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Cardiovascular > Cardiomyopathy > Flashcards

Cardiomyopathy Flashcards

1
Q

What is cardiomyopathy?

A

Cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium.

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2
Q

What is hypertrophic cardiomyopathy?

A

Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterised by left ventricular hypertrophy (LVH).

primary form of cardiomyopathy i.e. not in response to other underlying disease e.g. hypertension or valvular disease

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3
Q

Epidemiology of HCM

A
  • Second most common cardiomyopathy (after dilated)
  • 0.2% prevalence
  • May present at any age
  • Most common cause of sudden cardiac death in the young
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4
Q

What is the aetiology of HCM

A
  • Autosomal dominant trait: genetic missense mutation in one of the genes that encode proteins in the sarcomere of heart muscle.
  • Beta-myosin heavy chain mutation is the most common
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5
Q

RFs for HCM

A
  • Family history
  • Friedreich’s Ataxia (autosomal recessive neurodegenerative disease): patients with Friedreich’s ataxia often develop hypertrophic cardiomyopathy
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6
Q

What happens to the heart in HCM

A
  • Walls get thick, heavy and hypercontractile
  • muscles grow larger as new sarcomeres are added in parallel to existing ones.
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7
Q

Which ventricle is most affected in HCM

A

LV

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8
Q

What happens to the interventricular septum in HCM?

A

interventricular septum grows larger relative to the other ventricular wall

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9
Q

Consequences of HCM

A
  • Walls take up more room so the cavity is smaller and less able to fill with blood.
  • Walls are more stiff and less compliant so can’t stretch to fill with more blood.
  • This means less blood is pumped out of the heart - stroke volume is reduced. This can lead to heart failure.
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10
Q

What happens due to the muscle growth of the interventricular septum in HCM

A
  • gets in the way of the left ventricular outflow tract during systole.
  • This increases blood velocity through this smaller opening, and pulls the anterior leaflet of the mitral valve toward the septum.
  • This further obstructs the left ventricular outflow tract.
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11
Q

As blood is forced through a tiny opening in HCM what happens

A

crescendo-decrescendo murmur (louder as blood first rushes out, and then softer as less blood moves out).

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12
Q

Why might a patient have a bifid pulse in HCM

A

two pulses are felt because the mitral valve is moving toward the outflow tract and causing increased obstruction mid-systole.

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13
Q

Issue with thick powerful heart

A
  • Leads to disarray of cardiac myocytes.
  • This affects conduction and can lead to arrhythmias.
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14
Q

Overall pathophysiology of HCM

A

Heart thicker > Becomes hypercontractile > New sarcomeres > LV most affected > Increase O2 demand > Ischaemic tissue > Fast arrythmia

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15
Q

What happens as the interventricular septum gets larger relative to the wall?

A

Takes up more space > Less blood in Ventricles + Less compliance so less filling > Lower SV > Lower CO > Diastolic HF

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16
Q

Signs of HCM

A
  • Ejection systolic murmum
  • Bifid pulse
  • S4 sound
  • Fast arrhythmias
  • Hypertrophy on imaging
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17
Q

Symptoms of HCM

A

Dyspnoea
Syncope
Chest pain
Dizziness

18
Q

ECG signs for HCM

A

left ventricular hypertrophy with progressive T wave inversion and deep Q waves; may also be AF, WPW syndrome, ventricular ectopics, VT

Also do Echocardiogram investigation

19
Q

Treatment for HCM

A
  • BBs + CCBs
  • Anti-arrhythmic medication e.g. amiodarone
  • Consider defibrillator if at high risk of arrhythmias
  • Anticoagulation: if AF is present as there is higher risk of thrombus formation
20
Q

Why is digoxin contraindicated in HCM?

A

Digoxin is contraindicated because it tends to increase force of contraction, which can increase the obstruction.

21
Q

Complications of HCM

A
  • Left ventricular outflow obstruction
  • Heart failure
  • Arrhythmias: as there is disarray of cardiac myocytes as well as due to the heart becoming ischaemic
  • Sudden death: due to fast arrhythmias
22
Q

What is dilated cardiomyopathy? (DCM)

A

all 4 chambers of the heart dilate (but don’t get thicker).

