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cardiology > valve disorders > Flashcards

valve disorders Flashcards

1
Q

types of valve disorders

A

tricuspid
pulmonic
mitral
aortic

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2
Q

three thin leaflets open and close properly

A

healthy aortic valve

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3
Q

narrowing

A

stenosis

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3
Q

the leaflets become stiff and thickened limiting the amount of blood pumped out to the body

A

diseased stenotic valve

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4
Q

backflow

A

regurgitation

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5
Q

what does regurgitation look like

A

the chordae tendinae become floppy

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6
Q

3 leaflets – aortic and pulmonary

A

semi-lunar valves

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7
Q

mitral and tricuspid

A

AV valves

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8
Q

function of valves

A
  1. Keep blood moving in one direction through pumping chambers
  2. Each valve has leaflets that open easily and close fully in response to
    pressure changes and muscle contractions produced during systole
    and diastole to ensure forward progression of blood through the
    heart.
  3. An increase in forward pressure across a valve forces the leaflets to
    open. An increase in backward pressure against a valve forces the
    leaflets to close.
  4. The valves are stabilized and supported by the fibrous skeleton, a
    sheet like structure of dense fibrous connective tissue that separates
    the atria from the ventricles and encircles each valve, creating a ring or annulus. The annulus acts as an anchor to the heart muscle.
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9
Q

separates the left ventricle and the aorta

A

aortic valve

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10
Q

Leaflets close edge-to-edge by a fibrous collagen edge called

A

commisures

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11
Q

Surrounding the valve, at
the base of each leaflet is
the fibrinous ring, called the

A

annulus

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11
Q

Two of the sinuses house
the

A

R and L Ostia of the
coronary arteries

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12
Q

The walls of the aorta bulge
out slightly behind each
leaflet, called a

A

sinus of valsava

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13
Q

Coronary arteries fill during

A

diastole

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14
Q

what valves open during ventricular diastole

A

AV valves

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15
Q
  • Acquired
  • Calcium deposition (similar to that of athlerosclerotic disease of the coronary arteries)
  • 60- 75y/o
  • Rare in people younger than 50
A

degenerative/calcific aortic stenosis

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16
Q
  • Born this way
  • Symptoms usually occurs around 50 y/o, when
    degenerative processes begin to manifest
  • Younger when stenosis is severe
  • Often occurs with
     Dilated aortic root
     Coarctation of the aorta
  • Look for it in the family- parent, children
A

congenital/unicuspid or bicuspid valves

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17
Q

1) Bicuspid or unicuspid,
2) Fibrinous fused
commissures,
Symptoms age 50

A

congenital aortic stenosis

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18
Q

1) Nodular calcification
1) 3-cusp valve, no
commissural fusion
Limit leaflet movement,
Symptoms age 70

A

degenerative aortic stenosis

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19
Q

1) Fibrous thickening,
2) 3-cusp valve, mild
calcification, rheumatic
fever history in ½,
fused commisures

A

Rheumatic Aortic Stenosis

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19
Q

mild valve thickening or calcification
affects normal leaflet motion. As the disease progresses, leaflets become thicker, calcium nodules form, and new blood vessels appear.

calcium nodules located within the layers of the leaflet bulge outward toward the aorta and extend to
the sinuses of Valsalva, causing restricted leaflet motion and obstruction of left ventricular outflow during systole

A

aortic stenosis pathophysiology

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19
Q

what creates left ventricular hypertrophy

A

 As the aortic valve progresses from sclerosis to stenosis, it creates worsening resistance to LV blood outflow/ejection
 The ventricle must generate a higher systolic pressure to eject the blood out.
 the left ventricle encounters chronic resistance (over time) to systolic ejection (Increased Afterload)

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20
Q

LHV then causes an increase in the _____________ (best measured at the very end of diastole= LVEDP)… because the space available in the LV is now limited but must hold
the same amount of volume.

