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11.2 Denitions
C. E. Kulig
11.2.1
Heart failure can present in many different ways and is an umbrella term. Two
patients may both have the diagnosis of “heart failure” but have vastly different
cardiac structural changes and require different treatments.
a bare-bones denition.
patient to patient, the heart is unable to pump enough blood out to meet the
demands of the body.
as heart failure with reduced ejection fraction (HFrEF), and diastolic heart failure,
also known as heart failure with preserved ejection fraction (HFpEF). However, more
recently, new categories of heart failure have emerged, leaving us with some new
acronyms in our bowl of alphabet soup: heart failure with improved ejection fraction
(HFimpEF) and heart failure with mildly reduced ejection fraction (HFmrEF) [2].
the term ejection fraction (EF). Take a moment and ask yourself:
Heart
In order to really understand heart failure, it is best to rst strip this term down to
Heart failure is a condition where, for a variety of reasons that may differ from
The two historic denitions of heart failure are systolic heart failure, also known
To better understand this terminology, it is important to rst have a clear grasp of
Failure
11.2.2 What is Ejection Fraction?
As the name suggests, ejection fraction is a fraction, one number over another, and
is dened as stroke volume divided by the ventricular end-diastolic volume (VEDV).
Stroke volume
The amount of blood pumped =oout of the
ventricle in contraction
Ejection fraction
Stroke volume (SV) is the amount of blood that the ventricle pumps out per each
beat (aka in 1 contraction).
Ventricular end-diastolic volume (VEDV) is the total amount of blood in the
ventricle at the end of diastole (relaxation)—when the ventricle is at its fullest point
immediately prior to contraction.
Test Your Knowledge
At the end of diastole (relaxation), a patient’s left ventricle holds 100mL.During
systole (contraction), the left ventricle pumps 50mL of blood out to the aorta.
The vloume of blood in the ventricle at its fu
1
Ventricularend di
aastolic volume
lllest
11 Acute Decompensated Heart Failure
293
What is the patient’s:
A. Stroke volume
B. LVEDV
C. EF
The patient’s stroke volume is 50mL.The LVEDV is 100mL.Therefore the EF is
50/100=0.5=50%.
There are two phases of the cardiac cycle: systole (squeeze) and diastole (relaxation). Systole is the part of the cardiac cycle when both ventricles contract (and the
atria relax), and diastole is when both ventricles undergo relaxation (and the atria
contract).
Systolic heart failure, also known as HFrEF, occurs when there is an issue with
the force of contraction of the ventricle. As the name suggests, there is an issue with
the systole, or the squeeze, of the ventricle. The ventricular muscle is weakened and
can no longer squeeze as hard as it used to, to push that blood out of the ventricle.
Systolic heart failure is dened by an EF of <40% [2].
Diastolic heart failure, also known as HFpEF, occurs when there is an issue
with the relaxation of the ventricles. As the name suggests, there is an issue with
diastole or the relaxation of the ventricle. The ventricular wall can become stiff and
rigid, and no longer be elastic enough to relax and accommodate a normal blood
volume; in other patients, the left ventricular wall can hypertrophy and grow thicker
and thicker, decreasing the amount of space available to hold blood within the ventricle. In this way, diastolic heart failure is really an issue with the amount of blood
volume the ventricle can hold.
But what differentiates a healthy person from a patient with HFpEF? After all,
both ejection fractions are considered “normal” in both patients.
This can be best illustrated in an example.
Test Your Knowledge (*note: the volumes used in these examples are for
illustrative purposes only)
Patient A: Patient A’s left ventricle is able to hold 80mL at the end of diastole.
During systole, the LV pumps 40mL of blood out to the aorta.
Patient B: Patient B’s left ventricle is able to hold 30mL at the end of diastole.
During systole, the LV pumps 15mL of blood out to the aorta.
What is each patient’s:
A. LVEDV
SV
B.
EF
C.
P
atient A’s LVEDV is 80mL. Patient B’s LVEDV is 30 mL. Patient A’s SV is
40mL, and Patient B’s SV is 80mL. However, both patients have an EF of 50%.
As illustrated in the case above, although both these patients have an EF of 50%,
there is a big difference between the amount of blood that the body is receiving.
