Valvular Disease Flashcards
What are the indications for PMBC?
- Progressive MS (MVA > 1.5 cm2, T1/2 < 150 ms)
-
PMBC at CVC (Class IIb)
- Exertional symptoms →
- Stress test with hemodynamically significant MS →
- Pliable valve, no clot, < 2+ MR →
-
PMBC at CVC (Class IIb)
- Severe MS (MVA « 1.5 cm2, T1/2 « 150 ms)
-
PMBC at CVC (Class I)
- Symptomatic +
- Pliable valve, no clot, < 2+ MR
-
PMBC at CVC (Class IIb)
- Symptomatic +
- Pliable valve, no clot, < 2+ MR (does not meet) +
- Severe symptoms, NYHA III-IV
- NOT Surgical candidate
-
PMBC at CVC (Class IIa)
- Asymptomatic
- Pliable valve, no clot, > 2+ MR
- PASP > 50 mmHg
-
PMBC at CVC (Class IIb)
- Asymptomatic
- Pliable valve, no clot, > 2+ MR
- New onset A-fib
-
PMBC at CVC (Class I)
What are the indications for MVR in MS?
- Severe MS (MVA « 1.5 cm2 and T 1/2 ► 150 ms)
- Symptomatic –>
- No Favorable valve morphology, No LAA clot, < Mild MR
- Severe symptoms - NYHA Class III-IV symptoms
- Surgical candidate
***Class I recommendation
What are the contraindications to PMBV?
- Persistent LA or LAA thrombus
- Obstruction of IVC
- tumor, thrombus, therapeutic ligation, filter placement
- Bleeding diatheses
- Anatomic deformity resulting in rotation of the heart
- severe kyphoscoliosis
- previous pneumonectomy
- > Moderate MR
- Massive or bicommisural calcification
- Severe concomitant aortic valve disease
- Severe TS
- Severe functional TR with enlarged annulus
- Severe concomitant CAD requiring CABG
What is the recommended duration of Rheumatic Fever Prophylaxis?
- Rheumatic fever with carditis
- Residual heart disease (persistent valvular disease)
10 years
or
Until 40 years of age
- whichever is longer
- sometimes lifelong prophylaxis

What is the recommended duration of Rheumatic Fever Prophylaxis?
- Rheumatic fever with carditis
- No residual heart disease
10 years
or
until 21 years of age
- whichever is longer

What is the recommended duration of Rheumatic Fever Prophylaxis?
- Rheumatic fever without carditis
5 years
or
until 21 years of age
- whichever is longer

What are the medical treatment options for rheumatic fever prophylaxis?
- Benzathine PCN G
- PCN VK
- Sulfadizine
- Macrolide or Azalide
- only if allergic to PCN and Sulfadiazine
What is the medical therapy for chronic, primary MR?
no pharmacologic agent has been shown to slow progression toward surgical intervention
- ACE/ARBs –> decreased Regurgitant volume but no difference in clinical event rates
Why is MV repair recommended over MVR in primary MR?
- preservation of LV function
- lower operative mortality rate
- lower rate of long term complications associated with prosthetic valves
What subgroups of patients with primary MR have been found to have higher event rates or clinical deterioration?
- EROA ► 0.40 cm2 or
- Flail leaflets
What is the recommended medical therapy?
- chronic, primary MR
- LVEF < 60%
- surgery is not planned
- ACE/ARBs
- Vasodilator agents
****Class IIa recommendation
*****not indicated for normotensive, asymptomatic, LVEF ► 60%
Describe the management of chronic, severe MR
- Primary, Severe MR
- Asymptomatic
Describe the management of chronic, severe MR
- Primary, Severe MR
- Symptomatic
Describe the management of chronic, severe MR
- Primary, Severe MR
- Asymptomatic
What factors are required to proceed with TEER in primary severe MR?
- High or prohibitive surgical risk
- Anatomy favorable for transcatheter approach
- Life expectancy > 1 year
Describe the management of severe secondary MR
Describe the management of chronic, severe MR prior to proceeding with any surgical/procedural intervention
- Treat comorbidities:
- CAD Rx
- HF Rx
- AFib Rx
- Consider CRT
What is the treatment for acute, severe MR?
- Afterload reduction (may improve hemodynamic status by)
- reducing RV
- increasing LV forward SV
- increasing CO
- Sodium nitrorpusside
- Hypotension –> IABP
- Emergent Surgery = definitive therapy
What is the preferred treatment for chronic, secondary MR prior to surgical intervention?
- Medical therapy
- ACE, BB, Aldosterone antagonists –> treat LV systolic dyfunction and/or CAD
- reduces preload, afterload and reduces adverse LV remodeling –> secondary MR
- CRT
- to improve severe LV dysfunction with mechanical dyssynchrony
- may reduce MR severity
When is transcatheter (edge-to-edge) MV repair considered in chronic, severe, secondary MR?
- LV dysfunction (LVEF < 50%)
- NYHA class III-IV symptoms
- despite optimal therapy for CHF
- including Bi-V pacing
- Anatomy (favorable)
- LVEF 20-50%
- LVESD < 70 mm
- PASP < 70 mm
****Class IIa