A

diastolic pressure

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21
Q

 Cardiac output is maintained… UNTIL… the aortic valve becomes so severely stenosed, left ventricular can no longer generate enough pressure to overcome the afterload. this results in

A

 reduced LV systolic contractility (EF<50%)
 Or reduced diastolic volume: the LVH is so big, there is no volume to push out (EF>50%)
 Both of these scenarios= Hypoperfusion to other organs
 Syncope ( Not enough blood to the brain)
 Renal Failure ( Prerenal hypoperfusion RI)

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22
Q
  • condition characterized by widespread inflammation affecting a number of organs in the body, including the heart.
     It occurs after an infection of the throat caused by the bacterium
    Group A streptococcus.
     The resulting immune response targets both the bacteria and some
    of the body’s own tissues.
A

rheumatic fever

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22
Q

Rheumatic heart disease results from

A

persisting inflammation of the
heart after acute or recurrent episodes of rheumatic fever

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23
Q

gold standard for diagnosing aortic stenosis

A

noninvasive 2-dimensional Doppler echocardiography. (TTE)

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23
Q

peaks in early systole in mild aortic stenosis and progressively later as aortic stenosis becomes more severe.
 The crescendo-decrescendo late-peaking murmur is heard best at the upper right sternal boarder at the second intercostal space and may radiate to the carotid arteries.
 In older patients, the murmur may be less intense and may radiate to the apex of the heart rather than to the base
 In severe AS a palpable LV heave or thrill can present

A

systolic ejection murmur

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23
Q

what valves does rheumatic heart disease affect

A

the mitral and aortic valves. Chronic inflammation may cause narrowing of the valves resulting in decreased blood flow through the heart or
leakage of the valves causing blood to flow in the wrong direction

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24
Q

how to diagnose AS

A
  1. EKG-
     Show LVH
  2. Chest Xray-
     Cardiomegaly (Enlarged cardiac silhouette)
     Aortic Valve Calcification
     Aortic Root Dilation or Calcification
  3. Echocardiogram
     Visualize the Aortic valve leaflets, commissures, opening/closing
     Severity of LV thickness
     Overall ventricular function
     Aortic valve gradient
     Valve area estimation
  4. Cardiac Catheterization
     Measure pressures and gradients from inside the heart, and across the aortic valve
     Anatomy or coronary arteries
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25
Q

Aortic stenosis is graded:
mild, moderate, or severe.

A

Grading is based on 3 hemodynamic
parameters measured by using Doppler echocardiography:
 Aortic jet velocity
 Mean aortic valve pressure gradient
 Aortic valve area

Aortic stenosis is considered hemodynamically important when the :
 Valve area is less than 1.0 cm (per TTE or TEE) or
 Aortic jet velocity >4m/s (per TTE) or
 Mean gradient >40mmHg (per TTE or Cath)

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26
Q

aortic stenosis treatment

A

aortic valve replacement

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27
Q

how to treat cardiovascular risk factors

A

control:
 Hypertension (No Beta blockers - depress myocardial function and can induce left ventricular failure)
 diabetes mellitus
 smoking tobacco
 high cholesterol levels
 Overweight
 lack of exercise.

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28
Q

what is important to consider in AS treatment

A

Having patients compare current activity level with past activity level may indicate if usual activity has been altered to avoid signs and symptoms

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29
Q

what is the choice of replacement device of age <60 years

A

Mechanical prosthesis
Must be on anticoagulation!

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29
Q

 13% in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in African-Americans.
 Prevalence increases with Age in both genders.
 Of asymptomatic people >55 years of age, 13% have moderate or severe echocardiographic AR
with a total prevalence of 29% (including mild AR).
 The prevalence of AR appears to be similar across racial populations in the United States, although internationally there is significant
variation in the prevalence of predisposing conditions, such as rheumatic heart disease.

A

epidemiology of aortic valve insufficiency/regurgitation

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30
Q

what is the choice of replacement device of Age >60 years

A

Porcine or bovine pericardial tissue bio-prosthetic grafts
Last for average 10-15 years
Avoid the need for anticoagulation

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30
Q

The diastolic leakage of blood from the aorta into the left ventricle.

