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Cardio All My Notes > Cardiomyopathy > Flashcards

Cardiomyopathy Flashcards

1
Q

What are some causes of dilated cardiomyopathy?

A

Answer: , including
alcohol abuse, beriberi (wet), Coxsackie B myocarditis,
chronic cocaine use, Chagas’ disease, doxorubicin toxicity, peripartum cardiomyopathy,
**Takotsubo cardiomyopathy, **
tachycardic cardiomyopathy, and arrhythmia.

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2
Q

What is the mnemonic for remembering the causes of dilated cardiomyopathy?

A

Answer: A Bunch of stuff Can Cause Cardiac Dilation
oAlcohol abuse
oBeriberi (wet)
oCoxsackie B myocarditis
oChronic cocaine use
oChagas’ disease
oDoxorubicin toxicity

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3
Q

What are the three other causes of dilated cardiomyopathy?

A

Answer: The three other causes are
peripartum cardiomyopathy,
Takotsubo cardiomyopathy, and
tachycardic cardiomyopathy.

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4
Q

What is the most common cause of dilated cardiomyopathy?

A

Answer: idiopathic (unknown origin).

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5
Q

What are the causes of hypertrophic cardiomyopathy?

A

Answer: is usually caused by genetic mutations in
* HCM (heavy chain myosin),
* Frederick ataxia, and
* familial inheritance.

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6
Q

What is the characteristic feature of hypertrophic cardiomyopathy?

A

Answer: is asymmetric hypertrophy of the interventricular septum.

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7
Q

What are the causes of restrictive cardiomyopathy?

A

Answer: Girl PLEASH
* by post-radiation therapy,
* Loeffler’s syndrome (eosinophilic infiltration),
* endocardial fibroelastosis (in patients < 2 years old with congenital heart diseases),
* amyloidosis,
* sarcoidosis, and
* hemochromatosis.

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8
Q

What is the most common cause of restrictive cardiomyopathy?

A

Answer: The most common cause is idiopathic (unknown origin).

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9
Q

Can sarcoidosis and hemochromatosis cause both restrictive and dilated cardiomyopathy?

A

Answer: Yes, sarcoidosis and hemochromatosis can cause both restrictive and dilated cardiomyopathy.

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10
Q

What are the pathologic mechanisms in dilated cardiomyopathy?

A

Answer: In dilated cardiomyopathy, ventricular dilation occurs,
-> leading to thinner ventricular walls.
-> Sarcomeres are added in a linear fashion or in a series (eccentric hypertrophy).
-> This results in bigger ventricular chambers with a thinner wall.

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11
Q

What is eccentric hypertrophy?

A

Answer:

  • is the increase in the size of muscles in a lengthening fashion.
  • In dilated cardiomyopathy, it leads to the enlargement of ventricular chambers in diameter.
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12
Q

What are the pathologic mechanisms in hypertrophic cardiomyopathy?

A

Answer: I

  • , the interventricular septum is thicker than normal,
  • resulting in a smaller ventricular diameter.
  • Sarcomeres are added in a parallel fashion or on top of one another,
  • leading to an increase in the size of muscle cells in a concentric fashion.
  • However, this tends to favor the interventricular septum.
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13
Q

What is concentric hypertrophy?

A

Answer:
* is the increase in the size of muscles in a thickening fashion.
* Sarcomeres in “parallel”

  • In hypertrophic cardiomyopathy, it causes the thickening of the interventricular septum.
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14
Q

What are the pathologic mechanisms in restrictive cardiomyopathy?

A

Answer:

  • In restrictive cardiomyopathy, normal interstitial spaces in healthy cardiac tissues are replaced with fibrosis and infiltrative substances.
  • This destruction and infiltration of cardiac tissues lead to non-compliant (stiff) cardiac tissues, resulting in restrictive filling of the ventricles.
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15
Q

What are the clinical features and complications of dilated cardiomyopathy?

