Echo test 1

Aorta

1. if you are seeing more of the ascending aorta, you are too high (move down intercostal space) 2. if you are seeing less of the aortic root, you are too low (move up an intercostal space)

LV mass quantification

(basically is there hypertrophy or not (thickening)) 1. M mode 2. area length method 3. truncated ellipsoid method 4. subjective assessment -subjective assessment (also called "eye-balling" and gesalt viewing) is the most common method done by experienced sonographers

LV mass quantification 2

1. 2D, M mode method using parasternal short axis view or parasternal long axis view 2. assumes that LV is ellipsoid 3. measurment made at end diastole 4. ASE approved cube formula: LV mass index (g/m^2)= LV mass/BSA 5. small errors in M mode cause large errors in mass values. can have off axis/tangential cuts due to motion 6. dont use M mode with wall motion abnormality--> 2D accurate with WMA (don't memorize formula) 7. 1/3= minor demention, 2/3= major demention 8. normal LV mass index for males: 93 +/- 22 g/m^2 9. normal LV mass index for frmales: 76 +/- 18 g/m^2

HCMO M mode

1. ASH or another form of hypertrophy, such as concentric, midventricular or apical 2. SAM 3. LVOTO created by small hyperdynamic left ventricular cavity, ASH and SAM 4. mitral valve E point to septal contact 5. small left ventricle with hyperkinetic wall motion (chamber obliteration) 6. aortic valve notching (partial mid systolic closure) of the AoV due to sudden decrease in cardiac output 7. left atrial enlargement (LAE) resulting from mitral regurgitation and/or diastolic dysfunction due to noncompliant left ventricle

causes of LV systolic dysfunction

1. CAD 2. HTN 3. cardiomyopathy (iDCM, HCM, Etoh, Peripartum, viral, infiltrative, toxins, thyroid Dz., tachyarrythmias) 4. vascular disease

introduction

1. CHF affects over 3 million Americans 2. 400,000 new cases & 800,000 hospitalizations annually 3. CHF: primarily a disorder of the elderly 4. among the elderly, it is the most frequent hospital discharge 5. consumes over 10 billion health care dollars 6. major change in demographics in north america 7. mean age of population increasing significantly; fastest growth in 65 years and older 8. in the US, 40% of federal money spending goes to this population and the population of the elderly will increase x4 by 2030 9. CV (cardiovascular) disease is on of the most common causes of morbidity (illness) & mortality in this group, yet few studies exist and the ones that do the elderly were systemically excluded from the trials 10. thus cardiovascular specialists are not prepared to deal with an age group that includes most patients with cardiovascular disease

screen information

1. F= frequency 2. D= depth 3. G= gain 4. FR= frame rate -highest FR possible 5. persistence (frame averaging) -IP on top right, uses lot of images from older frames to make picture smoother 6. DR= dynamic range -determines how many shades of gray are displayed

LV systolic function variables

1. FS=(LVIDd-LVIDs)/LVIDdx100 2. percent change in LV dimension with systolic contraction 3. FS approximates EF if there are no significant wall motion abnormalities 4. SV=EDV-ESV EF=EDV-ESV/EDVx100 CO=SVxHR

diastolic heart failure

1. HF is the commonest hospital discharge diagnosis in the elderly 2. HF in the elderly is the major cause of death and disability in US: fatality up to 25%; 90 day hospital readmission up to 50% -50% readmitted with a stay of 90 days 3. DHF is a clinical syndrome manifested by HF symptoms and normal or even small LV cavity size with thickened walls and normal LV EF -systolic dysfunction with EF 4. systemic HTN increases afterload 5. LV diastolic relaxation is sensitive to increased afterload