Patient B illustrates a case of a patient with heart failure with a “normal” EF. Keep
in mind that ejection fraction is a relative term (because it is a fraction!), which is
why a patient with a healthy heart can have the same EF as a person with HFpEF.
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Fig. 11.1 Analogy: the difference between HFrEF and HFpEF
C. E. Kulig
For the visual learners, another way to visualize systolic vs. diastolic heart failure
is by the visual analogy of a hand squeezing a water bottle lled with water, where
the water bottle represents the ventricle, the hand squeeze represents the force of
contraction, and the water leaving the bottle represents stroke volume (Fig.11.1).
In a healthy heart, there is a good amount of water in that bottle—and there is
also a good squeeze. The end result is a lot of water exiting and spewing out of that
water bottle.
In a heart with reduced ejection fraction (aka HFrEF, aka systolic heart failure),
there is a good amount of water in that bottle—but the hand squeezing it is very
weak, unable to generate a good contracting force. The end result is less water leaving out that bottle.
In a heart with preserved ejection fraction (aka HFpEF, aka diastolic heart failure), there is not enough water in that bottle. You have a great squeeze, but because
there is not enough volume to begin with, and you end up with the same result as
you do in the HFrEF example, with less water leaving that bottle.
Let us delve into the different denitions of heart failure that were released with
the new 2022 American guidelines [2]. As stated earlier, HFrEF is dened as an EF
of <40%. Heart failure with mildly reduced ejection fraction (HFmrEF) is dened
by an EF of 40–49%; HFpEF is dened as an EF of ≥50%; and heart failure with
improved ejection fraction (HFimpEF), is dened as a patient with an previous EF
of <40%, but has since recovered.
11.3 Common Causes ofHFrEF vs. HFpEF
HFrEF is often caused by ischemia [2]. In other words, it is heart failure caused by
a lack of blood ow to the myocytes within the heart. If there is not enough blood
ow to the myocytes, the myocytes will start dying. The more muscle cells that die,
11 Acute Decompensated Heart Failure
295
the larger the extent of the damage, and the less squeeze that ventricle is capable of.
A common cause of HFrEF is a patient with a myocardial infarction. Other causes
of nonischemic HFrEF include autoimmune conditions, chemotherapy, cardiotoxic
medications, myocarditis, and substance abuse [2].
HFpEF can be caused by heart rhythm abnormalities, chronic hypertension,
severe aortic stenosis, and anemia, among others [2]. Keep in mind that your heart
is a muscle, just like other muscles within your body. If you went to the gym every
day and started lifting heavy weights, what would happen to your biceps? They
would grow. Your heart is no different. If your heart has to deal with a high chronic
afterload (aka the amount of pressure your left ventricle has to ght against to
ensure forward ow), your heart will also start to grow and hypertrophy. The greater
the amount of hypertrophy, the thicker the ventricle wall, and the smaller the area in
the ventricle that can ll with blood.
11.4 Understanding Blood Pressure
To understand acute decompensated heart failure (ADHF), a general overview of
the determinants of blood pressure would also be helpful. The easiest way to break
this idea down is by thinking of the garden hose sitting in your backyard. The higher
the pressure of the water leaving that hose, the further it will shoot out, right?
But how to make the water shoot further? Let us say the spout is completely off,
and you tweak the spout just a tad to let some water start going into that hose. At the
end of your hose, that water is barely going to go anywhere. It is just going to start
trickling out, and basically fall right onto the ground right next to the end of that hose.
But if we go back to that spout, and crank it all the way up to the max, that water
at the end of the hose will start picking up pace and shoot out in an arc and go much
farther.
In other words, the more the water - the more volume-, the higher the water
pressure.
Now, let us say the spout is already maxed out—you have a nice arc of water
owing from the end of the hose, but let us say you want to spray your unsuspecting
sibling who is across the yard. The hose is extended fully, so you cannot drag it out
anymore, and the water spout is already maxed out. What can you do to increase that
water pressure and get that water to shoot out farther?
For all those with siblings, you might know that putting your thumb to cover the
end of that open hose and blocking a lot of the water ow will allow the water exiting that hose to shoot out much farther in a smaller stream, now able to be ung
across the yard and soak the unsuspecting victim.
In other words, the smaller the space we allow water to go through, the higher the
pressure of the water leaving it.