A

Answer:
1. ventricular dilation with thinning of the walls leads to poor contractility,resulting in systolic heart failure or systolic dysfunction.
2. Patients may exhibit signs and symptoms of left heart failure, including paroxysmal nocturnal dyspnea, orthopnea, and dyspnea at rest or with exertion.
3. They may also present with signs of right heart failure, such as jugular venous distension, ascites, hepatomegaly, and pedal edema.

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16
Q

What are the pathophysiological mechanisms that contribute to decreased contractility in dilated cardiomyopathy?

A

Answer:
1. Decreased contractility in dilated cardiomyopathy is secondary to ventricular dilation, which stretches sarcomeres beyond their optimal length and reduces contractility.
2. Additionally, thinning of the ventricular walls also contributes to decreased contractility.

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17
Q

What is the Frank-Starling law and its relevance to dilated cardiomyopathy?

A

Answer:
1. The Frank-Starling law states that stroke volume increases as ventricular volume increases due to myocyte stretch, resulting in a more forceful systolic contraction.
2. In dilated cardiomyopathy, the dilated ventricles do not obey the Frank-Starling law, leading to decreased contractility.

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18
Q

What are the clinical features and complications of hypertrophic cardiomyopathy?

A

Answer: by
* asymmetric thickening of the interventricular septum, leading to diastolic dysfunction.

  • This can cause a decrease in cardiac output, which may result in symptoms such as angina (chest pain), dyspnea on exertion, and syncope.
  • In severe cases, decreased coronary artery perfusion can lead to sudden death through the acute onset of ventricular tachycardia or ventricular fibrillation.
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19
Q

What is the Venturi effect in hypertrophic cardiomyopathy?

A

Answer:
* In hypertrophic cardiomyopathy, the contracting interventricular septum creates a Venturi effect,

  • causing a decrease in pressure when blood flows through a stenosis at high velocity.
  • This can lead to decreased cardiac output and compromised coronary artery perfusion.
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20
Q

What are the symptoms and complications associated with restrictive cardiomyopathy?
.

A

Answer:
1. Rigid ventricles that cannot stretch, leading to diastolic dysfunction. Symptoms predominantly manifest as right heart failure,
2. including jugular venous distension, hepatomegaly, pedal edema, and ascites.
3. Left heart failure may also occur, leading to pulmonary edema

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21
Q

What are the characteristic heart sounds associated with dilated cardiomyopathy?

A

Answer:

  • Dilated cardiomyopathy is associated with the presence of an S3 heart sound, which occurs early in systole.
  • Additionally, mitral and tricuspid regurgitation can be heard as a holosystolic murmur due to the dilation of all chambers.
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22
Q

What are the heart sounds typically heard in hypertrophic cardiomyopathy?

A

Answer:

  • the presence of an S4 heart sound, which is caused by the rigid ventricles and low distensibility.
  • Additionally, a crescendo-decrescendo systolic ejection murmur can be heard at the left lateral sternal border. But not at the carotid
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23
Q

How does the presence of interventricular septum contraction affect the heart sounds in hypertrophic cardiomyopathy?

A

Answer:

  • When the interventricular septum contracts and bows inward in hypertrophic cardiomyopathy, it narrows the left ventricular outflow tract (LVOT), leading to the development of mitral valve regurgitation.
  • This contributes to the characteristic heart sounds associated with the condition.
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24
Q

What maneuvers can affect the intensity of the murmurs in hypertrophic cardiomyopathy?

A

Answer: The intensity of murmurs in hypertrophic cardiomyopathy can be affected by certain maneuvers.
For example,
* the Valsalva maneuver, standing, and leg lifts can decrease preload and intensity,
* while squatting and hand grips can** increase preload and intensity.**

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25
Q

What are the heart sounds and signs associated with restrictive cardiomyopathy?

A

Answer: In restrictive cardiomyopathy, the
* presence of S3 and S4 heart sounds can be observed.
* Additionally, mitral and tricuspid regurgitation occur due to the dilation of the atria, leading to stretching and pulling of the valve leaflets.
*
* Kussmaul’s sign, characterized by jugular venous distention that worsens or remains the same during deep inspiration, is also prominent in restrictive cardiomyopathy.