PLAX imaging goals

1. IVS and aorta are parallel and continuous of one another (have to find the break to measure IVS) -if walls thick but no high BP, check again 2. IVS and posterior wall parallel 2. all structures seen 3. mitral valve in the middle of sector 4. LV elongated, no apex seen 5. depth at the level of the DTA 6. focal zone at pericardium (starting out) 7. aortic valve has eccentric closure (even closure-close at center of vessel)

how to measure

1. LA measurement done at same angle as LVIDd and in end systole (maximum size) -measured posterior to AoV -anything above normal is considered LAE (left atrial englargement) 2. Ao diameter (root) when closed (end diastole), inner edge to inner edge 3. LVOT measured when Ao open (systole) and as close to aorta as possible -1.8-2.0cm (tall people may be over 2.0 or below for short) -important for Aortic stenosis patients -underestimation of the LVOT diameter will cause AVA (aortic valve area) to be overestimated -overestimation of the LVOT diameter will cause the AVA to be underestimated -LVOT number squared so if wrong- number will be way off (need LVOT diameter^2, LVOT peak velocity and aortic peak velocity

summary

1. LV mass quantification: M mode, area length method, truncated ellipsoid method, and subjective assessment 2. LV volume quantification: M mode, subjective assessment 3. LV function quantification: modified simpsons and subjective assessment by region... also by M mode, single plane are length method, velocity of circumferential shortening, mitral annular excursion, EPSS, index of myocardial performance, etc 4. modalities limited by: -quality of echo windows -accurate measurements are based on the ability to identify and capture ideal axis (recognize misleading off axis/tangential slices), and of course, sonographers experience

hypertrophic obstructive cardiomyopathy (HOCM)

1. LVH that is asymmetric, concentric, or midventricular with a LVOTO -idiopathic hypertrophic subaortic stenosis (IHSS) with asymmetric septal hypertrophy (ASH- on IVS) + systolic anterior motion (SAM-during systole anterior MV leaflet being pulled into LVOT) of the mitral valve leaflets and/or chordae tendineae --> LVOTO -HOCM with concentric LVH + SAM --> LVOTO -HOCM with midventricular LVH --> LVOTO 2. provocable HOCM: LVH with a LVOTO, but only when provoked with exercise, coughing, drugs, valsalva maneuver, stress echo, other 3. non-obstructive HCMO: (non-obstructive HCMO) LVH that is apical or other, without LVOTO 4. treatments: -septal myectomy: removal -alcohol septal ablation: ethyl alcohol injected to kill wall/thickness -ICD causes delay in contraction to decrease LVOTO

how do we quantify LV function

1. M mode * 2. modified simpsons method * 3. single plane area length method 4. velocity of circumferential shortening 5. mitral annular excursion * 6. E point to septal separation * 7. index of myocardial performance 8. subjective assessment * *=used the most

mitral annular excursion toward LV apex

1. M mode tracing in systole through septal mitral annulus 2. the magnitude of systolic motion is proportional to the longitudinal shortening of the LV 3. normal mitral annular systolic motion is 8mm+ (average 12+/- 2 on apical 4 or apical 2 views) -usually done in apical 4 4. if motion is <8mm, the EF is likely <50% 5. AKA MAPSE (mitral annular plane systolic excursion) 6. measure height of waveform (height of annulus toward apex)

DHF pathophysiology

1. Pts with this syndrome have an inability to increase stroke volume by frank-sterling mechanism despite severely increased LV filling pressure, indicative of diastolic dysfunction 2. severe exercise intolerance due to a reduction in exercise cardiac output and early lactate formation (cant exercise) 3. primary symptom, similar to systolic dysfunction, is exercise intolerance, manifested as exertional dyspnea fatigue 4. increased prevalence of systemic hypertension in diastolic HR 5. severe HTN is frequently present during the early phases of acute episodes of CHF in such pts

velocity of circumferential shortening

1. VCF is the mean velocity of LV shortening through the minor axis (IVS to posterior wall) 2. vcf= FS/ET (ejection time) 3. ET is the time between LV isovolumetric contraction and isovolumetric relaxation (systole in middle) 4. measure by obtaining M mode of AV opening to AV closure, aortic flow by doppler, or by an (external pulse recording of carotid artery-we don't do) 5. nl values are >1.0c/s -c/s= circumference/seconds 6. shlow vcf may suggest diminished systolic function <50%

dilated cardiomyopathy (DCMO)