Believe it or not, your body is not that different. In this analogy, the water represents your blood and the hose represents the vessels of your body.
The more blood volume, the higher the blood pressure. By giving patients uids,
we can help increase their pressure. Luckily for us, our body has built-in systems to
help increase blood volume if patients have low blood pressure (I am looking at you,
aldosterone).
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Fig. 11.2 Blood pressure
equation
C. E. Kulig
The smaller the vessels, the higher the blood pressure. Luckily for us, our body
is able to self-regulate by vasoconstricting or vasodilating our vessels. We can also
use medications to help us achieve these goals.
The variable we use to represent volume is cardiac output—or the amount of
blood volume that the body receives from our heart per unit of time. We use the term
systemic vascular resistance to represent the amount of squeeze (or size of) our
vessels are exerting (Fig.11.2).
11.5 Preload vs. Afterload
An integral part of understanding heart failure and the treatment of acute decompensated heart failure is having a clear idea of what the terms “preload” and “after-
load” mean.
Let us start with afterload, which I think can be a little easier to visualize.
Afterload is dened as the amount of pressure the heart has to exert in order to eject
blood out during ventricular contraction. For those who are visual, I would like you
to picture yourself inside of a patient’s left ventricle (LV). To orient you, on one
side, you have the mitral valve, where blood enters the LV from the left atrium
(LA). And looking ahead of you, you can see the aortic valve, which is where blood
must pass through in order to get out of the ventricle and into the aorta and systemic
circulation.
Now keep in mind that your aorta and arteries carry their own baseline pressure
even when the heart is relaxing (this is what we call your diastolic pressure). The
higher that pressure, the harder your heart will have to squeeze and contract in
order to ensure forward ow of blood. In other words, in order to get forward ow,
your heart—specically your left ventricle—must exert a pressure that is higher
than the pressure in your arteries/aorta.
In patients who are hypertensive with high systemic vascular resistance (SVR) or
have stenosis of their aortic valve, afterload will be higher, and your heart will have
to squeeze extra hard to get forward ow of blood.
In the context of left-sided heart failure, factors such as arterial vascular resistance (the size of your arteries) will determine that left ventricle’s afterload. Patients
with high arterial SVR will make forward ow harder for that left ventricle, while
patients with lower SVR with arterial dilation will make forward ow easier on that
left ventricle.
11 Acute Decompensated Heart Failure
The second term to understand is preload. The technical denition of preload is
ventricular end-diastolic pressure (VEDP) or the amount of stretch the ventricle
experiences at the end of diastole, prior to contraction. Two main factors can determine preload. The rst is volume. The more volume your patient has, the higher the
amount of pressure and stretch your ventricle will experience. Giving patients uids
will increase preload; diuresing patients will decrease preload. Besides volume
(since after all, most of the time patients remain with a fairly xed volume unless
we are actively giving them uids or if they are being diuresed or have blood loss),
the other thing that can inuence preload is the amount of pressure the blood enters
the heart with. This is inuenced by venous vascular resistance. For example, if we
vasodilate the veins, the pressure entering the heart will be decreased. A lot of
times, this may be confusing, but keep in mind that in a patient with constant volume, dilation will cause decrease in pressure (think back to your hose analogy). If
we constrict the veins, the pressure of the blood entering your heart will increase
and preload will be increased.
297
11.6 Acute Decompensated Heart Failure
11.6.1 Denition
In chronic heart failure, the heart has issues keeping up with the demands of the
body; however, with the use of medications, it is still able to meet the demands of
the body. However, in acute decompensated heart failure, the heart can no longer
meet those demands, and hospitalization may be needed to get that patient back to
their “baseline.”
11.6.2 Etiology
It is important when your patient comes in with a new decompensated heart failure
event that you assess for any precipitating causes and interview your patient. Some
of the common causes of acute decompensated heart failure (ADHF) include ischemia, infection, atrial brillation or other arrhythmias, pulmonary embolism, renal
failure, anemia, valvular issues, and aortic dissection, among others. Medications
can also precipitate ADHF.In HFrEF, any medication that has negative inotropic
effects (aka decreases the force of contraction of the heart) can induce an ADHF
event. A common example is the initiation of non-DHP calcium channel blockers,
such as verapamil or diltiazem [2]. Additionally, the use of high-dose NSAIDs can
also induce ADHF.In patients who come in with ADHF, these medications should
be discontinued and avoided [2].