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26
Q

What is the gold standard diagnostic tool for cardiomyopathies?

A

Answer: Echocardiogram

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27
Q

What are the characteristic findings of dilated cardiomyopathy on an echocardiogram?

A

Answer:
* decrease in wall thickness,
* an increase in ventricular cavity diameter, and reduced contractility leading to decreased stroke volume and ejection fraction.
* Mitral and tricuspid regurgitation can also be observed using Doppler to assess blood flow.

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28
Q

How does hypertrophic cardiomyopathy appear on an echocardiogram?

A

Answer:

  • increased wall thickness of the interventricular septum and asymmetric thickening of the ventricular myocardium.
  • Ventricular cavity diameter may be reduced, and there is an increase in contractility.
  • Mitral regurgitation can occur due to systolic anterior motion (SAM) of the mitral valve.
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29
Q

What are the echocardiographic findings in restrictive cardiomyopathy?

A

Answer:

  • There may be varied wall thickness, with some cases showing symmetric wall thickening.
  • The ventricular diameter may be normal or reduced due to increased thickness.
  • Ejection fraction is typically normal, but
  • ventricular compliance is decreased.
  • Mitral and tricuspid regurgitation can occur due to bilateral arterial enlargement
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30
Q

How do chest X-rays (CXR) help in diagnosing cardiomyopathies?

A

Answer
* In dilated cardiomyopathy, cardiomegaly (enlarged heart) and pulmonary edema due to left-sided heart failure can be observed.
* In hypertrophic and restrictive cardiomyopathies, the chest X-ray findings are usually normal.

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31
Q

What ECG findings are commonly seen in all types of cardiomyopathies?

A

Answer:
Atrial fibrillation, characterized by an increased size or thickness of the atrium, is a common finding in all types of cardiomyopathies.
This is due to the stretch and remodeling of the atria.
Additionally, all types of cardiomyopathies carry an increased risk of ventricular tachycardia and ventricular fibrillation.

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32
Q

What is the characteristic sound associated with constrictive pericarditis?

A

The characteristic sound associated with constrictive pericarditis is a “pericardial knock.”

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33
Q

Q2. What are the heart sounds typically heard in restrictive cardiomyopathy?

A

A2. The heart sounds typically heard in restrictive cardiomyopathy are mitral valve (MV) and tricuspid valve (TV) regurgitation.

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34
Q

Q3. What is the cause of low voltage QRS complex in both constrictive pericarditis and restrictive cardiomyopathy?

A

A3. The cause of low voltage QRS complex in both constrictive pericarditis and restrictive cardiomyopathy is deposition in the AV node and bundle branches.

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35
Q

Q4. Why does a ventricular septal bounce occur during diastole in constrictive pericarditis?

A

A4. A ventricular septal bounce occurs during diastole in constrictive pericarditis because when blood comes to a rigid pericardium, the ventricles cannot distend and are pushed contralaterally.

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36
Q

Q5. What is a common echocardiographic finding observed in both constrictive pericarditis and restrictive cardiomyopathy?

A

A5. A common echocardiographic finding observed in both constrictive pericarditis and restrictive cardiomyopathy is bi-atrial enlargement.

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37
Q

Q6. What is the difference in pericardial thickness between constrictive pericarditis and restrictive cardiomyopathy?

A

A6. Constrictive pericarditis is characterized by a thickened pericardium, while restrictive cardiomyopathy has a normal pericardium without any problems.

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38
Q

Q7. How does cardiac catheterization help differentiate between constrictive pericarditis and restrictive cardiomyopathy?

A

A7. Cardiac catheterization helps differentiate between constrictive pericarditis and restrictive cardiomyopathy by comparing ventricular pressures.
In constrictive pericarditis, the left ventricular end-diastolic pressure (LVEDP) is usually greater than the right ventricular end-diastolic pressure (RVEDP).

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39
Q

Q8. What is the relationship between end-diastolic pressures on both ventricles in constrictive pericarditis?

