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164 Cards in this Set
- Front
- Back
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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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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 happens to the MV with 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 are the complications of AS?
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-sudden death
-pulmonary edema -myocardial infarcts -arrythmias |
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what ar ethe causes of an aortic aneurysm?
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hypertension and congenital causes
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what may cause a flail AV?
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-leaflet destruction by endocarditis, trauma, or high frequency fluttering from AR
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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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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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WHat happens to the MV with acute AI?
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MV closes early because pressures are changing quicker.
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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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when would a RCC prolapse occur>
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with membranous VSD
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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 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 anatomical location of the TV?
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most inferior and lateral vlave
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etiology of tricuspid stenosis?
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-rhumatic
-carcinoid -congental-ebsteins -endocardial fibroelastosis |
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WITH TS, what is seen on M-mode, 2D, and doppler?
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M-mode:
-thick leaflets -decreased E-F slope -same letters as MV 2D: -thick leaflet -diastolic doming -decreased orifice size -enlarged RA DOPPLER: -area found by PHT or decel time(normal=7-9cm2) |
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What is the normal right ventricular systolic pressure? what does this equal?
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NOrmal=15-30mmHg
Equals pulmonary artery systolic pressure |
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what numbers represent mild and severe pulmonary hypertension? What is the formula we use for pulmonary hypertension?
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Mild-35mmHg
Severe>50mmHg FORMULA: RVSP=4V2+RAP |
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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 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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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 3 cusps of the PV?
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-posterior, right, and anterior
-left cust most often seen |
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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 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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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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what are the classifications of endocarditis?
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-rhumatic
-infective -nonbacterial thrombotic -atypical verrucous |
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Explain infective endocarditis
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-usually bacterial
-patients present with fever -positive blood cultrues and often a new murmur is heard |
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acute endocardidits
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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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why does congestive heart failure occure with endocarditis?
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due to severe regurge
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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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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 are the 3 I's? what is seen w/ each of them on ECG?
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Ishemia-inverted t wave
Injury-elevated ST segment Infarct-q below the baseline |
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what are some relative contraindications for stress echo?
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-lt main coronary artery stenosis
-moderate stenotic valvular heart disease -electrolyte balence -outflow tract obstructions -mental/physical imparement leading to inability to exercise (LE MOM) |
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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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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 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 is hypoxic injury?
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lack of oxygen suffereed by myocardial cells during acute ishemia(aka MI)
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what are the indications for an exercise stress echo?
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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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name the sequence of events of ishemia to myocardial infarction?
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ischemia
diastolic dysfunction systolic dysfunction ECG changes chest pain |
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end stage ischemic cardiac disease
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-repeated transmural and subendocardial infactions can result in a diffuse pattern of abnormal wall thickening and endocardial motion
-wen global systolic dysfunction is present, it is difficult to differential end stage ischemic disease ad systolic dysfunction due to long standing valvular disease or dialated cardiomyopathy |
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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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draw all wall segments and be able to tell which coronary artery supplies each
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do it!
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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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transumral infarction?
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>50% wall thickness
-results in definite area of akineses and wall thinning |
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Explain acute ishema?
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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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Myocardial infarction
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-irreversable injury to the myocardium due to prolonged ishemia
-myocardium initially becomes akinetic -overtime(4-6 wks), myocardial segments show thinning. - |
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ischemic heart disease
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narrowing of the coronoary artery so that blood supply is prevented from entering the myocardium=ishemia
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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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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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what is another drug used for stress echo?
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atrophine
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complications of myocardial infarction
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-mitral regurge
-VSD -vetricular rupture w/ pseudoaneurysm -pericardial effusion -RV infarction -LV aneurysm -LV thrombus (love prom) (LLVVPRM) |
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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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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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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 the types of myocardial ischemia?
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-acute
-chronic |
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what does the 2D of a normal post exercise echo look like? what images are taken? why?
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-decreased LV size
-hyperdynamic wall motion -increased EF IMAGES TAKEN: -PSLX -PSSA(pap level) -APICAL 4 -APICAL 2 So that all walls are demonstrated |
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what echo images are obtained w/ dobutamine?
