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162 Cards in this Set
- Front
- Back
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A systemic disorder resulting from increased deposits of iron in the cell tissues |
Hemochromatosis |
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Disorder of young infants and children characterized by a diffuse fibrosis or hyperplasia of the endocardium |
Endomyocardial disease or endomyocardial fibroelastosis |
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CW Doppler findings of HOCM |
•Calculate max pressure gradient using Bernoulli •Mean gradient much less in comparison to peak gradient |
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Restrictive cardiomyopathy IVRT |
Shortened |
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A diastolic pathology of the LV where filling is resisted or compromised |
Abnormal compliance |
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Prognosis of endomyocardial fibroelastosis |
•Poor depending on extent •95% die 2 years after diagnosis |
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Rare form of endomyocardial fibrosis clinically characterized by chronic elevation of eosinophils |
Lofflers endocarditis or endomyocardial fibrosis |
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How should an obstruction at the papillary muscle be evaluated? |
Color and PW |
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When should amyl nitrate never be given? |
If a patient has a resting gradient of 50 mmHg or 3.5 m/sec and higher |
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Restrictive physiology refers to... |
Nearly all filling occurs very rapidly in early diastole - a result of abnormal compliance |
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IHSS stands for |
Idiopathic hypertrophic subaortic stenosis |
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Restrictive physiology refers to... |
Nearly all filling occurs very rapidly in early diastole - a result of abnormal compliance |
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Color Doppler findings of SAM |
•Aliasing in outflow tract mid to late systole (color m-mode in PLAX) •MR very frequent •AI (small amount) |
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Pitfalls of Doppler with HOCM |
AS can coexist with subaortic stenosis - must obtain gradient from both |
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Color Doppler findings of SAM |
•Aliasing in outflow tract mid to late systole (color m-mode in PLAX) •MR very frequent •AI (small amount) |
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Patchy apoptosis of the RV and, to a lesser extent, LV |
Arrhymogenic right ventricular disease (ARVD) |
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Echo findings of ARVD |
•SVT and ventricular arrhythmias •Right heart failure •Increased risk of perforation and tamponade •Sudden death •Discovered postmortem |
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IHSS is at high risk for |
Sudden death |
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Uneven thickening of ventricular walls |
Asymmetric hypertrophy |
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Uneven thickening of ventricular walls |
Asymmetric hypertrophy |
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Uneven thickening of ventricular walls |
Asymmetric hypertrophy |
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Example of asymmetrical hypertrophy |
IHSS |
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Example of asymmetrical hypertrophy |
IHSS |
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Echo findings of IHSS |
•ASH •Speckled or glassy IVS |
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Echo findings of IHSS |
•ASH (asymmetrical septal hypertrophy) •Speckled or glassy IVS |
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Echo findings of IHSS |
•ASH •Speckled or glassy IVS |
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What can athlete's heart be misdiagnosed as? |
Either DCM or HCM |
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Restrictive cardiomyopathy pulmonary vein flow |
S smaller than D with larger and wider atrial reversal (greater than 35 m/s) |
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Dilated cardiomyopathies aka |
Congestive |
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How to tell the difference between DCM and ischemic dilated cardiomyopathy |
DCM will show segmental wall motion abnormalities, not global akinesis |
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Causes of DCM |
•CAD or MI •Pregnancy •Genetic •Viral •Idiopathic •Cardiac toxicity (chemo, alcohol, drugs) •Hypertension |
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2D findings of DCM |
•Spherical, enlarged LV and/or RV •Poor or absent systolic thickening (poor squeeze during systole) •LAE of varying degrees •Spontaneous contrast (smoke) •Possible thrombus layered along apex or any wall |
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Patient outcome/longevity with DCM depends on: |
•How good the RV systolic function is •The amount of MR or TR and the resultant secondary PHTN that is present |
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M-mode findings of DCM |
•Increased EPSS •Marked LVE, LAE •Decreased EF •Decreased FS or % of thickening |
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PW Doppler of DCM |
V1 (LVOT) is frequently decreased due to decreased systolic pressures in the LV and decreased CO |