298
C. E. Kulig
11.6.3 Presentation andClassication
Forrester’s classication is often used to classify the main ways a patient with
ADHF can present (Fig.11.3). The classication system is broken up into two main
concepts: What is my patient’s volume status? What is their perfusion status?
Let us start with the assessment of volume status. The “gold standard” of volume
assessment in terms of Forrester’s classication is known as pulmonary capillary
wedge pressure or PCWP [2].
Pulmonary capillary wedge pressure is a measurement taken by using an invasive catheter. The physician will make an incision at a major vein (usually the internal jugular vein, though there are other access options) and insert a long, thin, and
exible tube known as a catheter into the vein. They will then guide the tube up
through the vena cava, into the right side of the heart, through the right atria, through
the right ventricle, and out through the pulmonary artery. Once in the pulmonary
artery, the physician will place the tip of that catheter into a small pulmonary arterial
branch. The tip of that catheter has an inatable balloon on it; once in position, the
team will inate that balloon for a few seconds and “wedge” that branch closed
while reading the pressure at that moment in time. That pressure—the pulmonary
capillary wedge pressure—is a marker of volume status and left atrial pressure.
A typical PCWP in a “dry” or euvolemic ADHF patient is <18mmHg. Any measurement greater than 18mmHg is one marker that your patient may be presenting
with volume overload [2].
The other parameter of Forrester’s classication focuses on perfusion. The “gold
standard” marker of perfusion in terms of Forrester’s is cardiac index [2].
Cardiac index is a method of standardizing cardiac output, which, as we said
above, is the amount of blood that leaves the heart per unit of time. In other words,
it tells you how much blood your body is getting from the heart over a period of time.
Fig. 11.3 Forrester’s
classication system
11 Acute Decompensated Heart Failure
However, if we only looked at cardiac output, it would be very tricky to quickly
discern what a patient’s normal cardiac output should be for them. After all, a supermuscular 6′4″ male would likely require more blood per unit of time than let us say
a frail, small grandmother.
In order to “standardize” this term for any given patient, cardiac output is divided
by a patient’s body surface area. This means that a cardiac index (CI) of 2.0L/min/
m2 means approximately the same thing whether you are talking about a bodybuilder or someone’s Nana.
The “gold standard” for a patient that is adequately perfusing is a CI >2.2L/min/
m2. Anything below indicates that the patient may not be getting adequate perfusion
to their body [2].
299
11.6.4 Pulmonary Artery Catheters (PACs) forAll?
Now, not every patient is going to have invasive monitoring. In fact, most patients
do not require invasive monitoring. Surprisingly, despite the fact that we as clinicians love our data and values, there is not a lot of data supporting better outcomes
with the use of PACs in ADHF.
The 2022 AHA/ACC/HFSA Heart Failure Guidelines only recommend right
heart catheterization in the setting of persistent congestion despite treatment due to
the lack of compelling data [2].
If we do not have a PAC available, what are some other markers of either volume
overload or low perfusion?
Markers of volume overload to look out for include shortness of breath, rales,
pulmonary edema, pitting edema, and elevated BNP, among others. Ultrasound can
even be used to visualize the vena cava and assess if it is plump (volume up) or collapsible (volume down).
When we are thinking about perfusion, keep in mind what the whole point of
your heart is—to supply blood to the vital organs. Let us start with the brain—if the
brain is not getting enough blood supply, patients may present with confusion and
altered mental status. If the kidneys (which tend to be very sensitive to changes in
perfusion) are not getting enough blood ow, we can see increased serum creatinine
and decreased urine output in our patients. For the liver, we can see elevated liver
function tests. Lastly, if our extremities are not perfusing, we can see cold extremities to the touch, increased capillary lling time, and even ischemic digits.
11.7 Goals ofADHF Hospitalization
The rst thing to keep in mind with heart failure hospitalizations is that hospitalization is really a sentinel event in these patients, and we want to avoid hospitalizations
at all costs in these patients.
