Flashcards in Cardiomyopathy/Pericarditis Deck (35):
Mycarditis - etiology
1) Infection - VIRUS, parasite, fungal, bacteria
Fever, myalgia, muscle tenderness, chest pain with ECG arrhythmia, fatigue, dyspnea, CHF
pathology of viral myocarditis
imflammation with lymphocytes
more common in immunosuppressed
collagen vascular or CT disease systemic, (lupus, scleroderma, RA) to affect all three layers of heart
chemo drug to lead to toxic accumulation and myocarditis
What toxins cause mycarditis
Adriamycin, ethanol, cobalt, hemochromatosis
Protein deposition (beta pleated sheets) to cause myocarditis
Associated symptoms of dilated cardiomyopathy
normal HF, ventricular thrombus, M/T regurgitation, arrhythmia
Increased BNP in dilated cardiomyopathy
disproportionate Septum thickening to cause diastolic dysfunction.
Myocyte dissaray and concentric hypertrophy.
EF in dialated ver hypertrophic
dilated is reduced
hypertrophy - normal of hyperdynamic
Murmur is hypertrophic cardiomypathy
systolic murmur that increases with standing and valsava
Systolic anterior movement of mitral valve... gets stuck in outflow track to lead to mitral regurgitation murmur in systole.
Surgical tx of hypertrophic cardiomyopathy
myomectomy and alcohol ablation
diastolic dysfunction due to scar and fibrosis of heart. Most common cuases are amylodosis, sarcoidosis, hemochromatosis, raditiaion
Arrhythmogenic Right Ventricular cardiomyopathy
mycardium is replaced by fibroblast --> arrhythmia prone. More prevalent in RV than LV.
Secondary cuases of Hypertension
renal (diabetes, renal a. stenosis), endocrine, cardiovascualr
ECG finding of acute pericarditis
diffuse ST elevation
alteration of QRS amplitude between beats in pericardial effusion
decreased systolic BP >10 mm with inspiration - in pericardial effusion and cardiac tamponade.
ECHO in cardiac tamponade
effusion, RV and RA collapse, dialted IVC
Symptoms of constrictive pericarditis
elevated JVP, edema, ascites, tachy, hepatomegaly, 3rd heart sound.
Loss of function mutation in IKS - cannot hyperpolarize
loss of function mutation in IKR
gain of function in INa - does not inactivation
Gain of Function in Long QT
I Na - no inactivation
incomplete ICa inactivation to prolong phase 2
mutation in CaV1.2 (de novo) to have also immunodeficiency and cognitive abnormalities (autism)
G406R and G402S (exon 8 and 8A)
Sudden unexplained death syndrome that makes one prone to ventricular arrhythmias due to Na Channel mutation, ankryn mutation, and Cav1.2 to shorten QT
Mutation in IKs so it cannot bind to Yotiao. Yotiao binds PKA to Ca and K channels. Thus a mutation in IKs means that when increased sympathetic activity, there wont be enough K channels to match increased Ca current and leads to afterpolarizations.
how to overcome re-entry?
1) unidirection --> bidirectional block
2) prolong refractory time
how do you convert uni to bidirectional block?
1) slow conduction velocity so it cant propogate into depressred region
2) prolong refractory peroid
Catecholaminergic polymorphic Ventricular Tachy (CPVT)
no ECG abnormality, but apparent wit exercise of catecholamines.
RyR2 mutation that leads to Ca leaking from SR or increases RyR2 senstivity.
Calsequestrin mutation so it can no longer buffer and RyR2 is no longer regulated.