It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease
or dilation of the aortic root

A

aortic valve insufficiency/regurgitation

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31
Q

medical emergency with high mortality

 Most commonly it results from aortic dissection or endocarditis and, in rare cases, trauma.
 NO LV dilatation
 End-diastolic pressure in the left ventricle rises sharply. The heart tries to compensate by increasing the heart rate and increasing the contractility (Starling’s law) to keep up with the increased preload, but this is insufficient to maintain the normal stroke volume and fails

A

acute AR

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31
Q

Developed countries:
 Congenital bicuspid aortic valve
 Aortic root dilation

Developing countries:
 Rheumatic Fever

A

AI etiology

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31
Q

the most common
congenital -the most common cause of isolated AR

 Most patients remain asymptomatic for decades, as the left ventricle maintains forward stroke volume with compensatory
chamber enlargement and hypertrophy. Eventually, the left ventricular systolic dysfunction supervenes and left ventricular
end-diastolic pressure rises resulting in symptomatic congestive heart failure.
 Timing AVR before irreversible myocardial dysfunction develops is of critical importance.

A

chronic/progressive AR

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32
Q

Wide Pulse Pressure goes with

A

chronic AR

33
Q

 Symptoms: most patients remain asymptomatic for years
 Exertional dyspnea and fatigue
 May not worsen with exertion in the early stages due to compensatory tachycardia with shortened diastole
 Palpitations
 Chest pain
 Paroxysmal Nocturnal Dyspnea/ Pulmonary Edema
 Sudden cardiac death
 This is uncommon (< 0.2% per year) in asymptomatic patients with preserved LV functi

A

chronic AI

33
Q

 Sudden, severe shortness of breath
 Rapidly developing heart failure
 Chest pain if myocardial perfusion pressure is decreased (hypoperfusion ischemia) or an aortic dissection is present

A

acute AI

33
Q

caused by the regurgitant flow causing vibration of
the mitral apparatus, is lower pitched and short in duration

A

Austin flint murmur

34
Q

AI PE

A

Diastolic Decrescendo Murmur, usually as a high-pitched sound that is loudest at the
left sternal border.
 Heard best with the patient leaning forward in full expiration in a quiet room
 It is one of the cardiac murmurs most commonly missed.
 An Austin-Flint murmur, which is caused by the regurgitant flow causing vibration of
the mitral apparatus, is lower pitched and short in duration.
 Auscultation may reveal an S3 gallop if LV dysfunction is present

34
Q

characterized by narrowing of
the mitral valve orifice

A

mitral stenosis

34
Q

usually as a high-pitched sound that is loudest at the
left sternal border.
 Heard best with the patient leaning forward in full expiration in a quiet room

A

Diastolic Decrescendo Murmur,

35
Q

chronic aortic regurgitation PE

A

 The murmur of AR occurs in diastole, usually as a high-pitched sound that is loudest at the left sternal border.
 Manifestations of severe chronic AR are often the result of widened pulse pressure.

 Corrigan pulse (“water-hammer” pulse) - Abrupt distention and quick collapse on palpation of the peripheral arterial
pulse

Quincke sign - Visible pulsations of the fingernail bed with light compression of the fingern

35
Q

The PMI or Apical Pulse is prominent, laterally displaced, hyperdynamic, and may be
sustained

A

AI PE

35
Q

AI diagnosis

A

Transthoracic echocardiography

36
Q
  • Chordal Fusion
  • Papillary muscle malposition (Too close together
A

congenital mitral stenosis

36
Q

AI treament

A

Surgical replacement
 Mechanical vs. bioprosthetic
 Anticoagulation
 Age

TAVR

37
Q
  • Rheumatic Fever- Thickening of the leaflets, fusion of the commissures, retraction, thickening of the Chordae, calcium deposition
    in the valve
  • Inner to outer deposits/commissures to
    annulus
  • Mitral annular calcification (Old age and Dialysis)
  • Outer to inward deposits/ annulus to commissure
A

acquired mitral stenosis

38
Q

what is the most common cause of mitral stenosis

A

rheumatic fever

Mitral stenosis presents 20 to 40 years after an episode of rheumatic fever.