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-rest
-each infusion level -drug recovery |
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what is an alternate method for stress echo? explain it?
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Doubutamine(most common drug used):
-augments myocardial contractility=increasing the work of the heart and myocardial oxygen requirements -rapid onset of action within 2 minutes-peak at 10 minutes -safe and well tolerated -infused w/ infusion pump -HR and BP monitored every 3 minutes |
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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 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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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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infarction
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when the narrowing the the coronary artery progresses to the point that the heart muscle is damaged
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what does the 2D look like on an abnormal post exercise exam?
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-increased LV size
-myocardium has variable degrees of hypokinesis -reduced EF |
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RCA
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RCA
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what are 3 ways to calculate SV?
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-M-mode-EDV-ESV
-2D-simpsons and 2D measurement -Cardiac doppler-CSAxVTI |
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what is the formula for CI?what is the normal range?
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CO/BSA
normal range=2.4-4.2min/m2 |
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how are MVA and PHT calculated? what is the advantage of PHT?
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MVA=220/PHT
PHT=decel timex.29-independant of cardiac output or MR |
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what are the steps to calculate PISA
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-apical 4-color MV
-zoom MV -move baseline to 20-40 -freeze-measure radius from leaflet tips to where red meets blue -CW doppler through MR and trace -calculate |
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when can you not determine the ERO for MR?
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-if you have mild AI or if the MR jet is exentric
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what is the size of the vena contracta and PISA w/ severe MR?
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-vena contracta=6mm
-PISA>1cm |
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what is the pisa diameter for the different grades of MR?
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-1-<4mm
2-5-7mm 3-8-10mm 4->10mm(severe MR) |
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explain why diastolic dysfunction occurs before systolic dysfunction?
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-in early diastole, there is relaxation of the ventricle, then there is complience or stiffness of the ventricle in mid-late diastole
-therefor relaxation abnormaliities occur first followed by changes in compliance |
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Explain the phases of diastole
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IVRT-btw AV closure, and MV opening
Early filling-LV pressure falls below LA pressure Diastasis-pressures equalizing atrial filling phase-last kick at the cat |
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why does pseudonormalization occur?
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-because the increased LA pressure masks diastolic dysfunction
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what are the symptoms of the beck triad?
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-increased jugular venous pressure
-hypotension -diminished heart signs |
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what are the m-mode and 2D features of cardiac tamponade?
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-early diastolic RV collapse
-late diastolic RA collapse(inversion) -late LA collapse -swinging heart -IVC plethora -abnormal ventricular septal motion -respratory right and left ventricular chamber size variation -clotted blood in pericardiu |
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how does acure MR affect the MV and Aortic valve?
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mitral valve closes early and aortic valves opens late.
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what are the types of MVP/
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holosystolic
mid-late systolic |
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what are the primary and secondary causes of dialated cardiomyopathy
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Primary:
Infection, inflammation, and Idiopathic Secondary: -toxins(alcohol, or cobalt, snake bites) -diabetes -pregnancy |
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what is the m-mode appearence of dialated cardiomyopathy?
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-AO early systolic closure due to decreased CO(valve not held open because of blood flow)
->EPSS -hypokinetic LV -Decreased Post Ao root wall motion -may be b-mump on MV due to high end diastolic pressure |
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What is seen on doppler w/ Dialated cardiomyopathy?
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-MR-10% and TR-90%
-PR-50% AR-20% -dp/dt-systolic function -Grade of diastolic dysfunction(restrictive causes increased risk of mortality(50% within 2 years) -dull color flow(esp in apex) -determine SV and CO |
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what are the signs and symptoms of Dialated cardiomyopathies?
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-low BP
-evidence of heart failure -narrow pulse pressure -peripheral cyanosis -atrial fibrillation -cool clammy skin |
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How is dialated cardiomyopathy treated?
