echo exam 3 (combined)

what are the layers of the aortic wall? (3) which one is the most important and composes most of the wall?

• tunica intima

• tunica adventitia

• tunica media (most important, composes 80%)

what does the aortic wall do? (2)

• damping - stores force generated by ventricle in systole

• expulsion - expels stored energy in systole

(basically first dilates the aorta to allow blood in, then snaps back to push flow forward)

what are the aortic regions? (3) what does the aorta become after passing the diaphragm?

• ascending aorta

• aortic arch

• descending aorta

• becomes the abdominal aorta

what are the key segments of the ascending aorta? (4)

• annulus

• sinuses of valsalva

• sinotubular junction

• ascending aorta

what branches arise from the aortic arch? (3)

• innominate (brachiocephalic)

• left common carotid

• left subclavian

what is the aortic isthmus? what is it a common site for?

• part of aorta distal to left subclavian artery and descending aorta

• common site of coarctation

• common site of traumatic injury (bc aorta is fixed to thorax here)

where does the abd ao start? where does it run in comparison to the ivc? what is the average diameter?

• starts at diaphragm

• runs to the left of the ivc

• average diameter : 2 cm (1-3 cm is normal range)

what is supravalvular as?

• definition : congenital narrowing of the ascending aorta, just distal to coronary arteries

how common is obstructive lesion supravalvular as?

least common site for congenital as… very rare

what features usually accompany supravalvular as? (2)

• dilation of the coronary arteries, sometimes ostial obstruction (complete blockage of a vessel)

• thickening of the AoV cusps, with some AI

what are obstructive lesions?

general term for any abnormality that blocks or restricts blood flow

what are the types of supravalvular as? (3)

• hour-glass shaped

• discrete membrane

• hypoplastic asc ao

what are the characteristics of hour-glass type svas? (5)

• fibromuscular thickening, resulting in hourglass narrowing

• just above aortic sinuses

• most common type

• cusps may be thickened

• some degree of associated PA stenosis… (bc PA and Ao develop at same time) can be supravalvular or peripheral

what syndrome is hour-glass type svas associated with? what are the features of that syndrome? (4)

• williams syndrome

features:

• supravalvular as

• elfin facies

• mental retardation

• peripheral pulmonic stenosis

what are the characteristics of fibrous membrane svas? (2)

• seen in normal sized aorta

• located near sinotubular junction

what arteries does hypoplastic svas often also effect? what is it also known as? what syndrome is it associated with?

• often involves the origins of the brachiocephalic arteries

• aka : strand stenosis

• associated with hypoplastic left heart syndrome

what is the defining characteristic of each type of svas?

• hour-glass : aorta pinches right above valve

• discrete membrane : normal sized aorta with small membranous shelf

• hypoplastic : small aorta for an extended segment

where does coarctation occur?

• AORTIC ISTHMUS

• in descending aorta

• distal to left subclavian artery

• near ductus arteriosis

what is coarctation?

localized narrowing of the descending ao

what other congenital heart defects are usually associated with coarctation? (2)

• bicuspid AoV

• MV malformations

what is the ‘classic figure 3’ when talking about CXR?

it’s a sign of aortic coarctation.

• curved part = area of stenosis

• straight part = dilated subclavian artery

• double = post-stenotic dilitation

what are the signs of coarctation on CXR? (2)

• classic figure 3

• rib notching (from dilated vessels)

what are the types of subaortic valvular obstruction? (2)

• discrete membrane

• tunnel type

what are the characteristics of discrete membrane subaortic obstruction? where does it extend from and to? what is the echo appearance

• thin, membranous, crescent-shaped shelf formed right under AoV or in LVOT

• membrane usually extends from ANTE septum to AMVL

• echo appearance : thin linear echo in LVOT, perpendicular to IVS

what does the m-mode look like for a pt who has discrete membrane subaortic obstruction?

• coarse systolic flutter of Aov leaflets (fr turbulent and accelerated flow)

• midsystolic partial closure (fr LVOT obstruction)

what is aortic dilation? how common is it?

• increased diameter of aorta

• most common aortic abnormality

what are the causes for aortic dilation in asc ao? (5)

• htn

• atherosclerosis

• cystic medial necrosis

• post-stenotic dilation

• collagen vascular and inflammatory disorders

  • marfans

  • rheumatoid arthritis

  • SLE

  • reiter syndrome

when dilation becomes severe, it is then considered?

aneurysmic

what are aneurysms? what % increase in dilation would be considered anuerysmal?

