Heart failure’s used to describe a point
at which the heart can’t supply enough blood to meet the body’s demands. This can happen in two ways, either the heart’s
ventricles can’t pump blood hard enough during systole, called systolic heart failure,
or not enough blood fills the ventricles during diastole, called diastolic heart failure. In both cases, blood backs up into the lungs,
causing congestion or fluid buildup, which is why it’s also often known as congestive
heart failure, or just CHF. Congestive heart failure affects millions
of people around the world and since it means that the body’s needs are not being met,
it can ultimately lead to death. Part of the reason why so many people are
affected by heart failure, is that there are a wide variety of heart diseases like ischemia
and valvular disease that can impair the heart’s ability to pump out blood and—over time—can
ultimately cause the heart to fail. Alright, first up is systolic heart failure,
kind of a mathematical way to think this one is that the heart needs to squeeze out a certain
volume of blood each minute, called cardiac output, which can be rephrased as the heart
rate (or the number of beats in a minute) multiplied by the stroke volume (the volume
of blood squeezed out with each heart beat).

The heart rate is pretty intuitive, but the
stroke volume’s a little tricky. For example, in an adult the heart might beat
70 times per minute and the the left ventricle might squeeze out 70ml per beat, so 70 x 70
equals a cardiac output of 4900 ml per minute, which is almost 5 liters per minute. So notice that not all the blood was pumped
out right? And the stroke volume is a fraction of the
total volume. The total volume may be closer to 110 ml,
and 70ml is the fraction that got ejected out with each beat, the other 40ml kind of
lingers in the left ventricle until the next beat, right? In this example, the ejection fraction would
be 70ml divided by 110 ml or about 64%, a normal ejection fraction is around 50-70%,
between 40-50% would be borderline, and anything about 40% or less would indicate systolic
heart failure because the heart is only squeezing out a little blood each beat.

So in our example, if the total volume of
the left ventricle was 110 ml, but only 44 ml was pumped out with each beat (then you
have 44 ml divided by 110 ml which is 40%), and we would say that this person is in systolic
heart failure. Now in addition to systolic heart failure,
you’ve also got diastolic heart failure, which is where the heart’s squeezing hard
enough but not filling quite enough. In this case again the stroke volume is low,
but the ejection fraction’s normal…how’s that? Well it’s not filling enough so there’s
a low total volume, say about 69 mL, well even though both are low, 44 ml divided by
69 ml is still 64%. In this situation, the failure’s caused
by abnormal filling of the ventricle so that the chamber doesn’t get fully loaded or
stretched out in the first place.

Another term for this is having a reduced
“preload” which is the volume of blood that’s in the ventricle right before the
ventricular muscle contracts. An important relationship between systolic
and diastolic function is the Frank-Starling mechanism, which basically shows that loading
up the ventricle with blood during diastole and stretching out the cardiac muscle makes
it contract with more force, which increases stroke volume during systole. This is kinda like how stretching out a rubber
band makes it snap back even harder, except that cardiac muscle is actively contracting
whereas the rubber band is passively going back to its relaxed state. Heart failure can affect the right ventricle,
or the left ventricle, or both ventricles, so someone might have, right-sided heart failure,
left-sided heart failure, or both (which is called biventricular heart failure), each
of which can have systolic or diastolic failure. Having said that, if less blood exits either
ventricle it’ll affect the other since they work in series, so left-sided could cause
right-sided, and vice versa, so these terms really refer to the primary problem affecting
the heart, basically which one was first.

Usually left-sided heart failure is caused
by systolic (or pumping) dysfunction. This is typically due to some kind of damage
to the myocardium—or the heart muscle—which means it can’t contract as forcefully and
pump blood as efficiently. Ischemic heart disease caused by coronary
artery atherosclerosis, or plaque buildup, is the most common cause. In this case, less blood and oxygen gets through
the coronary artery to the heart tissue, which damages the myocardium. Sometimes, if the coronary’s blocked completely
and the person has a heart attack, they might be left with scar tissue that doesn’t contract
at all, which again means the heart can’t contract as forcefully. Longstanding hypertension is another common
cause of heart failure. This is because as arterial pressure increases
in the systemic circulation, it gets harder for the left ventricle to pump blood out into
that hypertensive systemic circulation.

To compensate, the left ventricle actually
bulks up, and its muscles hypertrophy, or grow so that the ventricle can contract with
more force. The increase in muscle mass also means that
there is a greater demand for oxygen, and, to make things even worse, the coronaries
get squeezed down by the this extra muscle so that even less blood’s delivered to the
tissue. More demand and reduced supply means that
some of the ventricular muscle starts have weaker contractions—leading to systolic
failure. Another potential cause would be dilated cardiomyopathy,
where the heart chamber dilates, or grows in size in an attempt to fill up the ventricle
with larger and larger volumes of blood, or preload, and stretch out the muscle walls
and increase contraction strength, via the Frank-Starling mechanism.

Even though this can work for a little while,
over time, the muscle walls get thinner and weaker, eventually leading to muscles that
are so thinned out that it causes systolic left-sided heart failure. Ultimately the ventricle walls need to be
the right size relative to the size of the chamber in order for the heart to work effectively. Any major deviation from that can lead to
heart failure. Even though systolic failure is most common
in left-sided heart failure, diastolic heart failure or filling dysfunction can also happen.