39
Q

 more common in females.
 onset usually between the third and fourth decade of life

A

rheumatic mitral stenosis

40
Q

There are several risk factors which support calcific degeneration such as ageing,
hypertension and mechanical stress, diabetes, atherosclerosis and systemic inflammation,
kidney disease and mineral disorders

A

mitral annular calcifications

40
Q

MS pathophysiology

A

 The normal mitral orifice area is 4 to 6 square centimeters.
 The mitral valve opens during left ventricular diastole to allow blood to flow from the
left atrium to the left ventricle.
 The pressure in the left atrium and the left ventricle during diastole are equal.
 The left ventricle gets filled with blood during early ventricular diastole. There is
only a small amount of blood that remains in the left atrium.
 With the contraction of the left atrium (the “atrial kick”) during late ventricular
diastole, this small amount of blood fills the left ventricle.
 Mitral valve areas < 2 square centimeters causes an impedimence to the
blood flow from the left atrium into the left ventricle.
 Mitral valve area less than 1 square centimeter = increase in
left atrial pressure. This left atrial pressure is transmitted to the pulmonary
vasculature resulting in pulmonary hypertension.
 As left atrial pressure remains elevated, the left atrium will increase in size. As the
left atrium increases in size, there is a greater chance of developing atrial fibrillation.
If atrial fibrillation develops, the atrial kick is lost.
 Thus, in severe mitral stenosis, the left ventricular filling is dependent on the
atrial kick/contraction.
 With the loss of the atrial kick, there is a decrease in cardiac output and
sudden development of congestive heart failure.

40
Q
  • Mitral stenosis with a measured valve area <1cm2 = Severe
  • Severe MS causes severe pulmonary hypertension
  • And further… then causes Right heart failure
A

MS pathophysiology

41
Q

MS most common cause of death

A

CHF

41
Q

 Exertional dyspnea and/or decreased exercise tolerance, Fatigue, proportional to the severity of the stenosis
 Chest pain – Pulm HTN
 Hemoptysis
 Palpitations – Atrial Fibrillation
 Thromboembolism- Atrial Fibrillation
 Orthopnea
 Paroxysmal nocturnal dyspnea
 Right Sided Heart Failure Symptoms- ascites, edema, and hepatomegaly

A

MS symptoms

41
Q

 A low pitched mid-diastolic rumbling murmur with presystolic accentuation is heard after
the opening snap.
 It is best heard with the bell of the stethoscope at the apex.
 The murmur accentuates in the left lateral decubitus position and with isometric exercise

A

MS physical exam

42
Q

MS diagnosis
-(Kerly B lines)

A

TTE (Echo)- Transthoracic Echocardiogram annually

42
Q

 Mean gradient (mmHg) less than 10
 Pulmonary artery systolic pressure (mmHg) greater than 50
 Valve area (cm2) less than 1.0

A

MS severe

43
Q

MS treatment

A

Currently, no medical therapy can relieve a fixed obstruction of the mitral valve.
 Medical therapy is focused on preventing endocarditis, decreasing new cases of rheumatic fever,
improving symptoms, and decreasing the thromboembolic risk.

43
Q

MS treatment high risk patients

A

Endocarditis prophylaxis should only be given to high-risk patients before dental procedures that involve manipulation of gingival tissue or perforation of the oral mucosa.
 High-risk patients are those patients with a prosthetic heart valve or prosthetic material used for valve
repair, previous history of infective endocarditis, and cardiac valvuloplasty

44
Q

MS treatment rheumatic fever prophylaxis

A

Benzathine penicillin is the primary prevention treatment in
patients with streptococcal pharyngitis

44
Q

MS treatment if the rhythm is normal sinus

A

Diuretics are utilized to help relieve pulmonary congestion. Beta-blockers and/or calcium channel
blockers help with exertional symptoms associated with elevated heart rate.

44
Q

MS treatment if rhythm is atrial fibrillation

A

 Ventricular rate control using AV node blocking agents such as beta blockers, calcium channel blockers,
and/or digitalis, to help with symptoms
 Anticoagulation to prevent stroke/embolus.(Warfarin/Coumadin)
 In an unstable patient, perform direct current cardioversion. If you cannot convert atrial fibrillation to
normal sinus rhythm, then the primary goal is rate control.