EKG definition:
- Pacemaker malfunction, not constantly capturing (atrium or ventricle) “failure to capture”
- Pacemaker stimulus without appropriate depolarization
- at a time when the myocardium refractory
- May be caused by:
- lead fracture
- increased pacing threshold secondary to myocardial scar
- medications (flecainide, amiodarone)
- perforation
- electrolyte abnormalities
- displacement
What are causes of “failure to capture” in pacemaker malfunction?
- lead fracture
- increased pacing threshold secondary to myocardial scar
- medications (flecainide, amiodarone)
- perforation
- electrolyte abnormalities
- displacement
What are the age cutoff’s for mechanical over bioprosthetic valve replacement?
- Aortic
- < 50 years –> mechanical
- 50-65 years –> either
- > 65 years –> bioprosthetic
- Mitral
- < 65 years –> mechanical
- > 65 years –> bioprosthetic

What are risk factors for poor outcomes in severe AR?
- Symptoms
- Increased LVEDD
- > 65 mm
- Increased LVESD
- > 50 mm
- Reduced exercise EF
- < 50%

What test should be ordered in a patient with incidental finding of dilated aortic root (4.2 cm)?
Why?
- TTE
- Bicuspid aortic valve
Describe the risk categories in selection of TAVR vs. SAVR

What mechanical prosthetic valves require bridging anticoagulation?
- Bileaflet aortic valve with increased thromboembolic risk factors
- Caged ball or tilting disc prosthesis
- Mitral valve prosthesis
- Recent CVA/TIA

What mechanical prosthetic valves do not require bridging anticoagulation?
Bileaflet AV without other risk factors of thromboembolism

What are risk factors for thromboembolism in the setting a mechanical valve?
- Hypercoaguable condition
- A-Fib
- LV dysfunction
- Thromboembolism (previous)
When is a target INR 3.0 (2.5-3.5) recommended in regards to mechanical prosthesis?
- Mechanical AVR + risk factors for TE
- Older generation mechanical AVR
- ball in cage
- Mechanical MVR
What are the INR recommendations for On-X valve in the aortic position?
VKA + ASA
- First 3 months –> INR 2.5
- > 3 months –> INR 2.0
What are the recommended anticoagulation strategies in pregnancy and prosthetic valves?
- Continued VKA
- 1st Trimester UFH or LMWH –> VKA (sequential therapy)
- UFH/LMWH (entire pregnancy)
*******UFH prior to delivery
What is the first step in assessment of prosthetic valve (AV or MV) with high gradients after surgery?
Calculate Indexed EOA
- Indicate Patient-Prosthesis mismatch:
- Aortic = EOA < 0.85 cm2 / m<strong>2</strong> (severe = < 0.65 )
- Mitral = EOA < 1.2 cm2 / m2 (severe = < 0.9 )

What is the second step in assessment of prosthetic valve (AV or MV) with high gradients after surgery?
TTE, TEE, Cinefluor –> to identify
- Gradient increased during follow-up
- Aortic > 10 mmHg
- Mitral > 5 mmHg
- abnormal leaflet morphology / mobility
- DVI:
- Aortic < 0.30
- Mitral > 2.2
- Difference between measured EOA and reference EOA > 0.30 - 0.4 cm2
- EOA and DVI decreased during follow up
YES –> consider prosthesis stenosis
NO –> consider
- High flow state
- Technical error
- Localized high gradient (bileaflet valve)