• localized areas of abnormal dilation of a vessel

• usually more than 50% increase in a vessel = aneurysmic

what is criteria to call an aortic aneurysmal?

• over 5 cm in asc ao

• over 4 cm in desc ao

• over 6 cm = high risk of rupture

what are the causes for aortic aneurysms? (7)

• atherosclerosis/degenerative causes (most common)

• syphilis

• trauma

• aortic stenosis

• genetically triggered (e.g. aortic coarctation)

• pda

• aortitis

what are the types of aneurysms?

• dissecting (tear, intima layer peels away)

• saccular (weakening of vessel wall at one point, results in pouch-like expansion)

• fusiform (most common, involves entire circumference of vessel and dilation is uniform)

what are the morphologic shapes of aneurysms?

• annuloaortic ectasia (pear-shaped ao root), involves annulus and SOV

• dilation involving annulus, SOV, and part of asc ao

• dilation beginning @ sinotubular junction, spares annulus and SOV

aneurysm type? what parts of the Ao does it involve?

• pear-shaped … involves annulus and SOV

• dilation at sinotubular junction and beyond

• dilation at annulus, SOV, and asc ao

for TTE eval, what view do we look at for aortic aneurysms? which exact parts do we measure? from where to where?

• aortic sizes, measured from plax, at end-diastole

• measure : annulus, SOV, sinotubular juntion, proximal part of asc ao

• can be leading edge to leading OR inner edge to inner

what is marfan’s syndrome?

disorder involving connective tissue, bones, muscles, ligaments, and skeletal structure

what are the echo findings for a pt with marfan’s syndrome? what is the most common?

• proximal aorta dilation

• multivalvular prolapse

• la compression

• ai, mr

• ao dissection (most common)

• lvvo

how common are atherosclerotic aneurysms? how much do they effect thoracic or abdominal ao?

• very common, most common

• 25% are thoracic, other 75% is abdominal

what are the most common sites for aneurysms for thoracic ao?

• aortic arch

• desc ao

how does the atherosclerotic process work on aortic aneurysms?

• weakens ao wall

• medial degeneration

• localized vessel dilation

how does hypertension effect the aorta?

• huge cause for disease of the aorta

• weakens the strength of aorta wall

• eventual expansion to aneurysm

symptoms of aneurysms (3)

• symptoms depend on size and location of the aneurysm

• symptoms are a result of compression on other structures

  • e.g. esophagus, laryngeal nerve, left bronchus

what symptoms arise from aortic aneurysms? (6)

• wheezing

• coughing

• dyspnea

• hemoptysis

• hoarseness

• dysphagia

which imaging modalities can be used for diagnosing anerurysms?

• chest xray (good for mediastinal widening)

• ct w/ contrast (good)

• mri (good, no contrast needed)

• angiography (the best! but can miss aneurysm if there is a thrombus)

treatments for aneurysmal aortas?

• follow ups

• medication

• surgery (when over 5-6 cm)

  • open chest surgery, remove enlarged area of ao and sometimes the valve too, replace with graft and mechanical/biological valve

  • evar (endovascular aortic aneurysm repair), tube inserted into blood vessel, usually groin, and guides to aorta. catheter places graft in aneurysmic site to reinforce weakened walls

what is a SOV aneurysm? how common is it? is it acquired or congenital? how does it present?

• dilation of sov

• rare

• can be acquired OR congenital

• can present ruptured OR unruptured

what are some congenital cause of SOV aneurysms? (4)

• bicuspid AoV

• connective tissue disease

• marfans

• ehler danlos

what are some acquired causes of SOV aneurysms? (3)

• infective endocarditis (veggies)

• atherosclerotic degeneration

• iatrogenic post cardiac surgery

if the left SOV had an aneurysm, where would it rupture? complications?

• would rupture into the LA or RA

• can cause la compression

if the non-coronary SOV had an aneurysm, where would it rupture?

• could rupture into LA, RA, LV, or IVS

if the right SOV had an aneurysm, where would it rupture? complications?

