Cardiomyopathies Flashcards

1
Q

Why is ECG used in DCM?

A

Mostly to rule out other things (sinus tachycardia, LBBB, arrhythmias)

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2
Q

What is the etiology of HCM?

A

Familial

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3
Q

Other management for RCM

A

CCB to improve diastolic compliance (CI in amyloid)
Anticoagultion
Consider transplant but some underlying diseases won’t let it

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4
Q

First line medication for DCM

A

ACE-i (reduce afterload by vasodilation to decrease BP)

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5
Q

Non-pharm management of DCM

A

Remove the underlying cause if possible
Limit activity based on functional status
Salt restriction <2-3 g/day
CPAP if sleep apnea

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6
Q

Management of stress CM

A

Just like acute MI so send to cath lab (but won’t find blockage)

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7
Q

Chemotherapy-induced DCM

A

Includes Adriamycin/Doxarubicin
Dose dependent and early detection is important
Treat the dysfunction and sxs
Get baseline echo to measure EF and monitor

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8
Q

Most common person for stress CM?

A

Post menopausal women

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9
Q

General signs of heart failure

A

Hypotension/tachycardia/tachypnea
Fatigue/weakness
Dyspnea (rest, exertional or at night) and orthopnea
Peripheral edema, elevated JVP, ascites

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10
Q

Sxs of HCM

A

Some are asymptomatic so found at death
Dyspnea on exertion mostly
Exertional angina
Fatigue, pre-syncope, palpitations

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11
Q

Mainstay for diagnosis of HCM

A

Echo with LV wall thickness > 15 mm

May have systolic anterior motion of mitral valve (measures obstruction gradient)

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12
Q

Etiologies of RCM

A

Infiltrative, storage diseases (hemochromatosis, glycogen storage disease), idiopathic, scleroderma, fibrosis from chemo, familial but rare here

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13
Q

What is the #1 cause of sudden death in competitive athletes 35 and younger?

A

Hypertrophic cardiomyopathy

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14
Q

Presentation of peripartum DCM

A

Mom is usually 36 wks gestation to 1 mo post partum
Usually transient dysfunction due to remodeling of LV so sxs probably better when not pregnant (dyspnea, hemoptysis, edema etc)

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15
Q

What is non-obstructive HCM?

A

Muscle hypertrophies in the wall and there is no blockage of the outflow tract

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16
Q

Initial management of HCM

A

Beta blockers

And exercise restriction obvi

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17
Q

Idiopathic DCM

A

Most common (50%)
Primary diagnosis for transplant
No cause obvi

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18
Q

Presentation of RCM

A

Right heart failure usually, angina, syncope, dyspnea

Prominent JVP, Kussmauls sign (increase in JVP with inspiration), maybe regurgitation murmur

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19
Q

What can RCM resemble?

A

Constrictive pericarditis (must differentiate)- scarring and consequent loss of normal elasticity of pericardial sac and impaired ventricular filling

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20
Q

In what diseases do you think about using Digoxin?

A

Afib, fatigue, dyspnea

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21
Q

When do you think of infectious DCM?

A

Presenting currently or previously with viral sxs (can be parasitic in Latin America-Chagas)
Most of the time when you clear the infection, the insult of the heart will improve

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22
Q

Factors that can worsen left ventricular outflow tract obstruction in obstructive HCM?

A

Tachycardia, hypovolemia, standing/valsalva (reduce cavity), + inotropes, diuretics, vasodilators

23
Q

What is a cardiomyopathy?

A

Heart disorder when heart muscle is abnormal in absence of CAD, HTN, valvular disease or CHD

24
Q

Risk factors of sudden cardiac death

A
Prior sustained ventricular tachycardia
Non-sustained v tach
Younger than 30
FH of sudden death due to this
Massive LVF (>30 mm)
Unexplainable syncope
Brady arrhythmias
25
Q

What do you see for diagnosis of peripartum DCM?

A

Increased BNP, echo shows EF<45

26
Q

What happens to the septum in obstructive HCM?

A

Assymetrically hypertrophies

27
Q

Pathophysiology of RCM

A

Non-dilated, rigid ventricles (deposits in muscle) that leads to diastolic dysfunction and restrictive filling
Preserved systolic function (HFpEF)
No hypertrophy usually
R and L atrial enlargement
Increased RA pressure leads to increased LA pressure and therefore forward failure (limited preload and SV, reduced CO and fatigue)

28
Q

Gold standard of diagnosis infectious DCM

A

Endomyocardial biopsy (but very invasive)

29
Q

What is stress/Takotsubo CM?