45
Q

MS treatment

A

 Anticoagulation prevents thromboembolic events.
 Anticoagulation is indicated in patients with mitral stenosis and atrial fibrillation
(paroxysmal, persistent, or permanent), previous embolic events, and the presence of left
atrial thrombus.
 At present, Warfarin is the anticoagulation of choice. Warfarin should be monitored using
international normalized ratio (INR) to target 2.0-3.0.
 The development or presence of symptoms or evidence of pulmonary hypertension
is the indication for intervention

45
Q

MS treatment intervention options

A

Percutaneous mitral balloon valvuloplasty (PMBV)

Valve Replacement Surgery –> symptomatic patients

46
Q

Affects a functional component of the valve apparatus
 often referred to as organic MR - (leaflets, chordae tendineae, papillary muscles, and/or annulus)
 Thus the valve component is responsible for the regurgitation

A

primary (degenerative) causes of mitral valve insufficiency/regurgitation

47
Q

In the developed world, the most common etiologies of MR are

A

degenerative disease with
mitral valve prolapse (a primary cause) and coronary heart disease (a secondary cause).

48
Q

 left ventricular (LV) dysfunction such LV dilation, or a cardiomyopathy (often caused by ischemic
heart disease), trauma, infective endocarditis
 Thus the valve is structurally normal but the regurgitation is caused by annular enlargement, papillary
displacement, leaflet tethering, or a combination
 Functional MR: refers specifically to LV dilation with incomplete coaptation of the mitral valve leaflets

A

secondary causes of mitral valve insufficiency/regurgitation

49
Q

A. Mitral leaflets are the most common structures involved
B. Rheumatic heart disease can manifest itself as mitral stenosis,
insufficiency or both (years later)
D. Rheumatic process includes:
1) leaflet thickening, calcification and retraction
2) periannular calcification with limitation of annular motion
3) leaflet fusion (esp. at the commussural regions) and “fish-mouthing”
4) chordal thickening , shortening, and fusion
5) papillary muscle inflammation

A

rheumatic fever

50
Q

a connective tissue disorder characterized by
thickening and elongation of the mitral leaflets and chordae and by dilatation of the
mitral annulus
 primarily affects the chordae and leaflets in older patients
 Causes redundancy of anterior and posterior mitral leaflets and the chordae
 Chordae elongate leading to MV regurgitation
 Myxomatous degeneration with prolapse is a common cause for mitral valve operation

A

myxomatous degeneration

51
Q

 leaflet tissue is commonly involved resulting in vegetations and destruction of leaflet
 may result in annular or periannular abscess
 destruction of leaflets, chordae, or papillary muscle may result in rupture and massive MV
regurgitation
 annular involvement of one valve may result in involvement of the other valve (aortic)

A

endocarditis

52
Q

A. myocardial ischemia from coronary artery disease affects
mitral valve function in many ways
1) ischemia leads to loss of contractility which affects mitral valve
competence
2) lateral ventricle wall and papillary muscle dysfunction
a) anterior papillary muscle is supplied usually by the LAD but can be
from a diagonal, ramus or proximal marginal arteries
b) posterior papillary muscle is usually supplied by RCA or distal CX
c) ischemia in these distributions can lead to papillary muscle
dysfunction
3) papillary muscle necrosis and rupture leads to acute cardiac
decompensation
4) left ventricular aneurysm may lead to valvular incompetence
5) the chordae tendinea and valve leaflets are avascular and not
directly affected by ischemia
6) annular dilatation can lead to MV incompetence
a) up to 20% of patients undergoing surgery for CAD will have some
MV regurgitation
b) often with correction of underlying CAD with improve MV
regurgitation

A

ischemic mitral valve disease

52
Q

most common form off valvular heart disease

A

mitral valve prolapse

52
Q

It is characterized by typical fibromyxomatous changes in the mitral leaflet tissue with superior
displacement of 1 or both leaflets into the left atrium

A

mitral valve prolapse

53
Q

 More common in women between ages of 15-30yrs.
 Increased familial incidence for some
 Varies in clinical presentation
 Most patients are asymptomatic and remain so
 Most common cause of isolated MR in North America
 Mid or late systolic “click”
 Generated by chordae tendinea tensing or prolapsing leaflet
 High pitched, mid-late systolic crescendo-decrescendo murmur which is occasionally
“whooping” or “honking” heard best at the apex