1. aka congestive CMO, most common, multi-chamber enlargement (increased volume) and decreased diastolic and systolic function 2. can be asymptomatic- no treatment 3. lifestyle adjustments, medical therapy, ICD (implanted cardioverter defibrillator, transplant 4. thin walls 5. spontaneous echo contrast (smoke) due to decreased flow patterm 6. possible thrombus at apex, use contrast if cant see apex or use CFD to see if fills apex , or TEE 7. M mode -thin walls with decreased function -increased chamber size -increased MV E point to septal separation that is >0.7cm -decreased MV D-E excursion (D-E leaning more) -decreased MV excursion-double diamond -B notch on MV due to increased left ventricular end diastolic pressure (LVEDP= or > 15mmHg) -means decreased EDP 8. regurgitation probable

endomyocardial fibrosis

1. an endocardial disease where fibrotic tissue lines the myocardium; may be diffuse or local 2. local areas of necrosis are prone to apical thrombus 3. left ventricular function is usually preserved 4. it may involve the valves, leading ti severe regurgitation and dilated atria

LV volume measurment with M mode

1. assuming normal ventricle morphology V=(LVID)^3 --> in machine 2. if ventricle is dilated (spherical): -teichholz equation (long equation don't need to know)

acoustic quantification

1. automatic detection of blood tissue border based on integrated back-scatter analysis 2. this is the difference in amplitude of back-scatter between myocardial wall and blood 3. blood tissue border is recognized by echo machine, and mark with dots 4. button called strain 5. new technology 6. area of study is quantified continuously in real time throughout cardiac cycle (don't have to freeze image) 7. therefore, the change in LV cavity area or volume with systolic contraction is calculated instantaneously, thereby providing LVEF 8. AO limited by its dependency on echo echo gain and image quality 9. echo gain: amplification of the returning signal which weakens with distance thereby decreasing accuracy....lateral wall is especially subject to error..... -if cant see, don't activate

HCMO doppler

1. if LVOTO present, the velocity will increase >2m/s, switch to CW to avoid aliasing (walk the dog) 2. the LVOTO is a late peaking systolic jet (dagger shape) 3. acquire the LVOTO peak velocity and mean PG -trace waveform (planimeter) for mean PG 4. when LVOTO and MR present, differentiate the two by waveform shape (MR longer- leaks last longer) 5. perform valsalva maneuver or adminiter medications while acquiring LVOT doppler samples if a provocable HOCM is suspected

RVOT/RVIT

1. if the RVOT is being seen you are aimed too superior -to correct aim inferior 2. if the RVIT is being seen you are aimed too inferior -to correct aim superior

assessment of regional function

1. based on grading wall motion divided into the 16 (17) segment model as proposed by the ASE 2. each segment can be viewed in multiple tomographic planes 3. breaks down LV into numbers 4. used in older labs with stress echo 5. 17 just means last segment is apical cap 6. lateral wall split into apical, mid, and basal sections 7. 1=normal 2=hypokinesis 3=akinesis 4=dyskinesis 5=aneursmal -wall motion scoring index 6. WMSI= sum of scores/number of visualized segments 7. WMSI> 1.7 may suggest perfusion defect > 20% 8. quantitative estimates errors due to : underestimation of EF due to endocardial echo drop out and seeing mostly epicardial motion -if we cant see entire endocardium border, >80% or else have to use contrast 9. underestimation of EF with enlarged LV cavity; a large LV can eject more blood with less endocardial motion (higher EF) 10. overestimation of EF with a smaller LV cavity-doesn't mean small in systole 11. significant segmental wall motion abnormalities

