Heart Failure Basics

by Dr. Elspeth Pearce

uploaded by Matthew Lam, MS2

Heart Failure for the Resuscitationist: The Basics

I don’t have to tell you that heart failure is a common condition in the general population and in patients presenting to the emergency department (ED). We see it on a daily basis. Even with this familiarity, there are still some conundrums in the care of these patients. My personal opinion is that a lot of the confusion starts with how we define and refer to these patients. When I say “acute decompensated heart failure,” you get a picture of a patient in your mind, but your “heart failure” patient might be someone else’s “flash pulmonary edema” patient. Language matters in how we talk to our colleagues, consultants, and the patients. In this post, I hope to identify clear definitions for heart failure exacerbations. The goal being that we can dissect the workup and treatment of the different presentation phenotypes.

Acute Decompensated Heart Failure

The first definition to tackle is Acute Decompensated Heart Failure (ADHF). Sounds easy enough; the name, itself, is pretty descriptive. The Heart Failure Society of America and the European Society of Cardiology both define ADHF by using the words acute, decompensated, heart, and failure in the definition, so not really that helpful. My favorite definition is this: a broad spectrum of clinical presentations that reflect the gradual or rapid worsening of signs and symptoms secondary to abnormal cardiac function that requires hospital admission for treatment. What are these signs and symptoms? The most common are dyspnea, fatigue, edema, and orthopnea.


So, what are these cute little names that we give to the different types of heart failure? HFrEF (typically pronounced hef-ref) stands for heart failure with reduced ejection fraction (EF ≤40%), and HFpEF (typically pronounced huf-puf) stands for heart failure with preserved ejection fraction (EF ≥55%). The main reason for these distinctions is because this is how we study heart failure patients. We have good data for therapies that improve mortality in patients with HFrEF. At this time we don’t have specific therapies for HFpEF, we target the underlying comorbid conditions.

It used to be that we used the terms “systolic dysfunction” and “diastolic dysfunction” for the different groups. This wasn’t as specific as these new labels. Patients who have HFrEF may also have diastolic dysfunction, and patients with HFpEF may have abnormalities of their systolic function, just not severe enough to cause reduction in ejection fraction. To make things more confusing, HFpEF patients may not have any diastolic dysfunction at all. Heart failure can be due to valvular, congenital, or electrophysiological abnormalities that do not change the ability of the ventricle to relax.

A big point I want to make is that heart failure is a clinical diagnosis. I will say it again: heart failure is a clinical diagnosis. History and exam are key for making the diagnosis. Labs, chest x-ray, and echocardiography (echo) findings are just additional evidence to support or refute the presumed diagnosis. A patient can have decompensated heart failure with no or minimal elevation in BNP, no pulmonary edema on chest x-ray, and no reduction in ejection fraction on echo. Even the terms HFrEF and HFpEF don’t tell us much about how a patient might present to the ED with acute decompensation.

Presentation Phenotypes

When we discuss treatment of ADHF, we typically only use this term to identify patients (i.e. “I have a decompensated heart failure patient for admission”). It is hard to make generalized statements about workup or treatment when ADHF could mean flash pulmonary edema to one physician and cardiogenic shock to another. An easy way to think about ADHF is to break it into two dysfunctions: congestion and perfusion.

Congestion breaks down into increased preload and left-sided filling pressures (wet) or normal preload (dry). Perfusion is broken down into reduced cardiac index (cold) or normal cardiac index (warm). Patients can fall into one of the four categories shown on the left based on their congestion and perfusion status. The warm/wet phenotype of patients have been broken into two subgroups based on time-course of symptoms. Let’s explore these categories some more.

Warm/Dry Phenotypes

These patients are easy for the EM doctor; they are compensated and should be managed in clinic. If they are HFrEF they should be on maximum doses of guideline directed medical therapy as tolerated.

Warm/Wet Phenotypes

These patients have normal perfusion but are volume overloaded. How they look clinically depends on how fast the fluid accumulated and the ability of the heart to handle the preload.

The warm/wet/slow phenotype is one we are very familiar with. These are the patients who present after forgetting to refill their medications for about a year, are 70 kg above their dry weight, and have edema up to their scalp. They usually have respiratory symptoms but typically are not unstable on presentation. They started sleeping sitting up a few months prior to presentation, and they finally came in because they stopped being able to make it to the bathroom without stopping to catch their breath. This may be a bit of an exaggeration but not much. The analogy is a bog or a swamp; there are tons of congested fluid and no easy way to get it out.

If the warm/wet/slow patients are like a bog, the warm/wet/fast patients are like a tsunami. These patients are familiar to EM physicians, and we have our own set of names for them: flash pulmonary edema, sympathetic crashing acute pulmonary edema, or hypertensive emergency. These patients have very little compliance of their left ventricle and quickly fall off the Frank-Starling curve when they start to retain fluid or have an acute increase in afterload. Since they cannot handle the extra preload, it gets dumped into the lungs rapidly, and they present with marked hypertension and rales up to their clavicles.

Cold/Wet Phenotype

This classification also has a common name: cardiogenic shock. These patients can present dramatically or insidiously. If they read the textbook, they have rales, hypotension, cool extremities, and narrow pulse pressure. If they didn’t read the textbook, they can easily be mistaken for sepsis, pulmonary embolism, or missed completely. Blood pressure in these patients is typically low, but they may have normal blood pressure and still not be perfusing appropriately. Tachycardia may be the only abnormal vital sign as the heart tries to compensate for the low stroke volume (cardiac output = heart rate x stroke volume). Watch out for patients who get shuttled down the sepsis pathway and get worse with fluid administration.

Cold/Dry Phenotypes

Not typically a patient type we would pick up on in the ED, but these patients do exist, often identified when they cannot be weaned from ionotropic support even after optimizing fluid status. If not already hospitalized, they present with cardiac cachexia, depressed mental function, worsening renal or hepatic failure and hypotension.


I know these phenotypes do not have great names or acronyms associated with them, so they would be cumbersome to use day to day on a shift, which is why we have the common names like cardiogenic shock and flash pulmonary edema. What I would encourage is getting away from using ADHF unless you clarify it with the perfusion status, the volume status, and the underlying etiology if you have all that information. For example, when admitting to the cardiology unit, you could tell them that you have a patient with HFrEF coming in with decompensated heart failure with significant volume overload but good perfusion.

You may be thinking to yourself, “Why? Why should we be differentiating the types of ADHF?” Mainly it has to do with the treatment. The mainstays of treatment for ADHF are afterload reduction and diuresis, but we employ them differently for the various presentation phenotypes. I’m sure you noticed I haven’t touched on treatment of any of the above; that is a subject for another post.