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135 Cards in this Set
- Front
- Back
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Explain the pressure curve for a Mild aortic regurge compared to one of severe AO regurge?
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MIlD AI:
-the pressure difference in early diastole is high -gradient decreases througout diastole due to a decline in diastolic pressure and an increase in LV end diastolic pressure -(flat slope) -SEVERE AI: -aortic pressure drops rapidly during diastole -LV EDP rises rapidly -causes rapid slope |
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what are the symptoms of AS?
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-Dyspnea and Fatigue
-Angina(coronary artery disease) -syncope-a and v-fib -auscultaion-dog bark |
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what are the stages of AI?
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1. LVVO(enlarged hyperdynamic LV)
2. Lage stage-slight LVH 3. Later stage-enlaged poorlymoving LV |
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disecting aortic aneurysm
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true lumen of the AO is separated from the false channel by an intimal flap.
-oscullation of the intimal flap can be a sure sign of a dissecting aneurysm |
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Aortic dissection:
What is it? What are the most common causes? What are some other causes? |
Tear in the intima where a column of blood enters the aortic wall. HIgh mortality rate
Common causes: -hypertension -atherosclerosis -marfans -pregnancy Other cuases: -endocarditis -syphillis -trauma |
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what are the causes of an aortic aneursym?
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hypertension and congenital causes
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2D and M-mode appearance of AS?
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-thick AO learflets
-restricted leaflet motion -LVH -Systolic doming of the aortic lealets -post stenotic dialation of AO root -Decrease LV comliance |
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what happens to the MV w/ chronic AI?
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the mitral valve closes later because the pressures are slowly changing. THis is why there is the b-bump(increased LV end diastolic pressures)
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what may cause a flail aortic valve?
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-leaflet destruction by endocarditis, trauma, or high frequency fluttering from AR
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What doppler measurements should be taken when evaluating for AO stenosis?
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Peak velocity
pressure gradient Aortic valve area |
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what is the etiology of AI?
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-rhumatic
-athereosclerotic changes -infetive endocardiditis -bicuaspid AV -aortic valve prolapes -AO root abnoralities |
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what are the complications of AS?
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-sudden death
-pulmonary edema -myocardial infarcts -arrythmias |
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what does a flail AV look like on m-mode?
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-eratic systolic leaflet motion
-fluttering leaflets during diastole -diastole MV flutter w/AI -enlarged LV in diastole, and AR in systole |
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What does AI look like on M-mode?
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-diastolic flutter of MV
-DIastolic flutter of AO valve -LVVO or LVH -B-bump if chronic |
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What are the predisposing factors for vegitations
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-rhumatic disease
-bicustpid AV -atheromatous changes |
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what are some cuases of aortic stenosis?
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bicuspid valve(congenital)
Rhumatic fever(aquired) degenerative(senile)(aquired) |
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what happens with a bicuspid AV? what are the long term complications of it?
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-most common cause of AS
-associated with coarctation of the AO. Long term complications: -AS, AI, and endocarditis |
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What happens to the heart as the AV orifice becomes narrower?
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-LVH due to increase pressure and afterload.
-LV and LA dialation(become hypokinetic) -Heart failure |
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With severe AI, where is flow reversal seen?
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-holostolic flow reversal in the proximal AO(seen in subcostal)
-holodiastolic flow reversal in the descending AO(seen in suprasternal notch) |
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when would a RCC prolapse occur>
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w/ a memebranous VSD
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what are the categories used to score MV stenosis?
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mobility
leaflet thickening subvalvular thickening calcification |
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symptoms of MR
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-fatigue
-dyspnea -angina -palpitations -congestive heart failure -peripheraledema -pulmonary edema may indicate acute MR |
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what indications are present on PW doppler for mitral regurge?
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-increased e-velocity
-decreased decel time - |
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PISA
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-proximal to the flow
-can quantitate severity of regurge |
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grades of MS
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mobility
thikening chordal involvement calcification |
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pisa formula
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2pieRsquared X PISA V =(ERO)(MR V)
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what are the possible complications of Mitral Regurge?
