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Clin Med 2 > Cardiomyopathies > Flashcards

Cardiomyopathies Flashcards

1
Q

What is cardiomyopathy

A

Myocardial disorder in which THE HEART MUSCLE IS STRUCTURALLY AND FUNCTIONALLY ABNORMAL in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease

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2
Q

What are the three main types of CM

A

Hypertrophic
Dilated
Restrictive

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3
Q

Dilated cardiomyopathy pathophysiology DCM

A

Symmetric left ventricular LV dilation
Impaired LV systolic function
Can involve the right ventricle RV

Not caused by CAD, valvular disease or HTN

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4
Q

DCM presentation both symptoms and possible PE findings

A 
Symptoms: 
EXERTIONAL INTOLERANCE WITH SOB, FATIQUE
Chest pain
Palpitations, presyncope/syncope
Peripheral edema
Abdominal pain
Posible PE findings:
Mitral/tricuspid regurg murmur 
S3 gallop
Increased jugular venous pressure
Basal crackles
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5
Q

Etiologies of DCM

A 
IDIOPATHIC
Familial
Infectious
Peripartum
Alcoholism
Drugs
[tachycardia-mediated
Endocrine dysfunction
Nutritional deficiencies
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6
Q

What is the most common etiology of DCM

A

Idiopathic DCM up to 50% (no identifiable cause

Primary indication for cardiac transplantation

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7
Q

Familial DCM criteria and important points

A

(+) FH of DCM in 2+ relatives

Seen >= 50% of patients with idiopathic DCM

Cardiac protein antibodies present in 30%

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8
Q

Infectious DCM important points

A

Myocarditis= inflammatory process 2 degree to infectious or non-infectious causes

Viral-most common in US
Parasitic (changes DZ) most common cause of DCM in Latin America
Present w/ viral sxs and/or heart failure sxs
Endomyocardial biopsy is GOLD STANDARD for diagnosis

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9
Q

Peripartum DCM risk factors and presentation

A 
>30 African descent
Multiparous
H/o preeclampsia, eclampsia, postpartum HTN
Maternal cocaine abuse
>4wks use of oral tocolytic

Presentation
Generally 36 wks of gestation - 5 mos. post-partum
Dyspnea, orthopnea, PND, pedal edema, cough, hemoptisis

*diagnosis: Inc. BNP, Echo= EF <45

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10
Q

Alcoholic DCM risk factors, presentation, prognosis

A

Risk factors: 6 drink/day for 5-10 years

Presentation: HF symptoms, signs of long-term EtOH use

Prognosis: abstinence can lead to significant improvement in heart failure
If continue EtOH = poor prognosis, mortality 50% at 3-6 years

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11
Q

Cocaine-related DCM

A

Toxic effects on myocardium

Causes myocarditis

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12
Q

Chemotherapy-induced DCM

A

Anthracyclines
-including adriamycin (doxarubicin) -> breast CA, sarcoma and lymphoma

Early detection improves outcomes
Can present with HF symptoms

*obtain baseline echo to measure EF and continue to monitor

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13
Q

Tachycardia mediated DCM cause and treatment

A

Caused by sustained rapid ventricular rates (130-200)
May follow any type of chronic cardiac arrhythmia
Treatment of tachycardia/arrhythmia reverses myocardial dysfunction

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14
Q

Endocrine dysfunction DCM

A

Diabetes
-initially myocardial fibrosis and diastolic dysfunction(restrictive CM) later stages systolic dysfunction

Thyroid dysfunction
-thyroid hormone can alter preload, afterload, heart rate and contractility

Pheochromocytoma
-adrenal tumor secreting catecholamines

*cardiac dysfunction usually can be reversed by correction of endocrine disorder

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15
Q

Nutritional deficiencies DCM

A

Thiamine B1 deficiency
-consider in alcoholic or malnourished pt (diarrhea, dialysis, poor intake)

Carnitine deficiency
-impairs oxidation of fatty acids, resulting in lipid accumulation in myocete cytomplasm

*cardiac dysfunction usually can be reversed by correction of nutritional deficiency

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16
Q

DCM diagnostics

A

EKG:
-non-specific changes -> sinus tachycardia, left bundle branch block, atrial/ventricular arrhythmia

CXR:
-cardiomegaly (globular heart), pleural effusions

Labs:
-BNP, TSH, CBC, CMP, (+/-) endomyocardial biopsy

ECHO***

  • dilated ventricle, reduced LV systolic function
  • exclude unsuspected valve disease
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17
Q

DCM management

A

Treat or remove underlying cause

  • d/c alcohol or cocaine use
  • evaluate chemo dosing

Lifestyle modification
Close f/u

18
Q

DCM med management

A 
ACE inhibitors **1st line**
-reduce afterload by vasodilation, BP reduction 
Diuretics
-used for volume overload/reduce preload
B-blockers
-decrease oxygen demand
Digoxin
(+) inotrope
Failure to respond to first line treatments
Used in afib, fatigue, dyspnea
19
Q

DCM management

A

Antiarrhythmics
-amiodarone if afib

Anticoagulation
-if afib, EF <30%, h/o thromboemboli, presence of mural thrombi (on wall of ventricle)

IMPLANTED CARDIOVERTER DEFIBRILLATOR
CARDIAC TRANSPLANTATION

20
Q

Hypertrophic cardiomyopathy pathophysiology

A

LEFT VENTRICULAR HYPERTROPHY (LVH) IN THE ABSENCE OF A CAUSE

  • diastolic filling abnormalities
  • small LV cavity

Leading cause of sudden cardiac death (SCD) in young persons

21
Q

HCM etiology

A

Familial

22
Q

What is obstructive HCM

A

Factors WORSENING left ventricular outflow tract (LVOT) obstruction:

