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Cardio Exam 4 > Cardiomyopathy > Flashcards

Cardiomyopathy Flashcards

1
Q

Cardiomyopathies are of 4 main types:

A

○ Dilated Cardiomyopathy
○ Hypertrophic Cardiomyopathy
○ Restrictive Cardiomyopathy
○ Takotsubo/Stress Cardiomyopathy

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2
Q

What is cardiomyopathy?

A

In general, Cardiomyopathy refers to primary
diseases of the myocardium itself.
○ This does not generally include structural cardiac disorders that can damage the myocardium, including coronary artery disease, valvular disorders, and congenital disorders.

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3
Q

The term _______ is commonly used and refers to the dilated, poorly contracting myocardium that can occur in patients with severe CAD with or without areas of infarction.

A

“Ischemic Cardiomyopathy”
○ It is NOT generally considered to be
one of the classic categories of
cardiomyopathy because it does not
describe a primary myocardial
disorder

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4
Q

Although some causes have been
identified, many cases of Cardiomyopathy
are ______

A

idiopathic

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5
Q

______ cardiomyopathy is by far the most
common type (95%)

A

Dilated

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6
Q

Dilated Cardiomyopathy

A

Large group of myocardial disorders
characterized by an enlargement of the left
ventricle, reduced myocardial contractility
in the absence of abnormal loading
conditions (such as with HTN or valvular
disease).

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7
Q

Frequent causes of Dilated Cardiomyopathy include:

A

○ Viral Myocarditis (Coxsackievirus B is most common)
○ Alcoholism or Cocaine abuse
○ Drugs and toxins (including chemotherapy)
○ Genetic abnormality (Familial in 20-35% of patients)
○ Pregnancy
○ Stress-induced (AKA Takotsubo Cardiomyopathy)

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8
Q

Dilated Cardiomyopathy

A

● Regardless of the cause, the myocardium dilates, thins, and develops
chronic fibrosis with variable hypertrophy.
● Often leads to functional mitral regurgitation or tricuspid regurgitation
and atrial dilation
● The disorder generally affects both
ventricles initially, but the atria dilate
as a result of systolic dysfunction

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9
Q

______ commonly occurs
as the left atrium dilates with Dilated Cardiomyopathy

A

Atrial fibrillation

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10
Q

Clinical presentation of dilated cardiomyopathy:

A

Occurs as a result of left or biventricular failure,
which presents as Systolic Heart Failure. Generally includes:
○ Exertional dyspnea (maybe pulmonary edema)
○ Cardiomegaly
○ Jugular Venous Distention
○ Peripheral edema
○ Functional AV valve regurgitation
○ S3 sound (and sometimes an S4)
○ Sudden cardiac death

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11
Q

Dilated Cardiomyopathy diagnosis

A

Echocardiogram will confirm ventricular wall
dilation (especially left), wall thinning, and global ventricular dysfunction
○ Echo shows low ejection fraction and may
show AV valve regurgitation
● Chest X-ray will reveal cardiomegaly due to the dilation and ballooning,
usually in all chambers of the heart
● EKG may show sinus tachycardia, atrial
fibrillation, and/or nonspecific ST-segment
changes. Other common findings includes
hypertrophy/enlargement and LBBB.

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12
Q

Dilated Cardiomyopathy treatment

A

○ If the cause can be identified, it should be treated.
○ Otherwise, the treatment for dilated cardiomyopathy is essentially the
same as treatment for Heart Failure in general.
■ May include ACEi or ARB, ARNI, Beta-Blocker, Diuretics, and an Aldosterone Antagonist (much more in later unit)
○ Anticoagulation may be necessary if atrial fibrillation is present.
○ Implantable cardioverter-defibrillator may be needed.
○ All patients should be seen by a cardiologist,

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13
Q

Dilated Cardiomyopathy prognosis

A

Prognosis generally has been poor for most groups.
○ About 20% die within the first year after diagnosis
○ Patients with peripartum cardiomyopathy or stress-induced cardiomyopathy appear to have a better prognosis than those with other
forms of dilated cardiomyopathy

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14
Q

Hypertrophic Cardiomyopathy

A

● Hypertrophic Cardiomyopathy (HCM) is a congenital or acquired
disorder characterized by marked left ventricular hypertrophy

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15
Q

How does HCM occur
without increased afterload?

A

● Ventricular hypertrophy can occur due
to increased afterload (such as aortic
stenosis, systemic HTN, coarctation,
etc), but this hypertrophy would not
qualify as hypertrophic
cardiomyopathy.

