right heart valves

causes of tricuspid stenosis (6)

-rheumatic heart disease (90%)

-systemic lupus erythmatosus

-carcinoid heart disease

-loeffler’s endocarditis

-metastatic melanoma

-congenital heart disease

is isolated rheumatic tv stenosis common

no, almost never occurs

normal tv orifice area

7-9 cm²

3 parameters to assess TS

valve area, mean transvalvular gradient, ra chamber size

rheumatic tv stenosis m mode appearance (3)

-diminished ef slope

-anterior displacement of posterior leaflet

-thickening of valve leaflet and apparatus

if undetected, tv stenosis complications include (3)

-increased operative morbidity and mortality in patients having left heart valve disease

-chronic elevation of ra pressure

-low cardiac output even if left heart valves are repaired

associated findings of tv stenosis (6)

-rae (due to increased ra pressure)

-ias bows to the left (from high ra pressure)

-increased diastolic tv pressure gradient

-dilated ivc

-pulmonary hypertension

-rvh (rvh and pulm htn can cause diminished ef slope)

high ra pressure leading to increased systemic venous pressure will cause (3)

-peripheral edema

-hepatic congestion

-fatigue

chronic ra dilation will cause (2)

-decreased sv

-possible afib w/ thrombus formation

2d criteria of tv stenosis (3)

-doming of tv leaflets in diastole (more toward leaflet tips)

-thickening and reduced excursion of posterior or septal leaflets (or both)

-reduced tricuspid orifice diameter relative to annulus diameter in same plane

what can obstruct rv inflow and mimic tv stenosis (3)

-ra tumors

-large vegetations

-large atrial thrombus (can be a result of embolization from venous bed)

doppler signs of TS (5)

-higher diastolic velocity than normal

-decreased ef slope

-turbulent flow

-prolonged reduction in velocity throughout diastole

-increased A wave on hepatic vein flow

tr and ts velocities

tr - <0.7 m/s

ts - >1 m/s

quantifiable data for tv stenosis (3)

-peak velocity

-peak gradient

-mean gradient

mild grading of tv stenosis (valve area, mean gradient, pulmonary artery pressure)

valve area >1.5 cm²

mean gradient <5 mmHg

pa pressure <30 mmHg

moderate grading of tv stenosis (valve area, mean gradient, pulmonary artery pressure)

valve area 1-1.5 cm²

mean gradient 5-10 mmHg

pa pressure 30-50 mmHg

severe grading of tv stenosis (valve area, mean gradient, pulmonary artery pressure)

valve area <1 cm²

mean gradient >10 mmHg

pa pressure >50 mmHg

carcinoid heart disease results from

presence of carcinoid tumors

how do carcinoid tumors affect right side of heart

produce vasoactive substance that causes endothelial damage to right side of heart

how many patients with carcinoid syndrome have cardiac involvement

1/2

how soon is the heart affected with carcinoid syndrome

late in disease progression

clinical symptoms of carcinoid heart disease (6)

-facial flushing with stimuli

-abdominal pain

-diarrhea

-renal failure

-hepatic failure

-hepatomegaly (in later stages)

cardiac signs of carcinoid heart disease (2)

-elevated venous pressure

-systolic and diastolic murmurs

2d appearance of carcinoid heart disease (6)

-rve

-abnormal septal motion indicating rvvo

-thickened tv leaflets that are retracted

-foreshortened chordae

-thickened retracted pv cusps

-tv leaflets don’t close completely and remain open throughout cardiac cycle

doppler signs of carcinoid heart disease (4)

-tr (most prevalent)

-increased diastolic tv velocities

-increased diastolic pv velocities

-pulmonary insufficiency

difference between rheumatic disease and carcinoid disease

rheumatic disease will have left sided valvular involvement but carcinoid will not

2 mechanisms that cause tricuspid regurgitation

-secondary to right heart chamber abnormalities (rae, rve, rv infarction)

-actual tricuspid valve disease

rve is associated with conditions that

cause rv volume or pressure overload

rve associated conditions (2)

-aortic valve disease

-mitral valve disease (especially MS bc it causes left sided pressure increase resulting in pulmonary htn)

tr causes (5)