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-vasodialator(ie. digoxin-makes heart contract by increasing cardiac output and increasing shortening fraction)
-beta blockers(eg. labetalol) -anticoagulation(eg. warfarin) -diuretics -02 therapy -bed rest -heart trasplant |
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name and explain the hemodynameic types of hypetrophic cardiomyopathy
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-Obstructive(HCOM)-subaortic due to mitral valve systolic anterior motion)
-Mid ventricular obstructive(occurs at papillary muscle level(without SAM)) -non-obstructive: -absence of resting gradient -normal LV systolic function -may have diastolic dysfunction -asymmetric apical hypetrophy(AAH) |
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what is the 2D appearacne of hypertrophic cardiomyopathy
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-brightened myocardium due to fiber disarray
-small hyperkinetic LV -Abnormal ventrical wall thickness(1-4) -SAM-may contribute to LVOT obstruction -IHSS=SAM=ASH -LA enlargement-due to MR -MV thickening and septal scarring because of leaflets striking the IVS -MAC |
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what is the m-mode appearance of hypertrophic cardiomyopathy?
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-ASH
-Concentric LVH -Apical hypertriphy -mid ventricular hypertrophy -small LV -SAM-may creast a LVOTO -B-notrch of MV-increased LV end diastolic pressure -mid systolic closure of the AO valve due to sudden decrease in CO |
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what is the treatment for hypertrophic cardiomyopathies?
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-myomectomy-partial exision of myocardium
-myotomy-cut or dissect tissue -drug-propanalol |
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what are the 3 characteristic findings of a person w/ hypertrophic cardiomyopathy?
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-ASH-asymmetrical septral hypertrophy
-SAM-systolic anterior motion of the MV in systole"ventrium effect" -mid systolc closure of the Aortic valve |
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what is restrictive cardiomyopathy characterized by?
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-normal LV systolic function
-impared diastolic function(due to stiff, hypertrophied LV) -atrial enlargement -signs of secodary pulmonary hypertenion -paradoxical septal motion -high velicity TR jet |
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what causes symptoms of heart failure w/ restrictive cardiomyopathy?
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-elevated LVEDP
-inability to increase cardiac output due to impared diastolic function |
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what is the 2D and m-mode appearance of restrictive cardiomyopathy?
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-no definitive 2D findings
-biatrial diation -AV valves may be involved(bright leaflets) -can have LVH-amyloidosis -can have apical obliteration |
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doppler of restrictive cardiomyopathy
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-av regurge
-determine diastolic dysfunction grade |
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what are some complications of restrictive cardiomyopathies?
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-congestive heart failure
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Lofflers syndrome
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-aka loffler's endocarditis or tropical endomyocardial fibrosis
-form of restrictive cardiomyopathy -endomyocardial disease fibrotic tissue lines the myocardium -parasitic -decrease LV function -focal nectosis -mural thrombi and enomyocardial fibrotic thickening |
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arrhythomgenic right ventricu.lar cardiomyopathy(dysplasia)
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-rare
-characterized by progressive firbro-fatty replacement or right ventricular myocytes -some cases=familial(autosomal dominant) -more common in young adult males -enlarged RV w/ decreased RV function |
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takotsubo
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-octapus trap
-stress related -usually affects post menopausal women -transient myocardial stunning -acute reversable cardiomyopathy SONOGRAPHICALLY: -apical ballooning w/ akinetic apical segments -preserved basal inferior wall systolic function -70-80% post menopausal women |
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Endocardial Fibroelastosis
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aka hypersinophilic syndrome
-congenital -inflammed endocardium -thick endocardial layer -overlying thrombus and appearance of obliterative apical process |
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what is the appearance of the aortic valve w/ IHSS?
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speckled; mid-systolic closure
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If an echo perfomed in a patient w/ suspected dialated cardiomyopathy showns no significant impairment of the LV systolic dysfunction, what are some other possible causes?
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-coronary artery disease
-valvular disease -hypertensive heart disease -pericardial disease -pulmonary heart disease |
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what type of hypertrophy is indicated w/ an inverted T-wave
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apical hypertrophy
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name and breifly explain the forms of restrictive cardiomyopathies?