Describe the risk/benefits in anticoagulation strategies used in pregnancy with prosthetic valves?
- VKA
- Lowest likelihood of maternal complications
- Highest likelihood of fetal complications (1st trimester (particularly) + dose > 5 mg) –>
- miscarriage
- fetal death
- congenital abnormalities
- Reduced dose < 5mg/day –> decreased (not eliminated) fetal complications
- Reduced thromboembolic complications (compared to UFH/LMWH)
- UFH/LMWH
- increased maternal complications
- greatest number of successful live births
What are the anticoagulation recommendations following bioprosthetic valve placement?
- ASA daily
- indefinitely if no contraindication
- SAVR
- VKA –> 3-6 months (Class IIb)
- TAVR
- VKA –> 3 months (Class IIb) or
- DAPT –> 3-6 months (Class IIb)
What is the recommended anticoagulation strategy in patients receiving TAVR who are unable to be anticoagulated?
DAPT x 6 months
- dc Clopidogrel after 6 months and continue ASA indefinitely
What is the recommendation regarding ASA in patients with valve replacement?
ASA daily (indefinitely) + VKA
- decreases incidence of:
- major embolism or death (1.9% vs. 8.5% per year; p < 0.001)
- stroke rate (1.3% vs. 4.2% per year)
- overall mortality (2.8% vs. 7.4% per year)
- Increased bleeding (not statistically significant)
What findings on exercise stress testing, in a patient with asymptomatic, severe AS, would merit intervention?
Symptoms
or
Inability to augment BP by 20mmHg
or
Decrease in BP at peak exercise
What murmur is related to the Gallavardian phenomenon?
Describe the murmur
- AS (degenerative or age-related)
- harsh murmur at the base + musical murmur at the apex
- due to the high-frequency components of the AS murmur radiating to the LV apex
- often confused with MR
How can these murmurs be differentiated?
- AS (age-related or degenerative)
- MR
- AS (age-related or degenerative)
- Systolic ejection murmur
- harsh at base
- musical at apex
- increases with bradycardia or after a pause (PVC)
- Systolic ejection murmur
- MR
- holosystolic
- not affected by HR, PVC
Describe the valvular lesion associated with these hemodynamic findings
- Large LV to aorta pressure gradient
AS
Calculate posthetic valve EOA
CSA LVOT x VTI LVOT
VTI jet
Describe the valvular lesion associated with these hemodynamic findings
- large V wave on PCWP
MR
Describe the valvular lesion associated with these hemodynamic findings
- large V wave on the RA
TR
Describe the valvular lesion associated with these hemodynamic findings
- increased PA O2 saturation
Left-to-right shunt / VSD
Describe the valvular lesion associated with these hemodynamic findings
- large RVOT to PA pressure gradient
PS
Describe the effects on cardiac auscultation and murmur as AS worsens
- diminished ejection sound/intensity of A2
- murmur peaks later in systole
*****PVC –> murmur increases

What can cause the murmur of AS to intensify or worsen?
PVC
Describe key differences between the murmurs:
- Acute AR
- Chronic AR
- Acute AR
- diastolic murmur may be short
- mitral valve might close prematurely (S1 softens) and
- mid-diastolic rumble of relative mitral stenosis (Austin-Flint murmur) may occur
- Chronic AR
- holodiastolic murmur

Describe the effects of cardiac auscultation/murmur with worsening MS
- A2-opening snap interval in MS shortens –>
- as LA pressure rises and
- approaches that of the aortic early diastolic pressure

What is one finding of bicuspid aortic valve fusion that carries prognostic implications?
Right-Noncoronary cusp fusion –> higher incidence of aortic dilation
What is the monitoring recommendation for BAV?
Annually (if)
- significant aortic dilatation > 4.5 cm
- rapid rate of change in aortic diameter > 0.5 cm/year
- FH of aortic dissection
What is the cutoff for aortic imaging with Echo?
visualization of the aorta up to 4 cm distal to the valve
What are the indications for surgical intervention in regards to aortic abnormalities in BAV?
-
Class I
- aortic diameter > 5.5 cm
-
Class IIa
- aortic diameter 5.1 - 5.5 cm + rapid growth ( > 0.5 cm/year) or FH aortic dissection
- aortic diameter 4.5 cm + valve surgery (severe AS or AR)

