Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
53 Cards in this Set
- Front
- Back
|
Dilated CMO is a ___________ disease. |
Systolic |
|
|
Primary causes of Dilated CMO |
- Idiopathic causes (unknown origin) - Familial causes |
|
|
Secondary causes of Dilated CMO |
#1- Coronary Artery Disease #2- Alcohol Induced Others: chemotherapy, peripartum, systemic disease, AIDS, stress induced, etc. |
|
|
Takotsubo CMO |
- Broken heart syndrome - Temporary CMO brought on by stressful situations - Apex of heart balloons and is dysfunctional - Condition reverses itself |
|
|
Anatomy of Dilated CMO |
- Systolic disorder - Decreased ejection fraction (usually lower than 30%) - Dilated LV and RV (biatrial enlargement may occur) - Increased cardiac weight due to chamber dilation - Increased LV volume and LV mass |
|
|
LV Dilation in DCM is due to: |
- The heart trying to compensate in order to try to achieve a normal cardiac output. - Only works for a short time--eventually it won't help anymore (Frank Starling's Law: too much stretch is not a good thing) |
|
|
Symptoms of Dilated CMO |
- Symptoms of heart failure - Breathing difficulties - Fatigue/exercise intolerance - Angina - Ascites, edema - Coughing - Tachycardia |
|
|
Clinical Findings of DCM |
- Congestive heart failure - Conduction abnormalities - Murmur (and regurgitation) due to valve annulus stretching with ventricle dilation - Enlarged heart on x-ray - Pleural effusion - Pulmonary Congestion |
|
|
Dilated CMO 2D Echo Findings |
- RV and LV enlargement - Impaired systolic function (low CO, SV, EF, CI) - Global hypokinesis - Walls may be thinned due to dilation or be normal thickness - Elevated LVEDP (due to chronic increase in LAP, diastolic dysfunction, B-notch on m-mode) |
|
|
B-Notch on M-mode means: |
Increased LVEDP |
|
|
Biplanes Simpsons EF Formula |
LVEDV (avg. of 4C and 2C) - LVESV (avg. of 4C and 2C) EF (%) = --------------------------------------------------------------------------- * 100 LVEDV (avg. of 4C and 2C) |
|
|
Which CMO may we see smoke in the LV? |
DCM |
|
|
DCM M-Mode Findings |
- Increase in LVEDD/LVESD - B-notch - Increased EPSS (> 7mm points to DCM) - Decreased D-E excursion (= low CO) - Decreased motion of aortic root |
|
|
RVSP Formula |
RVSP = 4 * (Peak TR velocity ^2) + RA pressure |
|
|
What does dP/dT tell us? What are normal values? |
- The estimated myocardial contractility. - Measures the rate of LV pressure rise over time - Normal: >1200 mmHg - Abnormal: <1000 mmHg |
|
|
Diastolic Function Patterns in DCM |
- Normal (I): early in disease course - Impaired relaxation (II): small E, big A, long DT - Pseudonormal (III): tissue doppler abnormal - Restrictive (IV): big E, small A, short DT *poor prognosis* |
|
|
Hypertrophic CMO Definition |
- Massive hypertrophy of the myocardium without an underlying cause. - Three types: non-obstructive, obstructive, and provokable obstructive |
|
|
Non-Obstructive HCM |
- Uniform distribution of hypertrophy - No LVOT obstruction |
|
|
Obstructive HCM |
- Asymmetric hypertrophy - Obstruction of the LVOT |
|
|
Provokable Obstructive HCM |
- Obstruction is latent at rest - Obstruction present when provoked by: maneuvers (ex. valsalva), medications, exercise |
|
|
Asymmetrical Septal Hypertrophy |
- Most common distribution - Anterior portion of IVS |
|
|
Concentric Hypertrophy |
- Increased wall thickness is equal along the whole LV |
|
|
Free Wall Hypertrophy |
- Increased wall thickness on the LV free wall only |
|
|
Mid-Ventricular Hypertrophy |
- Increased LV wall thickness at base and mid levels - Thinned or aneurismal at LV apex |
|
|
Apical Hypertrophy |
- Increased LV wall thickness at apex only - "Ace of Spades" |
|
|
Which CMO is the leading cause of sudden cardiac death in people under the age of 30? |
Hypertrophic CMO |
|
|
Anatomy/Pathology of HCM |
- Small LV cavity size - Hyperdynamic LV function (EF > 70%) - Thickened LV walls - LVOT obstruction (in obstructed HCM) - Systolic Anterior Motion of the MV (SAM) - Primarily a diastolic disorder - Myocardial ischemia--decreased CO - Arrhythmia's - Atrial fibrillation |
|
|
Symptoms of HCM |
- Dyspnea - Syncope - Angina - Pulmonary edema - Sudden death - May be assymptomatic |
|
|
Clinical Findings of HCM |
- Cardiomegaly - Increased QRS voltage on ECG - Arrhythmia's - In apical HCM: giant negative T waves in V leads - Murmurs |
|
|
2D/M-mode/Doppler Echo Findings of HCM |
- Small LV Cavity size - Hyperdynamic function - SAM - B-notch - Mid-systolic notching/closure of AV - Doppler: need to pulse up the septum with PW till it aliases and then switch to CW |
|
|
LVOT Doppler Signal with CW |
- The peak intraventricular pressure gradient looks like a dagger - Dagger shaped because of late peaking signal - Use provokable maneuvers to make sure you get the peak gradient |
|
|
Provokable Maneuvers |