A

MR- MVP

53
Q

 Acute pulmonary edema
 Due to sudden increase in LA pressure
 Acute dyspnea
 Chest pain
 Pan-systolic Murmur heard best at the
Apex

A

acute MR

54
Q

 Can be asymptomatic if mild to moderate isolated
MR for years
 Fatigue
 Orthopnea
 SOB, DOE
 CHF
 Pulmonary congestion
 Leads to R sided HF – ascites, ankle edema,
distended neck veins from
 LA enlargement/ LV enlargement
 Pan-systolic Murmur heard best at the Apex
 Listen for mid systolic CLICK

A

chronic MR

55
Q

 Left ventricular enlargement- MPI!!!
 High pitched apical pansystolic murmur that radiates to the axilla
 Holosystolic murmurs = severe MR
 Murmur intensity will vary with ischemia and papillary muscle dysfunction
 Right LV failure in advanced disease
 LA pressure and volume, backed up the pulmonary system. Pulmonary Congestion backs up
the Right ventricle= RV failure!
 Ascites
 Hepatomegaly
 DOE

A

MR PE

55
Q

MR diagnosis

A

ECHO/TTE- mainstay of mitral valvular pathology diagnosis
1) reveals leaflet thickening and abnormal excursion
2) doppler ECHO can estimate transvalvular gradient
3) detection of atrial thrombi and valvular vegetations

55
Q

MR treatment medical

A

 Depends upon the cause to a degree
 Atrial Fibrillation – place on Coumadin, INR goal 20-3
 Treatment of heart failure
 Diuretics
 BB
 ACE
 Digitalis

55
Q

MR treatment: indications for operation

A

 Indications for operation are more complex than mitral stenosis
 Endocarditis and acute ischemic mitral regurgitation are clear indications= YES! SURGERY!
 Chronic non-ischemic severe MR
 Once symptomatic due to CHF – Persistent NYHA Class III - IV
 New onset AF
 Pulmonary HTN - PAP > 50mmHg at rest and/or >60mmHg w/exercise
 EF <60%

55
Q

A. low incidence of thromboembolism
B. average durability is 10-15 years
C. porcine valves may be chosen in
females who desire to become
pregnant
D. glutaraldehyde-preserved stented
porcine tissue valves are the most
common
E. bovine pericardial valves were
found to degenerate rapidly
H. some recommend patients should
receive 3 months of anticoagulation
therapy until endocardial healing is
completed

A

bioprosthetic valves

56
Q

A. durable with valve life up to 20 years
B. requires anticoagulation (INR 2.5 -3.0)
C. usually indicated in young patients or patients with chronic atrial fibrillation
D. bileaflet (St. Jude, Carbomedics) most common mechanical valve used in the U.S.
E. Higher risk on thromboembolism in the mitral position

A

mechanical valves

57
Q

A. Septal, posterior and anterior leaflets
B. Annulus- sphincter-like function
C. Septal annulus- fixed
D. Dilatation only in anterior and posterior
annulus

A

tricuspid valve anatomy

58
Q

 Less common
 Rheumatic in origin in developing
countries
 In US, due to carcinoid disease or
previously placed prosthetic failure
 Women >Men
 Does NOT occur in isolation
 Usually associated with MS
 Echocardiogram is diagnostic

A

tricuspid stenosis

59
Q

 Usually masked by MS symptoms – due to MS proceeding TS
 Pulmonary congestion
 Fatigue
 Severe Tricuspid Stenosis
 Blood congested in the Venous system
 Hepatomegaly, ascites, edema
 Can result in cirrhosis
 Physical Exam
 Murmur has many qualities of MS – best heard along the left sternal border and over xiphoid
process; Mid-diastolic rumble with presystolic accentuation (worse with inspiration)
 Opening snap
 JVD and giant a-wave

A

tricuspid stenosis

59
Q

EKG
 RA enlargement, tall peaked P waves in Lead II and upright P waves in lead V1
 Afib

CXR
 Prominence of the RA and SVC w/o enlargement of the PA

Echo
 Valve is thickened and domes in diastole
 Valve area < 1.0cm2
 RA and IVC are enlarged

Cardiac cath - not routinely necessary

A

diagnosis for tricuspid stenosis

59
Q

TS treatment

A

 Decreased Right sided HF symptoms with Diuretics to relieve fluid congestion
 Surgery is not terrible effective, because it often causes TR as a consequence.