What is recommendation regarding Warfarin use throughout pregnancy?
Continued throughout pregnancy if dose « 5 mg/day
- embryopathy from warfarin appears to be dose dependent
- switch to UFH just prior to delivery
- Class IIa recommendation
What equation can be used to obtain MVA during cardiac catheterization?
- Hakki equation
- MVA = CO (L/min) / √mean pressure gradient (mm Hg)
What are common errors / problems when obtaining MVA during cardiac catheterizaton (Hakki equation)?
- subject to errors in estimation of CO
- failure to simultaneously measure left atrial (LA) and LV pressure
- Concomitant regurgitation
What is the problem when utilizing PCWP in place of LA pressure to determine MVA during cardiac catheterization (Hakki equation)?
measurement of PCWP in place of LA pressure may
- overestimate gradient and
- underestimate MVA
Define patient prosthesis mismatch (PPM)
effective orifice area (EOA) of a prosthesis is too small
relative to the patients body size –>
resulting in abnormally high postoperative gradients
What are two situations in which bioprosthetic valves are utilized over mechanical valves?
- Pregnancy (anticipating)
- History of IVDA
What are 3 priniciples that must be understood by both sonographer and interpreting echocardiographer in the assessment of prosthetic vavles?
- All prosthetic valves have some inherent obstruction (which varies based on valve type and size), which can make differentiating between normal and pathologic gradients challenging.
- Prosthetic valves have inherent transprosthetic regurgitation that must not be confused with pathologic regurgitation.
- Acoustic shadowing and other artifacts such as reverberations can make evaluation of the structure of the valve and presence/degree of regurgitation difficult
What is the EOA (indexed) cutoff in regards to PPM for a prosthesis in the aortic position?
EOA indexed ≤ 0.85 cm2 / m2
- smaller areas –> rapid increase in transvalvular gradients
What is the EOA (indexed) cutoff for severe PPM for a prosthesis in the aortic position?
EOA indexed ≤ 0.65 cm2 / m2
What are the major adverse outcomes associated with PPM?
short-term and long-term survival
- particularly if associated with LV dysfunction
What peak velocity should prompt further evaluation in assessment of aortic prosthetic valves?
> 3 m/s
What is the severity scale for aortic prosthetic valves?
- Peak velocity
- Normal < 3 m/s
- Possible stenosis 3-4 m/s
- Significant stenosis > 4 m/s
Assessment of peak and mean gradients across the mitral/tricuspid valve prostheses are greatly dependent upon this?
Heart rate
- gradients across mitral and tricuspid prostheses are very HR dependent
What is the severity scale for mitral prosthetic valves?
- Peak velocity
- Normal < 1.9 m/s
- Possible stenosis 1.9-2.5 m/s
- Significant stenosis > 2.5 m/s
What is the severity scale for mitral prosthetic valves?
- Mean gradient
- Normal ≤ 5 mmHg
- Possible stenosis 6-10 mmHg
- Significant stenosis > 10 mmHg
What is the severity scale for aortic prosthetic valves?
- Mean gradient
- Normal < 20 mmHg
- Possible stenosis 20-35 mmHg
- Significant stenosis > 35 mmHg
What is the severity scale for aortic prosthetic valves?
- DVI
- Normal ≥ 0.30
- Possible stenosis 0.29 - 0.25
- Significant stenosis ≤ 0.25
What is the severity scale for mitral prosthetic valves?
- VTIPrMV / VTILVOT
- Normal < 2.2
- Possible stenosis 2.2 - 2.5
- Significant stenosis > 2.5
What is the severity scale for mitral prosthetic valves?
- EOA
- Normal ≥ 2cm2
- Possible stenosis 1-2 cm2
- Significant stenosis < 1 cm2
What is the severity scale for aortic prosthetic valves?
- EOA
- Normal > 1.2 cm2
- Possible stenosis 1.2 - 0.8 cm2
- Significant stenosis < 0.8 cm2
What is the severity scale for mitral prosthetic valves?
- PHT
- Normal < 130 ms
- Possible stenosis 130 - 200 ms
- Significant stenosis > 200 ms
What is the severity scale for aortic prosthetic valves?
- Acceleration time (AT)
- Normal < 80 ms
- Possible stenosis 80 - 100 ms
- Significant stenosis > 100 ms
What are findings suggestive of prosthetic TS?
- PV ≥ 1.7 m/s
- MG ≥ 6 mmHg
- PHT ≥ 230 ms
What is the severity scale for aortic prosthetic valves?
- jet velocity contour
- Normal - triangular, early peaking
- Possible stenosis - triangular to indeterminate
- Significant stenosis - rounded, symmetrical contour
What do microcavitations (in harmonic imaging) indicate in prosthetic valve assessment?
normal prosthetic valve
What prosthetic valves demonstrate the greatest degree of pressure recovery?
Bileaflet (small)
and
Ball and cage
Define Ejection clicks
- high-pitched sounds that occur at the moment of maximal opening of the aortic or pulmonary valves
- heard just after the first heart sound
- sounds occur in the presence of:
- a dilated aorta or pulmonary artery of in the presence of
- a bicuspid or flexible stenotic aortic or pulmonary valve
What are the recommendations in regards to PHT in assessment of prosthetic valves?
Should not be used / Inaccurate
In which mitral valve prosthesis is the largest degree of physiologic regurgitation seen?
Bileaflet valves
- central and peripheral jets
Describe EKG findings in hyperkalemia (K 6.5 - 7.5)
- 1st degree AV block
- flattening and widening of the P wave
- ST-depression
- QRS widening
What is recommended whenever paravalvular regurgitation is suspected?
TEE
- essential to the evaluation of paravavular regurgitation
What are mimickers of constriction?
- Restrictive cardiomyopathy
- Severe TR
- Ventricular interdependence (other causes)
Describe the algorithm in evaluating aortic prosthesis with PV > 3 m/s