A

Transient LV systolic and diastolic dysfunction in absence of attributable CAD
Preceded by emotional/physical trigger usually
NE and epi released and stress heart so transient abnormality

30
Q

Alcoholic DCM

A

Normal sxs of DCM with hx
Elevated LFTs
Tx of abstinence can lead to much improvement (if not then poor prognosis at 3-6 yrs)

31
Q

Pathophysiology of DCM

A

Symmetric LV dilation, impaired LV systolic function and decreased EF (might involve RV)

32
Q

Other medications for DCM

A
Diuretics (volume overload)
B-blockers (decrease oxygen demand)
Digoxin (+ inotrope, used in failure of other tx)
Antiarrhythmics (amiodarone wwith afib)
Antiocoagulation (afib, EF<30, thrombi)
Implanted cardioverter defibrillator
33
Q

Types of surgery for HCM

A

Indicated for symptomatic LVOT obstruction with advanced CHF refractory to medical therapy
Surgical septal myectomy
EtOH ablation
Mitral valve surgery

34
Q

Distinguishing the murmur of HCM

A

Increases with valsalva and standing (v is decrease of preload and afterload, s is just preload)
Decreases with squat and isometic handgrip (squat is increase preload and afterload, i is just afterload)
*this is the same murmur in aortic stenosis but these maneuvers have a different effect

35
Q

Potential exam findings in HCM

A

May be normal
Bifid carotid pulse (mitral valve coming close to septum), brisk radial pulse, audible S4, harsh crescendo-decrescendo murmur

36
Q

Most common cause of RCM

A

Amyloidosis (infiltrative) which is abnormal amyloid protein in cardiac muscle

37
Q

Other management of HCM

A

Non-dihydropyridine CCB
Diuretics but caution if significant obstruction
Manage arrhythmias
ICD implantation if high risk for SCD

38
Q

Which is the most common CM?

A

Dilated

39
Q

How do you see familial DCM?

A

Use the history of course
Seen in >50% of idiopathic pts
Cardiac protein antibodies in 30% of pts and in 20-30% of 1st/2nd degree relatives

40
Q

Diagnostics for stress CM

A

Increased troponin and BNP (drop quicker then after MJ)
Look like MI on ECG
Decreased EF
Wall motion abnormalities on MRI

41
Q

Presentation of stress CM

A

ACUTE ONSET

Present like acute coronary syndrome with sxs of HF

42
Q

What is the leading cause of cardiac transplantation?

A

Dilated cardiomyopathy

43
Q

Risk factor for alcoholic DCM

A

7-8 drinks/day > 10 yrs because alcohol is toxic to myoctyes

44
Q

How do you rule out restrictive paricarditis?

A

Cardiac MRI

45
Q

Mainstay of management for RCM

A

Low dose loop diuretics

Treat underlying cause obvi

46
Q

Presentation of cardiac amyloidosis

A

Elevated JVP, hepatomegaly, ascites

Periorbital purpura wth HF- pathognomonic

47
Q

How might DCM present?

A

Like heart failure
Mostly exertional intolerance with SOB and fatigue
Crackles, JVP, edema, regurgitation murmurs etc

48
Q

Risk factors for peripartum DCM

A

> 30, African, multiparous, h/o preeclampsia (HTN, edema, proteinuria)/eclampsia (those with seizures)/postpartum HTM, maternal cocaine abuse, >4 wks of oral tocolytic to stop contractions

49
Q

Pathophysiology of HCM

A

Diastolic filling abnormalities
Asymmetric septal hypertrophy
Small LV cavity
Maybe intramural vessel abnormalities and ischemia
Might be secondary to HTN or aortic stenosis

50
Q

Criteria for familial DCM

A

+FH of DCM in 2+ relatives

51
Q

Drug-related DCM

A

Causes myocarditis and toxic effects on myocardium
Cessation of cocaine can reverse dysfunction (it has hyperadrenergic affects on body)
Think of this when young person has sxs of HF for no reason

52
Q

Long term management of stress CM

A

Depends on if LV dysfunction persists
ASA, BB and ACE-i until recovers
Anticoagulate for 3 mos with warfarin if thrombus
Most recover systolic function within 4 wks

53
Q

What does it mean when RCM becomes symptomatic?

A

Usually a rapid decline (underlying dz progresses slowly)

54
Q

Possible etiologies of DCM

A

Idiopathic, familial, infectious, alcoholism, peripartum, drugs, tachycardia-mediated, endocrine dysfunction, nutritional deficiencies