Dilated cardiomyopathy

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Dilated cardiomyopathy

CARDS

CARDS

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
Cardiac conduction system
Action potentials in pacemaker cells
Cardiac conduction velocity
ECG basics
ECG axis
ECG rate and rhythm
Anatomy of the heart
Cardiovascular system anatomy and physiology
Cardiac cycle
Pressure-volume loops
Normal heart sounds
Coronary circulation
Cardiac work
Action potentials in myocytes
Excitability and refractory periods
Cardiac excitation-contraction coupling
Baroreceptors
Renin-angiotensin-aldosterone system
Ventricular arrhythmias: Pathology review
Brugada syndrome
Atrial flutter
Premature atrial contraction
Atrial fibrillation
Wolff-Parkinson-White syndrome
Class II antiarrhythmics: Beta blockers
Atrioventricular nodal reentrant tachycardia (AVNRT)
Compliance of blood vessels
Resistance to blood flow
Laminar flow and Reynolds number
Blood pressure, blood flow, and resistance
Frank-Starling relationship
Pressure-volume loops
Stroke volume, ejection fraction, and cardiac output
Changes in pressure-volume loops
Cardiac contractility
Excitability and refractory periods
Atrioventricular block
Bundle branch block
Ventricular tachycardia
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Hypertension
Class I antiarrhythmics: Sodium channel blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Calcium channel blockers
Ischemia
Free radicals and cellular injury
Endocarditis
Myocarditis
Endocarditis: Pathology review
Infective endocarditis: Clinical
Clinician's Corner: Endocarditis
Dilated cardiomyopathy
Cardiomyopathies: Pathology review
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Cardiomyopathies: Clinical
Heart failure: Pathology review
Vasculitis
Vasculitis: Pathology review
Vasculitis: Clinical
Kawasaki disease
Positive inotropic medications
Heart failure: Clinical
Valvular heart disease: Clinical
Heart blocks: Pathology review
Mitral valve disease
Aortic valve disease
Congenital heart defects: Clinical
Cyanotic congenital heart defects: Pathology review
Acyanotic congenital heart defects: Pathology review
Atrial septal defect
Ventricular septal defect
Tetralogy of Fallot
DiGeorge syndrome
Patent ductus arteriosus
Turner syndrome
Cardiac tumors
Vascular tumors
Cardiac and vascular tumors: Pathology review
Angiosarcomas
Shock
Shock: Clinical
Shock: Pathology review
Advanced cardiac life support (ACLS): Clinical
Prerenal azotemia
Anaphylaxis
Lung volumes and capacities

Transcript

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Cardiomyopathy translates to “heart muscle disease,” so cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium, or heart muscle.

When cardiomyopathy develops as a way to compensate for some other underlying disease, such as hypertension or valve diseases, it’s called secondary cardiomyopathy. When it develops all by itself, it’s called primary cardiomyopathy.

Now, the most common type is dilated cardiomyopathy, which can cause all four chambers of the heart to dilate, or get bigger. Specifically, new sarcomeres, or muscle units, in the walls are added in series, and the chambers grow larger, which leaves the walls relatively thin compared to the large chamber size, with less muscle to use for contraction.

In other words, they have really weak contractions, which means less blood is pumped out each contraction. This also means that there’s a lower stroke volume, and if the heart’s failing to pump out as much blood to both the body from the left ventricle, and the lungs from the right ventricle, patients develop biventricular congestive heart failure. Since contraction happens during systole, we say this is a type of systolic heart failure.

Also, when the chambers get larger, they tend to stretch out the valves that separate the atria and ventricles. When they are stretched, the valves can’t close all the way, so they start to regurgitate blood back into the atria. This is called mitral valve regurgitation on the left side, and tricuspid valve regurgitation on the right. Mitral valve regurgitation might be heard on auscultation as a holosystolic murmur, meaning that it happens throughout systole.

Additionally, you might also hear an S3 heart sound on auscultation, which is the result of blood rushing and slamming into the dilated ventricular wall during diastole.

Another complication can be arrhythmias, because stretching out the muscle walls can irritate the cells in the conduction system, which are within those walls. Sometimes, an X-ray can be helpful for a diagnosing dilated cardiomyopathy.

As far as causes go, primary dilated cardiomyopathy is most often idiopathic, meaning there isn’t a clearly identifiable cause. Some cases, however, can be traced back to specific genetic mutations or genetic conditions, such as Duchenne Muscular Dystrophy and hemochromatosis. Also, in some cases it can be caused by an infection, like coxsackievirus B, which causes myocarditis — inflammation of the heart muscle — or Chagas disease, a protozoal infection.

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. "The Diagnosis and Evaluation of Dilated Cardiomyopathy" Journal of the American College of Cardiology (2016)
  5. "Idiopathic Dilated Cardiomyopathy" New England Journal of Medicine (1994)
  6. "Dilated cardiomyopathy" Nature Reviews Disease Primers (2019)