Describe the timing of heart sounds

In which mitral valve prosthesis is a large central jet most consistent with normal valve function?
Medtronic-Hall single disc valve

What is the diagnosis and next best step?
- 52 year old man with prior Type A aortic dissection s/p mAVR and root repair presents with 1 week of progressive dyspnea and orthopnea
- HR 92 bpm, BP 148/92, RR 22, O2 90% on RA
- PE: elevated JVP, rales and scattered wheezing, distant heart sounds, 1+ LE edema
- EKG: NSR with lateral ST depressions
- Labs: Cr 1.2, INR 2.2, BNP 1200, Troponin 0.40
- TTE: Normal LVEF with poor windows
- CXR: bilateral, patchy infiltrates
-
TEE
- TTE (class I) indication –> TEE utilized due to poor windows
- TEE more sensitive for the detection of valve dysfunction and thrombosis
- CCTA (Class IIa) can also be utilized
-
Valve thrombosis
- suspect in patients with interrupted anticoagulation or subtherapeutic INR
What is the most helpful distinguishing feature of a pulmonary ejection sound?
Inspiration –> decreased intensity / dissappearnce
- inspiration –> increased venous return –> partial opening of the pulmonary valve prior to systole –> lack of a sharp opening movement of the pulmonary valve
- maximal intensity of the ejection sound
-
expiration –> valve opens rapidly from its fully closed position –> sudden “halting” of this rapid opening –> maximal intensity of ejection sound
*
-
expiration –> valve opens rapidly from its fully closed position –> sudden “halting” of this rapid opening –> maximal intensity of ejection sound
What are four criteria used to identify constrictive pericarditis?
- Ventricular inderdependence (septal motion abnormality)
- Mitral inflow velocity ≥ Grade 2
- Mitral annulus medial e’ ≥ 8 cm/s
- Hepatic vein diastolic expiratory flow reversal

Why is severe AS associated with a single S2 heart sound?
A2 component of the second heart sound (due to AV closure) is delayed –>
occurs simultaneously with the pulmonic component (P2)
When does S2 become paradoxically split in AS?
severe AS + LV dysfunction
Describe the frequency of monitoring in AR
- Progressive (stage B)
- Mild –> every 3-5 years
- Moderate –> every 1-2 years
- Severe (stage C)
- Severe –> every 6-12 months
- Dilating LV –> more frequently

Describe the frequency of monitoring in MS
- Progressive (stage B)
- MVA > 1.5 cm2 –> every 3-5 years
- Severe (stage C)
- MVA 1 - 1.5 cm2 –> every 1-2 years
- Very severe
- MVA < 1.0 cm2 –> every 1 year