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16
Q

_____ is a common cause of sudden cardiac death in young athletes

A

HCM

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17
Q

HCM results in _____ Heart Failure

A

Diastolic
● The hypertrophic ventricular and/or septal wall result in decreased intraventricular space (decreased end-diastolic volume)

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18
Q

What happens to ejection fraction in HCM?

A

Because the ventricular wall is still functional myocardial tissue, contractility remains normal, resulting in a normal ejection fraction.
○ Later in the disease process, the ejection fraction might actually be increased

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19
Q

HOCM

A

Hypertrophic obstructive cardiomyopathy

20
Q

How does HCM result in HOCM?

A

● Generally, the hypertrophy is asymmetrical, rather than evenly distributed throughout the LV walls.
● The interventricular septum is significantly
hypertrophied in the most common phenotype.
○ This, along with systolic anterior motion of the mitral valve, result in Left Ventricular Outflow Obstruction during systole. (“HOCM”

21
Q

signs and
symptoms often appear during
exercise or tachyarrhythmias with _____

A

HCM

22
Q

Carotid pulse often has a bifid peak (“Bisferiens Carotid Pulse”) with _____

A

HCM

23
Q

S/S of HCM:

A

○ Dyspnea
○ Chest pain
○ Palpitations
○ Syncope

24
Q

Murmur of Hypertrophic Cardiomyopathy

A

systolic ejection
murmur as the blood rush past the septal obstruction (does not radiate).
○ Heard best at the 3rd/4th intercostal space along the left sternal borde
● Mitral regurgitation murmur might be heard.
● A 4th heart sound (S4) is often heard due to
atrial contraction (kick) against a poorly
compliant LV wall in late diastole.
● A sustained PMI may be palpated

25
Q

How do you distinguish the HCM murmur from a murmur of Aortic Stenosis?

A

○ Have the patient perform a Valsalva Maneuver and listen.
○ This will increase the intensity of the murmur because valsalva
decreases the venous return to the heart, decreasing the left ventricular
volume, thereby increasing the outflow obstruction and increasing the
intensity of the murmur.
○ The murmur of HCM is the only systolic murmur that increases in
intensity during the strain phase of valsalva. Decreases with squatting

26
Q

HCM diagnosis

A

● CXR is usually normal (mild or no cardiomegaly).
● Echocardiogram or Cardiac MRI:
○ Hypertrophied left ventricle (>1.5 cm thick),
often times asymmetrically septal
● EKG reveals evidence of LV hypertrophy and LA enlargement.
● Asymmetric septal hypertrophy may cause deep “dagger-like” Q waves in leads I, AVL, V5 and V6.
● T waves are often inverted in lateral leads

27
Q

Hypertrophic Cardiomyopathy Treatment

A

Beta blockers and/or rate-limiting calcium channel blockers (like Verapamil) are used to decrease myocardial contractility and slow the heart rate.
■ This prolongs diastolic filling and decreases outflow obstruction
○ Avoid drugs that decrease preload (ACEis, ARBs, diuretics, nitrates) as these decrease LV size and can increase obstruction.
○ Surgical septal myomectomy or alcohol septal ablation can be
performed when medical management is insufficient.

28
Q

prognosis of HCM

A

○ Prognosis overall is highly variable; consult with Cardio is best.
■ There is a 1-2% annual risk of sudden cardiac death.

29
Q

Restrictive Cardiomyopathy

A

● Restrictive Cardiomyopathy (RCM) is characterized by noncompliant
ventricular walls that resist filling.
● The least common cardiomyopathy results from fibrosis or infiltration
of the ventricular walls because of collagen-defect disease.

30
Q

Causes of Restrictive cardiomyopathy

A

○ Amyloidosis (most common)
○ Hemochromatosis

31
Q

Restrictive Cardiomyopathy pathophysiology

A

● Myocardial infiltration, with iron in hemochromatosis or amyloid fibrils in
amyloidosis, causes myocardial cell death and scarring/fibrosis
● Endocardial thickening, due to other
cell injury, also results in myocardial
cell death and fibrosis.
● Both myocardial infiltration and
endocardial thickening result in rigid,
noncompliant ventricular walls.
○ Results in Diastolic Dysfunction
and Pulmonary Hypertension

32
Q

Presentation of Restrictive Cardiomyopathy

A

Restrictive Cardiomyopathy
● Patients present with exertional dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, and peripheral edema.
○ May see JVD
○ May hear pulmonary rales
● Fatigue is common because of fixed cardiac output