-pacer wire in right heart

-cardiac transplant

-tv disease

-rv infarction

-rv dilation

tr caused by rv infarction involves which pap muscle and why

posterior, attaches to posterior and septal leaflets of tv

types of tv disease (7)

-rheumatic tv disease

-tv prolapse

-endocarditis

-ruptured pap muscle or chordae

-carcinoid heart disease

-trauma

-congenital defects of tv (tv dysplasia or abstains anomaly)

physical findings of tr (4)

-jvd w/ prominent v wave

-jaundice

-thrill in lower left sternal border)

-hyperdynamic rv impulse along left sternal border

2 ways of color assessment of tr

-ratio of ra area/jet area

-hepatic vein and ivc flow (flow into ra during systole, pressure falls w/ atrial relaxation)

severe tr color doppler will show (2)

-retrograde flow in hepatic veins and ivc

-systolic flow reversal

2 reasons to determine tr severity

-determine systolic pulmonary pressures

-deciding to repair or replace tv in patients having other cardiac surgeries

what equation to use to calculate tv pressure gradient

Bernoulli (4v²)

systolic pa pressure (spap) vs right ventricular systolic pressures (rvsp)

same as long as there is no pv stenosis

how to obtain right ventricular systolic pressure (RVSP) (equation)

4v² + rap

normal ra pressure (TC)

normal ivc diameter

<=2.1 cm

dilated ivc diameter

>2.1 cm

systolic pa pressure equation

(tv pg x 25%) + tr gradient

tv prolapse is common to see with

mvp

what view is tv prolapse visualized from

rv inflow or a4c

tv endocarditis is usually seen with (3)

-iv drug use

-alcoholism

-congenital defects (ie vsd)

clinical sbe findings (3)

-temperature >100 degrees

-murmurs of tr and pi

-positive blood cultures (usually staphylococcus aureus)

2d sbe findings (4)

-dense mass

-highly mobile

-shaggy appearance of entire valve

-polypoid structure attached to single leaflet

differential diagnosis of tv sbe (2)

-myxoma (attach to ias by stalk)

-vegetaions

complications of tv sbe (2)

-tr

-flail tv

rheumatic pv disease is rare, always associated with _, and typically manifests as _

ms, stenosis

severe rheumatic ps has a peak velocity of

>4 m/s

severe rheumatic ps has a mean gradient of

>35 mmHg

3 areas involves with pulmonic valve stenosis

-valvular

-supravalvular

-subvalvular

3 morphologic types of pv stenosis

-dome shaped (40-60% of cases)

-bicuspid or multicuspid pv (associated w/ congenital syndromes)

-dysplastic pv (20% of cases)

doming from pv stenosis characteristics (4)

-doming of valve in systole

-fusion of raphe

-post stenotic dilatation of the pa

-balloon valvuloplasty can correct

3 characteristics of dysplastic pv

-severely thickened valve tissue

-immobile cusps from thickened myxomatous tissue

-associated with noonan’s syndrome which includes dysmorphic features

supravalvular stenosis can be difficult to diagnose with the if _ are involved

peripheral arteries

supravalvular pulmonary stenosis occurs where

infundibular level

supravalvular stenosis is usually part of

more complex congenital disease

isolated subvalvular pulmonary stenosis may occur from

obstruction of a windsock vsd bulging into rvot (SOVA)

physical exam signs in ps (6)

-prominent jugular a wave

-significant ps (palpitation of precordium finds a systolic thrill at upper left sternal border or rv lift or heave)

-widely split s2 (caused by prolonged pulmonic ejection time and delayed closure of the pvs)

-ejection click (commonly audible in mild ps)

-w/ increasing ps severity, click approximates the first heart sound

-severe cases may have an inaudible click and a harsh crescendo-decrescendo ejection murmur can be heart at left upper sternal border which increases in intensity w/ inspiration)

symptom of mild or moderate ps

mostly asymptomatic

symptoms of significant ps (4)

-dyspnea

-exertional chest pain

-dizziness

-syncope

mild pv stenosis (peak velocity, peak gradient)

peak velocity <3 m/s

peak gradient <36 mmHg

moderate pv stenosis (peak velocity, peak gradient)

peak velocity 3-4 m/s

peak gradient 36-64 mmHg

severe pv stenosis (peak velocity, peak gradient)

peak velocity >4 m/s

peak gradient >64 mmHg

pulmonic regurgitation/pi involves turbulent flow into rvot during _

diastole

clinical significance of pulmonic regurgitation

not known

valve characters of pi in a normal patient (4)

