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22 Cards in this Set
- Front
- Back
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What's the pathophysiology of DCM?
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injury (CAD/ EtOH/ chemotox/ infl/ genetic/ peripartum) leads to diastolic and systolic dysfxn, myocardial toxicity, neurohormonal changes, remodeling and hemodynamic changes.
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What do you see clinically with DCM?
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volumer overload (congestion) sympts, low CO sympts, arrhythmias, end-organ dysfxn, thromboemboli, tachycardia,RV heave, lat PMI, S3, S4, TR/MR, rales/wheezing, incr JVP, cachexia
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Prognosis for DCM
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depends on etiology, severity, fxnal impairment. 20-50 % 5-yr survival.
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Evaluation of DCM
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echo: thin dilated ventricle, enlarged chambers
ECG: LBBB, infract pattern CXR: enlarged silhouette labs: metabolic, CBC, thyroid, iron, HIV |
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Management of DCM
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meds: diuretics, ACEI, ARB, bB, adoctone, NO, digoxin, anticoag.
device: biV pacemaker, ICD. surg: revascularization, valve repair, cardiac transplants, V assist device |
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What's HCM?
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Usually genetic, LVH w/o loading conditions to account for it. asymmetrical (usually) or concentric hypertrophy. LVH --> impaired relaxation/filling and subendocardial ischemia. If asymmetric --> LV outflow obstruction. may progress to DCM.
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Clinical signs of HCM
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asymptomatic usually, dyspnea, angina, palpitations/ dizziness/ syncope, bifid pulse, forceful LV, S4, sys cres-descresc murmur
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Evaluation of HCM (lab tests)
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ECG: LVH
echo: V hypertrophy, small V cavity, SAM --> MR Holtermonitoring: atrial and/or V arrythmias. |
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Management for HCM
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avoid vigorous exercise
meds: bB, CCB (incr diastole), dysopyramide (neg inotrope), antiarrythmics device: dual chamber pacemaker, ICD myectomy (alcohol ablation, surgical) heart transplantation |
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What's RCM?
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imparied V filling with ~normal systolic function. primary or secondary. from infiltration/fibrosis --> stiff noncompliant ventricle
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Clinical manifestations of RCM
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volume overload, low CO, thromboembolism, atrial arrhythmias, conduction system abn, S3, holosys TR/MR murmur, incr JVP, Kussmaul's, enlarged liver, ascites, edema.
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Tests for RCM
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EKG: bilat enlargement, low QRS voltage (amyloid)
echo: atrial enlargement, normal V, "speckled myocardium" (amyloid) CT/MRI: infiltrates in pericardium cardiac cath: distinguish RCM from constrictive with hemodynamics labs: Fe, CBC, serum/usine |
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Management of RCM
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if Fe: phlebotomy/chelation.
sarcoidosis: steroids Loeffler's endocarditis: steroids, cytotoxic agents med: decr preload, anticoag prophylaxis amyloidosis returns with a heart transplant |
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What's arrhythmogenic RV dysplasia?
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RV muscle is replaced by fibro-fatty tissue, 30-50 % familial. apoptosis, infl and myocardial dystorphy --> RV fxnal and structural changes --> electrical instability and RV/biV dysfxn.
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Clinical manifestations of arrhythmogenic RV dysplasia
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often asymptomatic, palpitations, syncope, SCD, HF. 2.5 % mortality/yr.
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Tests for arrhythmogenic RV dysplasia
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ECG: epsilon wave and inversted t-wave in V1-V3
echo: dilated hypokinetic RV MRI: mainstay to evaluate patients |
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Management for arrhythmogenic RV dysplasia
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meds: bB, anti-arrhythmics, HF Rx
radiofrequency ablation of V-arrhythmias ICD |
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What's ventricular noncompaction?
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Spongiform cardiomyopathy.
intrauterine arrest of compaction, have deep traculations in V walls, so myocardium appears thickened with hypokinetic segments w/ thin compacted myocardium and thick noncompated layer (endo). familiar and nonfamilial. --> sys dyfxn, HF, thromboemboli, arrhythmias, high mortality |
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What's tachycardia-induced cardiomyopathy?
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potentially reversable DCM, LV sys dysfxn secondary to SVT or V-tach. systolic function normalized with cessation of tachycardia.
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Tako-tsubo CM
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Stress-induced, mimics STEMI in absence of CAD.
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What's mitochondrial cardiomyopathy?
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mutations in DNA/proteins. progressive myocardial hypertrophy, dilation and arrhythmias. Generally systemic (MELAS, Kearns-Sayre Syndrome)
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What's endocardial fibroelastosis?
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Rare, infancy or early childhood.
Thickened LV or L cardiac valves. |
