Jack of all trades, master of… some?

Off-service rotations can provide humbling instances of opportunities to improve our patient care in the ER. But, occasionally, they also serve as a reminder that as emergency physicians, we frequently are first best at certain things.

On the first day of my telemetry rotation, I saw a patient who had just been admitted to our service - a 64-year-old female that had presented to the ED for sudden onset shortness of breath. She was in extremis, with tachycardia, tachypnea, and a BP of 220/120. She had bilateral rales on lung exam but no lower extremity edema or JVD.

Respiratory was called to start the patient on BiPAP as she was speaking in one to two word sentences. She was given three sublingual nitrates while IV access was obtained, a nitroglycerin drip was set up, and she was placed on BiPAP with the head of the bed almost straight up.

The nitro drip was started at 100 mcg/min and rapidly titrated to 400 mcg/min for two minutes. Then maintenance was started at 100 mcg/min and titrated with frequent BP checks. Within fifteen minutes the patient, who was previously on the brink of intubation, is now breathing comfortably.

It knows many names: severe decompensated heart failure, sympathetic crashing acute pulmonary edema (SCAPE) or “flash” pulmonary edema, as our colleagues upstairs tend to refer to it. Whatever you choose to call it (I choose SCAPE), it’s one of my favorite pathologies (don’t lie, you have them too). It is an entirely clinical diagnosis that we often fix before our consulting cardiologists have even made it downstairs to evaluate the patient.

SCAPE is usually the result of a hypertensive emergency: an acute increase in afterload results in elevated cardiac filling pressures and rapid accumulation of fluid in pulmonary interstitial and alveolar spaces. Intense sympathetic activity causes increased systemic vascular resistance leading to worsened cardiac pump function and drastic increases in both preload and afterload.

We can stop this vicious cycle of sympathetic upsurge by decreasing afterload. Nitroglycerin is your friend here. It will rapidly reduce both preload and afterload and can be easily titrated. But the classic 0.4 mg sublingual doses won’t cut it. At these doses, nitroglycerin reduces preload but has little effect on afterload (remember that the vicious sympathetic cycle in SCAPE is primarily the consequence of an afterload issue).

Research has shown that bolus nitroglycerin doses (400 mcg/min over 1-2 minutes) reduces intubation rates, ICU admission rates, and hospital lengths of stay. After the bolus you want to drop your drip to 100 mcg/min and titrate to effect (effect being resolution of symptoms - target SBP should generally be around 140-160). As the patient improves, you need to sharply decrease this drip rate. You obviously will need to be at bedside while using these doses.

It is important to note that SCAPE patients are very different than our chronically fluid overloaded CHF exacerbations, who may present with gradual onset of 2+ pitting edema, weight gain, or worsening dyspnea/orthopnea. In contrast, SCAPE develops acutely and severely over minutes to hours with accompanying malignant hypertension. SCAPE patients may not necessarily have increased total body volume, and the majority will actually be euvolvemic, as was the case with my patient.

Forgetting the 13th law of the House of God (the delivery of medical care is to do as much nothing as possible), my eager cardiology colleague had started this seventy-kilogram lady with normal kidney function on 80 mg IV Lasix BID. After three doses her creatinine had jumped from 0.9 to 1.4.

The key learning point here is that the physiology underlying SCAPE is one of fluid redistribution rather than fluid overload. While there may be a role for diuretics for certain patients, it is generally not helpful in the acute setting and further research should be conducted. Reach instead for your nitroglycerin and your BiPAP, and go save another life.

There’s a lot to be said on this subject. I highly recommend the very first episode of EMCrit, which focuses on SCAPE. Other SCAPE pearls:

· Start patient on BiPAP with a PEEP of 6-8 and quickly titrate to PEEP of 10-12

· 0.4 mg SL nitro tabs over the course of 5 min = ~80 mcg/min, 2 tabs = 160 mcg/min, etc

o SL tabs can be useful as you set up your drip

· The standard nitro mix is 200 mcg/ml. To give your bolus you can draw up 4 mL of nitro and 6 mL of NS and give over 2 minutes

· If your shop has them, IV Ace Inhibitors are fast acting agents that can work on the RAAS system to continue to reduce afterload

· Your CXR may show acute pulmonary edema, or it may be normal. Trust your clinical exam skills

· Following stabilization, search for potential underlying causative factors/precipitating triggers (MI, acute valvular dysfunction, cardiomyopathy, etc)

References

Agrawal N, Kumar A, Aggarwal P, Jamshed N. Sympathetic crashing acute pulmonary edema. Indian J Crit Care Med. 2016;20(12):719–723. doi:10.4103/0972-5229.195710

Cotter G, Kaluski E, Moshkovitz Y, Milovanov O, Krakover R, Vered Z. Pulmonary edema: new insight on pathogenesis and treatment. Curr. Opin. Cardiol., (3):159-163. MED: 11357010

Levy P, Compton S, Welch R, et al. Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis. Ann Emerg Med, 2007; 50: 144–52.

Nohria A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA, (5):628-640. MED: 1182970.

Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure. Am J Emerg Med, 2017; 35: 126–31.