Truly appreciate your efforts. Have incorporated many of your teachings into checkless and protocols in our department.

    Thoughts regarding CPAP versus BiPAP in CHF (and COPD for that matter)? I understand the basic differences between the two, but wanted to hear your thoughts about when they should be used for specific conditions.

    • PEEP for Oxygenation Issues (CHF, Pneumonia)
      PSV or IPAP for ventilatory (COPD/Asthma)

      very few pts benefit from both. Perhaps only palliative care patients.

      I have a podcast on NIV on this site.

      • Just listened, precisely what I was seeking. Thank you.

        How often, if ever, do you deploy CPAP for non severe acute pulm edema without frank oxygenation issues… that is just to ‘treat’ the APE (knowing there isn’t that clear mortality benefit from the lit), and perhaps provide some comfort to the patient? If you do use, what is your end-point to d/c?

  21. Hi Scott,

    Thanks for the great podcast! I have a question. What if patient was really tachycardic, like 140-180, have history of thyrotoxicosis, should NTG be used? Or it would worsen the heart? Thanks!

  22. DocXology says:

    A few points I would like to make.

    1) I have never had to resort to bolus dosing GTN for flash APO and yet I can’t remember having to intubate one either
    2) The pathophysiology of flash APO is complex and probably is not related to fluid overload (unlike the slow burn decompensated heart failure who is sub-acutely accumulating fluid). The inciting event includes (but not limited to) ^recumbency during the night > ^ congestion > hypoxia + early morning sympathetic surge > ^BP > ^stroke work index > myocardial ischaemia > acute diastolic dysfunction > ^LV preload > pulmonary congestion > hypoxia > myocardial ischaemia (vicious circle). In fact a sudden rise in PAOP is often indicative of acute myocardial ischaemia
    3) GTN at lower doses works predominantly on the venous side to decrease preload (where it has major beneficial effects for APO) and at higher doses affects arterial side and afterload (the reason why drops in BP are not infrequent in S/L administration)
    4) There is a risk of precipitous fall in MAP, worsening coronary perfusion and myocardial ischaemia if injudicious amounts of GTN are used particularly when one does not know the baseline MAP of the patient
    5) I don’t see a major need to bolus dose. I immediately commence CPAP to improve oxygenation, improve lung water redistribution by altering FRC and obtain the haemodynamic advantages of decreasing preload (and after load). I then begin low dose GTN and rapidly titrate upward 5-10 mcg/min every 5 minutes closely monitoring BP. A moderate lowering of MAP suggests that significant preload reduction has occurred with some afterload decrease as well. At this point I stop escalating dose and plateau the infusion rate. Importantly, a large part of therapy is just to redistribute blood into the capacitance vessels on the venous side and the congestion is relieved. As frightening as flash oedema can seem, I believe this method is more controlled and safer and does not necessarily prolong response times significantly or increase intubation rates.

  23. DocXology says:

    A few points I would like to make.

    1) I have never had to resort to bolus dosing GTN for flash APO and yet I can’t remember having to intubate one either
    2) The pathophysiology of flash APO is complex and probably is not related to fluid overload (unlike the slow burn decompensated heart failure who is sub-acutely accumulating fluid). The inciting event includes (but not limited to) ^recumbency during the night > ^ congestion > hypoxia + early morning sympathetic surge > ^BP > ^stroke work index > myocardial ischaemia > acute diastolic dysfunction > ^LV preload > pulmonary congestion > hypoxia > myocardial ischaemia (vicious circle). In fact a sudden rise in PAOP is often indicative of acute myocardial ischaemia
    3) GTN at lower doses works predominantly on the venous side to decrease preload (where it has major beneficial effects for APO) and at higher doses affects arterial side and afterload (the reason why drops in BP are not infrequent in S/L administration)
    4) There is a risk of precipitous fall in MAP, worsening coronary perfusion and myocardial ischaemia if injudicious amounts of GTN are used particularly when one does not know the baseline MAP of the patient
    5) I don’t see a major need to bolus dose. I immediately commence CPAP to improve oxygenation, improve lung water redistribution by altering FRC and obtain the haemodynamic advantages of decreasing preload (and after load). I then commence 5-10mcg/min GTN and rapidly titrate upward 5-10 mcg/min every 3-5 minutes closely monitoring BP. A moderate lowering of MAP suggests that significant preload reduction has occurred with some afterload decrease as well. At this point I stop escalating dose and plateau the infusion rate. Importantly, a large part of therapy is just to redistribute blood into the capacitance vessels on the venous side and the congestion is relieved. As frightening as flash oedema can seem, I feel this method is more controlled and safer and does not necessarily prolong response times significantly or increase intubation rates.

  24. Duane Ordiway says:

    I am a RN working in an ICU and am also a REACT RN for the hospital (Rapid response ) Just wanted to say although I am not an MD I find many of your podcast relevent to my work as I also intubate crashing pts and respond to many situations where your info has been most beneficial. Just wanted to say thanks.. Your material is well appreciated

  25. Ekaterina says:

    Hello, I saw my staffs use a very much more dose of NTG in bolus.
    They go to use máximum drop infusión (like 999 mL/hr) with administration of total 50.000 mcg. They only stop when the patient is better. That was very good tolerare by the patient with good arterial pressure. Something in 15 minutes they was absolute a new patients.

    My question, what is you opinión abouth this bolis?

Trackbacks

  1. [...] EMCrit is an excellent podcast blog with nice short podcasts. More important than being nice and short, the podcasts are science-based and address many of the issues that EMS treats. The first podcast from EMCrit is 10:33. [...]

  2. [...] [11] EMCrit Podcast 1-Sympathetic Crashing Acute Pulmonary Edema by EMCRIT on April 25, 2009 Link to Podcast page [...]

  3. [...] discussion of a patient presenting with SCAPE (Sympathetic Crashing Acute Pulmonary Edema – coined by Weingart) as the inaugural Canadian FOAM of the Week. She earned bonus points for incorporating a fantastic [...]

  4. [...] discussion of a patient presenting with SCAPE (Sympathetic Crashing Acute Pulmonary Edema – coined by Weingart) as the inaugural Canadian FOAM of the Week. She earned bonus points for incorporating a fantastic [...]

  5. [...] the virtues and practical use of nitrates espoused further, take a stroll down memory lane with EMCrit Podcast #1 by Mr. ED Critical Care, Scott Weingart. Holy crap, that was 4 years [...]

  6. [...] person has what Weingart calls SCAPE. (creepily Dave Menzies used the exact same phrasing in his comment…) This is acute pulmonary [...]

  7. […] Go listen to the very first EMCrit podcast.   […]

  8. […] her a SCAPE patient  (Sympathetic Crashing Acute Pulmonary Edema, trademark Scott Weingart – EMCrit podcast episode #1). As long as you label it something and identify how to treat it, then you’ve achieved goal #1. […]

  9. Acute Pulmonary Edema - Nitro vs Lasix? | The Chart Review says:

    […] her a SCAPE patient  (Sympathetic Crashing Acute Pulmonary Edema, trademark Scott Weingart – EMCrit podcast episode #1). As long as you label it something and identify how to treat it, then you’ve achieved goal #1. […]

  10. […] her a SCAPE patient  (Sympathetic Crashing Acute Pulmonary Edema, trademark Scott Weingart – EMCrit podcast episode #1). As long as you label it something and identify how to treat it, then you’ve achieved goal #1. […]

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