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GLOSH:
-GLycogen storage disease-carbohydrate/globular/young people -loffler's-fibrotic tissue lines myocardium/parasitic/focal nectosis -other-carcinoid, neuromuscluar, lupus, rhumatoid, toxins -sarcoids-granuloma deposits/ inflammatory disease/affects other organs -hemochraomatosis-iron/bronze skin/causes liver disease and diabetes/arrythimas and heart failure |
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name and explain the misc. cardiomyopathies?
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(SCALP E)
-Stress related takatsubo-octapus/post meno/reversable -chagas myocardiits-infection/apical aneurysm/south america -arrythogenic RV-coronary artery dysplasia-rarely fattly dise[lacement/young males w/ enlarged RV and deacrease RV function -Endocardial fibroelastosis-congenital/tropical(or not)/inflammed endocardium/obliterated apex |
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what is seen on ECG w/ amyloidosis? what else may occur?
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demonstrates a low voltage on ECG
-common to have a PE |
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transverse sinus
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-where the pericardium extends along the great vessels superiorly, and surrounds the vessels posteriorly.
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oblique sinus
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-pericardial space extends lateral to the LA, and a blind pocket extends posterior to the LA btw the four pulmonary veins.
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explain small, moderate, and large pericardial effusions?
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SMALL PE:
-<100ml -seen post to LV, distal to AV groove -<1cm separation btw pericardial layers MODERATE: -100-150ml -circumferential accumulateion that extends posteriorly to the LA -pericardial layer separation<1cm LARGE PE: ->500ml -circumfrential fluid accumulation ->1cm separation of pericardial layers -ant-post, or med-lat heart is swinging |
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intrapericardial stands
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-aka fibrous bands
-aggigates of fibrin, thrombus, or tumors, and indicitive of inflammation -extend from visceral to parietal pericarduium -linear, undulated or hyper mobile appearance |
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what are the causes of pericardial effusions?
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(LPNP CTR)
-lupus -pericardial inflammation -neoplastic invasion -post cardiac surgery -chronic renal failure -TB -radiation and trauma |
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what are the clinical signs and symptoms as well as the complications of PE's?
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-PE reduces cardiac output by restricting filling of chambers
-RV wall is thinned and may appear compressed COMPLICATIONS: -cardiac tamponade -chronic pericarditiis, may lead to constrictive pericarditis |
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swinging heart syndrome; what may it cause?
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-occurs w/ large PE
-heart sways in pericardial fluid MAY CAUSE: -malse MVP and TVO -false sam -electric alterans-ECG change-varrying height of R wave |
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what are the clinical findings with a pleural effusion?
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-enlarged cardiac silhouette
-distant heart sounds(pericardial rub) |
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what are the causes of acute pericarditis?
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-infection
-idiopathic -metabolic -collagen vascular/autoimmune disease -post injury -neoplastic |
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name and explain the 3 groups of pericardial disease?
|
1.INTTRISIC:
-myocardial infarction -myocarditis -trauma -rhumatic fever 2.DISEASE IN ADJACENT STRUCTURES: -TB -CA of lung -CA of esophagus -Psneumonia and emphysema 3.GENERALIZED DISORDERS: -viral -renal failure -connective tissue dosorders |
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what are the causes of constrictive pericarditis
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-TB
-Trauma -Radiation -Viral disease -CA -cardiac surgery -Certain drugs |
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what is the 2D appearance of constrictive pericarditis?