Describe the frequency of monitoring in MR
- Progressive (stage B)
- Mild –> every 3-5 years
- Moderate –> every 1-2 years
- Severe (stage C)
- Severe –> every 6-12 months
- Dilating LV –> more frequently

Describe the findings

Parachute mitral valve
- mitral valve attached to a single papillary muscle with
- redundant leaflet tissue

Describe the findings

Severe AR on M-Mode –> early surgical intervention
- rapidly rising LV diastolic pressure –>
- premature closure of the mitral valve
- soft S1 heart sound

Describe the valvular abnormality:
- Prominent carotid pulsations
- apical impulse is slightly enlarged and laterally displaced to the anterior axillary line
- S1, S2 are normal
- S3 present
- early systolic click that does not change with inspiration
- left sternal border
- soft (grade 2/6) crescendo-decrescendo systolic murmur
- soft (grade 2/4) decrescendo diastolic murmur
Bicuspid aortic valve with regurgitation
- sudden cessation of valve opening –> ejection click
- findings of AR / volume overload
- enlarged and laterally displaced apical impulse
- wide aortic pulse pressure
- S3 gallop
What test should be performed prior to AVR in S. Bovis endocarditis?
Why?
- Colonoscopy
- Colon cancer screening
What is the next best step?
- 30 year old female with progressive SOB worsening over 2 years
- PE: opening snap with low-frequency murmur
- Echo:
- thickening of mitral valve leaflets with doming
- MG 5 mmHg (HR 60 bpm)
Exercise Stress Echo
- helpful when discrepancy between:
- symptoms
- Doppler echo findings
- Positive test findings: increased
- MG
- PASP
What is the next best step?
- Aysmptomatic, BAV s/p repair 20 years ago
- Echo:
- LVEF 57%
- LVEDD 6.5 cm
- LVESD 4.2 cm
- Severe AR (RV 70 mL, RF 60%, AR diameter 4.2 cm)
Serial monitoring - TTE in 6-12 months
- Asymptomatic, severe AR –> surgery only if:
- LVEF < 50% (class I)
- Other cardiac surgery (class I)
- LVESD > 50 mm (class IIa)
- Progressive decline on 3 consecutive studies:
- LVEF < 55-60% or
- LVEDD > 65 mm
- low surgical risk (class IIb)
What accounts for the majority of cases of severe TR?
80% are functional (secondary) due to RV remodeling
- Result of pressure and/or volume overload –>
- leaflet tethering
- annular dilation
Describe EKG findings in hyperkalemia (K 5.5 - 6.5)
- Tall, peaked, narrow-based T waves
- QT interval shortening
- Reversible LAFB or LPFB
What are findings consistent with severe TR secondary to Carcinoid syndrome?
- 5-HIAA –> unique characteristic findings of the RV
- short, thick, retracted leaflets (posterior and septal) with systolic and diastolic restriction
What are common causes of TR
80% are secondary (functional)

What leads to increased S1?
- maximal opening of the MV and TV leaflets at the onset of ventricular systole
- Loud closure sound requires a mobile valve and at least moderate excursion
What are causes of increased S1?
- MS
- MVP
- Short cycles in A-Fib
- Short PR interval
- Rapid HR (anemia, thyrotoxicosis)
What is the only right-sided ausculatory event that diminishes with inspiration?
Pulmonary ejection click - associated with PS
What is the “sail sound?”
When is it seen?
- midsystolic click in Ebstein’s anomaly
- sound emanating from the broad anterior TV leaflet
Describe EKG findings in hyperkalemia (K > 7.5 )
- Dissappearance of P-waves
- LBBB, RBBB, or markedly widened and diffuse IVCD resembling a sine wave pattern
- Arrhytyhmias and conduction disturbances
- VT, VF, Idioventricular rhythm, Asystole