measurements

1. can be taken on 2D or M mode 2. can differ per facility 3. anything outside of normal range is abnormal 4. normal 2D (all cm) -RVd: 1.9-3.6 -IVSd: 0.6-1.1 -LVIDd: 3.5-6.0 -LVPW: 0.6-1.1 (diastole) -Ao root: 2.0-3.7 -ACS: 1.5-2.6 -LVIDs: 2.1-4.0 -LA: 2.3-3.8 5. normal M mode values (all cm) -RVFW: 0.5-0.8 -RVd: 1.9-2.6 -IVSd: 0.6-1.1 -LVIDd: 3.7-5.6 -LVIDs: 2.0-3.8 -LVPW: 0.6-1.1 -Ao root: 2.0-3.7 -ACs: 1.5-2.6 -LA: 1.9-4.0 6. usually don't measure ascending Ao unless root is dilated

Grade I (delayed relaxation)

1. decrease in LV pressure bu increase in LA pressure 2. altered LV filling pattern delayed relaxation -reduced peak rate and amount of early filling (E) -relative importance of atrial filling is enhanced resulting in reversed E/A -decreased peak rate of early filling owing to a decreased early diastolic LA to LV pressure gradient, caused by a slowed rate of LV relaxation -etdec >200ms (still normal decel time) 3. can be seen in pts with LVH, arterial HTN, CAD 4. most are asymptomatic and vigorous atrial contraction compensates for the reduced early filling caused by impaired LV relaxation 5. this pattern is normally seen in healthy older persons, so not abnormal for them -in younger=abnormal

cardiomyopathy

1. diseases of the heart muscles 2. the heart muscle becomes enlarged, thick, or rigid. in rare cases the muscle tissue becomes scar tissue 3. as it worsens the heart becomes weaker and can lead to heart failure or edema in lungs and body or even heart valve problems 4. can be acquired (not born with it but devolve due to another disease, condition, or factor) or inherited (passed down) or idiopathic (unknown) 5. can effect all ages and certain ages are more likely to get certain types 6. some people have no signs and symptoms and need no treatment for other people symptoms are severe 7. treatments: lifestyle changes, medications, surgery, implanted devices to correct arrhythmias, nonsurgical procedures -treatments control symptoms, reduce complications, and stop from progressing

pattern summary

1. each abnormal pattern results from a variable combination of delayed early relaxation, increased LA pressure, and increased LV chamber stiffness 2. a continuum from normal to severe diastolic dusfunction 3. unifying themes: increasing LV chamber stifness and decreasing etdec

diagnostic goals

1. evaluate a heart murmur 2. diagnose valve conditions 3. find changes in the heart structure 4. assess motion of the chamber walls and damage to the heart muscle after a heart attack 5. assess how different parts of the heart work in people with chronic heart disease 6. determine if fluid is collecting around the heart 7. identify growths in the heart 8. assess and monitor congenital defects 9. test blood flow through the heart 10. assess heart or major blood vessel damage caused by trauma 11. test heart function and diagnose heart and lung problems in very ill patients 12. assess chest pain 13. look for blood clots within heart chambers

DHF (diastolic heart failure)

1. first described bu Luchi et al in 1982, Luchi suggested this syndrome could account for 1/3 to 1/2 of cases if CHF 2. it has also been found that compared with those with reduced EF, those with a normal EF were much more likely to be women 3. population-based database suggest that over 50% of the elderly with CHF have normal EF

importance of PLAX

1. first view in protocol 2. can immediately tell if there is pericardial and or pleural effusion 3. physicians will refer to this view first for EF 4. has to be diagnostic (if able to obtain)

Ao measurements

1. focus on aortic root and it is measured at the level of the sinus of valsalva 2. it is made with the angle of the aorta (perpendicular) 3. it is made when the aorta is at maximum size (ED) 4. this is when it is filling with blood in diastole 5. normal range: 2.9-3.7cm 6. same for 2D and M mode 7. anything above 3.7 is dilated and should be noted -measure ascending Ao should be measured 8. inner edge to inner edge

