She Called 911 for Back Pain and Weight Gain... Not Her Florid CHF Exacerbation.

"P2, can you head to 123 Main St., apt. 512, for the female party who feels like she is gaining weight after injuring her back."

Interesting dispatch for sure... My partner and I chuckled and headed to the address.

When we entered the apartment we found a Spanish-speaking (only) 68-year-old female who was very much in distress... Turns out there were some facts lost in translation. While yes, she had in fact gained around 12 lbs in the last week or so with swelling in her legs and abdomen, she was also very short of breath and had been complaining of worsening difficulty breathing and fatigue over the last 4-5 days.

This changed things.

Her son had arrived on the scene minutes before us and was able to translate. Essentially, the patient fell a couple of weeks ago and injured her back. She'd been taking ibuprofen like candy for the last week and a half for this. She has an extensive cardiac history - including heart failure - and despite this, assumed her SOB and weight gain were due to her back pain and recent inactivity. She called 911 for back pain and weight gain... Not her florid CHF exacerbation.

On exam, she was speaking 2-3 word sentences and appeared very SOB. She had audible rales and a non-productive cough. She was breathing around 30 breaths per minute with all of the accessory muscles, and her room-air SpO2 was only 80%. She had JVD present while sitting straight up with warm extremities and strong radial pulses. She had +2 pitting edema to her lower legs with abdominal edema appreciated by her son. My partner took a pulse and got a BP: 120 and 184/100.

Her son asked, "What do you think is going on?"

This lady is in obvious heart failure. She has an extensive history of ischemic cardiomyopathy and takes all the heart failure meds. Her HPI and physical exam both support this working diagnosis and she is obviously in extremis at this point.

Heart failure is complex.

When we think "heart failure" in EMS we tend to think of this scenario, congested heart failure. However, there are far more classifications and subtypes than just that.

The heart is a two-pump system, right? Each pump can fail individually or together. So you can have an isolated right heart failure, like in a massive PE patient, or you can have an isolated left heart failure. More commonly, however, the patient has both left and right failure as the number one cause of right heart failure is in fact left heart failure.

There are a bunch of terms thrown around for heart failure - most of which are being phased out. Congestive heart failure, for one, systolic heart failure, diastolic heart failure, chronic heart failure, acute heart failure, decompensated heart failure, etc.

This patient has chronic heart failure. So she has a history of heart failure and is being treated for it chronically. More technically, she has heart failure with a reduced ejection fraction (HFrEF). This used to be referred to as systolic heart failure, but that term has fallen by the wayside after some more research. The other major flavor of heart failure is heart failure with preserved ejection fraction (HFpEF), which used to be referred to as diastolic heart failure.

These terms can all be confusing, so let's try to simplify it. The heart relaxes and fills with blood and then contracts and shoves blood out, right? That relaxation phase is called diastole and the contraction phase is called systole. The ejection fraction (EF) is measured by an echocardiogram. It's the percentage of blood the LV ejects with each beat. Preload comes in, usually around 110 mL, and then some of that blood - not all of it -  is ejected when the heart squeezes, usually around 70 mL. A normal EF is around 55-70%. An EF <45% is considered a systolic failure. Essentially, the EF represents how much blood the heart can squeeze out each beat in proportion to the amount of blood that fills it. A normal EF with a small stroke volume (the volume of blood ejected) in the setting of heart failure is a diastolic issue or a filling issue. 

So, this patient has a low EF and thus HFrEF. She has this issue at baseline and takes meds, etc. for it. Today, she is having an acute exacerbation, or worsening, of her chronic failure. In case you missed it - it's due to the ibuprofen. Ibuprofen is an NSAID. NSAIDs work by inhibiting prostaglandins which are part of pain/inflammation pathways. You also have prostaglandins in your kidneys. Too many NSAIDs can cause sodium - and thus water - retention. By treating her back pain the last week and a half, she's caused her kidneys to retain water, increasing her intravascular volume, causing her already failing heart to be overworked, acutely decompensate, and backup, causing congestion/edema. She is in what's called acute decompensated heart failure.

So, we recognize this, place her on an NRB, and get her down into the truck where she is placed on the monitor while CPAP is initiated.

Heart failure patients tend to fit into one of four hemodynamic profiles. These are clinically useful to think about because they can guide treatment pathways.

I put a picture of this diagram in the comments below, so check that out - this will make more sense after looking at it.

