Valvular Disease

Front 1

Mitral stenosis

Back 1

-most commonly a result of chronic rheumatic heart dz secondary to 1 or more episodes of rheumatic fever
-the valve inflamm associated with RF leads to an abnml flow pattern across the valve causing inc tension coupled with fibrin deposition after yrs leads to fibrosis and thickening
-left atrial enlargement

Front 2

mitral stenosis ssx

Back 2

1. dyspnea on exertion
2. pulmonary edema
3. hemoptysis
4. A-fib
5. systemic embolism
6. dysphagia, hoarsnes
7. RV failure
8. infective endocarditis

Front 3

mitral stenosis PE

Back 3

1. malar flush
2. JVD b/c of RV failure
3.** A loud first heart sound, early diastolic opening snap, rumbling DIASTOLIC murmur!!
-best heard at the apex with pt in LLD position, use bell

Front 4

mitral stenosis imaging

Back 4

Echocardiography- TTE/TEE- Calcification, fibrosis, limited leaflet excursion

Front 5

mitral stenosi medical therapy

Back 5

-plays no role in altering the natural history
-Diuretics: pulmonary congestion and edema
-Anticoagulants: especially those that are in a-fib due to increased risk of thromboembolic event
-infective endocarditis prophylaxis

Front 6

mitral stenosis- interventional

Back 6

-Percutaneous transvenous valvotomy- risk of thrombus
-balloon catheter advanced across the stenotic mitral valve from the left atrial side and inflated separating the stenotic leaflets

Front 7

mitral stenosis- surgical

Back 7

1. prosthetic valves (mechanical) - must anticoagulant for life!
2. Biprosthetic valves (porcine) - 20-40% fail over 10 yrs
3. mitral valve repair (commisurotomy)- the goal is to restore the pliability of the leaflets

Front 8

Mitral reguritation- causes

Back 8

Acute:
1. trauma, dysfunction of a papillary muscle, valve malfxn
2. infectious endocarditis, acute RF
3. Chordal rupture
Chronic:
1. RDH, SLE, progressive systemic sclerosis
2. degeneration and calcification
3. Marfans
4. infectious endocarditis
5. acute causes progressing to chronic
6. congenital

Front 9

mitral regur pathophys

Back 9

-a portion of each systolic stroke vol is ejected retrograde into the left atrium, as a result there is left atrial dilation and left ventricular hypertrophy with progressive inc in LV volume
-ischemic, non-ischemic, and functional

Front 10

MR- chronic ssx

Back 10

-time to sx- decades
1. asymptompatic
2. enlarged L atrium
3. nml to inc filling pressures
4. nml to dec Q
5. compensated CV system
6. LVH on EKG
7. LV/LA enlargement on CXR
-non-emergent med/surg tx

Front 11

MR- acute ssx

Back 11

- time to sxs immediated
1. nml LV/LA size
2. inc filling pressures
3/ dec Q
4. uncompensated CV system
5. no LVH on EKG
6. no cardiac enlargement on CXR, but pul edema
-urgent surgical tx

Front 12

MR ssx

Back 12

Acute:
1. dyspnea
2. orthopnea
3. cardiogenic shock
Chronic:
1. exercise intolerance
2. DOE
3 orthopnea
4. PND
5. CHF

Front 13

MR - PE

Back 13

1. sharp carotid upstrokes
2. hyperdynamic apical impulse
3. ** Murmur - best heard in the apical position and often radiating to the axilla - high pitched blowing holosystolic murmur
4. S4 sometimes

Front 14

MR imaging

Back 14

-Echocardiography: used for diagnosing, severity and cause
1+ mild
2+ moderate
3+ moderately severe
4+ severe
-Cath- useful for diagnosing concomitant CAD

Front 15

MR medical therapy

Back 15

Acute: nitroprusside, diuretics
Chronic: endocarditis prophylaxis, antocoagulation, vasodilators, digoxin, diuretics, nitrates

Front 16

MR surgery

Back 16

-timing is imperative
-Consider LV size and fxn, exercise capacity and LV fxn at peak stress, repairability of valve, severity of MR, pulmonary artery pressures, atrial fibrillation, age and other comorbidities
-Repair vs Replacement - data suggests better post-op LV fxn/survival w/repair – depends on valve lesion and skill of surgeon

Front 17

mitral valve prolapse (MVP)

