Heart failure

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Heart failure

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 76-year-old woman presents to the emergency department for evaluation of increased lower extremity swelling and shortness of breath. The patient has had progressive lower extremity swelling over the past several weeks to the point where she can no longer fit into her normal shoe size. In addition, she can no longer walk half a city block before becoming short of breath. Past medical history includes hypertension, diabetes, and a deep vein thrombosis after a long flight ten years ago. The patient has been smoking one pack of cigarettes per day for thirty-five years. Temperature is 36.1°C (97.0°F), pulse is 78/min, respirations are 16/min, blood pressure is 156/92 mmHg, and O2 is 90% on room air. Physical examination demonstrates a loud P2, jugular venous distension, faint bilateral end-expiratory wheezing, and 2+ pitting edema in the bilateral lower extremities. A chest X-ray is obtained and shown below. Which of the following best describes the pathophysiology of this patient’s lower extremity findings?  


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ACE inhibitors p. 628

heart failure p. 316

Angiotensin II receptor blockers p. 628

heart failure p. 316

β -blockers p. 245

heart failure p. 316

Cardiomyopathy p. 315

heart failure with p. 316

Diastole

heart failure and p. 316

Diuretics

heart failure p. 316

Dyspnea

heart failure p. 316

Edema

heart failure and p. 316

Fatigue

heart failure and p. 316

Heart failure p. 316

ACE inhibitors for p. 628

acromegaly p. 341

acute tubular necrosis with p. 620

amiodarone p. 327

angiotensin II receptor blockers p. 628

aortic regurgitation as precursor p. 296

associations p. 733

atrial septal defect p. 303

β -blockers for p. 245, 327

B-type natriuretic peptide in p. 299

calcium channel blockers p. 361

carcinoid syndrome p. 586

cardiac glycosides for p. NaN

chronic ischemic heart disease p. 308

contractility in p. 290

diabetic ketoacidosis p. 355

disopyramide p. 326

dobutamine for p. 241

dopamine for p. 241

Ebstein anomaly p. 302

ejection fraction in p. 290

ESR in p. 210

fludrocortisone and p. 360

hydralazine for p. 320

hypertension p. 304

hypertension treatment in p. 320

hypertensive emergency and p. 304

jugular venous pulse in p. 293

loop diuretics for p. 624

MI p. 309

Paget disease of bone p. 468

pleural effusion p. 699

potassium-sparing diuretics p. 627

pulmonary hypertension p. 697

pulse pressure in p. 290

readmissions with p. 276

renal failure causing p. 620

shock caused by p. 320

in sleep apnea p. 697

systolic vs diastolic p. 290

thiazides for p. 627

ventricular septal defect p. 303

Hydralazine p. 323

heart failure p. 316

Hypertension p. 304

heart failure p. 320

Loop diuretics p. 624

for heart failure p. 316

Myocardial infarction (MI) p. 308

heart failure caused by p. 316

Peripheral edema

heart failure p. 316

Pulmonary edema

heart failure p. 316

Spironolactone p. 627, 663, 673, 676

for heart failure p. 316

Thiazide diuretics

heart failure p. 316

Transcript

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Content Reviewers

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 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.

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 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, 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 considered 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.

Alright, so 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.

And, 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 to 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 actually 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.

Alright, 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.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "The Impact of Frailty and Comorbidities on Heart Failure Outcomes" Cardiac Failure Review (2022)
  6. "Effects of Digoxin in Heart Failure (HF) With Reduced Ejection Fraction (EF)" Cureus (2022)
  7. "Advanced heart failure: guideline‐directed medical therapy, diuretics, inotropes, and palliative care" ESC Heart Failure (2022)