Grade III (reversible restrictive) and Grade IV (fixed restrictive)

1. grade IV=restrictive CMO and waveform foes not change in valsalva so it is fixed 2. early filling is increased abnormally, even above that seen in young normals, exceeding the filling velocity seen during atrial contraction 3. E/A increased abnormally, often greater than two 4. increased early filling results from an increase in LA pressure that more than offsets delayed LV relaxation 5. the decel time state of early flow is rapid because of increased LV stiffness 6. short etdec (<160ms RR (reversible), <<160ms FR (fixed))-much less 7. this pattern is seen in pts with sever diastolic dysfunction, pulmonary congestion, end stage DCM 8. imparts substantially increased mortality 9. its prognostic power persists regardless of age 10. decrease in prognosis no matter the age

DHF summary

1. hallmarks of the syndrome: older age, female preponderance, a history of HTN, normal or small LV cavity size with significant hypertrophy, normal or supernormal contractility, increased LV filling pressure, and increased neurohormonal activation 2. therapeutic goals should include: mild reduction in LV filling pressure, controlling systemic arterial pressure, LVH regurgitation, improving LV diastolic dispensability (improve relaxation), and mitigating the effect of neuroendocrine activation

utilizing zoom

1. hit zoom button to bring up movable box 2. use the trackball to move the box over the ROI (region of interest) 3. use right kidney (set) to change the size of box 4. hit zoom again to zoom

hypertrophic cardiomyopathy (HCMO)

1. hyperdynamic, thick, non dilated left ventricle that is sometimes associated with LVOTO (left ventricular outflow tract obstruction 2. due to a sarcomere protein gene mutation, researchers using TDI of the mitral annulus to detect the mutation through DD 3. sudden death especially with exertion 4. leading cause of heart related sudden death in those under the age of 30 5. high blood pressure, small chamber

aging and cardiovascular function

1. increased systolic blood pressure and systemic vascular resistance -ex. plaque in arteries 2. increased LV stiffness 3. change in diastolic LV filling pattern; reduce early diastolic filling & increased late atrial filling -short E, tall A= E to A reversal

Restrictive/infiltrative cardiomyopathy

1. infiltration of the myocardium that results in stiff, rigid ventricular walls that impede diastolic filling and cause biatrial enlargement; typically results in heart failure -small to normal LV size with normal to decreased LV systolic function -regurgitation of all valves probable (mitral inflow=large E wave and small A wave without respiratory variation) -additional findings: pericardial effusion, endocardium and AV valves may be scarred or echogenic 2. resembles constrictive pericarditis, however constrictive pericarditis usually surrounds the entire heart; whereas, R/I CMO primarily affects the ventricles 3. least common 4. myocardium very bright (ground glass appearance) 5. both ventricles hypertrophy, pericardium stops ventricles from relaxing bc the layers adhere to each other 6. biopsy to confirm diagnosis, possible transplant

evaluation of diastolic dysfunction what do we want to know

1. is relaxation impaired 2. what are the filling pressures 3. etiology of DD 4. disease severity and prognosis

how many pictures should i have

1. it will be required of you to do all LV measurements first -RV, IVS, LV, and LVPW (systole and diastole) 2. then scroll to diastole and make Ao measurement 3. then scroll to systole and make LV and LVOT measurements 4. this will result in 4 pictures (you are allowed to use the same frozen image, just use the trackball to toggle between frames) 5. eventually you will be doing all diastolic and all systolic measurements together for a total of 2 pictures

sarcoidosis

1. marked by abnormal inflammatory masses (granulomas) that infiltrate multiple organ systems 2. heart complications include heart failure, pulmonary hypertension, and irregular rhythms

amyloidosis

1. most common 2. extracellular deposition of myloid protein in multiple organ systems causing damage and malfunction; produces heart stiffening that prevents complete filling 3. common to have an accompanying pericardial effusion and irregular rhythms 4. can mimic constrictive pericarditis

hemochromatosis

1. most common iron overload disease that may result in multiple organ and tissue damage 2. heart biopsy reveals iron deposition in the myocytes (muscle cells) 3. heart complications include heart failure and irregular rhythms

