Heart failure: Pathology review

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Case Study0:00–0:50

On the cardiology ward, there were two people who had been admitted to the hospital repeatedly. The first one is 70 year old Lidia, who had a myocardial infarction about 3 years ago.
She presents with fatigue, and dyspnea. She says that she usually wakes up at night because of shortness of breath, but using more pillows when sleeping helps relieve it somewhat.
On examination, she has pitting edema in her legs and on auscultation, an S3 sound is heard. The other person is 81 year old Richard who has been a smoker for the past 50 years.
He is also experiencing fatigue, and has pitting edema, but on further examination, there’s also jugular venous distention and hepatomegaly.
Okay, so, both these individuals suffer from heart failure. Heart failure is a clinical syndrome used to describe the inability of the heart to pump enough blood or a point at which the heart can’t supply enough blood to meet the body’s demands.

Pathology0:50–1:31

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 into 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.
Alright, first up is systolic heart failure. One way to think about this is that the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which can be calculated as the heart rate multiplied by the stroke volume.

Systolic Heart Failure1:31–3:43

The heart rate is pretty intuitive, but the stroke volume is a little tricky. For example, an adult heart might beat 70 times per minute and 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.
Now, the stroke volume is only a fraction of the total volume. The total volume might 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.
In this example, the ejection fraction would be 70ml divided by 110 ml or about 64%, a normal ejection fraction is around 50-70%.
Now, in systolic heart failure, there’s decreased contractility of the left ventricle, which causes a decreased cardiac output because the stroke volume is low.
This means there’s also a decreased ejection fraction. During diastole blood returns to the ventricles and combines with the leftover blood that didn’t get pumped out during systole, and this is called the EDV or end diastolic pressure volume.
With systolic heart failure, don’t forget that EDV is high, because there’s more blood leftover after each heartbeat. Regarding the end diastolic pressure or EDP, which is the pressure that’s found in the ventricle at the end of diastole, this will also be high, because the volume at the end of diastole is high as well.
Systolic heart failure is mainly caused by low contractility which can happen with ischemia caused by myocardial infarction, where a part of the cardiac tissue is damaged so it won’t contract properly anymore.
Another cause is dilated cardiomyopathy, where the ventricle is dilated and weakened. Now in addition to systolic heart failure, you’ve also got diastolic heart failure, which is where the cardiac contractility is sufficient but not enough blood is returning to the ventricles.

Diastolic Heart Failure3:43–5:09

In this case, again, the stroke volume is low, but the ejection fraction is normal. So for example, the total volume might be lower than normal, say about 69 mL, and we pump out 44 mL, so if we divided 44 by 69, we get 64%, which is in the normal range.
With diastolic heart failure, we need to look at the end diastolic pressure, or the EDP, as well. The problem is that the left ventricle isn’t compliant enough, so when the ventricle is filling during diastole, the pressure within will rise, so keep in mind that EDP is elevated during diastolic heart failure.
Also remember that with diastolic heart failure, EDV is normal, at least in the beginning, because the atria are capable of squeezing more blood into the ventricle.
One cause of diastolic heart failure is ventricular hypertrophy, where the ventricular myocardium gets thicker, and this decreases the ability of the chamber to stretch when filling.
Alright, so heart failure can be systolic or diastolic and can affect the right ventricle, or the left ventricle, or both ventricles, which is called biventricular heart failure.

Left Heart Failure5:09–9:37

Having said that, if less blood exits either ventricle it’ll affect the other since they work in series. So these terms really refer to the primary problem affecting the heart, basically which one was first.
For your exams, it’s important to remember that the main cause of right heart failure is left heart failure. When right heart failure isn’t caused by left heart failure, but by a pulmonary cause, we refer to this as cor pulmonale.
In terms of symptoms, in left heart failure the blood starts to back up into the lungs, specifically in the pulmonary veins and capillary beds which can increase the pressure in these vessels.
This leads to fluid moving from the blood vessels to the interstitial space causing pulmonary edema, or congestion. This is a very important sign and must be remembered!
In the alveoli of the lungs, all the extra fluid makes oxygen and carbon dioxide exchange a lot harder, and therefore patients have dyspnea or trouble breathing.
Another symptom is orthopnea, which is difficulty breathing when lying down flat. This is because there’s more venous return from the legs and the gut to the heart, which increases the amount of blood backing up into the pulmonary circulation.
This also explains why these people experience paroxysmal nocturnal dyspnea, which is when the sensation of not being able to breathe wakes a person at night.
Such individuals often sleep using more pillows in order to keep their upper body a bit elevated. This will lower the venous return and ease lung congestion.
The extra fluid in the lungs causes crackles or rales on auscultation. If enough fluid fills the capillaries in the lungs, they can rupture, causing blood to leak 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 called “hemosiderin-laden macrophages”, also known as “heart failure cells”. Next, since there’s decreased cardiac output, not enough blood is reaching vital organs.
As a result, an individual with heart failure may also present with fatigue. Decreased blood flow to the kidneys activates the renin-angiotensin-aldosterone system, which will increase sodium and water reabsorption in the kidneys, ultimately causing fluid retention.
You’d think this is good, because it increases blood volume which increases end diastolic volume and based on the frank starling mechanism, it will increase contractility.
Unfortunately, in the long term large portions of this extra fluid will end up leaking into the tissues, which worsens the pulmonary edema and it will also lead to peripheral edema.
This is sometimes called “pitting edema” because the tissue is visibly swollen and when you apply pressure to it - it leaves a “pit.” Apart from this, the low cardiac output will also activate the sympathetic nervous system, which increases left ventricle contractility, but also activates the renin-angiotensin-aldosterone system.
Finally, an important thing to remember is that with left heart failure, on auscultation, you can hear an extra sound, either S3, or, less commonly, S4.
S3 is a low-pitched sound that comes right after S2. This occurs when there’s a lot of blood filling of the ventricle rapidly.
Normally, you wouldn't hear this, but in systolic heart failure, the ventricle is overly compliant, allowing more blood to gush into the chamber, so S3 is also called ventricular gallop.
S4, on the other hand, comes right before S1. Once again, this is normally not heard, but in diastolic heart failure, when the ventricles are extra stiff, the atria have to contract extra hard to push that blood in, when this blood is forcefully pushed into the ventricle and hits the chamber wall, it produces a S4, or atrial gallop.