• could rupture into RA, RV, MPA, or pericardium

• can cause:

  • RVOT obstructions,

  • RCA dissection or compression and acute MI

  • compression on conduction system → heart block

  • tamponade

what do the signs and symptoms (clinical symptoms) of SOV aneurysms depend on? (4)

• size

• location

• compression

• rupture

for a pt with a SOV aneurysm, what would you expect from their physical exam?

• wide pulse pressure (from AI)

• Long diastolic murmur

• LVH on EKG

• CXR

  • signs of CHF (fluid in leg, lung, etc)

  • cardiomegaly (enlarged heart)

  • unfolding of Ao (not as curvy aortic arch)

what are possible treatments for SOV aneurysms?

• surgery (for ruptured and unruptured)

• transcatheter repair

what is aortitis?

group of conditions that cause inflammation to walls of aorta

what are the types of aortitis? (4)

• infectious

• noninfectious

• radiation induced

• idiotpathic

what are the clinical signs of aortitis?

• nonspecific pain

• fever

• malaise (feeling of bleh)

• elevated levels of acute phase reactants

• other systemic manifestations

what is acute aortic syndrome? (7)

• acute onset of chest pain

• disruption of ao wall motion

• need for urgent medical attention

• Aortic dissection

• intramural hematoma penetrating atherosclerotic ulcer (when plaque explodes, clot forms on top causing even more stenosis

• traumatic aortic rupture due to blunt deceleration trauma

• aortic aneurysm leak and rupture

what is aortic dissection? which gender is more affected?

• sudden tear in intima layer of aortic wall, allowing blood to enter the wall and destroy media and further strip intima from adventitia

• more common in male

what are the names of the systems used to classify aortic dissections?

• deBakey

• stanford

how does stanford classify aortic dissections?

by location

• type a = ascending ao

• type b = any other dissection

how does DeBakey classify aortic dissections?

by location

• type 1 = ascending, transverse, and descending ao involved (70%)

• type 2 = ascending ao involved, but stops before brachiocephalic (5%)

• type 3 = descending ao and may extend into abd ao (25%)

what are the causes of ao dissection? (11)

• htn

• atherosclerosis

• marfan’s

• aging

• pregnancy

• trauma

• iatrogenic injury

• inflammatory diseases

• cocaine

• renal disease

• strenous physical exercise

what are the symptoms for ao dissection? (6)

• excruciating pain

• severe at onset

• radiate in path of dissection

• clammy

• shock-like

• hypertensive (or hy

what is the echo hallmark for ao dissection?

• flap in between the intima and media layer of aortic wall… best seen in short axis

• creates false and true lumen

what is the criteria for diagnosing aortic dissection?

• oscillation independent of ao

• visualized in multiple views

• disctintion from other structures (calcification, plaque, wires…)

• pericardial effusion

• aortic insufficiency

• false lumen is larger than true lumen

• flap moves towards true lumen in diastole (true lumen expands during systole, vice versa diastole)

• spontaneous contrast in false lumen

• slow flow in false lumen

• more rapid flow in true lumen

• contrast agents opacify true lumen first

• turbulence at entry site

what complications are associated with false lumens in ao dissections? (3)

• compresses true lumen

• extends into other branch vessels

• thrombosis (esp. aortic wall thickness > 15 mm)

what are the other complications associated with ao dissection? (not dealing w false lumen)

• malperfusion (coronary, cerebral, spinal, limb, or abdominal ischemia)

• ruptures (pericardial, pleural, peritoneal space, tamponade)

what is the most common cause of aortic isthmus?

trauma from high speed deceleration of mva

what are the views for tricuspid valve? (5)

• inflow

• psax

• apical 4

• subcostal 4

• non-imaging

what are the causes of tricuspid stenosis? (6)

• rheumatic heart disease (most common, 90%)

• SLE

• carcinoid heat disease

• loeffler’s endocarditis

• metastatic melanoma

• congenital heart disease

t/f : rheumatic TS usually occurs with rheumatic mitral or aortic stenosis

true, isolated rheumatic tv stenosis is VERY rare

what is the NORMAL tv orifice area?