33
Q

Diagnosis of Restrictive Cardiomyopathy

A

● Arrhythmias and AV Blocks are commonly found on EKG.
● A 3rd and/or 4th heart sound (S3, S4) may be noted on auscultation.
● Murmurs of mitral regurgitation and/or tricuspid regurgitation may be
heard as a result of endomyocardial fibrosis or infiltration changing the
geometry of the chordae tendineae or the ventricular wall
● Echocardiogram reveals a small, thickened LV with poor diastolic
ventricular wall compliance and bright myocardium (speckled).
● Cardiac MRI may show a distinctive pattern of diffuse gadolinium hyperenhancement in amyloidosis
● To definitively diagnose infiltrative RCM, we can perform a right heart
cath with Endomyocardial Biopsy

34
Q

Murmur in Restrictive Cardiomyopathy

A

Murmurs of mitral regurgitation and/or tricuspid regurgitation may be
heard as a result of endomyocardial fibrosis or infiltration changing the
geometry of the chordae tendineae or the ventricular wall.

35
Q

Restrictive cardiomyopathy should be
considered in patients with ______

A

heart failure
and preserved ejection fraction

36
Q

To definitively diagnose infiltrative RCM, we can perform a _____

A

right heart cath with Endomyocardial Biopsy
● Demonstration of tissue infiltration
on biopsy specimens using special
stains and histologic studies will
confirm cardiac amyloidosis

37
Q

Restrictive Cardiomyopathy prognosis

A

generally poor because the diagnosis is often not made
until very late in the disease process (late stage).
○ There is a high rate of conduction defects and sudden death

38
Q

Restrictive Cardiomyopathy treatment

A

● No specific treatment is available for other RCM patients, other than
symptomatic, supportive care.
● Treatment is otherwise directed at the cause of the RCM if possible
(not commonly possible), such as phlebotomy for hemochromatosis.
● For patients with peripheral edema, diuretics may be used with
caution, but may decrease preload too much
● In late 2019, a new drug called Tafamidis was approved by the FDA and treats a specific type of Amyloidosis (transthyretin amyloidosis)

39
Q

Takotsubo/Stress Cardiomyopathy

A

● Takotsubo Cardiomyopathy gets its name from the takotsubo pot, a Japanese octopus pot, because the shape of the Left Ventricle deforms into a rounded ampulla shape similar to the takotsubo pot
● This condition generally follows a significant
catecholamine discharge and acutely results in the deformed LV

40
Q

Sometimes can be called “broken-heart syndrome.”

A

Takotsubo/Stress Cardiomyopathy

41
Q

Takotsubo/Stress Cardiomyopathy pathophysiology

A

● As the severe stress response occurs, large amounts
of epinephrine and norepinephrine are released
from the Adrenal Medulla and sympathetic fibers.
● This surge of catecholamines results in damage to
the myocardium in multiple ways:
○ Microvascular coronary vasoconstriction/spasm
○ Direct catecholamine toxicity
○ Adrenoceptor-mediated damage
○ Increased cardiac workload
● Creates a unique dysfunction and shape of the LV

42
Q

Takotsubo/Stress Cardiomyopathy Presentation

A

● This condition presents acutely, with signs and symptoms essentially
identical to any Acute Coronary Syndrome (ACS).
○ Chest pain, chest pressure, shortness of breath, etc

43
Q

Diagnosis of Takotsubo/Stress Cardiomyopathy

A

● EKG generally reveals ST elevation and deep
anterior T-wave inversion.
● Troponin biomarkers are generally positive but often normalize quickly.
● As the patient is evaluated in the Cardiac Cath Lab for MI evaluation, the coronaries will appear normal.
● While in the Cath Lab, left ventriculogram will reveal the characteristic apical LV ballooning deformity,

44
Q

Takotsubo/Stress Cardiomyopathy Tx

A

● Initially, standard MI treatments should be started (before it’s realized
that it’s Takotsubo) - antiplatelets, heparin, pain meds, etc
● Once the diagnosis is established, the initiation of long-term
treatment depends on how long the LV dysfunction persists.
○ Most patients should receive aspirin, beta-blocker, and ACE
inhibitor therapy until the LV fully recovers
● Interestingly, ACEis or ARBs (not beta-blockers) have improved
long-term survival support.
● Most patients recover completely

45
Q

Takotsubo/Stress Cardiomyopathy prognosis

A

● While overall prognosis is good, some serious complications can occur,
such as mitral regurgitation, ventricular tachycardia, ventricular
rupture, shock, and death

Cardio Exam 4 (5 decks)

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