Right Heart Failure9:37–11:31

Now let’s switch gears and talk about right-sided heart failure, and remember, the most common cause is left heart failure.
Since left heart failure increases the pressure in the pulmonary artery, this will make it harder for the right ventricle to pump blood into it.
Other causes of right-sided heart failure include chronic lung disease. Lung diseases, such as emphysema or pulmonary embolism, make oxygen exchange harder.
In response to low oxygen levels, or hypoxia, the pulmonary arterioles constrict, and the pulmonary blood pressure rises.
This makes it harder for the right side of the heart to pump against and can lead to right-sided hypertrophy and heart failure.
In right-sided heart failure, blood gets backed up to the body, and so individuals will have congestion in the veins of the systemic circulation.
One common manifestation of this is jugular venous distention, where the jugular vein that’s relatively close to the heart becomes enlarged and distended.
Also in the body, when blood backs up to the liver, it causes venous congestion there and eventually, fluid can move into its interstitial spaces, causing the liver to become enlarged, which is called hepatomegaly.
There’s a special name for this particular type of hepatopathy, called congestive hepatopathy. On pathology, there’s a so called “nutmeg liver”, because you can see the congested hepatic venules and veins as dark spots and it actually looks like a grated nutmeg!
If the liver is congested for long periods of time, patients can eventually develop cirrhosis and liver failure, which is called cardiac cirrhosis.
Finally, fluid that backs up into the interstitial space in the soft tissues of the legs causes pitting edema. In terms of treatment, a high-yield topic for your exams is the list of medications that decrease mortality and slow down the progression of heart failure.

Treatment11:31–12:54

This includes Angiotensin-converting enzyme or ACE inhibitors, Angiotensin Receptor Blockers or ARBs, aldosterone receptor antagonists, like spironolactone, and certain beta blockers, specifically carvedilol, bisoprolol and metoprolol.
Bear in mind though that beta blockers must be used with caution in decompensated heart failure, which is when heart failure rapidly worsens.
That’s because of their ability to decrease heart rate and their negative inotropic effect, meaning that they decrease the force of heart’s contraction.
Also, a new type of mortality decreasing medication are the neprilysin inhibitors. These work by inhibiting neprilysin, an enzyme that breaks down the helpful endogenous peptides that normally promote urine sodium excretion and vasodilation.
In contrast, thiazide or loop diuretics may be used to relieve symptoms by reducing the overall fluid buildup in the body.
And then, hydralazine combined with nitrates, as vasodilators, has been shown to improve both symptoms and mortality in select patients.
Okay, let’s review! Heart failure is a clinical syndrome where the heart is unable to pump enough blood or a point at which the heart can’t supply enough blood to meet the body’s demands.

Review12:54–14:22

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 into the ventricles during diastole, called diastolic heart failure.
Heart failure can affect the right ventricle, or the left ventricle, or both ventricles. 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.
Actually, the main cause of right heart failure is left heart failure. When right heart failure isn’t caused by left heart failure, but by a pulmonary cause, we refer to this as cor pulmonale.
Now, since both ventricles are affected, let’s remember that symptoms of heart failure include dyspnea, orthopnea, fatigue due to low perfusion, rales, jugular venous distention, pitting edema, and an S3 or rarely an S4 heart sound on auscultation.
Treatment includes medications that decrease mortality and ones that are used for symptom relief. Now, back to our cases!

Summary14:22–15:25

Lidia came in with a history of myocardial infarction. She’s experiencing fatigue, shortness of breath.
Examination shows pitting edema and an S3 sound. An echocardiogram showed that her ejection fraction was pretty low, which indicates systolic heart failure.
Her other symptoms point towards a left heart failure and the key symptoms were dyspnea, paroxysmal nocturnal dyspnea and orthopnea.
Next is 81 year old Richard, who presents with fatigue, pitting edema, jugular venous distention and hepatomegaly. His echocardiogram showed that his ejection fraction is normal, but there’s hypertrophy in his right ventricle.
This and his symptoms like jugular venous distention and hepatomegaly point towards right-heart failure with a pulmonary cause.
Now, since Richard has been a smoker for the past 50 years, pulmonary emphysema could be the cause of his right-sided heart failure, so the next steps involve doing a chest X-ray and spirometry.