Trigger - Cardiomyopathy Flashcards
often missed or underappreciated on echo
diastolic dysfunction
characterized by Abnormal LV relaxation and filling
as well as Elevated filling pressures
diastolic dysfunction
results in necrosis and degeneration of myocytes as well as dilated Cardiomyopathy
myocarditis
can be caused by cytotoxic effects or immune responses
myocarditis
how long does the acute phase of myocarditis last? chronic phase?
acute 2 weeks
chronic (aeverything after 2 weeks)
Presents with chest pain, SOB, fever, HF s/s, and arrhythmias (palps, syncope, death)
acute infective myocarditis
PE shows pleural friction rub, S3/S4 gallop, volume overload and mitral/tricuspid regurg murmur
myocarditis
CXR showing cardiomegaly, pul edema
EKG showing PVCs, sinus tach and dysrhythmias
infective myocarditis
may also see elevated troponins
Elevated ESR, CBC showing eosinophilia, elevated BNP
infective myocarditis
this imaging can aid in assessing the extent of inflammation, myocyte necrosis and scarring and also shows ventricualr size/shape
Cardiac MRI in infective myocarditis
T/F - if there is diastolic dysfunction, there is ALWAYS systolic dysfunction
FALSEEEEEEEE
systolic always leads to diastolic dysfunction.
BUT diastolic dysfunction is not always CAUSED by systolic dysfunction
definitive dx for infective myocarditis
histology with endomyocardial biopsy.
NOT COMMONLY USED unless it will change management for case
treatment for myocarditis
- cardiology consult
- LVEF <40% = ACE and BB
- NSAIDS (colchicine) for pain
- manage arrhythmias
characterized by LVEF <40% with NO CAD or valvular disease.
Dilated CM (dilation and impaired contraction of one or both ventricles)
3x more common in black patients
DCM
primary cause is idiopathic
DCM
caused by chagas disease and lyme disease
DCM
TB, Meningococcal, and pneumococcal bacteria
DCM
autosomal dominant trait
DCM
HCM
involves antibodies to a variety of cardiac proteins
autosomal dominant inherited DCM
thryoid dysfunction
pheochromocytoma
cushings
GH excess/deficiency
DCM
How does Peripartum CM present
SCA or CHF in late pregnancy or early postpartum
PE shows ascites, peripheral edema, elevated JVD
DCM
also PE:
S3/S4 gallop
Rales
Ascites
Peripheral edema
Elevated JVD
murmur or tricuspid/mitral regurg
PE shows rales, S3/S4 gallop and tricuspid or mitral regurg murmur
DCM
also PE:
S3/S4 gallop
Rales
Ascites
Peripheral edema
Elevated JVD
murmur or tricuspid/mitral regurg
EKG shows tachy, LBBB and/or pulsus alternans
DCM
if a CM patient has dyspnea, what test should you order and why?
BNP or NT-ProBNP for prognosis and disease severity
what confirms vnetricular dilation and excludes vascular disease in a DCM patient
Echo!
also dx LV systolic fxn and Pulm HTN
presents with tricuspid or mitral regurg murmur
Infective myocarditis or DCM
i think maybe possible HCM too but im not sure
diastolic dysfunction is associated with which cardiomyopathys
Restrictive and hypertrophic
non-dilated ventricles with impaired filling. fibrosis of ventricular wall.
restrictive cardiomyopathy
biatrial enlargement
restrictive cardiomyopathy
Most Uncommon type of cardiomyopathy
restrictive cardiomyopathy
caused by infiltrative diseases or storage diseases
restrictive cardiomyopathy
can also be caused by radiation, chemo (MCC), carcinoid HD, hypereosinophillic syndrome
MCC in the US is chemo
restrictive cardiomyopathy
treatment for restrictive cardiomyopathy
- treat underlying cuase
- diuretics for edema and congestion
characterized by LV hypertrophy and interventricular septum dysfunction
hypertrophic cardiomyopathy
genetic mutations of sarcomere genes
hypertrophic cardiomyopathy
Presents with fatigue, Chest pain, CHF, and syncope
HCM
also see:
Carotid pulses bisferiens d/t mimicked aortic stenosis.
increased risk for arrhythmias
Carotid pulses bisferiens d/t mimicked aortic stenosis.
HCM
Mid-systolic, harsh, 3rd-4th intercostal that is louder with valsalva
HCM
this murmur is QUIETER with SQUATTING
EKG shows LVH
HCM
Echo showing LV wall >1.5 cm thick
HCM
in this diagnosis we AVOID diuretics and vasodilators. Why?
HCM. because they lower preload and we do not want that
treated with BB and verapamil
HCM
procedures considered for this diagnosis is septal myectomy and alcohol septal ablation
HCM
in this diagnosis, it is reccomended to screen 1st degree relatives annually with an echo until they are 20. then Q5 years after.
HCM
characterized by systolic dysfunction presenting as CHF (edema, JVD, Dyspnea)
ischemic cardiomyopathy
EKG with possible Q waves and CXR showing pulmonary edema
ischemic cardiomyopathy
echo showing decreased LVEF and regional wall motion abnormalities
ischemic cardiomyopathy
RV free wal myocardium replaced by fibrous/fatty tissue leading to RV dilation and abnormal function of RV
Arrhythmogenic RVCM
Causes sudden death in young adults in Europe primarily
Arrhythmogenic RVCM
presents as Chest pain
Palpitations, Syncope, SCA
arrhythmogenic RVCM
Altered myocardial wall d/t intrauterine arrest of compaction of loose interwoven meshwork
LV noncompaction CM
Presents as CHF, Ventricular arrhythmias, thromboembolisms
LV noncompaction cardiomyopathy
Causes ACS due to high catecholamine surge
takotsubo cardiomyppathy aka broken heart syndrome
MC in postmenopausal women
takotsubo cardiomyppathy aka broken heart syndrome
LV apical ballooning on echo or LV angiography
takotsubo cardiomyppathy aka broken heart syndrome
treated with BB for one year
takotsubo cardiomyppathy aka broken heart syndrome
yayyyyy donezo