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Calculations performed for DCM |
•TR - RVSP •Modified Simpson's for EF (4 and 2 chamber); especially if due to ischemia •diastolic function (restricted late in disease) •dP/dT for systolic function using MR •rule out thrombus (contrast) |
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How to calculate dP/dT for systolic function using MR |
Using MR tracing: •Place a caliper at 1 m/s and again at 3 m/s •Machine calculates dP/dT |
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Ranges for dP/dT |
1000 mmHg and greater = normal Less than 1000 mmHg = abnormal |
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The most commonly identified specific cause of dilated cardiomyopathy |
Ischemic cardiomyopathy |
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Ischemic cardiomyopathies are due to an MI, which causes localized necrosis and scarring, which results in... |
Loss of contractile function in the ventricular segments |
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Chamber dilation in ischemic cardiomyopathies is due to... |
The myocytes distal to the area of infarction undergo increased wall stress |
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What is seen with ischemic cardiomyopathies? |
•MR due to papillary dysfunction •Chronic MR results in volume overload which increases myocardial demands and eventually worsens systolic dysfunction •Atrial and ventricular arrhythmias are common |
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Ischemic cardiomyopathy treatment |
•Pacemaker for arrhythmia •CABG can be performed to try and improve ventricular function |
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When does peripartum cardiomyopathy develop? |
In the last month of pregnancy or within 5 months postpartum |
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When do most cases of peripartum cardiomyopathy occur? |
75% of cases occur in the first two months after delivery |
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Peripartum cardiomyopathy most commonly occurs with: |
•Women older than 30 •Twin pregnancy •African descent •Family history |
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Peripartum cardiomyopathy etiologies |
•Unknown •Possibly related to a reduced suppressor T-cell activity which occurs during pregnancy and results in an autoimmune type of myocardial inflammation |
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Peripartum cardiomyopathy recovery |
•Usually within 6 months •Occurs in 50% of patients •Patients advised not to have further children •If heart fails to recover within 6 months, it usually won't recover at all |
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Alcoholic cardiomyopathy accounts for what percentage of all cardiomyopathies? |
Approximately 4% |
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Alcohol cardiomyopathy is more common amongst who? |
Men |
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Alcoholic cardiomyopathy occurs when? |
With heavy drinking for more than 15 years |
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Cocaine and amphetamines can result in DCM when? |
Single or chronic use |
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What should be done when DCM is due to doxorubicin or other cancer treating agents? |
•Continually monitored •Discontinued if necessary |
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Toxic cardiomyopathy characteristics |
•Diastolic dysfunction precedes systolic dysfunction •LVE is an early finding •HTN •A-fib •CAD |
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Alcoholic DCM treatment |
•Abstinence - can improve systolic function •Heart failure medications - as long as abstinence is involved |
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What can athlete's heart be misdiagnosed as? |
Either DCM or HCM |
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How does the athletic heart contract at rest? |
•Very slowly and without a lot of force •In the habit of being in a state of near hibernation when not in "exercise mode" |
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LV chambers in athlete's heart are larger than normal due to what? |
The extra volume of blood it has become accustomed to having when the person exercises |
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What is seen with athlete's heart? |
•LVE (greater than 6 cm); 20% never decrease back to normal •EF 45-50% at rest •RVE (can cause misdiagnosing of ARVD) •Enlarged aorta •LAE •RAE |
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The added muscle mass of an athletic heart can sometimes be misdiagnosed as... |
Non-obstructive hypertrophic cardiomyopathy |
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Diastolic filling in athlete's heart demonstrates what? |
A restrictive pattern with most filling occurring early |
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When does acute Chagas disease occur and how long does it last? |
•Occurs immediately after infection •May last up to a few weeks or months •Parasites may be found in the circulating blood |
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Chagas disease symptoms |
•Mild or asymptomatic - many remain asymptomatic for life and never develop Chagas-related symptoms •Fever or swelling around site |
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Rarely, acute Chagas disease infection may result in... |
Severe inflammation of the heart muscle or the brain and lining around the brain |