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-LV dialation
-LA thrombus -pulmonary hypertension -pulmonary edema -infective endocarditis -congestive heart failure -right heart failure |
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how can color help in determining severity of MR
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-determines jet area
-ratio of jet to LA -diameter of vena contracta |
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what 4 specific things should you check on 2D while determining MS?
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-Determine if there is an ASD(lutembacker's syndrome)
-Determine if ther is AO, Tricuspid, or pulmonic stenosis -measure MV area in short axis -determine score index |
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what is the most common cause of MVP?
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myxomatous degeneration
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MVP on m-mode
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-thick MV leaflets
-mid-late systolic sagging -abnormal late systolic dip in the left ventricle wall -LA and LV dialation -pulmonary hypertension |
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how does the heart look when MS progresses?
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-LA gets bigger
-increased pulmonary venous pressure which goes back to the lungs(this is why there is SOB) -causes increase size of RV and RA. |
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what are some changes on M-mode with mitral stenosis?
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-thick leaflets
-decreased E-f slope -anterior motion of post leaflet -decreased A-wave -decreased diastolic separation -LA dialation -Pulmonary hypertension -RVH -Paradoxical septral motion |
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what are some symptoms of mitral stenosis?
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-Dyspnea at rest
-pulmonary edema -palpations -fatigue(due to A-fib) -chest pain -hemoptysis(blood stain sputum -hoarseness |
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what differences are there in 2D with a mitral stenosis?
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-thick leaflets
-hockey stick appearence -fibrous chordae -commissural fusion(PSSA) -LA dialation, smoke, and thrombus -Pulmonary hypertension -RVH, Right atrial dialation, small LV |
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what should be determined with doppler in search of a MVP?
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-direction of regrgitant jet(AMVP has a post. jet, and vice versa)
-timing of regurgitant jet(mid-late systolic vs. holostolic) -severity of regurge |
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what are the symptoms of MVP?
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-typically no symptoms
-palpitations -chest pain -dyspnea -fatigue -exercize intolerence -anxiety, panic attacks -syncope -TIA -CVA -congestive heart failure due to regurge |
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what is different on PW and CW doppler with mitral stenosis?
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-turbulent flow
-increased E- velocity(>1.3) -decreased slope and increased Pressure half time. |
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lutenbacher syndrome
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mitral stenosis with an ASD
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what things need to be done to obtain a PISA?
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-obtain radius of PISA
-aliasing velocity -MR velocity |
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what are some diseases associated with MAC?
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-high blood pressure(most common)
-renal disease -AO stenosis -hypertrophic cardiomyopathy |
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what indications are present on CW doppler for mitral regurge?
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-spectral strenght indicates severity
-assymetrical flow pattern indicates acuteness |
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what can mac mimic?
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mitral stenosis
pericardial effusions masses |
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what are the disadvantages of TDI?
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-cannot be used w/ prosthetic or MAC
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what are the factors that affect doppler evaluation of LV distolic funtion? normal, and physiologic factors?
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normal:
-respiration -heart rate -age and PR interval PHYSIOLOGIC: -preload-pressire -volume flow rate -LV systolic function and atrial contraction |
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what are the factors that effect contractility?
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-preload
-afterload -intrinsic contractile function -heart rate |
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what are causes of diastolic dysfunction w/ preserved systolic function?
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-LVH due to hypertension
-Hpertrophic cardioyopathy -restrictive cardiomyopathy -ischemic disease w/out prior infarction |
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WHAT ARE the parameters of diastolic function?
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-ventricular relaxation
-myocardial or chamber complience -filling pressures |
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auxotonic regulation
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-the last 3 phases of diastole where the MV is open
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what determines the magnitude and duration of flow reversal in the PV?
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transmitral and atriovenous pressure gradients which are influenced by the LA systolic function and LA and LV compliance
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what are examples of active and passive forces of LV filling?
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active:
-early diastole -rate of myocardial relaxation and elastic recoil(suction) PASSIVE: -late diastole -chamber compliance -chamber stiffness -LA pressure |
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how can we tell if there is pseudonormalization?