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-thickened pericardium
-flat LV inf. wall motion in diastole -abn. systolic motion of LV wall -premature PV opening due to and increase in RV diastolic pressure greater than PV pressre -LV normal size-septal bounce |
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constrictive pericarditis-dopple
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-increase in RV filling and decrease in LV filling w/ inspiration(tamponade hemodynamics)
-restrictive diastolic function(prominant e; rapid decel slope; decrease IVRT, increased A-velocity of pulmonary veins) |
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explain the types of pericardial tumors
|
METASTATIC:
-5% of patients w/ CA will develop it in their hearts -more common than primary -caused by lung cancer in men and breast cancer in women -other-lymphoma, melanoma, leukemia, and rarely: colon, kidney, ovary, and prostate PRIMARY: -cause-mesothelioma-most common -rare-lymphangioma, hemangioma, teratoma |
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what are the clinical and 2D findings of a metastatic pericardial tumor?
|
CLINICAL:
-PE most common -Tamponade -BLoody PE 2D: -echodense areas w/out distince borders -locarlized on the pericardial surface - |
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what is the 2D appearance of congenital absence of the pericardium?
|
-RV enlargement(RVVO)
-exagerated heart motion -paradoxical septal motion -elarged LA appendage -heart shifted to the LT |
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what is an absent pericardium associated w/?
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-ASD's
-bicuspid AV -bronchognic cysts |
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what are the clinical signs of tamponade?
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-Elevated central nervouse pressure
-hypotension -pulsus paradoxus -beck traid -kussmaul sign -eward sign |
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Beck triad
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-increased venous pressure, hypotension, and diminished heart sounds
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kussmaul sign
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-paradoxical increase in venous distension and pressure during inspiration
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ewart's sign
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-aka pins sign
-dullness of percussion and breathing sounds at the tip of the Lt scapula where the effusion is LG enough to compress the Lt lower lung. |
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acute tamponade
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-less common
-caused by trauma, catheterization, rupture of the heart(ie. myocardial infarction, or aortic rupture) |
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subacute tamponade
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-idiopathic
-viral pericarditis -neoplastic |
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what is the 2D appearance of tamponade?
|
-pericardial effusion
-RA and RV diastolic collapse -decreased LV size on inspiration -decreased MV E-F slode due to decreased LV filling |
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acute pericarditis
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-small to moderate PE
-pericardial thickening -fibrosis -uncommonly calcification can occur |
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what can the transverse and ovlique sinus's be confused with?
|
-trx sinus can be confused with the coronary artery dialation
-oblique sinus can be confused wiith the coronary sinus |
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what does increased pericardial pressures cause?
|
effects the filling of the heart
-effects lower pressures first |
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what is the most common type of primary CA in the heart?
|
mesothelioma
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what are the similarities and differences in the clinical findings with restrictive cardiomyopathies, and constrictuve pericarditis?
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SAME:
-possible kussmauls sign -low voltage ECG and A-fib -edema -ascites -hepatomegaly RC: -biventricular failure -no pericardial knock CP: pleural effusion pericardial knock |
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what are the similarities and differences in the doppler with restrictive cardiomyopathies, and constrictuve pericarditis?
|
SAME:
-distolic dysfunction(CP=restrictive RC=not necessarily restrictive) RC: -little respiratory variation -increased TR jet CP: -respiratory velocity changes with MV and TV -Pulm and HV flow respiration changes -normal TR jet -rapid early LV filling |
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plethora
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SVA and IVC are dialated
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mild, moderate, and severe systemic hypertension
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mild-diastolic blood pressure btw 90 and 105 mmHg
moderate-diastolic BP btw 105-114mmhg Severe-diastolic BP btw115-129mmHg(medical emergency) |
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What should be determined with doppler for systemic hypertension?
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-determine grade of diastolic dysfunction(important)
-determine LV global systolic function -severity of AP and MV regurge |
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What are the degrees of systolic pulmonary arter pressure(SPAP)
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NOrmal-18-25mmHg
MIld-30-4-mmHg Moderate-40-70mmHg Severe>70mmHg Eisenmenger's>120mmHg/ and or exceed systolid pressure |
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what does the m-mode of PH look like?
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-Pv-flying w sign
-RVVO pattern |
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the degree of LV systolic dysfunction is a good predictor of what?
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-clinical outcome for cardiovascular diseases such as:
-ishemic disease -valvular disease -cardiomyopathis -congenital heart disease |
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Explain preload
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(VOLUME)
-affects the ventricle during distole -increased preload=increased force of contraction |
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explain afterload
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(PRESSURE)
-aortic resistance/impedance/wall stress -increase afterload=redced ventricular foce and volocity of contraction(reduced myocardial fiber shortening) -affects the ventricle during systole |
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what will increase myocardial intrinsic contractility?