- Maneuvers that decrease the LV volume or increase the contractility that will increase the severity of the obstruction and the intensity of murmurs - Valsalva, squatting, leg raises, etc. |
|
|
Treatment of HOCM |
- Avoid strenuous exercise - Cardioversion for A-fib - Medications - Pacemaker - Alcohol septal ablation - Myectomy |
|
|
Restrictive CMO Definition |
Characterized by normal LV size and systolic function, marked atrial enlargement, and impaired filling of the ventricles due to poor compliance--myocardial stiffening. Diastolic disorder of the heart. Least common CMO. |
|
|
Primary Causes of RCM |
Idiopathic Endomyocardial fibrosis: scarring of the heart |
|
|
Secondary Causes of RCM |
For these, Doppler/diastolic function is similar to primary RCM but the 2D findings are diagnostic of underlying pathology. Different diseases cause RCM, and a biopsy is needed to differentiate which one. |
|
|
2D and M-mode Findings of RCM |
- Biatrial enlargement - Normal LV size - Normal LV systolic function - Normal wall thickness - Due to LA pressure, RV size may increase - Depending on the cause, different pathologies cause different findings |
|
|
Doppler Findings of RCM |
- Abnormal diastolic function - MV Inflow: * Increased high E vel >1.0 m/sec * Decreased low A vel < 0.5 m/sec * Increased E/A ratios > 2.0 * Decreased/Short decel times < 150 m/sec * Decreased IVRT < 70 msec |
|
|
Constriction vs Restriction |
Constriction: thickened and noncompliant pericardium, and will have respiratory variation on tissue doppler Restriction: stiff and noncompliant ventricular myocardium, and rarely shows respiratory variation. |
|
|
Amyloidosis |
- Secondary RCM - Deposition of amyloid (waxy, translucent, abnormal protein) in the heart - Leads to increased wall thickness - Most common form of RCM - ECG's QRS has normal/low voltage |
|
|
Doppler findings of Amyloidosis: |
- Regurgitation of all cardiac valves - Increased RVSP - Low CO - Diastolic function worsens as disease progresses - Tissue doppler: Low E |
|
|
2D findings of Amyloidosis: |
- Normal LV size and function - Increased LV and RV wall thickness - Biatrial enlargement - Thickened valves - Pericardial effusion (small) - Pleural effusion (may be large) - Ground glass appearance of myocardium - Diffuse RWMA |
|
|
Prognosis and Treatment of Amyloidosis |
- Increased mortality if DT time < 150 msec - Fatal prognosis due to fatal arrhythmias, congestive heart failure - Challenging to treat |
|
|
Sarcoidosis |
- Secondary RCM - Infiltrative granulomatous disease of unknown etiology involving multiple organs - Often includes pulmonary involvement (PHTN, right heart failure, pulmonary fibrosis) |
|
|
Echo Findings of Sarcoidosis |
- Need good TR velocity to assess PHTN - Increased wall thickness early in disease process, segmental wall thinning late in disease process - RWMA inconsistent to coronary involvement - Aneurysm - Enlarged LV with decreased function - Pericardial effusion |
|
|
Hemochromatosis |
- Secondary RCM - Storage disease of excess accumulation of iron in the tissues - Can damage heart, liver, pancreas, pituitary, gonads, and joints - Genetic - Results in heart failure |
|
|
2D Echo Findings of Hemochromatosis |
- Normal/dilated LV - Normal LV wall thickness - Systolic dysfunction - Normal valves - Biatrial enlargement--MR/TR |
|
|
Pompe's Disease |
- Secondary RCM - Glycogen storage disease - Excessive glycogen storage in heart tissue - Occurs early in life - Echo findings: cardiomegaly, hypertrophy, decreased LV function |
|
|
Hypereosinophilia |
- Secondary RCM - Idiopathic systemic illness presenting with elevated eosinophil counts in the blood - Persistant eosinophil count > 1500 cells/mm^2 - Eosinophils infiltrate the end and myocardium--often found in the apex - May look like apical HCM |
|
|
Echo Findings of Hypereosinophilia |
- Normal LV size and systolic function - Atrial enlargement - Apex of the heart is obliterated by thrombus-eosinophilic material - Posterior mitral valve leaflet affected - MR/TR |
|
|
Carcinoid Heart Disease |
- Carcinoid tumor usually starting in GI tract or liver metastasized to the heart - Right-sided heart failure - Glistening deposits may be seen on TV and PV - Echo findings: thickened TV, severe TR, RAE, RVE, pericardial effusion |
|
|
Arrythmogenic RV Cardiomyopathy |
- Rare congenital abnormality with abnormal development of the tissue of the RV, resulting in a form of RV CMO - Progressive loss of RV myocardium that is replaced with fiber-fatty tissue - Ventricular arrythmias and sudden death - Dilated RV and decreased RV function - Familial |
|
|
Non-Compaction Syndrome |
- Genetic CMO - Thick, prominent trabeculated LV myocardium with deep recesses (fingerlike projections in LV apex) - Similar clinical findings to other CMO's (heart failure, embolic events, arrthymias) |