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if the PV a-wave reversal is >35cm/s
-if PV a-wave duration is> MV inflow a-wave |
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what is the formula for mean velocity of circumfrential fiber shortening?
what is the normal? |
mean Vcf=(LVIDd-LVIDs)/(LVIDd)(LVET)
Norm=1-1.9cir/sec |
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what does the severity of acute ishemia depend on?
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site of obstruction
size of infarction collateral circulation |
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what are the causes for false negatives in stress echo/dobutamine?
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-uncommon
-unable to reach max heart rate -inadequate exercise-dobutamine -rapid reperfusion as a reprofusion as a result of extensive collaterals |
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What are the causes of ischemic heart disease?
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-atherosclerosis
-coronary artery spasm -embolus |
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acute ishemia
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-commonly caused by coronary thrombus at the site of atherosclerosis
-rapidly occluded vessel, and myocardial cells suffer hypoxic injury(MI) -severity depends on the site of obstruction, size of infarction, and collateral circulation -ishemia is reversible in myocardial O2 demand |
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stress echo indications
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-evaluate patients w/ known CAD
-evaluate patients w/ symptoms of CAD -ambiguous stress EKG exam -Evaluate LV systolic function -identify viable, hybernating, or stunned myocardium -evaluate hemodynamics in valvular/cardomyopathic heart diaseas(Ao stenosis, MR) |
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why are some patients unable to exercise?
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-peripheral vascular disease
-musculoskeletal or neurological disorders -pulmonary disease -obesity |
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CAD strategies
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Thrombolysis during angiography
Transluminal angioplasty Severe obstruction requires coronary bypass surgery |
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What are the absolute contraindications for stress echo?
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-Acute MI(within 2 days)
-unstable angina uncontrolled cardiac arrythimias -severe Aortic stenosis -aortic dissection -pregnancy -congental anomalies -significant PE or tamponade |
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pericardial effusion
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-seen as nonspecific respons to trasral infarction
-may be asymptomatic or associated w/ chest pain -temponade can occur |
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when can acute pericarditis occur?
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in the first few days following an infarction; when the infact extends to the epicardial surface
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what are the pitfalls and artifacts associated w/ stress echo?
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-reqires quick and precise sonographer
-Left bundle branch block causes abnormal septal wall motion(looks like a bounce) -LVH -atypical acoustic windowns-low parasternal window=anteroseptal hypokinesis -apex seen best at apical view(don't forshorten)-false RV dialation -gain settings need to be constant -subconstal view best for RV size. |
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what are false positives for strss echo?
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-uncommon, but more common than false negatives
-cardiomyopathy -inadequate exercse in elderly -early myocardial dysfunction -LVH-LV fibrosis -aging of the heart -high BP -severe hypertension |
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hibernating myocardium
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prolonged persistence of wall motion abnormalities that can be reversed by reperfusion
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chronic ishemia
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atheroscerosis and non-occlusive thrombi cause slow progressivenarrowing of arterial lumen
-allows myocardial cells to partially adapt to hypoxia -allows anastamosis to develop btw ishcemic and normal vessels -necrosis occurs, and myocardial cells are replaced by fibrous tissue decreasing compliance and contractility |
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what are the pathophysiologic events that occur w/ stress to the heart
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1. Myocardial perfusion becomes nonhomogenious, decreasing in myocardium- supplied by the obstructed vessel
2.Change in diastolic function 3.Slowed relaxation, increased stiffness, increased end-diastolic pressure 4.Contractile failure = segmental hypokinesis 5.Significant shifts of the ST segment ECG 6.Chest pain |
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what are false positives for strss echo?
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-uncommon, but more common than false negatives
-cardiomyopathy -inadequate exercse in elderly -early myocardial dysfunction -LVH-LV fibrosis -aging of the heart -high BP -severe hypertension |
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what are some contraindications for dobutamine?
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-class 3 and 4 heart failure
-high grade AV block -angina at rest |
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HOw are myocardial infartions classified
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-subendocardial(only inner layer of the myocardium)
-subepicardial(involving both inner and middle layers) -trasural(extending through all layers of the myocardial wall) |
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kawasaki's disease
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congenital mucocutaneous lymph node syndrome
-virl in nature=coronary aneurysm |
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dressler's syndrome
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-delayed form of acute pericarditis
-occurs up to several months after the infarct -(usually 6-12 wks after) |
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what are the pitfalls in diagnosis thrombus?