23
Q

Epidemiology of DCM

A
  • Most common type of cardiomyopathy
  • Prevalence: 0.2%
24
Q

Causes of DCM

A
  • Idopathic
  • Autosomal Dominant
  • Alcohol
  • Infections
  • Drugs
  • Genetics
25
Q

RFs for DCM

A
  • Family history
  • Certain conditions e.g. haemochromatosis
  • Alcohol abuse
  • Drug abuse
  • Chemotherapy
  • Certain infections
  • Thyroid disorders
  • Increased BP
26
Q

What causes DCM?

A
  • Caused by cytoskeletal gene mutations which result in new sarcomeres being added in series to enlarge the chambers.
  • However, the walls are relatively thin compared to the large chamber size.
27
Q

Pathophysiology of DCM

A

Increased sarcomeres > However thinner walls so less muscle for contraction > Leads to weak contractions and less blood being pumped out with each contractions > Decreased CO + SV > Leads to Biventricular congestive HF

28
Q

What happens when chambers get larger?

A

Stretch out AV valves

29
Q

What happens as valves become stretched?

A

Cant close all the way > Cause regurgitation > Hollow systolic murmur > S3 sound on auscultation

30
Q

Signs of DCM

A
  • Larger heart on imaging
  • Systolic murmur
  • S3 gallop
  • Increased pulse
  • Decreased BP
  • Arrhythmias
31
Q

Symptoms of DCM

A
  • Fatigue
  • Dyspnoea
32
Q

Investigations for DCM

A
  • Bloods: BNP elevated; low Na+ implies poor prognosis
  • CXR: cardiac enlargement; pulmonary oedema
  • ECG: tachycardia, non-specific T wave changes and poor R-wave progression; may be AF or VT
  • ECHO: shows dilated heart and low ejection fraction
33
Q

Management of DCM

A
  • Bed rest
  • Diuretics: to deal with oedema
  • Beta blockers: to control heart rate
  • ACE inhibitors: dilate vessels to improve blood flow
  • Anticoagulation: due to increased risk of thrombus
    Left ventricular assist device (LVAD): mechanical pump that assists the heart in distributing blood
34
Q

Complications of DCM

A
  • Heart failure
  • Mitral and tricuspid valve regurgitation
  • Arrhythmias
  • Risk of thromboembolism
  • Sudden death
35
Q

What is restrictive cardiomyopathy?

A

Restrictive cardiomyopathy describes when the heart muscle becomes stiffer and less compliant.

36
Q

Causes of RCM

A
  • Amyloidosis: amyloid deposition in the heart making it less compliant
  • Sarcoidosis: formation of granulomas in the heart tissue
  • Endocardial fibroelastosis
  • Loffler syndrome
  • Haemochromatosis
  • Scleroderma
37
Q

What happens in RCM

A

heart muscle is restricted, meaning that it becomes stiffer and less compliant. However, the muscles and size of the ventricles stay roughly the same size, or only get slightly enlarged.

38
Q

Pathophysiology of RCM

A
  • Normally, when blood fills the ventricles they stretch out and allow more blood to fill in.
  • When blood fills restricted ventricles, however, they can’t expand as much. This means the ventricles fill with less blood and therefore pump out less blood. This eventually leads to heart failure.
  • Ventricles dont stretch > Less filling (Diastolic HF) > Less blood pumped out > HF
39
Q

Signs of RCM

A
  • 3rd and 4th heart sounds
  • Signs of heart failure
    • Increased JVP
    • Elevation of venous pressure with inspiration
    • Oedema
    • Hepatomegaly
40
Q

Symptoms of RCM

A
  • Dyspnoea
  • Fatigue
  • Embolic symptoms
41
Q

Investigations for RCM

A
  • ECG: low amplitude QRS
  • ECHO
  • CXR
  • MRI
  • Cardiac catheterisation
42
Q

Management of RCM

A
  • Treat underlying cause e.g. removing excess iron in case of haemochromatosis
  • Heart transplant

Cardiovascular (14 decks)

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