Heart failure: Pathology review

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Heart failure: Pathology review

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Introduction to the cardiovascular system
Introduction to the lymphatic system
Cardiovascular system anatomy and physiology
Coronary circulation
Lymphatic system anatomy and physiology
Abnormal heart sounds
Normal heart sounds
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Cardiac cycle
Cardiac work
Changes in pressure-volume loops
Pressure-volume loops
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac afterload
Cardiac contractility
Cardiac preload
Frank-Starling relationship
Law of Laplace
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Cardiac conduction velocity
Cardiac conduction system
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Control of blood flow circulation
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Compliance of blood vessels
Laminar flow and Reynolds number
Pressures in the cardiovascular system
Resistance to blood flow
Action potentials in myocytes
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Excitability and refractory periods
Adrenergic antagonists: Beta blockers
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
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Lipid-lowering medications: Fibrates
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Positive inotropic medications
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Endocarditis
Myocarditis
Rheumatic heart disease
Cardiac tumors
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Ventricular septal defect
Hypoplastic left heart syndrome
Tetralogy of Fallot
Total anomalous pulmonary venous return
Transposition of the great vessels
Persistent truncus arteriosus
Cor pulmonale
Heart failure
Cardiac tamponade
Dressler syndrome
Pericarditis and pericardial effusion
Shock
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
Unstable angina
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Arteriole, venule and capillary histology
Artery and vein histology
Cardiac muscle histology
Development of the cardiovascular system
Fetal circulation
Anatomy of the coronary circulation
Anatomy of the heart
Anatomy of the inferior mediastinum
Anatomy of the superior mediastinum
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Mediastinum
Introduction to pharmacology
Chest X-ray interpretation: Clinical sciences
Electrolyte disturbances: Pathology review
Anatomy clinical correlates: Breast
Anticoagulants: Heparin
Thrombolytics
Congestive heart failure: Clinical sciences
Approach to ascites: Clinical sciences
Approach to dyspnea: Clinical sciences
Approach to lower limb edema: Clinical sciences
Coronary artery disease: Clinical sciences
Chronic obstructive pulmonary disease: Clinical sciences
Tobacco use: Clinical sciences
Approach to chest pain: Clinical sciences
Approach to hypertension: Clinical sciences
Acute coronary syndrome: Clinical sciences
Carotid artery stenosis screening: Clinical sciences
Diabetes mellitus (Type 1): Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Dyslipidemia: Clinical sciences
Essential hypertension: Clinical sciences
Peripheral arterial disease and ulcers: Clinical sciences
Abdominal aortic aneurysm: Clinical sciences
Aortic dissection: Clinical sciences
Approach to bradycardia: Clinical sciences
Approach to postoperative hypotension: Clinical sciences
Approach to tachycardia: Clinical sciences
Atrioventricular block: Clinical sciences
Cardiac tamponade: Clinical sciences
Central line-associated bloodstream infection: Clinical sciences
Hypovolemic shock: Clinical sciences
Infectious endocarditis: Clinical sciences
Pericarditis: Clinical sciences
Ventricular tachycardia: Clinical sciences

Transcript

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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.

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.

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.

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.

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.

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. "Heart failure" Lancet (2005)
  4. "Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association" Circulation (2018)
  5. "2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines" J Am Coll Cardiol (2013)