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What percentage of Chagas infected people will develop debilitating, sometimes life-threatening, medical problems over the course of their lives? |
20-30% |
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Complications of Chagas disease include: |
•Heart rhythm abnormalities that can cause sudden death •Dilated esophagus or colon leading to difficulties eating or passing stool •Dilated heart and poor EF |
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In which people can Chagas disease reactivate with parasites found in the circulating blood, causing severe disease? |
People with suppressed immune systems (AIDS or chemotherapy) |
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The leading cause of heart failure in elderly women |
Hypertensive dilated cardiomyopathy |
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What is present with hypertensive dilated cardiomyopathy? |
•LVH initially which progresses into DCM over time •Diastolic dysfunction •A-fib is commonly associated |
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Treatment for hypertensive dilated cardiomyopathy |
Medication to treat the hypertension |
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A syndrome of unknown cause and diverse clinical features |
Takotsubo cardiomyopathy |
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A syndrome of unknown cause and diverse clinical features |
Takotsubo cardiomyopathy |
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Onset symptoms of takotsubo cardiomyopathy |
Resemble acute MI: •Apical akinesis •Basal hyperkinesis •T wave inversion and QT prolongation following MI-like ST elevation on EKG |
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Myocardial enzyme release and angiographical stenosis in takotsubo |
•Minimal myocardial enzyme release •No angiographical stenosis in the coronary arteries |
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Myocardial enzyme release and angiographical stenosis in takotsubo |
•Minimal myocardial enzyme release •No angiographical stenosis in the coronary arteries |
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When is there reversible left ventricular dysfunction in takotsubo? |
After several days |
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Risk factors of takotsubo |
•Mental and/or physical stress (mcc) •Chronic and acute alcohol intake •Hypertension •Diabetes mellitus •Hyperlipidemia •Smoking |
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Etiologies of takotsubo |
•Precise cause is idiopathic •Simultaneous multivessel coronary spasm at the epicardial artery or microvascular levels may contribute to the onset of takotsubo like LV dysfunction •Emotional stress can precipitate severe LV dysfunction in patients without coronary disease •Exaggerated sympathetic stimulation is central to the cause of this syndrome •Most often effects middle aged women |
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An unexplained thickening of a non-dilated LV |
Hypertrophy |
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Etiologies of HCM |
Genetic disease of the heart characterized by excessive overgrowth or thickening of the septum •bulging muscle obstructs normal flow from LV to body •causes increase in LV pressure and puts strain on pumping chamber •causes MV to move abnormally which further blocks the blood flow from LV |
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HCM symptoms |
•Symptoms vary •Appear at any age •SOB (at rest or with exertion) •Chest pain, fainting, fatigue, palpitations •Vary from asymptomatic to mild to severe or have all symptoms •Sudden death (small number) |
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IVS and PW are similar in thickness |
Symmetrical LVH (concentric) |
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2D findings of symmetric LVH |
•Small LV with LVH and/or large sigmoid septum that encroaches upon outflow tract •Small LVOT (less than 1.9cm) •Hypertrophy (symmetric or asymmetric) •Hyperdynamic systolic function with occasional decrease in IVS systolic thickening present (EF greater than 75%) •Possible systolic virtual cavity obliteration d/t symmetric hypertrophy |
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Uneven thickening of ventricular walls |
Asymmetric hypertrophy |
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Example of asymmetrical hypertrophy |
IHSS |
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IHSS stands for |
Idiopathic hypertrophic subaortic stenosis |
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IHSS mcc |
•Idiopathic •Thought to be genetically predisposed (family history) |
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IHSS caused by |
IVS being disproportionately thickened compared to posterior wall |
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IHSS is at high risk for |
Sudden death |
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Echo findings of IHSS |
•ASH (asymmetrical septal hypertrophy) •Speckled IVS or glassy appearance |
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Normal IVS to PW ratio and ASH |
Normal = 1.3:1 ASH = septum greater than 1.3 |
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ASH is seen which diseases? |
•IHSS •AS •Systemic HTN •Posterior MI •Amyloidosis |
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The Venturi effect causes |
SAM |
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What happens with SAM |
Venturi effect pulls the MV apparatus anteriorly towards the septum during systole while MV is closed, obstructing the LVOT |