A

A8. Equal end-diastolic pressures on both ventricles are observed in constrictive pericarditis.

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40
Q

Q9. How does the compliance of the ventricles differ between constrictive pericarditis and restrictive cardiomyopathy?

A

A9. The compliance of the ventricles is reduced in constrictive pericarditis due to the rigid and non-distensible pericardium, while in restrictive cardiomyopathy, the ventricles have slightly reduced compliance but can still distend.

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41
Q

Q10. What is the primary difference in the involvement of the pericardium between constrictive pericarditis and restrictive cardiomyopathy?

A

A10.

  • The pericardium surrounds the heart and is rigid in constrictive pericarditis, causing limited expansion during diastole.
  • In restrictive cardiomyopathy, there is no problem with the pericardium, and the condition is primarily related to the compliance and function of the ventricular myocardium.
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42
Q

Q1. What is the management approach for dilated cardiomyopathy with a focus on controlling volume and venous return?

A

A1.
The management approach for dilated cardiomyopathy involves
1. diuretics to control hypervolemia, fluid restriction, and
2. compression stockings to enhance venous return.

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43
Q

Q2. How can afterload be reduced in dilated cardiomyopathy?

A

A2.
1. using medications such as ACE inhibitors/ARBs and
2. direct vasodilators like hydralazine and isosorbide dinitrate.

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44
Q

Q3. What medication can be used to increase contractility in dilated cardiomyopathy?

A

A3. Digoxin can be used to increase contractility of the heart in dilated cardiomyopathy.

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45
Q

Q4. What is the recommended treatment for dilated cardiomyopathy patients at high risk of ventricular tachycardia or ventricular fibrillation?

A

A4.
with an ejection fraction (EF) less than 35% should receive an
* automated implantable cardioverter-defibrillator (AICD).

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46
Q

Q5. How can cardiac remodeling be reduced in dilated cardiomyopathy?

A

A5. Cardiac remodeling can be reduced in dilated cardiomyopathy by using
1. beta blockers,
2. ACE inhibitors/ARBs, and
3. aldosterone antagonists.

47
Q

Q6. Why is anticoagulation necessary in dilated cardiomyopathy?

A

A6. Anticoagulation is necessary in dilated cardiomyopathy due to the increased risk of atrial fibrillation and decreased ejection fraction, which can lead to thromboembolic events.

  • Medications such as warfarin and DOACs (direct oral anticoagulants) can be used.
48
Q

Q7. What are the treatment options for patients with refractory crises in dilated cardiomyopathy?

A

A7. Patients with dilated cardiomyopathy who are refractory to other treatments, especially those with low EF and AICD, may be considered for heart transplantation.

49
Q

Q8. How should preload, afterload, and contractility be managed in hypertrophic cardiomyopathy?

A

A8. In hypertrophic cardiomyopathy,

  • adequate hydration is important to increase preload.
  • Afterload should be decreased, so medications like ACE inhibitors/ARBs, hydralazine, isosorbide dinitrate, and dihydropyridine CCBs should be avoided.
  • Contractility should not be increased, so digoxin should be avoided as well.
50
Q

Q9. Why are patients with hypertrophic cardiomyopathy at risk of ventricular tachycardia or ventricular fibrillation?

A

A9. Patients with hypertrophic cardiomyopathy, especially those who are dehydrated and exert themselves, are at increased risk of sudden cardiac death due to acute ventricular tachycardia or ventricular fibrillation.

51
Q

Q10. What are the invasive procedures that can be considered for patients with hypertrophic cardiomyopathy?

A

A10. Invasive procedures like myomectomy (surgical excision of the interventricular septum) and
alcohol ablation (endovascular perfusion of high concentrations of alcohol) can be considered for patients with hypertrophic cardiomyopathy who are candidates for these procedures.

52
Q

Q11. How should the treatment approach be adjusted for restrictive cardiomyopathy?