7-9 cm²

what should the severity of tricuspid stenosis be graded on? (3)

• valve area

• mean PG

• ra chamber size

if a pt has tricuspid stenosis, what would you expect from their m-mode? (3)

• diminished EF slope (caused RVH and pulm HTN)

• anterior displacement of posterior leaflet

• thickening

if tricsupid stenosis goes undetected, what could it lead to? (3)

• increased chance of mortality when undergoing operations

• chronic elevation of RA pressure

• low CO (even if left valves are functioning well… bc low venous return)

what are the associated findings of tv stenosis? (6)

• RAE

• bowing IAS

• increased diastolic TV PG

• dilated IVC

• pulmonary HTN

• RVH

what will high RA pressure lead to?

• increased venous pressure:

  • peripheral edema

  • hepatic congestion

  • fatigue

• chronic RA dilation

  • decreased SV

  • a fib, thrombus

what is the 2d criteria for grading TV stenosis?

• doming of tv leaflets in diastole

• thickening and reduced excursion

• smaller orifice

what can mimic TV stenosis?

anything that obstructs RA…

• RA tumors

• large veggies

• large atrial myxomas

what would you expect from a doppler on a pt with TV stenosis? (5)

• faster diastolic velocities

• decreased ef slope

• turbulent flow

• prolonged reduction in velocity (normal: fast decline)

• increased a wave for hepatic vein

what should TV velocities be?

• with tr, tv velocities equal or less than 0.7 m/s

• with tv stenosis, velocities are greater than 1.0 m/s

how do we grade tv stenosis?

• NOT planimetry

• NOT RLLY pht (not proven) … TVA = 190/PHT

• quantifiable data (what we mostly grade on):

  • peak velocities

  • peak PG

  • mean PG

if a pt has mild TV stenosis, what would their valve area, mean PG, and pulm artery pressure be?

• TVA : >1.5 cm²

• mean PG : <5 mmhg

• pulm artery pressure : <30 mmhg

if a pt has moderate TV stenosis, what would their valve area, mean PG, and pulm artery pres

• TVA : 1-1.5 cm²

• mean PG : 5-10 mmhg

• pulm artery pressure : 30-50 mmhg

if a pt has severe TV stenosis, what would their valve area, mean PG, and pulm artery pres

• TVA : <1 cm²

• mean PG : >10 mmhg

• pulm artery pressure : >50 mmhg

what is carcinoid heart disease?

• result of carcinoid tumors (mostly found in GI tract)

• effects right side of heart (TV and PV)

how do carcinoid tumors affect the heart?

• tumors produce a vasoactive substance that causes endothelial damage to the right side of heart

• primary tumors can be small

at what part in the carcinoid disease does it affect the heart? what is the rate of people with carcinoid disease that get some sort of heart involvement?

• heart is effected late into the progression

• ½

what are the symptoms of carcinoid heart disease? (6)

• flushed face

• abdominal pain

• diarrhea

• renal failure

• hepatic failure

• hepatomegaly (later stages)

what are the cardiac signs of carcinoid heart disease?

• elevated venous pressure

• diastolic and systolic murmurs (from the regurgitations and stenosis)

what is the 2d appearance of a pt with carcinoid heart disease?

• RVE

• abnormal septal motion, indicating RVVO

• thickened, retracted TV

• foreshortened chordae

• thickened, retracted PV

• TV never fully coapts

what are the doppler signs for carcinoid heart disease?

• TR (most prevalent)

• increased TV velocities

• increased PV velocities

• PI

what are the echo findings for carcinoid heart disease?

• similar to echo findings for rheumatic TV stenosis

what differentiates the echo findings of carcinoid heart disease from rheumatic disease?

rheumatic has left sided valvular involvement. carcinoid heart disease only effects right side valves.

what mechanisms cause TR? (2)

• right heart chamber abnormalities

• actual tricuspid valve disease

what causes TR? (4)

• pacer wires in right heart

• cardiac transplant

• TV disease

• RV infarction

how is TR caused by RV dilation?

• congenital heart disease (e.g. partial anomalous venous return)

• RVVO (alters TV apparatus)

how is TR caused by RV infarction?

• involved posterior papillary muscle which is attached to posterior and septal leaflet of TV

what tricuspid valve diseases cause TR? (7)

• rheumatic TV disease

• TV prolapse

• endocarditis

• ruptured pap/chordae

• carcinoid heart disease

• trauma

• congenital defects (e.g. tv dysplasia and ebstein’s anomaly)