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
What do you see for diagnosis of peripartum DCM?
Increased BNP, echo shows EF<45
26
What happens to the septum in obstructive HCM?
Assymetrically hypertrophies
27
Pathophysiology of RCM
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
Gold standard of diagnosis infectious DCM
Endomyocardial biopsy (but very invasive)
29
What is stress/Takotsubo CM?
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
Alcoholic DCM
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
Pathophysiology of DCM
Symmetric LV dilation, impaired LV systolic function and decreased EF (might involve RV)
32
Other medications for DCM
``` 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
Types of surgery for HCM
Indicated for symptomatic LVOT obstruction with advanced CHF refractory to medical therapy Surgical septal myectomy EtOH ablation Mitral valve surgery
34
Distinguishing the murmur of HCM
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
Potential exam findings in HCM
*May be normal* Bifid carotid pulse (mitral valve coming close to septum), brisk radial pulse, audible S4, harsh crescendo-decrescendo murmur
36
Most common cause of RCM
Amyloidosis (infiltrative) which is abnormal amyloid protein in cardiac muscle
37
Other management of HCM
Non-dihydropyridine CCB Diuretics but caution if significant obstruction Manage arrhythmias ICD implantation if high risk for SCD
38
Which is the most common CM?
Dilated
39
How do you see familial DCM?
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
Diagnostics for stress CM
Increased troponin and BNP (drop quicker then after MJ) Look like MI on ECG Decreased EF Wall motion abnormalities on MRI
41
Presentation of stress CM
ACUTE ONSET | Present like acute coronary syndrome with sxs of HF
42
What is the leading cause of cardiac transplantation?
Dilated cardiomyopathy
43
Risk factor for alcoholic DCM
7-8 drinks/day > 10 yrs because alcohol is toxic to myoctyes
44
How do you rule out restrictive paricarditis?
Cardiac MRI
45
Mainstay of management for RCM
Low dose loop diuretics | Treat underlying cause obvi
46
Presentation of cardiac amyloidosis
Elevated JVP, hepatomegaly, ascites | Periorbital purpura wth HF- pathognomonic
47
How might DCM present?
Like heart failure Mostly exertional intolerance with SOB and fatigue Crackles, JVP, edema, regurgitation murmurs etc
48
Risk factors for peripartum DCM
>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
Pathophysiology of HCM
Diastolic filling abnormalities Asymmetric septal hypertrophy Small LV cavity Maybe intramural vessel abnormalities and ischemia Might be secondary to HTN or aortic stenosis
50
Criteria for familial DCM
+FH of DCM in 2+ relatives
51
Drug-related DCM
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
Long term management of stress CM
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
What does it mean when RCM becomes symptomatic?
Usually a rapid decline (underlying dz progresses slowly)
54
Possible etiologies of DCM
Idiopathic, familial, infectious, alcoholism, peripartum, drugs, tachycardia-mediated, endocrine dysfunction, nutritional deficiencies