Heart failure

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Heart failure

ETP CVS

ETP CVS

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Hypertension
Hypertensive emergency
Conn syndrome
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
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Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Hypoplastic left heart syndrome
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Tetralogy of Fallot
Ventricular septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Pulmonary hypertension
Aortic aneurysms and dissections: Clinical
Raynaud phenomenon
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

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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)