300
Heart failure is very similar to chronic obstructive pulmonary disease (COPD) in
that once a patient has an exacerbation, they often never return to their true baseline
prior to hospitalization [2]. Besides triggering negative overall outcomes for our
patients, ADHF hospitalizations are also a huge burden on both a patient’s quality
of life and the healthcare system. Rehospitalizations within 90days of discharge are
unfortunately very common, and the frequency of hospitalizations increases as the
patient’s heart function deteriorates [2].
A big goal of ADHF hospitalizations, besides stabilizing the patient, is to get
“guideline-directed medical therapy,” also known as GDMT, onboard for these
patients [2]. These agents are extremely effective at preventing death and hospitalizations in these patients. We will be focusing on GDMT at the end of this chapter.
Lastly, another goal of hospitalization is to try to determine the patient’s
euvolemic weight, relieve their decongestion, and treat their symptoms.
C. E. Kulig
11.7.1 Treatment ofADHF
When thinking about treating acute decompensated heart failure, it is important to
gauge which of Forrester’s classication your patient falls into and assess wet vs.
dry and warm vs. cold. This classication will help guide treatment.
11.8 Treating Volume Overload
If your patient is volume overloaded—they come in with rales, shortness of breath,
pitting edema, pleural edema on chest X-ray, elevated CVPs, pro-BNP, and
PCWPs—it is important to help patients take this excessive volume off the heart and
also to reduce symptoms such as dyspnea.
11.8.1 Loop Diuretics
The long-time mainstay decongestion in these patients, which is echoed in the 2022
AHA/ACC/HFSA Heart Failure Guidelines, continues to be intravenous loop diuret-
ics [2]. IV loop diuretics provided the most rapid and effective method of deconges-
tion in these patients, and although they are not associated with clinical outcomes
such as mortality, they are extremely effective at improving symptoms of volume
overload in these patients [2]. Every patient coming in for a heart failure hospitalization should have a discharge plan that includes the adjustment of their diuretics [2].
Because of the phenomenon of “diuretic resistance” that involves nephron
remodeling causing resistance with a need to continue escalating doses to reach the
“diuretic threshold,” loop diuretic dosing is not a “one-size-ts-all” approach [2].
11
Acute Decompensated Heart Failure
301
The 2011 DOSE trial investigated the question of optimal dosing in these patients
as well as examined whether or not it is more effective to administer these doses as
IV boluses or continuous infusions at a low dose [5]. The trial showed that “high”dose diuretics (dened as 2.5× the home dose administered as IV) was more effective than “low-dose” diuretics and found no difference between the routes of
administration (e.g., bolus dosing was no different than the continuous infusion
dosing) [5].
A few things are important to note about this trial:
1. The trial did not account for the bioavailability of PO:IV furosemide (which is
2:1). For example, if a patient was on 40mg PO QD at home, they would receive
100mg IV furosemide. This really does support the claim that we should be
aggressive and use “high-dose” diuretics.
2. The trial did not give an initial bolus prior to starting continuous infusion
diuretics. Keep in mind that in order to see diuresis in these patients, the concentration of the diuretic must be above that patient’s own “diuretic threshold.”
Because continuous infusion diuretics are given at such a low dose per time, it
would take a long time to reach that threshold without the help of an initial
bolus. If considering starting a continuous infusion, always keep in mind to
give an initial bolus up front to prevent this delay in effect. Additionally,
continuous infusion may be benecial in patients sensitive to quick uid
shifts, as it causes slow but prolonged diuresis and prevents things like
hypotension.
We have three loop diuretic agents: furosemide, torsemide, and bumetanide.
These agents all differ in potency so need to be converted if interchanging between
drugs. Tables 11.1 and 11.2 illustrate both oral and intravenous diuretic options;
Table11.3 illustrates equivalent diuretic doses.
Table 11.1 Commonly used oral diuretics [2]
Drug Starting dose Max daily dose Duration of action
Loop diuretics
Bumetanide 0.5–1.0mg QD or BID 10mg 4–6h
Furosemide 20–40mg QD or BID 600mg 6–8h
Torsemide 10–20mg QD 200mg 12–16h
Thiazide diuretics
Chlorothiazide 250–500mg QD or BID 1000mg 6–12h
Chlorthalidone 12.5–25mg QD 100mg 24–72h
Hydrochlorothiazide 25mg QD or BID 200mg 6–12h
Indapamide 2.5mg QD 5mg 36h
Metolazone 2.5mg QD 20mg 12–24h