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Focal thickening of the septum; sigmoid or catenoid IVS |
Basal hypertrophy |
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More accurate measurement for patients whose hearts are "booted up" |
2D |
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Spade like LV |
Apical hypertrophy |
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Apical hypertrophy aka |
Yamaguchi disease |
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Obstruction to flow from out of the ventricle |
HOCM Hypertrophic obstructive cardiomyopathy |
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Apical hypertrophy can result in... |
AS |
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Venturi effect is brought on by: |
•Small LV •Small LVOT •LVH (hypertrophy of septum) •Hyperdynamic LV (EF greater than 75%) |
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HOCM can occur from |
•AMVL •PMVL •Both MV leaflets •Chordae •Hypertrophied papillary muscles in small chambers |
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Venturi effect is brought on by: |
•Small LV •Small LVOT •LVH (hypertrophy of septum) •Hyperdynamic LV (EF greater than 75%) |
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SAM is best seen with which mode? |
M-mode |
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A longer duration of SAM means... |
The more significant the obstruction |
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Obstruction to outflow occurs when... |
MV is in contact with the IVS for at least 30% of systole |
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No fixed cause of obstruction and increased pressure gradient throughout systole is referred to as... |
Dynamic |
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Septal brightness with SAM is due to... |
Scarring where MV strikes the septum |
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Severe LVOT obstruction shows what on m-mode |
Mid-systolic closure of AV |
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Color Doppler findings of SAM |
•Aliasing in outflow tract mid to late systole (color m-mode in PLAX) •MR very frequent •AI (small amount) |
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PW Doppler findings of HOCM |
•Dynamic dagger - peak gradient occurs in mid to late systole •PW for diastolic function (usually abnormal; systolic is usually Hyperdynamic) filling patterns can vary |
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CW Doppler findings of HOCM |
•Calculate max pressure gradient using Bernoulli •Mean gradient much less in comparison to peak gradient |
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When is HOCM gradient "V" shaped (like AS) |
When obstruction is due to a fixed obstruction from a membrane |
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If no obstruction exists at rest, how can it develop? |
Exercise or maneuvers |
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Where can obstructions occur? |
LVOT or RVOT |
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Obstruction at the papillary muscle level is seen how? |
Systolic aliasing of color at the papillary muscle level |
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How should an obstruction at the papillary muscle be evaluated? |
Color and PW |
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What are papillary muscle level obstructions called? |
Intra-cavitary gradients, not obstructive gradients |
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What vasodilator is given for HOCM and what does it do? |
Amyl nitrate - decreases preload (RV then LV filling) creating a smaller cavity and worsens obstruction |
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When should amyl nitrate never be given? |
If a patient has a resting gradient of 50 mmHg or 3.5 m/sec and higher |
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Pitfalls of Doppler with HOCM |
•AS can coexist with subaortic stenosis - must obtain gradient from both •MR waveform can easily be obtained |
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HOCM treatments |
•Beta blocker - keeps HR down and contractility of ventricle low and relaxed •Septal myectomy - overgrown muscle of septum is cut out •Pacemaker - for abnormal septal or RV contraction (not as effective) •Alcohol ablation - complete heart block is most common side effect (requires permanent pacemaker implantation) |
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Restrictive cardiomyopathy aka |
Infiltrative |
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Restrictive cardiomyopathies are due to... |
Metabolic problems which allow cardiac muscle to become infiltrated by abnormal substances |
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Restrictive physiology refers to... |
Nearly all filling occurs very rapidly in early diastole - a result of abnormal compliance |
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A diastolic pathology of the LV where filling is resisted or compromised |
Abnormal compliance |
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Systolic function in restrictive cardiomyopathy |
Can be normal or near normal |
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Restrictive cardiomyopathy pressure tracing |
Dip and plateau or square root |
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Restrictive cardiomyopathy pressure tracing of dip and plateau is caused by... |
Early diastolic pressure drop followed by a rise in pressures |
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Infiltrative cardiomyopathies include: |