EPSS

1. normal E point to septal seperation is <6mm with reduced LVEF, EPSS may be increased 2. smaller number= better EF 3. measure peak of E wave to LV wall

diastolic function parameters

1. notebook pg 108 2. E/A ratio nl 1.0-1.5 3. deceleration time 160-240ms 4. "A" wave duration >pulmonary vein arterial reversal wave (PVa) nl >150ms 5. pulmonary vein interrogation (111) 6. IVRT 7. tissue doppler (TDI or TVI)- 109

sonographer position

1. one hand only 2. face machine 3. remember POC and EOB 4. feet shoulder width 5. shoulders even 6. patient head inclined or pillow -pillow under head only

dimensions and area

1. parasternal short axis at level of left ventricle -from a sonographers perspective slightly distal to the MV leaflet tips 2. parasternal long axis at level of LV -from a sonographers perspective slightly distal to the MV leaflet tips --2D and M mode measurements 3. apical 4 chamber 4. apical 2 chamber

challenges

1. patient habitus 2. poor skin contact 3. gel 4. patient positioning 5. implants and/or scar tissue

corrective measures

1. patient habitus: change frequency, utilize contact, utilize B color 2. poor skin contact: press harder 3. gel: add or remove gel 4. patient positioning: position more lateral 5. implants and/or scar tissue: avoid and or maneuver around. document

Grade II (pseudo-normalization)

1. pseudo means false 2. abnormal 3. E/A> 1 as seen in young normals (only the young pattern can be normal) 4. pattern seen in pts with more severe impairment of diastolic function 5. results from an increase in LA pressure that compensates for the slowed rate of LV relaxation 6. increase in late atrial filling increases E wave and looks normal 7. restores early diastolic LV pressure gradient to the baseline level seen in younger persons 8. shortened early deceleration time (etdec <160ms) owing to increased LV stiffness 9. animal studies have shown that there is a fixed relationship between etdec and LV chamber stiffness (shortened etdec) -inversely related 10. "false-positive" pattern seen with significant MR, which is more common in the elderly 11. in false positive pseudo normalization etdec is normal (160-200ms)

color kinesis by 2D echo to evaluate wall motion

1. real time color coded displays of LV endocardial motion on sequential frames 2. color is added to pixels that are identified as changing from blood to tissue in systole 3. create a color map of endocardial border 4. this method limited by poor endocardial definition and translational motion of heart 5. TDI (TVI) tissue doppler

diastolic function

1. refers to the ability of the ventricles to relax and fill 2. this is referred to as ventricular relaxation and compliance 3. diastolic function indicates whether the ventricular filling is normal or increased 4. decreased function indicates (diastolic dysfunction DD) can precede systolic dysfunction 5. DD is defined as a failure of the ventricle to relax and allow normal filling 6. similar to decreased systolic function, DD can be an indicator of heart disease and related symptoms

DD in heart disease

1. relaxation is impaired and the heart fills more slowly, asynchronously or only with an increase in filling pressure

normal pattern

1. seen in healthy young and middle aged persons 2. in sinus rhythm, there are 2 peaks in doppler diastolic filling profile (E and A) 3. peaks occur in response to the pressure gradient between the LA and LV 4. early in diastole following mitral valve opening when LV pressure falls below LA pressure 5. late in diastole when atrial contraction increases LA pressure above LV pressure 6. predominant rapid filling early in diastole with modest additional filling during atrial contraction 7. quantified by measuring the peak early diastolic flow velocity (E) & peak low velocity during atrial contraction (A), E/A>1 (1.0-1.5-unitless)

left ventricle

1. should be perpendicular 2. if the left ventricle is angled from right to left you are too high (move down an intercostal space) 3. if the left ventricle is angled from left to right you are too low (move up an intercostal space)