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-drugs and hormones and sympatheic nervous sytem
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what are the problems with quantification of systolic function?
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-endocardial dropout
-forshortening LV(will overestimate) -reginonal wall abnormalities -disco orination of contration |
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how is wall motion scored? how then is the WMSI obtained?
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1. normal
2. hypokinesis 3. akinesis 4. dyskineses 5. aneurysmal WMSI=average score normal=1; abnormal=1.7 |
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auxotonic relaxation
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-the last 3 phases of diastole where the MV is open
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What is LV filling determined by?
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active and passive forces:
-Early diastole-e=active relaxation(cells recoil from elastic energy) and determine LV filling -Late diastole-a-passive properties(myocardial compliance-inverse of stiffness) |
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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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ventricular relaxation(early diastole)
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-systolic filling during IVRT
-active process involiving energy from myocardium -factors that affect IVRT=internal loading forces and inactivation of myocardial contraction -abnormal IVRT=prolonged rate &reduction in peak filling rate |
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ventricular compliance
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-change in volume over change in pressure
-influenced by ventricular size, shape and characteristics of the myocardium -elevation is based on diastolic passive pressure |
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what echo findings suggest diastolic dysfunction?
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-LVH
-enlarged LA -dialated IVC w/ reduced respiratory collapse |
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what echo findings suggest diastolic dysfunction?
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-LVH
-enlarged LA -dialated IVC w/ reduced respiratory collapse |
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what is the IVRT, DT, E/A, mitral duration, and PVs/d comparasin for normal, impared relaxation, pseudonormal pattern, and restrictive diastolic dysfunction?
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IVRT:
N-70-90 I=>90 Ps=<90 R=<70 DT: N-160-240 I=>240 P=160-240 R=<160 E/A: N-1-2 I-<1 Ps-1-2 R->1.5 Pvs:Pvd: I-Pvs>PVd Ps-Pvs<Pvd R-Pvs<Pvd Mitral duration: N=>PV A duration I=either or depending on LVEDP Ps-<PV a duration R-<PV a duration |
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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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dP/dT
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measure of the rate of rise of ventricular pressure during IVCT
-using CW -measures time interval btw 2 points -measures the change in pressure over time(time it takes the LV to generage 32 mmHg of pressure during IVCT) |
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what is the formula for dP/dt?
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dP/dt=32/change in time
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HOw does diastolic dysfunction produce signs of heart failure?
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-elevated LV pressure which causes:
-increase LA pressures -this is reflected back to pulmonary circulation which: -causes SOB and pulmonary congestion |
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Restrictive
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-severe reduction in LV compliane, and increased LA pressures
-PV higher than 30cm/s -MV opens earlier=short IVRT increased LA pressure increases transmitral gradient causeing increase E wave -short DT -Increased LVEDP -E/A ratio=>2 -PV-increased d wave, and decrease s wave, increased duration and velocity of atrial contraction(a duration) |
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what will the E/A ration e on a reversable diastolic dysfunction compared to irreversable?
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<1, valsalva does not change EA ration(most serious form of diastolic dysfuction)
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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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how is LV mass determined? what is normal for males and females?
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LV mass= volume of myocardiumxspecific gravity of myocardium(1.04g/ml)
norm M-125-130g/m2 F-105-120g/m2 |
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with dp/dt, what does the velocity of MR reflect? assuming LA pressure does not increase significantly durin IVRT, what does the rate of rise of the doppler velocity reflect?
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-Velocity of MR reflects the instantaneous pressure gradient btw LA and LV during systole
-rate of rise of Doppler velocity reflefts the rate of rise of LV pressure. |
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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 some complications of diastolic dysfunction?
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-exercise intolerance
-dyspnea(most common) -PH -volume overload=edema ascites -tachycardia=a-fib=clot and CVA |
