Module 15 : Dilated and Hypertrophic Cardiomyopathies Flashcards
definition of cardiomyopathy CMO
- primary disease of the myocardium
- excluding myocardial dysfunction due to ischemia or chronic valve disease
what are the 2 classifications of CMOs
- 1st physiology
- 2nd etiology
what are the 4 main types of CMOs
- dilated
- hypertrophic
- restrictive
- other
what are 2 main characteristics of dilated CMO DCMO
- biatrial and biventricular dilation
- ventricular systolic and diastolic dysfunction of the LV and RV
what are 2 main characteristics of hypertrophic CMO. HCMO
- idiopathic asymmetric hypertrophy of heart
- hypertrophic hyper dynamic non dilated left ventricle
what are 3 main characteristics of restrictive CMO RCMO
- increased resistance to ventricular filling due to lack of compliance
- heart failure with increased LVEDP, LAP
- global systolic function preserved
what are 3 main characteristics of other CMOs
- arrhythmogenic RV dysplasia
- LV non compaction
- idiopathic
what is dilated CMO called when there is no known cause
- idiopathic dilated CMO
what will all 4 chambers of the heart look like with dilated CMO
- all 4 may be dilated
what will the systolic and diastolic function be of the LV and RV with dilated CMO
- reduced CO and EF
- elevated LVEDP
- grade 3 DD
what are the 8 main causes of DCMO
- infectious
- toxic
- peripartum
- metabolic
- genetic
- endocrine disease
- idiopathic
- stress induced
what are 3 infectious causes of DCMO
- viral myocarditis
- parasitic
- AIDSq
what are 3 toxic causes of DCMO
- alcohol abuse
- chemotherapy
- drugs
what is perpartum DCMO caused by
- immune system reaction
what is metabolic DCMO caused by
- thiamine deficiency
what is genetic DCMO caused by
- x linked familial disorder
what are the 3 causes of endocrine DCMO
- hypothyroidism
- hyperthyroidism
- pheochromocytoma
what are the signs and symptoms of DCMO related to CHF
- Low BP, fatigue, weaknes
- peripheral cyanosis
- dyspnea/SOB
what are 5 other symptoms of DCMO related to underlying disease
- chest pain
- palpitations
- afib/PVCs
- wet cough
- embolic events
what are 4 complications of DCMO
- systolic embolization
- sys-synchrony of contraction
- cardiac death
- consequences of underlying disease
what will the ECG look like with dCMO
- sinus tach
- conduction defects
- LVH (large QRS complex)
- afib
- LAE
- ventricular arrhythmias
what 2 characteristics will an X-ray have of DCMO
- cardiomegaly
- pulmonary congestion
what are the 2 different treatments of DCMO
- medical
- surgical
what are the medical treatments of DCMO
- treat etiology if known
- dietary changes (less salt)
- alcohol cessation
- drugs
- biventricular pacing
- cardioverter
what are the surgical treatments of DCMO
- mitral valvulolasty/replacemtn
- ventricular reduction
- revascularization
- LVAD
- cardiomyoplasty
- transplant
what are 4 general echo findings of DCMO
- 4 chamber dilation
- pericardial effusion
- aneurysmal apex
- decreased global LV and RV systolic and diastolic function
what are 5 m mode findings of DCMO
- reduced wall excursion (PW < 10mm)
- MV B bump from high LVEDP
- increased EPSS (e point to septum separation)
- decreased AV cusp excursion or opening
- early AV closure
what is the normal EPSS meauremtn
- < 7mm
what would an EPSS of > 20mm indicate about the EF
< 30%
what are 8 2D findings associated with DCMO
- increased LV diameter both systolic and diastolic
- RV enlarged
- decreased EF,FS,CO
- sphericity index > 0.76
- spontaneous contrast in LA and LV
- LV thrombus
- MV tenting
- biatrial enlargement
what are 7 doppler findings with DCMO
- MR 100% of the time
- TR
- PR
- AR
- decreased LVOT velocity
- color doppler fill reduced
- decreased PV acceleration time
what are the 5 doppler measurements for DCMO
- CO
- severity of regurge
- SPAp, MPAP, PAEDP
- LV EDP
- LV Dp/Dt