Tachycardia
Hypovolemia
Standing
Valsalva
\+ inotropes
Diuretics
Vasodilators

My words: mitral valve is close to septum and gets stuck. This causes regurg, and obstructed aortic outflow

Can be asymptomatic until exertion

23
Q

HCM presentation

A

Asymptomatic
Found on echo
Death

Symptomatic
Dyspnea on exertion
Exertional angina 
Fatigue
Pre-syncope, syncope
Palpitations
24
Q

HCM presentation continued

A

POTENTIAL PE FINDINGS W/ LVOT OBSTRUCTION
Brisk, bifid carotid pulse
Audible S4
Crescendo-decrescendo systolic ejection murmur

INCREASES with valsalva and standing
DECREASES with squat and isometric handgrip

25
Q

HCM diagnostics

A

EKG

  • LV hypertrophy w/ strain
  • increased incidence of both supraventricular and ventricular arrhythmias
  • ECHO*
  • INCREASED LV WALL THICKNESS >= 15mm is diagnostic
  • asymmetric septal hypertrophy
  • systolic anterior motion of mitral valve

Stress/exercise echo:
-risk stratification assess LVOT

26
Q

Sudden cardiac death risk factors

A

Prior sustained ventricular tachycardia (VT)
Non-sustained VT
Young age <30 years
Family history of sudden death due to HCM
Massive LVH (wall thickness >= 30mm)
Unexplainable syncope, especially in young patients
Brady arrhythmias

27
Q

HCM and physical activity restriction

A

Avoid most competitive sports

Avoid high-intensity sports

28
Q

HCM management

A

Asymptomatic: ->no prophylactic therapy

Symptomatic:
BETA BLOCKERS BB or NON-DIHYDROPYRIDINE CALCIUM CHANNEL BLOCKERS (Nd-CCB)
- (-) inotrope
-may improve chest pain and dyspnea

Diuretics w/ caution if significant LVOT obstructin and symptoms
Manage arrhythmias
ICD implantation if high risk for SCD, sustained ventricular tachyarrhythmia

29
Q

Surgery for HCM

A

Indicated for SYMPTOMATIC LVOT obstruction w/ advanced heart failure refractory to medical therapy

Surgical septal myectomy

EtOH ablation

Mitral valve surgery (mitral valve replacement or plication)

30
Q

Restrictive cardiomyopathy RCM pathophysiology

A 
Non-dilated, rigid ventricles
Diastolic dysfunction 
Restrictive filling
Preserved systolic function 
HFpEF
R and L atrial enlargement
31
Q

RCM most common Etiology

A

Infiltrative

  • Amyloidosis -> most common
  • sarcoidosis

Storage diseases
-hemochromatosis
Glycogen storage disease

Other
Idiopathic
Scleroderma
Fibrosis 2nd chemotherapy, radiation

32
Q

RCM presentation symptoms and PE

A

Symptoms:
Right > left heart failure
Edema, abdominal discomfort, ascites
Angina, syncope, dyspnea

PE
*S3 gallop not heard in constrictive pericarditis
Prominent JVP
+/- kussmaul’s sign (distensión of jugular vein during inspiration)
Possible MR/TR murmur (regurg)

33
Q

Cardiac amyloidosis presentation and diagnostic studies

A

Presentation:
Elevated JVP
Hepatomegaly, ascites
Periorbital purpura with heart failure is pathognomonic (late finding)

Diagnostic studies:
Echo -> inc left ventricular wall thickness with diastolic dysfunction, later right ventricular diastolic dysfunction develops
Endomyocardial biopsy —> definitive

34
Q

RCM diagnostic

A

EKG- non-specific findings

ECHO
Bi0atrial enlargement
Normal to small ventricular cavity (amyloid may result in wall thickness)
Nml Ef, abn filling

CARDIAC MRI
Chamber size, wall thickness, presence/absence of infiltration, inflammation, fibrosis

Endomyocardial biopsy
Diagnostic

35
Q

RCM Managment

A 
TREAT UNDERLYING CAUSE
LOW DOSE LOOP DIURETICS
- decrease systemic and pulmonary congestion 
Heart transplant consideration
Poor prognosis
36
Q

What is takotsubo cardiomyopathy (TCM)

A

“Ballooning”

TRANSIENT LV systolic and diastolic dysfunction in the absence of attributable coronary artery disease (CAD)

  • preceded by emotional or physical trigger
  • typically occurs in postmenopausal women
37
Q

TCM presentation

A

-abrupt onset
Present like acute coronary syndrome
SUBSTERNAL CHEST PAIN, dyspnea, syncope
Symptoms of heart failure

38
Q

TCM diagnostics

A

Labs: increased troponin, BNP
EKG: St-segment elevation, deep anterior T-wave inversions (which gradually resolve)
CXR: normal or pulmonary congestion
Echo: decrease EF, possible LVOT obstruction, eval for thrombus
Cardiac MRI: wall motion abnormalities

39
Q

TCM managment

A

IMMEDIATE: similar to any acute MI, including cath lab
Resolve trigger
At discharge
-ASA, BB, and ACE-I until the LV fully recovers
-(+) thrombus = anticoagulation for minimum of 3 months

Long-term: depends on whether LV dysfunction persists
Prognosis: most recover systolic function w/in 4 wks. May have variable EKG changes for several months following event

40
Q

Diagnostic criteria Takotsubo cardiomyopathy

A
  1. There is transient hypokinesis, dyskinesia, or alpines is of the left ventricle
  2. No obstructive coronary artery disease (CAD) or angiographic evidence of an acute plaque rupture
  3. New EKG abnormalities (ST-segment elevation and/or T-wave inversion) or modestly elevated levels of cardiac troponin
  4. Absence of pheochromocytoma or myocarditis

Clin Med 2 (6 decks)

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