We want to think about 2 main issues when using these profiles: The patient's congestion and perfusion status. Ask yourself, "How congested is this patient?" Do they have rales, crackles, edema, etc.? Then ask yourself, "Is this patient perfusing?" Personally, I like to feel their extremities - knees, feet, hands, etc. Are they warm? Cold?

This patient is warm and wet - she is perfusing, so she hasn't taken a cardiac output hit yet, but she is congested. She has both pulmonary and peripheral edema. This is the traditional "CHF patient" and the most common heart failure profile we see - hence why our education tends to focus on it almost exclusively.

The big treatment goals here are supporting ABCs while reducing preload and afterload. It's kinda the name of the game in CHF.

First things first, we have a B-emergency, right? She is hypoxic on room air and has difficulty breathing. So we need to perform a breathing intervention right away - here, in the form of CPAP. BiPAP is also an option and is fine, but really, CPAP is all you need here - it's a pure oxygenation problem, not really a ventilation one.

So how does CPAP work?

This patient has an accumulation of fluid, edema, in her alveoli. Basically, there is a traffic jam in the left ventricle that causes an increased pressure there. The fluid then gets backed up into the pulmonary circulation where, due to Starling forces, it leaks into the interstitial space. From there, the pressure can increase, causing the fluid to eventually leak into the alveoli themselves and, in more advanced cases, into the lower airways where it can be coughed up as pink, frothy sputum.

This fluid causes 2 big problems: (1) It creates a barrier to gas exchange. O2 needs to now move through the fluid to get to the capillaries. (2) The fluid in the alveoli increases the surface tension and can result in atelectasis, or the closure of lung units. Pulmonary edema can lead to both shunt and dead space ventilation.

CPAP does a few things for patients with congestive heart failure.

CPAP prevents the leakage of fluid from the vascular compartment into the interstitium and alveoli by changing the pressure gradients. Contrary to popular belief, CPAP does not "force the fluid out of the lungs." It's all a complicated pressure game. CPAP also increases functional residual capacity. CPAP acts to shunt open those collapsed alveoli and maintain them, preventing further atelectasis.

CPAP also affects thoracic hemodynamics by both reducing right heart preload and left heart afterload. CPAP increases intrathoracic pressure which reduces the amount of venous return coming back from the body to the right heart. This reduction in preload reduces the amount of blood joining that backed-up highway. CPAP also reduces LV afterload by affecting something called transmural pressures.

So the big intervention here: CPAP (or BiPAP, if you have it). That's the number one thing to do for these patients. Be early and aggressive about it.

While placing the patient on CPAP we obtained a 12-lead ECG to rule out STEMI/ischemia as a cause of the failure (no STEMI) and placed an IV.

At this point, my partner gave SL nitro. Nitroglycerin is a vasodilator. It works by stimulating nitric oxide in the vasculature. At lower doses, nitro primarily affects the venous side, reducing preload. At higher doses it loses its selectivity and affects the arterial side as well, reducing afterload. These actions make nitro a helpful agent in heart failure. Nitro also comes in a titratable IV variety which some EMS services carry - if you carry it, this is the preferred method.

We also gave furosemide.

Now, this used to be a really popular drug and was a staple in heart failure treatment for EMS. However recently this has become controversial. Most patients with chronic heart failure tend to take daily diuretics. This patient is no different, she takes furosemide at home. Furosemide, or lasix, is a loop diuretic. Loop diuretics block the Na/Cl/K transporter in the kidney which results in more water (among other things) being excreted by the kidneys. Furosemide also has vasodilator effects which can further reduce preload.

The jam with this is that most of the time, the patient is not actually volume overloaded - they are volume misplaced. The patient is euvolemic and shifted their fluid into the intravascular space so by diuresing them we run the risk of actually causing hypovolemia. It can also be an issue if the patient has concomitant renal failure, in which case shredding the kidneys would not be helpful... It's more complicated than this, but hey, it's a FB post and I'm already running out of room.

With that said, I'll end it here... We talked to med control and gave some furosemide. Where I worked at the time, this med was a med control-only order given the above. Within 10 minutes we got the patient to the ED and turned over care. Ultimately, she did well. After 6-8 hours of NIV she was weaned and admitted for a few days to get some things regulated. She was then discharged to a rehab - turns out she fractured a rib and slipped a disk when she fell.

What are your protocols for heart failure? Share them below!

Thanks for reading!

-Dean Stockley