Heart failure: Pathology review

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Heart failure: Pathology review

ETP Cardiovascular System

ETP Cardiovascular System

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
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
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
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial 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

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)