Back 17

-one or both of the mitral leaflets are enlarged/myxomatous/floppy and they prolapse into the left atrium during systole
-primary- appears to have a genetic predis
-secondary-young women, ASD, hyperthyroidism, HCM

Front 18

MVP ssx

Back 18

1. most NONE
2. Most sx’s are associated with significant MR
3. arrhythmias- SVT, VT, bradyarrhythmis
4. anxiety, easy fatigue, palpitations, orthostatic hypotension

Front 19

MVP- PE

Back 19

1. Pectus excavatum, straight back and scoliosis; low body weight and hypotension
2. use the diaphragm: LLD position
3. ****Mid-systolic click, usually late systolic murmur heard best at the apex (high pitched, crescendo, cooing/honking/whooping)

Front 20

MVP imaging

Back 20

-EKG: nml or nonspecific St-T wave changes
-CXR: usually nml
-ECHO: greater than 2 mm displacement of one or both mitral leaflets into the left atrium during systole

Front 21

MVP- therapy

Back 21

-most need only clinical f/u and reassurance
-f/u therapy for sig MR
-Bblockers may help the autonomic sx
-tell pt to avoid caffeine, alcohol, tobacco
-Aspirin for those with h/o TIA, coumadin post stroke or recurrent TIAs
-Mitral valve repair for mitral insufficiency

Front 22

Aortic stenosis

Back 22

-obstruction of flow at the level of the valve and restricted systolic opening
-with progressive obstruction of the left ventricular outflow tract there is hypertrophy of the left vent and sx of heart failure, syncope and angina

Front 23

AS causes

Back 23

-age-realted calcific degeneration
-bicuspid valves- present in 1-2% of the pop; M>W
-rheumatic AS- coexists with AI and mitral valve lesions
-subvalvular- congenital

Front 24

AS-pathophys

Back 24

Pressure overload in an attempt to maintain cardiac output due to a narrowed LVOT = LVH
Diastolic dysfunction (DD)- this is determined by LV relaxation and LV compliance; increased afterload and LVH reduce compliance
Supply-demand mismatch - LVH and DD lead to an inc. in LVEDP which in turn leads to decreased perfusion pressure across the coronary bed and causes endocardial compression of intramyocardial arteries - possible ischemia with exertion

Front 25

AS ssx

Back 25

-asymptomatic: "latent phase"- risk of sudden cardiac death is <2%/yr
Pressure overload in an attempt to maintain cardiac output due to a narrowed LVOT = LVH
Diastolic dysfunction (DD)- this is determined by LV relaxation and LV compliance; increased afterload and LVH reduce compliance
Supply-demand mismatch - LVH and DD lead to an inc. in LVEDP which in turn leads to decreased perfusion pressure across the coronary bed and causes endocardial compression of intramyocardial arteries - possible ischemia with exertion
-angina, syncope, heart failure

Front 26

AS PE

Back 26

1.***systolic ejection murmur heard best at the RUSB radiation to the neck
2. S4 common due to LVH and poor compliance
3. apical impulse nondisplaced, diffuse and sustained

Front 27

AS imaging

Back 27

-EKG: L atrial abnormality
-CXR: nml or boot shaped
-ECHO: Annually for severe AS, q 2 years for moderate and q 5 for mild; cause/location/severity - nl valve area of 2-4 cm2, mild >1.5, mod. 1-1.5, severe <1.0 and critical <.75

Front 28

AS therapy

Back 28

1. replacement
2. primary prevention of CAD, maintaing sinus rhythm, BP control
3. heart failure therapy
4. vasodilators and nitrates are used with extreme caution
5. ?stain use to slow progresison

Front 29

AS surgical intervention

Back 29

1. Percutaneous aortic balloon valvuloplasty (PABV)
2. AVR (best choice)

Front 30

Aortic insufficiency (AI)

Back 30

-diastolic regurgitation of LV stroke vol thereby increasing LV end-diastolic vol, raising wall tension by compensatory eccentric hypertrophy of the myocytes
1. chronic compensated phase
2. chronic decompensated phase

Front 31

AI (causes)

Back 31

1. Leaflet: RF, endocarditis, trauma
2. Aortic root/Asc. aorta- age-related, HTN,

Front 32

AI ssx

Back 32

-often asymptomatic, starts with fatigue, dec exercise tolerance
-If LV dysfxn exists pts develop sx’s related to pulmonary congestion - DOE, orthopnea, and PND
-Some may feel chest discomfort related to LV enlargement exacerbated by lying supine or w/PVCs; forceful heart beat (may be noted by spouse)