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-Fibrous bands across apex
-ruptured pap muscle -abnormally placed pap muscle -near field artifact -prominent LV trabeculation (FRAN P) |
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MItral regurge murmur
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-most common cause of MR murmur is papillary muscle dysfunction or papillary muscle rupture
-requires immediate surgery |
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hibernating myocardium
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prolonged persistence of wall motion abnormalities that can be reversed by reperfusion
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stunned myocardium
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wall motion abnormalities persist for 24-72 hours even though irreversable damage has not occured
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what is another name for thrombolytic therapy?
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reprofusion therapy
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LBBB
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left bundle branch block
-causes abnormal septal wall motion; looks like a bounce |
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Systolic murmur after MI is indicitive of what?
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VSD
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Marfan's syndrome
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-congenital/connective tissue disorder that leads to:
-AO root dialation -usually found in tall and skinny guys -graft @ 5.5cm -complications are dissection AO root |
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what would cause a new systolic murmur on a persone w/ a myocardial infarct?
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pap muscle defect
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carcinoid
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associated w/ isolated TS/PS, but normal MV. Comes from the ilium
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what is the best view to see the RV free wall?
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subcostal
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A-dip
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-associated w/ pulmonary valve
-represents atrial systole -not seen on the Lt because of higher pressures in diastole -PS=increased a-dip -PHT-no a-dip, and mid systolic closure(flying w) |
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how do you obtain a pressure half time when you are given a decel time?
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x .29
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what components are needed to obtain a pisa?
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-aliasing velocity(from color bar)
-MR jet velocity -Radius of PISA |
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w/ severe MR, what happens to the pulmonary veins?
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-reversed systolic PV flow
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if a person has reduced CO, what does this look like on m-mode?
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-flat septum, walls, root movement, and LA movement
-reduced color -dialated LV, reduced EF, and increased EPSS |
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Name the order of how endocarditis affects the valves?
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MV, AO V, TV, PV
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When does the posterior leaflet move w/ the anterior leaflet?
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w/ Mitral stenosis 90% of the time
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What view is MVP best seen in? What is seen? what are the complications?
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-best seen in PSLX
-bowing(systolic) -complications are regurge and flail |
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when is doming seen?
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Mitral stenosis
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Compare RVVO and LVVO
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RVVO-paradoxical septal motion
LVVO-big LV, and hyperdynamic |
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When is AI severe?
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when the slope is steep
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what side of the valve are veggies seen?
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on the upstream side(they move w/ the leaflets)
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What are the main causes of flail MV?
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MVP or MI of pap muscles
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does starlings law affect preload or afterload?
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preload
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ebsteins
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posterior displacement of the TV
-big heart; big rt side first |
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What PG is indicitive of sever MS?
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>12mmHg
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raffe
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makes bicuspid AV look like tricuspid in diastole
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layers of the heart
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pericardium, myocardium, endocarditis
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what are the long term complicatoins of a bicuspid valve?
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AI, AS, and endocarditis
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where is the IVRT measured?
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prediastole-btw AV closure and MV opening
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what is normal Pulmonary valve velocity?
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.6-.9cm/s
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what are the stages of AI vs. the stages of AS?
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AI=normal, dialation, slight hypertrophy, big sac
AS=normal, LVH, Big sac |
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where are pseudoaneurysms usually seen?
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infertior wall
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how is dp/dt measured?
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by measureing the IVCT of MR to determine systolic LV function.
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explain embolization w/ endocarditis?
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-occurs when vegge breaks off
-higher incidence with vegge>5mm, mobile and pedunculated |
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Name the m-mode, 2D, and Doppler appearence of TR?
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M-mode:
-increase RV -Paradocical septal motion(RVVO) -b-bump(increased RVEDP) 2D; -RVVO -Paradoxical septal motion -dialated right side -theick leaflets -dialated IVC Doppler: -the more seer the TR waveform, the less symetrical it is because of increased RA pressure. -reverse systolic flow in hepatic veins. |
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what are the causes of PR?