-pv cusps are thinner than ao valve

-pv has a less fibrous ring

-pv has shallower sinuses

-retorgrade pressure from pa may not be enough to close valve right

pi characteristics (4)

-long duration in diastole

-centrally located jet

-originated from valve computation point into rvot

-flow velocities are nearly the same as trans pulmonary pressure difference

causes of pi (6)

-pulmonary htn

-bacterial endocarditis

-pulmonary valvotomy

-congenital defects

-carcinoid heart disease

-trauma

is it possible to differentiate between pi from physiologic causes vs pathology

yes

velocity of pi jet reflects _ difference during _

transpulmonary pressure, diastole

physiologic pi approximate gradient and velocity

gradient 9 mmHg

velocity 1.5 m/s

in a patient w/ normal pa pressure <18 mmHg, pw shows that pi _ in early diastole and _ in late diastole

peaks, slows

pa pressures >25 mmHg pw velocity profile shows

wideband spectrum that is sustained throughout diastole

characteristics of patients w/ physiologic pi (or no significant cardiac abnormalities) (4)

-normal pv and pa

-normal chamber dimension

-normal pa pressures

-pi distance <10mm (or 1 cm in length) and not holodiasatolic in duration

pi distance is

maximum distance traveled by pi using pw and color flow doppler

pi distance in patients w/ borderline pi

1-2 cm in length and holodiastolic in duration

pi distance and velocity in patients w/ clinically significant pi or w/ underlying cardiac pathology ie pulmonary htn

>20mm (2cm) in length w/ peak velocity >=1.5m/s and holodiastolic in duration

grading of pi w/ cw spectral strength of regurgitation jet

grade 1 (mild) - spectral tracing stains sufficiently for detection but not enough for clear delineation

grade 2 (moderate) - complete spectral tracing can just be seen

grade 3 (mod sev) - distinct darkening of spectral tracing is visible but density is less than antegrade flow

grade 4 (sev) - dark stained spectral tracing

severe pr jet width/annulus diameter, pr jet pht, and deceleration time

jet width >=70%

pht <100 ms

deceleration time <260 ms

pulmonary htn is increased pulmonary pressure due to (2)

-reduction in caliber of pulmonary vasculature

-increase in pulmonary blood flow

(sometimes both)

pulmonary htn is an increase in pulmonary arterial pressure above

30mmHg systolic (some sources say >20 mmHg)

rv pulmonary htn response order (5)

-hypertrophy

-rve

-tr

-pi

-rae

primary pulmonary htn cause

unknown

secondary pulmonary htn found in patients w/ (5)

-mitral stenosis

-heart failure w/ elevated lv end diastolic pressures

-cor pulmonate (right hear failure due to pulmonary disease

-thrombolic emboli to lungs

-congenital heart disease w/ a left to right shunt (elevated la pressures)

m mode appearance of pulmonary htn (3)

-midsystolic closure of pv (flying w sign)

-rvh

-paradoxical septal motion

methods of grading pulmonary htn severity (3)

-AcT/RVET ratio

-SPAP values

-RVOT acceleration time

acceleration time pulmonary htn severity

normal >= 120ms

mild 80-100 ms

mod 60-80 ms

severe <60 ms

rvet is time from _ to _

onset of flow to end systolic flow

normal AcT/RVET ratio

0.45

significant pulmonary htn ratio (act/rvet) is reduced to

0.25

common causes of rvvo (4)

-tr

-pi

-asd

-partial or total anomalous venous return

less common causes of rvvo (3)

-vsd w/ lv-ra shunt

-ruptured sov

-coronary artery fistula w/ communications to ra or ventricle

rvvo echo signs (4)

-dilated rv

-flattened septum or d sign on 2d

-rv appeaers more oval than usual crescent shape

-rv apex may extend past lv apex

eccentricity index is used for

separation of right ventricular volume and pressure overload

rv pressure overload results from (2)

-increase in rv volume

-obstruction to rv blood flow (primarily from pulmonary embolism)

course of rv pressure overload (6)

rv dilation, tr, rv fails, resulting hypokinesis of rv, ra ivc mpa dilate, rvh may also occur