In hypertension, remember how the left ventricular
hypertrophied? Well that hypertrophy is concentric, which
means that the new sarcomeres are generated in parallel with existing ones. This means that as the heart muscle wall enlarges,
it crowds into the ventricular chamber space, resulting in less room for blood, meaning
that in addition to contributing to systolic dysfunction, hypertension also can cause diastolic
heart failure. Concentric hypertrophy leading to diastolic
failure can also be caused by aortic stenosis, which is a narrowing of the aortic valve opening,
as well by hypertrophic cardiomyopathy, an abnormal ventricular wall thickening often
from a genetic cause. Restrictive cardiomyopathies are yet another
cause. In this case the heart muscle gets stiffer
and less compliant, and therefore the left ventricle can’t easily stretch out and fill
with as much blood, which leads to diastolic heart failure. When the heart doesn’t pump out as much
blood, there’s decreased blood flow to the kidneys, which activates the renin-angiotensin-aldosterone
system, ultimately causing fluid retention.

Which fills the heart a bit more during diastole
and increases preload, which increases contraction strength again by the Frank Starling mechanism. Unfortunately, just like the other strategies,
in the long term, retaining fluid so that more fluid remains in the blood vessels typically
leads to a large portion of it leaking into the tissues and can contribute to fluid buildup
in the lungs and other parts of the body, which can worsen the symptoms of heart failure. Aright so a major, major clinical sign of
the heart not being able to pump enough blood forward to the body, is that blood starts
to back up into the lungs. A backup of blood in the pulmonary veins and
capillary beds can increase the pressure in the pulmonary artery and can also result in
fluid moving from the blood vessels to the interstitial space causing pulmonary edema,
or congestion. In the alveoli of the lungs, all this extra
fluid makes oxygen and carbon dioxide exchange a lot harder, since a wider layer of fluid
takes more time for oxygen and carbon dioxide to diffuse through, and therefore patients
have dyspnea—trouble breathing, as well as orthopnea – which is difficulty breathing
when lying down flat since that allows venous blood to more easily flow back from the legs
and the gut to the heart and eventually into the pulmonary circulation.

This extra fluid in the lungs causes crackles
or rales to be heard on auscultation while the patient breathes. If enough fluid fills some of these capillaries
in the lungs, they can rupture, leaking blood into the alveoli. Alveolar macrophages then eat up these red
blood cells, which causes them to take on this brownish color from iron build-up. And then they’re then called “hemosiderin-laden
macrophages”, also known as “heart failure cells”. For left-sided heart failure, certain medications
can be prescribed to help improve blood flow, like ACE inhibitors which help dilate blood
vessels, as well as diuretics to help reduce the overall fluid buildup in the body which
helps prevent hypertension from worsening the heart failure. Now let’s switch gears and think about right-sided
heart failure, which is actually often caused by left-sided heart failure.

K remember how fluid buildup increased pressure
in the pulmonary artery? Well this increased pulmonary blood pressure
makes it harder for the right side to pump blood into. In this case the heart failure would be biventricular,
since both ventricles are affected. Someone can also have isolated right-sided
heart failure, though, and an example of this would be a left-to-right cardiac shunt.

In these cases, there might be a cardiac shunt
like an atrial septal defect or a ventricular septal defect, that allows blood to flow from
the higher-pressure left side to the lower-pressure right side, which increases fluid volume on
the right side and can eventually lead to concentric hypertrophy of the right ventricle,
making it more prone to ischemia—which is a systolic dysfunction, and have a smaller
volume and become less compliant—which is a diastolic dysfunction. Another potential cause of isolated right-sided
failure is chronic lung disease. Lung diseases often make it harder to exchange
oxygen, right? Well in response to low oxygen levels, or
hypoxia, the pulmonary arterioles constrict, which raises the pulmonary blood pressure. This, just like before, makes it harder for
the right side of the heart to pump against and can lead to right-sided hypertrophy and
heart failure. When chronic lung disease leads to right-sided
hypertrophy and failure, it’s known as cor pulmonale.

With left-sided failure, blood gets backed
up into the lungs. With right-sided failure, blood gets backed
up to the body, and so patients have congestion in the veins of the systemic circulation. One common manifestation of this is jugular
venous distention, where the jugular vein that brings blood back to the heart takes
on more blood and becomes enlarged and distended in the neck. Also in the body, when blood backs up to the
liver and spleen, fluid can move into the interstitial spaces within those organs and
they can both become enlarged, called hepatosplenomegaly, which can be painful, and if the liver is
congested for long periods of time, patients can eventually develop cirrhosis and liver
failure, which would be called cardiac cirrhosis.

Excess interstitial fluid near the surface
of the liver and spleen can also move right out into the peritoneal space as well, and
since that cavity can take a lot of fluid before there is any increase in pressure,
a lot of fluid can build up in the peritoneal space which is called ascites. Finally, fluid that backs up into the interstitial
space in the soft tissues in the legs causes pitting edema, where the tissue is visibly
swollen and when you apply pressure to it it leaves a “pit” and takes awhile to
come back to its original place. This generally affects the legs in most people,
because gravity generally causes the majority of fluid to “pool” in the dependent parts
of the body, which is the legs when you’re standing and the sacrum, essentially the lower
back, when you’re lying down.

Right-sided heart failure will be treated
similarly to left-sided heart failure, especially because it’s often a result of left-sided
heart failure. Therefore, medications like ACE inhibitors
and diuretics may be prescribed. With heart failure, we saw that sometimes
the muscle wall can stretch and thin out, or sometimes it can sometimes thicken and
become ischemic. In either case, those heart cells get irritated,
in both scenarios the cells get irritated, and this can lead to heart arrhythmias. With an arrhythmia, the ventricles don’t
contract in sync anymore making them less able to pump out blood and worsening the whole

In some cases, patients might be treated with
cardiac resynchronization therapy pacemakers, which can stimulate the ventricles to contract
at the same time and potentially improve the blood pumped out. Alternatively, for heart failure in general,
some people might have ventricular assist devices implanted, or VADs, which literally
assist or help the heart pump blood may also be implanted. In end-stage situations where other forms
of treatment have failed, patients might have a heart transplant..



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