A

A11.
In restrictive cardiomyopathy, similar measures are taken as in dilated cardiomyopathy but with gentler management.
Diuresis should be done cautiously to avoid excessive reduction in preload, afterload should be gently reduced, and
anticoagulation should be considered due to the increased risk of atrial fibrillation and bi-atrial enlargement.

53
Q

Q12. What is the final treatment option for patients with refractory crises in restrictive cardiomyopathy?

A

A12. If all measures have been tried and there is irreversible fibrosis and infiltration, heart transplantation may be the final treatment option for patients with refractory crises in restrictive cardiomyopathy.

54
Q

Dilated cardiomyopathy is associated with an increased risk of thromboembolic eventsdue to decreased ejection fraction (EF) and an increased risk of atrial fibrillation (A-Fib).

A
55
Q

Hypertrophic cardiomyopathy can lead to sudden death, particularly in young athletes. It is important to be aware of this risk and consider appropriate screening measures.

A
56
Q

In restrictive cardiomyopathy, jugular venous distention (JVD) may manifest as Kussmaul’s sign, which is the paradoxical rise or lack of decline in jugular venous pressure during inspiration. This is due to impaired filling of the right ventricle during diastole.

A
57
Q

Q3: What type of inheritance pattern is associated with familial dilated cardiomyopathy?

A

A3: Autosomal dominant

58
Q

Q5: What is the mnemonic “A Bunch of stuffs Can Cause Cardiac Dilation” used for?

A

A5: It helps remember some causes of dilated cardiomyopathy:
Alcohol abuse,
Beri-beri (wet),
Coxsackie B myocarditis,
chronic cocaine use,
Chagas disease, and
doxorubicin & daunorubicin.

59
Q

Q6: How is dilated cardiomyopathy characterized in terms of ventricular size and wall thickness?

A

A6: Enlarged ventricular size with decrease ventricular wall thickness.

60
Q

Q7: What happens to the contractility of the heart in dilated cardiomyopathy?

A

A7: Contractility decreases, leading to reduced ejection fraction.

61
Q

Q8: How does dilated cardiomyopathy affect preload and afterload?

A

A8:

  • Preload increases beyond the point of optimal contractility, and
  • afterload increases due to RAAS activation and sympathetic nervous system activity.
62
Q

Q9: What is the difference between hypertrophic remodeling and dilated remodeling in terms of sarcomere addition?

A

A9: In volume stress, sarcomeres are added in series, while in pressure stress, sarcomeres are added in parallel.

63
Q

Q10: What happens to the collapsing pressure in dilated cardiomyopathy?

A

A10: The collapsing pressure decreases, indicating the ventricle’s inability to generate sufficient force for effective blood ejection.

64
Q

Q2: What are some complications of dilated cardiomyopathy?

A

A2: Complications include right-sided heart failure symptoms such as
jugular vein distension,
hepatomegaly, and
pedal edema,
as well as left-sided heart failure symptoms such as
hypotension and
pulmonary edema.

65
Q

Q3: What heart sound is typically associated with dilated cardiomyopathy?

A

A3: The S3 heart sound is often heard in dilated cardiomyopathy
due to the increased stretchiness (high compliance) of the ventricles during diastolic filling.

66
Q

Q4: Why does dilated cardiomyopathy cause a holosystolic murmur?

A

A4:
* The dilation of the ventricles in dilated cardiomyopathy leads to the stretching of the anulus ring, where the tricuspid and mitral valves attach.
* This stretching can result in regurgitation of blood, causing a holosystolic murmur.

67
Q

Q5: Why is dilated cardiomyopathy associated with atrial fibrillation (AF) and supraventricular tachycardia (SVT)?

A

A5:

  • The dilation of the ventricles causes increased blood volume and backs up into the atria.
  • This leads to remodeling of the atria, including electrical remodeling, which can predispose to the development of AF and SVT.
68
Q

Q6: What imaging modality is considered the gold standard for diagnosing dilated cardiomyopathy?

A

A6: Echocardiogram is the gold standard imaging modality for diagnosing dilated cardiomyopathy, as it can demonstrate the dilation of the left and/or right ventricle and assess contraction function.