Front 33

AI PE

Back 33

1. wide pulse pressure
2. water-hammer or corrigans pulse
3. Traube's sign: Pistol shot sounds heard over the femoral arteries in both systole and diastole
4. diminished S1, S3 w/severe LV dysfunction
5. DIASTOLIC MURMUR- Blowing, decrescendo immed. after S2 best heard sitting up and leaning forward in full expiration (use diaphragm)
6. Austin flint murmur- middle to late diastolic rumble

Front 34

AI lab eval

Back 34

-EKG: LVH, LAD, LAE
-CXR: may reveal cardiomegaly, w/inferior and leftward displacement, pul congestion
-ECHO: used for cause and severity ; 1+, 2+, 3+, 4+
-Blowing, decrescendo immed. after S2 best heard sitting up and leaning forward in full expiration

Front 35

AI (causes)

Back 35

1. Leaflet: RF, endocarditis, trauma
2. Aortic root/Asc. aorta- age-related, HTN,

Front 36

AI- medical therapy

Back 36

1. abx prophylaxis
2. vasodilators
3. ACE inhibitors
4. CCBs
5. Acute AI - IV vasodilators, ? Inotropes, surgical consult
6. bblockers

Front 37

AI ssx

Back 37

-often asymptomatic, starts with fatigue, dec exercise tolerance
-If LV dysfxn exists pts develop sx’s related to pulmonary congestion - DOE, orthopnea, and PND
-Some may feel chest discomfort related to LV enlargement exacerbated by lying supine or w/PVCs; forceful heart beat (may be noted by spouse)

Front 38

Tricuspid valve disease

Back 38

-tricuspid stenosis- 90% result of RHD and the mitral valve is almost always involved
-ssx: easily fatigability and edema; fluttering sensation in neck; RUQ pain

Front 39

AI PE

Back 39

1. wide pulse pressure
2. water-hammer or corrigans pulse
3. Traube's sign: Pistol shot sounds heard over the femoral arteries in both systole and diastole
4. diminished S1, S3 w/severe LV dysfunction
5. DIASTOLIC MURMUR- Blowing, decrescendo immed. after S2 best heard sitting up and leaning forward in full expiration (use diaphragm)
6. Austin flint murmur- middle to late diastolic rumble

Front 40

tricuspid valve dz- PE and imaging and tx

Back 40

-diastolic murmur along the LSB, low pitched and the intensity increase with inspiration
-image by echo
-tx: Diuretics and sodium restriction to help the edema; valvuloplasty or tricuspid valve replacement

Front 41

AI lab eval

Back 41

-EKG: LVH, LAD, LAE
-CXR: may reveal cardiomegaly, w/inferior and leftward displacement, pul congestion
-ECHO: used for cause and severity ; 1+, 2+, 3+, 4+
-Blowing, decrescendo immed. after S2 best heard sitting up and leaning forward in full expiration

Front 42

Tricuspid regurgitation

Back 42

-Any process that changes the normal valve fxn
-ssx: Mostly well tolerated; edema, hepatic congestion, and fatigue from reduced Q

Front 43

AI- medical therapy

Back 43

1. abx prophylaxis
2. vasodilators
3. ACE inhibitors
4. CCBs
5. Acute AI - IV vasodilators, ? Inotropes, surgical consult
6. bblockers

Front 44

tricuspid regur PE, imag, tx

Back 44

-Pansystolic murmur heard best at the 3rd/4th ICS, LSB and again increased w/inspiration; right sided S3/S4; w/pulm. HTN an accentuated P2; systolic pulsation of the liver
-image by echo
-tx:Diuretics; Repair vs replacement

Front 45

Tricuspid valve disease

Back 45

-tricuspid stenosis- 90% result of RHD and the mitral valve is almost always involved
-ssx: easily fatigability and edema; fluttering sensation in neck; RUQ pain

Front 46

pulmonary valve dz- stenosis

Back 46

-Most commonly congenital, RHD, carcinoid and pseudo-pulmonary stenosis from RV outflow tract obstruction
-ssx: Present in their 40-50s with RV failure and DOE
-PE: Systolic ejection murmur decreased by inspiration; decreased P2; RV failure
-tx: Severe stenosis w/RV failure then balloon valvuloplasty is the procedure of choice