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-pulmonary hypertension
-endocarditis -rheumatic disease-rare -carcinoid -congenital -ausultation(murmur resembles AI, but lounder with inspiration) |
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which views demonstrate what leaflets of the TV?
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PSSX-septal and anterior
RV inflow-Ant and post apical 4-septal and ant. |
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what is the physiology of tricuspid regurge?
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-enlarged RA
-A-fib -increase IVC, hepatic vein, SVC, and neck vein size -leg and abdominal swelling -increase liver size -portal hypertension -high pitched blowing sound in systole that increases with inspiration |
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endocarditis classifications
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-rhumatic
-infective -nonbacterial thrombotic -atypical verrucous |
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reasons for TR
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-ebsteins
-rhumatic disease -carcinoid ruptured chordae and TVP |
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what will pulmonary regurge look like on doppler?
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-red flame
-small PR is normal -normal PR=.6-1.3 |
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infective endocardidtis
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infection involving the endothelial latyer of the heart
-most commonly affects valves -may affect lining |
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cause of endocarditis
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-introduction of pathogen into circulation via oral cavity, respiratory tract, GI tdact, female reproductive tract
-causes bacteremia, or fundemia -veggie is th classic manifestation -once veggie is attached, microorganisms attach and proliferate -becomes a cyst-like structure that defens the colony from defensive cells |
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what is the M-mode and 2D appearence of PR?
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-dialated RV
-Diastolic flutter on TV -paradozical septal motion -premature openng of PV -RVVO |
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what is the classic trid for clinical diagnosis of infective endocarditis?
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-fever
-enemia -new murmur |
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how is pulmonary stenoss evaluated with m-mode, 2D, and Doppler?
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M-mode:
-deep a wave -RVH -Presystolic opening of PV if severe 2D: -systolic doming of PV -RVH -post stenotic dialtion -flattened septum due to the increase in RV pressure DOPPLER: -bernouli equation gives PG -surgery recommended if Peak PG is >50mmHg |
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what are the causes of pulmonary stenosis?
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-COngenital-most common(valvular, subvalvular, supravalvular)
-rhumatic-rare -carcinoid(most common) -sinus of valsalva aneurysm |
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rhumatic Tricuspid stenosis
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-rhumatic MS always seen before TS
-most common aquired TS |
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why does congestive heart failure occure with endocarditis?
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due to severe regurge
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where are aortic valve vegges most often detected?
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in PSLX and PSSX.
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What is the anatomical location of the TV?
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most inferior and lateral vlave
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acute endocarditis
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-powerful pathogens that display rapid destruction
-invasion of normal valve -caused by the bacteria STAPHYLOOCCUS AUREUS -may have embolic event -blood cultures are positive -night sweats -arthrolagia -weight loss -anemia, tachecardia |
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what are the pitfalls of dealing with endocarditis?
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Some findings may be mistaken for aortic valve vegetation like the following:
-beam width artifact: -calcified nodule -prosthetiv valve -normal leaflet thickeingin -coaptation region -nodule of aratius -lable's excrescence |
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what should be obtained with endocarditis and severe regurge usuing doppler and color flow?
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-valvular stenosis calculations
-MV-PHT -AV-continuity equation -regurge -examine turbulent flow -examine flow through and around the abscess. |
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Tricuspid valve prolapse; where is it usually found?
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-usually associated with mitral valve prolaps
-usually found in patients with marfan's syndrome, ASD's and ebsteins. |
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what are the complications of endocarditis?
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-embolization
-structural and hemodynamic changes -abscess -congestive heart failure |
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when is Right ventricular systolic pressure not equal to pulmonary artery systolic pressure?
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-embolization
-structural and hemodynamic changes -abscess -congestive heart failure |
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when is Right ventricular systolic pressure not equal to pulmonary artery systolic pressure?
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when there is a RVOT obstruction
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what occurs first: a wave, or a-dip?
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a-wave because it is happening in the TV which occurs before the mitral valve
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what is the ausculation sound of the PA? when is it heard?
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stenosis=harsh systolic murmur
-heard over the left costal border. |