69
Q

Q7: What can a chest X-ray (CXR) show in dilated cardiomyopathy?

A

A7: A CXR may show signs of left ventricular systolic failure, such as
* cardiomegaly and
* pulmonary congestion.

70
Q

How can preload be reduced in the management of dilated cardiomyopathy?

A
  • Achieve less fluid/less volume within the blood.
  • Fluid and sodium restriction.
  • Diuretics to eliminate excess fluid.
  • Inhibit angiotensin II using ACE inhibitors (ACE-I) and angiotensin receptor blockers (ARBs).
  • Nitroglycerin to reduce venous return.
71
Q

How can afterload be reduced in the management of dilated cardiomyopathy?

A
  • ACE inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) to inhibit the renin-angiotensin-aldosterone system (RAAS).
  • Vasodilators such as hydralazine and isosorbide dinitrate to dilate arteries and reduce afterload.
72
Q

How can contractility be increased in the management of dilated cardiomyopathy?

A

Increase inotropic effect and inhibit chronotropic effect using digoxin.

73
Q

How can cardiac remodeling be inhibited in the management of dilated cardiomyopathy?

A
  • Inhibit the RAAS by using ACE inhibitors (ACE-I), angiotensin receptor blockers (ARBs), and
  • aldosterone antagonists (such as spironolactone and eplerenone).
  • Inhibit the sympathetic nervous system (SNS) by using beta blockers.
74
Q

When should Warfarin be considered in the management of dilated cardiomyopathy? 2

A

If the patient has a valvular issue, such as a mechanical heart valve, which increases the risk of thromboembolism.

75
Q

What is an AICD?

A
  • AICD stands for Automatic Implantable Cardiac Defibrillator.
  • It is used in certain situations where a patient is at high risk of ventricular tachycardia or ventricular fibrillation, and their left ventricular ejection fraction is below 35%.
76
Q

Q: What is the most common cause of sudden cardiac death in young people?

A

A: Hypertrophic cardiomyopathy (HCM)

77
Q

Q: What is the primary etiology of hypertrophic cardiomyopathy?

A

A: Autosomal dominant genetic mutation in sarcomeric genes HCM (60% of patients)

78
Q

Q: What are the characteristic features of hypertrophic cardiomyopathy? 3

A

A:
1. Left ventricular hypertrophy (LVH),
2. impaired diastolic filling, and
3. abnormalities of the mitral valve.

79
Q

Q: How does hypertrophic cardiomyopathy lead to diastolic dysfunction?

A

A:
1. The thickened portion of the heart reduces compliance,
2. resulting in a narrowed lumen,
3. decreased preload, and
4. decreased stroke volume.

80
Q

Q: What is the term used to describe the dynamic interventricular septum obstruction seen in hypertrophic cardiomyopathy?

A

A: Systolic anterior motion (SAM) of the anterior leaflet of the mitral valve.

81
Q

Q: What are the symptoms associated with hypertrophic cardiomyopathy?

A

A:
* Angina (myocardial ischemia),
* dyspnea on exertion,
* systolic ejection murmur, and
* S4 heart sound.

82
Q

Q: How does sudden cardiac death occur in hypertrophic cardiomyopathy?

A

A:
1. Ischemia causes increased permeability of myocardial cells,
2. leading to hyperexcitability and
3. fatal arrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF).

83
Q

Q: What is the characteristic systolic murmur heard in hypertrophic cardiomyopathy?

A

A: Harsh crescendo-decrescendo murmur.

84
Q

Q: What is the underlying cause of the S4 heart sound in hypertrophic cardiomyopathy?

A

A: Atrial hypertrophy resulting in blood pushing into the small left ventricular lumen during diastole, causing the S4 sound.

85
Q

Q: What is a common associated finding in hypertrophic cardiomyopathy?

A

A: Mitral regurgitation.

86
Q

Q: How is hypertrophic cardiomyopathy often detected in asymptomatic individuals?

A

A: It can be detected through family screening of an affected individual or routine ECG examinations.