Front 47

tricuspid valve dz- PE and imaging and tx

Back 47

-diastolic murmur along the LSB, low pitched and the intensity increase with inspiration
-image by echo
-tx: Diuretics and sodium restriction to help the edema; valvuloplasty or tricuspid valve replacement

Front 48

Tricuspid regurgitation

Back 48

-Any process that changes the normal valve fxn
-ssx: Mostly well tolerated; edema, hepatic congestion, and fatigue from reduced Q

Front 49

tricuspid regur PE, imag, tx

Back 49

-Pansystolic murmur heard best at the 3rd/4th ICS, LSB and again increased w/inspiration; right sided S3/S4; w/pulm. HTN an accentuated P2; systolic pulsation of the liver
-image by echo
-tx:Diuretics; Repair vs replacement

Front 50

pulmonary valve dz- stenosis

Back 50

-Most commonly congenital, RHD, carcinoid and pseudo-pulmonary stenosis from RV outflow tract obstruction
-ssx: Present in their 40-50s with RV failure and DOE
-PE: Systolic ejection murmur decreased by inspiration; decreased P2; RV failure
-tx: Severe stenosis w/RV failure then balloon valvuloplasty is the procedure of choice

Front 51

Drug induced valvular disease

Back 51

-phentermin and fenfluramine
-methysergide
-ergotamine
-likely caused by inc serotonin levels
-those on drugs >6mo
-regurgitant valve dz most commone

Front 52

infective endocarditis (IE)

Back 52

-infx of the cardiac endothelium seen as vegitations
-injury to the endocardial surface attracts fibrin and plts
-bacteremia seed this process with microorganisms which attract more plts and fibrin
-mitral valve most commonly effected valve

Front 53

IE- acute

Back 53

-highly virulent organisms
-often infecting nml valves
-rapid onset fever w/rigors and malaise
-embolic complications
-50-60% mortality rate

Front 54

IE- subacute

Back 54

-low to mod virulence
-often infectin abnml valves
-less destruction, smaller vegitations
-insidious onset, low-grade fever

Front 55

IE ssx

Back 55

-onset of sx within 2 wks
-range of sx- subtle to CHF w/severe valvular regurgitation
-fever and a new murmur or change in old murmur!
-the pt c/o fatigue, wt loss, malaise, chills, nt sweats, +/- myalgias

Front 56

IE physical findings

Back 56

1. CHF
2. cerebral emboli
3. mucosal petechiae
4. splinter hemorrhages
5. osler nodes (painful nodes in the pads of fingers and toes)
6. janeway lesions (red painless spots on palms and soles)
7. clubbing
8. splenomegaly
9. roth spots! (retinal hemorrhaes with central clearing)

Front 57

IE pathogens

Back 57

1. Native valve IE: S. aureus
2. Right sided IE (tricuspid valve)- most common in IV drug users, s. aureus
3. Austrian Triad: S. pneumoniae
4. PVE- 10-20% of all cases; greatest risk within 6 mo of surgery

Front 58

IE lab eval`

Back 58

-BLOOD CULTURE (do not delay therapy for more than 2-3 hrs). Dx if there is a positive cx drawn 12 hrs apart or 3 of 4 + drawn 1 hr apart
-modest leukocytosis
-normochromic, normocytic anemia
-elevated ESR, CRP, RF
-Histopathologic evaluation of valve tissue is the gold standard
- neg culture IE (2-30%)

Front 59

IE imaging

Back 59

1. Echo- transthoracic
2. TEE if IE is strongly suspected- more sensitive than TTE
3. CXR, CT and EKG

Front 60

IE- duke criteria

Back 60

-positive valve culture or histology or
-2 major criteria:
-5 minor
-1 major and 3 minor

Front 61

IE tx

Back 61

-combo therapy most effective
ex. B-lactam + aminoglycoside
-surgery- indicated in 25-30% of cases with complicated IE or 20-40% in subacute case
-indications include: CHF, unresponsive to abx, PVE, fungal IE, abcess

Front 62

IE prophylaxis

Back 62

-only those at highest risk of adverse outcomes
1. prosthetic cardiac valve
2. previous endocarditis
3. congenital heart dz
4. cardiac transplant pts with valve dz