60
Q

 Secondary to dilation of the annulus from RV enlargement due to PA HTN. NOT
primary valve disease.
 Secondary to pacemaker lead placement
 Late stages or Rheumatic Fever or Congenital heart disease
 Cardiomyopathies
 Infarction of the papillary muscles
 TVP
 Carcinoid heart disease
 Infective endocarditis
 Leaflet trauma

A

tricuspid regurgitation

61
Q

 Often due to other underlying cause
 Fatigue
 DOE
 Cervical pulsations
 Abdominal fullness
 Diminished appetite
 Muscle wasting

A

TR symptoms

61
Q

 R sided HF
 Distended neck veins
 Marked hepatomegaly, ascites, pleural effusions, edema
 Blowing holosystolic murmur along the lower left sternal margin – which may be
intensified during inspiration and reduced during expiration or the Valsalva maneuver
 Atrial Fibrillation

A

TR physical

61
Q

TR diagnosis

A

Echo
 RA dilation
 RV volume overload with abnormal interventricular wall movement
 Prolapsed leaflet

62
Q

TR treatment

A

Medical
Diuretics – for Right sided heart failure Sx
Treatment of pulmonary HTN

Indications for Surgery
Tricuspid regurgitation
1) Clinical decision- improvement with repair of left-
sided lesion
2) Moderate to severe TR or any structural TR
3) RV volume overload
4) Right-sided heart failure
5) Repair vs replacement
Endocarditis
1) Severe TR
2) Persistent sepsis
3) Recurrent PE
4) Excision vs replacement vs repair

62
Q
  1. Uncommon
  2. Congenital etiologies (vast majority)
  3. Adult acquired
    A. Endocarditis, rheumatic
    B. Secondary to previous procedures
    A. Congenital (Tetralogy of Fallot)
    B. Adult (Ross)
A

pulmonary valve disease

63
Q

dynamic or fixed anatomic obstruction to flow from
the right ventricle (RV) to the pulmonary arterial vasculature.
 Commonly pediatric patients
 Female greater than male
 Isolated PS - 10% of all congenital heart disease.

 the valve commissures are partially fused and the 3 leaflets are thin and pliant, resulting in a
conical or dome-shaped structure with a narrowed central orifice.

 10-15% of individuals have dysplastic pulmonic valves.
 These valves have irregularly shaped, thickened leaflets, with little, if any, commissural
fusion, and they exhibit variably reduced mobility.
 A bicuspid valve is found in as many as 90% of patients with tetralogy of Fallot

A

pulmonary stenosis

63
Q

Symptoms
1) Infants have less symptoms than neonates
2) Older than 1 year–murmur only
3) Second, third, and fourth decade of life chronic right heart failure
4) 30-40% with severe pulmonary stenosis are asymptomatic when first examined
5) Dyspnea of exertion is most common
Signs
A. Loud, Harsh systolic murmur, radiates towards the left shoulder, decreased with
inspiration
B. With a possible thrill in the left 2nd and 3rd intercostal space
C. Ejection click
D. Right ventricular lift due to RVH

A

pulmonary stenosis

63
Q

PS diagnosis

A

ECHO
diagnostic TTE

64
Q

PS treatment

A

percutaneous balloon valvuloplasty

64
Q

 Most patients are asymptomatic.
 Mild to moderate
 PA HTN usually dominates the picture.
Symptoms:
 Right heart volume overload and RHF symptoms
Signs: Murmur
 High pitched, decrescendo diastolic murmur hear along the
left sternal border, may become louder with inspiration.
Diagnosis:
 TTE for diagnosis

A

pulmonic regurgitation

64
Q

PR treatment

A

 Surgical repair is rare
 Focuses on the underlying cause
 Reduce PA vascular resistance/Pulm HT

cardiology (6 decks)

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