87
Q

Q: How can maneuvers involving preload affect the intensity of the murmur in hypertrophic cardiomyopathy?

A

A:
* Increasing preload (venous return) decreases obstruction and the intensity of the murmur,
* while decreasing preload increases obstruction and the intensity of the murmur.

88
Q

Q: What are the maneuvers used to increase preload in hypertrophic cardiomyopathy?

A

A: Squatting and passive leg raise.

89
Q

Q: How can maneuvers involving afterload affect the intensity of the murmur in hypertrophic cardiomyopathy?

A

A:
* Increasing afterload (systemic vascular resistance) decreases obstruction and the intensity of the murmur,
* while decreasing afterload increases obstruction and the intensity of the murmur.

90
Q

Q: What maneuver can be used to increase afterload in hypertrophic cardiomyopathy?

A

A: Hand grip.

91
Q

Q: What maneuver can be used to decrease afterload in hypertrophic cardiomyopathy?

A

A: Vasodilators to decrease systemic vascular resistance.

92
Q

Q: What type of obstruction is seen in hypertrophic cardiomyopathy?

A

A: Dynamic/functional obstruction that can be manipulated by maneuvers.

93
Q

Q: What are the ECG changes commonly seen in hypertrophic cardiomyopathy?

A

A: ECG changes can include VTach/VFib, AFib,

  • left ventricular hypertrophy (large R waves in V4, V5, V6 and deeper S waves in V1, V2, V3),
  • deep Q waves in inferior and lateral leads, and
  • giant inverted T waves.
94
Q

Q: When should patients with hypertrophic cardiomyopathy be assessed for insertion of an ICD (Implantable Cardioverter-Defibrillator)?

A

A:
Patients with 2 or more risk factors for sudden cardiac death, such as massive left ventricular hypertrophy, prior unexplained syncope, and family history of sudden cardiac death.

95
Q

Q: How are chest pain and dyspnea treated in hypertrophic cardiomyopathy?

A

A: They are treated with
* beta-blockers and
* verapamil, either alone or in combination. Verapamil has an inotropic effect on the heart.

96
Q

Q: How can preload be increased in the management of hypertrophic cardiomyopathy?

A

A: Volume expansion with fluids and avoiding drugs that decrease fluid volume.
Diuretics can be used to reduce fluid volume.

97
Q

Q: How can afterload be reduced in the management of hypertrophic cardiomyopathy?

A

A: Avoiding drugs that cause arterial dilation, such as ACE inhibitors and nitrates, as they decrease systemic vascular resistance (SVR) and thus afterload.

98
Q

Q: How can contractility be avoided or decreased in hypertrophic cardiomyopathy?

A

A: Avoiding drugs that increase contractility, such as digoxin, and
using beta-blockers or non-dihydropyridine calcium channel blockers (CCBs) like diltiazem or verapamil.

99
Q
  • How to decrease arrhythmia in hypertophic cardiomypthay
A

Automated Implantable Cardioverter Defibrillator (AICD) Automatically delivers shocks to stop fatal arrhythmias DRUGS TO BE AVOIDED HAVE A STRIKETHROUGH! EX:Drug A

100
Q

Q: How does sarcoidosis contribute to restrictive cardiomyopathy?

A

A: In sarcoidosis,
1. the immune system creates non-caseating granulomas that deposit on various tissues, including the myocardium.
2. The subsequent fibrosis and infiltration of the myocardium lead to decreased ventricular compliance.

101
Q

Q: What is the pathophysiology of restrictive cardiomyopathy?

A

A: In restrictive cardiomyopathy, the walls of the
1. ventricles become stiff, but not necessarily thickened.
2. This reduces ventricular compliance during diastolic filling
3. , leading to limited expansion of the ventricles during the middle and late phases of diastolic filling.
4. This results in decreased ventricular cavity size and low cardiac output.

102
Q

Q: Which phases of diastolic filling are affected in restrictive cardiomyopathy?

