A 60 year old male with a history of HTN comes in with acute onset shortness of breath.

(Clinical details altered).

He was in profound respiratory distress. He was tachypneic with intercostal retractions. He had rales halfway up his chest. His initial BP was 250/110 mmHg. He was hypoxic with a room air sat of 77%. Quick review of records showed CHF with an EF of 35%

I quickly called for RT to bring the BiPAP machine and to get a stat portable chest x-ray. The staff appeared anxious and anticipated that this patient would eventually require intubation.

The xray confirms SCAPE. Sympathetic Crashing Acute Pulmonary Edema—a vicious cycle where the heart, due to catecholamine surges, peripheral vasoconstriction & increased afterload has to work harder to maintain cardiac output.

Reduced cardiac output results in decreased renal perfusion. The kidneys secrete renin, which coverts angiotensinogen to angiotensin I. Angiotensin I gets converted to Angiotensin II by ACE (angiotensin converting enzyme) and does TWO important things.

Angiotensin II acts directly on blood vessels, stimulating vasoconstriction (and increasing afterload). It also acts on the adrenal glands to secrete aldosterone, which acts the level of the kidney to reabsorption of salt + water.

Why is this important? Because the increased afterload makes the failing heart have to work harder. While this is happening and the patient feels like they’re drowning, the kidneys are working to reabsorb fluid which is only compounding the problem.

A knee jerk reaction is to intubate these patients. But, if managed correctly, these patients turn around almost instantaneously. We immediately placed the patient on BiPAP. His settings were 16/8 cm H2O (won’t go into CPAP/BiPAP for type I vs II resp. failure here).

We coached him through what was about to happen. He was able to tolerate the mask. BiPAP helped his oxygenation and his work of breathing. The positive pressure dropped his preload & helped to reduce the work that his failing heart had to do.

Next, we started him on a nitroglycerin drip. This is always a point of contention. What should the dosing of the drip be? Nitro, like the positive pressure, helps to decrease preload and reduces the work done by the heart

However, high dose nitroglycerin has been shown to reduce AFTERLOAD as well as preload. This makes it easier on the failing heart to pump and perfuse the vital organs.

Traditionally, sublingual nitro is dosed at 0.4 mg = 400 mcg every 5 minutes. That is equivalent to 80 mcg/minute. So, when starting a nitro drip at 50 mcg/min on these pulmonary edema patients, which is less than the dose of SL nitro, you aren’t doing jack for them!

These patients require high dose nitro. What do we do with all drips? Traditionally we give a bolus. Cardizem drip? Give 1-2 dose of cardizem first. Heparin drip? Give a bolus first. Same concept. You want to saturate the system & allow drip to have an immediate effect.

That is exactly what we did. We started the drip high. Dosing is usually anywhere from 200-400 mcg/min. I DID NOT LEAVE THE BEDSIDE WHILE THIS WAS HAPPENING. I stood there and monitored the patient.

Within minutes this mans work of breathing significantly improved. You could tell he was feeling better & wasn’t struggling as hard to breathe. It was then that we dropped the nitro dosing to 50 mcg/min and kept him on the BiPAP. His repeat BP was 180/95 mmHg.

These interventions reduced his preload + afterload, improved oxygenation, & helped his WOB. A nice pearl is to give a dose of IV ACE inhibitor like Enalapril to help break the RAAS system. This is why its so important to understand the pathophysiology of this disease.

An hour passed and the patient was looking so much better. He could carry a full conversation and didn’t have 1-2 word dyspnea. He thanked us. We were even able to turn off his nitro drip and transitioned him from BiPAP to nasal cannula.

This man was never intubated. He was admitted to the step down unit on nasal cannula. He did extremely well and was discharged home with his family on the following day.

Without these key interventions, I am certain that he would have required intubation for respiratory failure. This is a high risk procedure in the critically ill patient with associated morbidity/mortality with no guarantees of coming off the vent.

Please remember these key concepts in the treatment of APE (acute pulmonary edema) and share them with your colleagues. People often ask me why I teach on twitter. This is why. #savelives #meded #FOAMed #emergencymedicine #MedTwitter #criticalcare

You can follow @BabakBehgam.
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