timing

1. sometimes there can be lung and rib artifact clouding/covering image -to correct ask patient to inhale/exhale and hold their breath -or you may have to move to another intercostal space

what we find out from echos

1. systolic function: refers to the ability of the ventricle to efficiently eject the blood out of the heart and into the systemic and pulmonary circulatory systems 2. ejection fraction: represents the volumetric fraction of blood pumped out of the ventricle (heart) with each heartbeat or cardiac cycle. RVEF and LVEF may vary widely from one another incumbent upon physiological state -RV normal EF=45% -LV low normal EF= 50-55% -LV normal= 60-65% -LV high normal= 70-75% 3. fractional shortening is the function of any diastolic dimension that is lost in systole (fiber shortening) -M mode function

remember

1. there is a difference between thick walls and a big heart (dilated) 2. there is also a difference between volume and dimensions

ETDEC-early transmitral deceleration time

1. time required for deceleration of the early diastolic flow (etdec) and the rate of deceleration are additional elements that help characterize LV filling pattern 2. in normal young and middle aged subjects, etdec > 190ms (range>160ms 3. normal range 160-240ms 4. etdec most helpful 5. etdec increases slightly with age 6. peak of E wave to baseline, only on MVI

pompes

1. typically occurs early in life (hereditary factor) 2. excessive glycogen storage in the tissues; the heart becomes enlarged and heavily thickened

modified simpson's method (disc summation method)

1. use apical 4 chamber and apical 2 chamber views to measure dimension and area 2. trace borders manually or by acoustic quantification (does it by itself) 3. divides area (LV chamber) into 20 cylinders of equal height -most accurate -with RWMA or not 4. LVEF= EDV-ESV/EDVx100

M mode quantifications

1. use parasternal short axis (Mayo) or long axis (ASE) views to measure LVEDD (D=dimensions) and LVESD 2. may take several measurements at different levels and calculate average 3. assumes no significant regional wall motion abnormalities present... 4. uncorrected LVEF (no RWMA)= (LVEDD)^2- (LVESD)^2/(LVEDD)^2x100 -if apical contractility is normal 5. corrected LVEF (has RWMA, usually in apex)= uncorrected LVEF + ((100-unc LVEF)x15%) -5% hypokinetic, 0% akinetic, -5% dyskinetic (wall moving in opposite direction), -10% aneurysm (wall buldging) 6. want to measure within same frame or cardiac cycle

index of myocardial performance (Mayo clinic)

1. uses of systolic and diastolic time intervals to evaluate global ventricular performance (IVRT & IVCT) 2. systolic dysfunction causes prolonged IVCT and a shortened ejection time. systolic and diastolic dysfunction causes a prolonged IVRT 3. IMP (index of myocardial performance) =(IVCT+IVRT)/ET 4. LV -normal= 0.39 +/- 0.05 -DCM= 0.59 +/- 0.10 --> dilated cardiomyopathy 5. RV -normal= 0.28 +/- 0.04 -primary pulmonary hypertension= 0.93 +/- 0.34 --> TR+RAP=PAP 6. use PW of AV valves inflow signal, or CW to get AV regurgitation signal...Also need to measure interval between AV closure and opening (A Vco) 7. then, need to use PW or CW to capture semilunar outflow signal to measure ejection time. after all of this, IMP can be calculated 8. IMP= (A Vco-ET)/ET 9. equation most important

survey scan

1. usually performed as the first sonographic image 2. it takes a look at structures outside the heart 3. mainly done to check for effusion 4. can be obtained initially or after finding appropriate PLAX first

components of systolic function evaluation

1. wall thickening- LVH (probably from hypertension) 2. wall motion 3. chambers size and 4. ventricular end diastolic pressure

probe manipulations

rotate, sweep or tilt, sliding or centering, rocking

moral

same skilled sonographer/doctor can still result in varied opinion