A

A:

  • The early phase of diastolic filling, which involves the normal expansion of the ventricles, may remain relatively unaffected.
  • However, the middle and late phases of diastolic filling, which involve limited expansion of the ventricles, are compromised in restrictive cardiomyopathy.
103
Q

Q: What are the clinical presentations of restrictive cardiomyopathy?

A

A: Clinical presentations of restrictive cardiomyopathy include

  • dyspnea, fatigue,
  • elevated jugular venous pressure (JVP),
  • edema, hepatomegaly, and
  • the development of atrial fibrillation (AF).
104
Q

: What are the two main reasons for thrombotic events in restrictive cardiomyopathy?

A

A: The two main reasons for thrombotic events in restrictive cardiomyopathy are
1. atrial dilation, which leads to atrial fibrillation (AF) and altered electrical activity, and
2. conditions involving the endocardium, which can cause endocardial inflammation and injury, increasing the risk of mural thrombi formation.

105
Q

Q: What investigations can be performed to diagnose restrictive cardiomyopathy?

A

A:

  • ECG findings in restrictive cardiomyopathy may include
  • reduced QRS,
  • left bundle branch block (LBBB), and
  • atrioventricular blockades.
  • Echocardiography can reveal symmetric thickening of the ventricular walls without enlargement, as well as bi-atrial enlargement.
  • Endomyocardial biopsy can also be performed.
106
Q

Q: What causes an S3 heart sound in restrictive cardiomyopathy?

A

A:

  • In the early diastolic filling phase,
  • the ventricular pressure is at its lowest.
  • The rapid and turbulent filling of blood from the dilated atrium into the ventricle produces an
  • S3 heart sound.
107
Q

: How is restrictive cardiomyopathy managed?

A

A: Management of restrictive cardiomyopathy involves the management of heart failure symptoms. The underlying cause, if identified (such as amyloidosis or sarcoidosis), should be managed accordingly.
1. Preload reduction is performed slowly and gently by restricting water and sodium intake and using diuretics.
2. Mild reduction of afterload can be achieved by gently reducing systemic vascular resistance (SVR) using medications such as ACE inhibitors, ARBs, and hydralazine.
3. In patients with significant atrioventricular (AV) block, beta-blockers and calcium channel blockers should be avoided, and cardiac pacing may be necessary.

108
Q

Q: What is the name of the uncommon inherited condition that predominantly affects the right ventricle with fatty or fibro-fatty replacement of myocytes?

A

A: The condition is called arrhythmogenic right ventricular cardiomyopathy (ARVC).

109
Q

Q: What is the genetic inheritance pattern of arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

A: ARVC can have both
1. autosomal dominant and
2. autosomal recessive forms. Mutations mostly involve desmosomal genes.

110
Q

Q: What is the pathophysiology of arrhythmogenic right ventricular cardiomyopathy?

A

A: The pathophysiology involves fibro-fatty replacement of cardiomyocytes in the right ventricle, with left ventricular involvement seen in over 50% of cases.

111
Q

Q: What are the clinical presentations of arrhythmogenic right ventricular cardiomyopathy?

A

A: Most patients with ARVC are symptomatic.
The common symptoms include
* symptomatic ventricular arrhythmia,
* syncope, and
* sudden death.

112
Q

Q: What investigations are typically performed to diagnose arrhythmogenic right ventricular cardiomyopathy?

A

A:
1. ECG findings in ARVC are usually normal.
2. Imaging techniques such as echocardiography and cardiac MRI can provide valuable diagnostic information.
3. Genetic testing can also be conducted to identify relevant mutations.

113
Q

Q: What is the management approach for arrhythmogenic right ventricular cardiomyopathy?

A

A:
1. β-blockers are the first-line treatment for patients with non-life-threatening arrhythmias associated with ARVC.
2. Symptomatic arrhythmias may require the use of antiarrhythmic medications such as amiodarone or sotalol.
3. In cases of refractory or life-threatening arrhythmias, an implantable cardioverter-defibrillator (ICD) is required.

Cardio All My Notes (13 decks)

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