why is the LV Dp/Dt measurement so important for DCMO
- MR always present and reduced afterload which will make EF higher than is
- can asses global systolic function way better
how does the angle of MV inflow change with DCMO
- normal = inflow < 20º lateral to apex
- dilates = inflow up to 40º from apex
what are 3 other structs that might occur at the apex other than thrombi
- aberrant chordae
- ruptured chordae or pap
- prominent LV trabeculations
what are 7 tips for detecting LV thrombus
- highest frequency
- harmonics
- reduce depth
- focal zone
- pan through LV
- confirm thrombus in 2 or more planes
- color doppler
what is the etiology of hypertrophic CMO HCMO
- inherited disease = X linked autosomal dominant
- increased muscle mass due to myofibril disarray producing symmetric hypertrophy of the heart
what are the 2 sub groups of HCMO and what are they based on
- non obstructive
- hypertrophic obstructive CMO
+ HOCMO - base on whether hypertrophy is causing any LV outflow obstruction
which area of the heart will most likely result in HOCMO
- basal anterior septum
what are 3 characteritcs of non obstructive HCMO
- LVOT PG < 30mmHg at rest
- potential for LVOT obstruction to develop wth time
- VALSALVA EVERY PATIENT
what are 4 characteritcs of HOCMO
- dynamic obstruction
+ occurs when MV leaflets com in contact with thick IVS - LVOT PG > 30mmHg at rest
- latent obstruction discoverable with valsalva
- if obstruction present at rest then present always
what are 7 clinical signs of HCMO
- angina
- exercise intolerance
- arrhythmias
- AV blocks
- systolic murmur
- syncope
- sudden death
what are 3 M mode characteristics of HCMO
- systolic anterior motion of MV SAM
- wall thickness IVS basal vs LVW basal
+ high risk > 30mm - mid systolic closure of AV
what are the 2D findings of HCMO
- ASH
- narrowed LVOt
- IVS > 1.3
- IVS:LVPW > 1.3
- thickened ground glass IVS
- decreased systolic IVS thickening
- hyper dynamic LV motion
what are the 3 forms of HCMO
- basal IVS segment
- mid ventricular hypertrophy
- apical hypertrophy
what are the 3 types of HOCMO
- persistance obstruction
- provocable obstruction
- latent obstruction
what is persistant HOCMO
- obstruction at rest no provocation
- high velocity LVOT
what is provable HOCMO
- mild obstruction at rest that increases with provocation
- gets worse with valsalva
what is latent HOCMO
- near normal velocity at rest that increases with provocation
- obstruction only during valsalva
what 2 factors is obstructive CMO dependant on
- preload
- afterload
what will increase the obstruction
- lower preload lower LV volume increased contractiliyc and decreased afterload
what are the 3 provocative maneuver to uncover latent obstruction
- amyl nitrate
- valsalva
- stress test
what will a dynamic flow obstruction look like on doppler
- mid to late systolic peaking of LVOT flow
- gradient across LVOT
- use PW to map level of obstruction
- CW to display peak velocity
- as gradient increases the degree or severity increases
characteristics of mid ventricular HCMO
- entire LV extremely thick \+ concentric - obstruction in mid ventricular cavity - LV contracts on itself - lv cavity obliterates duding systole -
echo findings of mid ventricular HCMO
- very thick LV
- small LV cavity
- color doppler increase velocityes
- MR
- LVOT obstruction at higher heart rates
- saw tooth waveforms
characteristics of apical HCMO
- similar to mid ventricle
- need to image true apex
- heart cavity globular inchape
- color doppler to identify obstruction
- look for apical infarction, clot, aneurysm
what are the 2 main treatments of HCMO
- medical
- surgical
what are the 2 medical treatments of HCMO
- improve diastolic function with meds
- prevention of sudden death (Cardiac defibrillator)
what are the 3 surgical treatments of HCMO
- spatial ablation
- myectomy
- percutaneous intervention