•Amyloidosis - mcc •Sarcoidosis •Hemochromatosis •Endocardial fibroelastosis •Eosinophilic endomyocardial disease aka lofflers endocarditis •Arrythmogenic right ventricular disease (ARVD) |
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Signs and symptoms of restrictive cardiomyopathy |
•Elevated RA pressures (mcc) •JVD •Hepatomegally/pulsative liver •Peripheral edema |
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Restrictive cardiomyopathy IVRT |
Shortened |
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Restrictive cardiomyopathy deceleration time |
Extremely short - less than 150 msec |
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Restrictive cardiomyopathy E to A ratio |
E wave much taller than A E to A ratio is 2.2 or more |
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Restrictive cardiomyopathy pulmonary vein flow |
S smaller than D with larger and wider atrial reversal (greater than 35 m/s) |
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Can TDI and color m-mode be performed on restrictive cardiomyopathies |
Yes |
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Nature of restrictive filling patterns |
Malignant |
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Restrictive filling patterns can be seen in patients with... |
DCM in end stage Failing heart transplants |
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Prognosis of restrictive filling patterns |
Poor |
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An eosinophilic fibrous protein that invades the heart becoming deposited between the myocardial fibers |
Amyloidosis |
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What nature is amyloidosis and what is it associated with? |
Familial in nature Associated with myeloma |
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Echo findings of amyloidosis |
•Concentric LVH and RVH •Thickened valves d/t infiltration •Infiltration of coronation and pericardium (granular) •Small pericardial effusion •Biatrial enlargement with small amount of MR and/or TR •Poor systolic function •Diastolic pattern is restrictive filling
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Amyloidosis treatment |
None |
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A systemic disorder resulting from increased deposits of iron in the cell tissues |
Hemochromatosis |
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Echo findings of hemochromatosis |
•LVE •Moderate to severe systolic dysfunction •Fuzzy appearance to the myocardium •Biatrial enlargement •Diastolic function is varied |
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Treatment for hemochromatosis |
Repeated phlebotomy |
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Caused by granulomas involving the heart, eyes, lungs, skin, and other organs |
Sarcoidosis |
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How can sarcoidosis be diagnosed? |
When other organs are affected besides the heart |
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Echo findings of sarcoidosis |
•Thinning of myocardial walls - aneurismal appearance •Biatrial enlargement •V-tach and other arrhythmias, especially heart block, which cause syncope or sudden death |
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Sarcoidosis treatment |
•Steroids - not always effective •Pacemakers for arrhythmias |
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Inherited disorder of young infants and children that live in tropical areas, characterized by a diffuse fibrosis or hyperplasia of the endocardium |
Endomyocardial disease or endomyocardial fibroelastosis |
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Echo findings of endomyocardial fibroelastosis |
•Dilated LV (primary) •LVH •Fibrotic AV and MV with MR •Mural thrombi •Biatrial enlargement |
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Prognosis of endomyocardial fibroelastosis |
•Poor depending on extent •95% die 2 years after diagnosis |
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Endomyocardial fibroelastosis treatment |
Attempted with steroids - not usually successful |
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Rare form of endomyocardial fibrosis, most common in first 2 years of life, clinically characterized by chronic elevation of eosinophils |
Lofflers endocarditis or endomyocardial fibrosis |
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Lofflers endocarditis 2D findings |
•Normal to small cavity sizes •Fibrosis of TV and MV subvalvular areas resulting in MS or TS •Apical thickening with normal systolic motion •Pericardial effusion •Cardiac dysfunction in half of patients •Death d/t CHF |
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Lofflers endocarditis treatment |
Attempted with steroids |
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Patchy apoptosis of the RV and, to a lesser extent, LV |
Arrhymogenic right ventricular disease (ARVD) |
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ARVD aka |
Fat cardiomyopathy- d/t fatty infiltration of RV |
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When do patients present with ARDV |
Early adulthood; familial trait |
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Echo findings of ARVD |
•SVT and ventricular arrhythmias •Right heart failure •Increased risk of perforation and tamponade •Sudden death •Discovered postmortem |
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ARVD treatment |
•Anti-arrhythmia Meds first •Radio frequency ablation •Cardioverter-defibrillators •Heart transplant |