What leads to decreased S1?
reduced mobility of the MV or TV
or
early partial closure
What are causes of decreased S1?
- worsening MS
- Acute AR with preclosure of the MV
- Long P-R interval
- LBBB
- Body habitus issues (obesity, large breasts)
What leads to early systolic sounds?
- generally from the semilunar valves (aortic or pulmonary)
- due to sudden abrupt cessation of a doming valve
What are causes of early systolic sounds?
- BAV
- PS
- Dilated aorta
- Abnormal (or stiff) AV from systemic hypertension
- Abnormal (or stiff) PV from pulmonary hypertension
What causes mid-late systolic sounds?
- emanate from the MV (most commonly) or TV
- clicks coincide with the maximal MV excursion into the LA
- thought to be due to abrupt tensing of the redundant leaflets or chordae
- at times, multiple clicks are audible
What are causes of mid-late systolic sounds?
- MVP
- Ebstein’s anomaly
- Pericardial rub
What is the indication and recommendation for PMBV in pregnant patients?
- Severe MS (MVA < 1.5 cm2, PHT > 150 ms)
- favorable valve morphology
- NYHA Class III or IV HF symptoms + despite medical therapy
- PMBV - (Class IIa) if:
- < Mild MR
- Favorable Wilkins score « 8
Describe the findings:

A. - A4C vies
B. - Color-flow display
C. - Measure of PISA
D. - CW doppler of TR jet allowing calculation of EROA and RVol

Describe the findings:

Hepatic vein flow reversal in Severe TR
- A and B
- Color Doppler demonstrating systolic flow reversal into the vena cava ad hepatic vein
- C
- spectral doppler recording from the hepatic vein
- also showing the systolic retrograde flow

Describe the findings

Diastolic gradient RA-RV should be noticed (associated TR)
and
absence of A wave due to A-fib

When is the Dobutamine infusion stopped in LF-LG, reduced EF, AS evaluation?
- Maximum dose of Dobutamine reached
- Positive result obtained
- HR rises 10-20 bpm over baseline or exceeds 110 bpm
- Symptoms, BP drop or concerning arrhythmias

Describe the mumur:
- Heart murmur since childhood
- Normal JVP and contour
- high-pitched sound just after S1, followed by a murmur
- auscultation along left sternal border
Pulmonary stenosis
- Right-sided ejection click and ejection murmur
What are considered positive results for Dobutamine stress echo in LF-LG, reduced EF, AS evaluation?
-
Pseudostenosis
- Increase in effective AVA > 1.0 cm2
-
True stenosis
- PV > 4.0 m/s or MG > 40 mmHg +
- AVA < 1.0 cm2 (at any flow rate)
-
Absence of contractile reserve
- failure to exceed stroke volume by > 20%
- predicts poor surgical outcomes

What are causes of a single S2?
- Congenital absence of the pulmonic valve
- Transposition of the great vessels
- Inaccurate auscultation
- body habitus, emphysema, pericardial effusion
- Pulmonary HTN
- PS
- Severe AS
When should TTE monitoring be performed following valve implantation?
Why?
- 6 weeks - 3 months
- establish baseline for comparison should complications or deterioration occur later
What is the only right-sided ausculatory event that diminishes with inspiration?
Pulmonary stenosis
What is the recommendation regarding perioperative anticoagulation management?
- mechanical (bileaflet) AVR
- no TE risk factors
- Surgery: nephrectomy
- discontinue VKA 3-4 days prior to surgery
- continue ASA 81mg daily
What is the differential?
- paced P-wave is not followed by either a paced or native QRS complex
- Dual-chamber PPM programmed to DDD mode
- failure of ventricular output
- sensing is appropriate but the pacemaker is not able to deliver a packemaker spike owing to a problem internal to the pacemaker
- oversensing
- the pacemaker senses something in the AV interval that it misidentifies as ventricular activity, such as a T wave or external artifact
- failue to capture
- pacemaker spike is generated at the appropriate time but fails to capture the ventricle
Why do transvalvular gradients increase during pregnancy?
- increased HR
- increased plasma volume
- increased stroke volume
Describe the treatment algorithm for:
- Severe AS
- Asymptomatic
Describe the treatment algorithm for:
- Severe AS
- Symptomatic
Describe the treatment algorithm for:
- Abnormal aortic valve with reduced systolic opening
- Moderate AS
- Asymptomatic
What is the rate of progression of aortic stenosis?
- PV
- MG
- PV
- 0.1 - 0.4 m/sec/year
- MG
- 3-7 mmHg / year
Describe the stepwise approach for AS Severity
Describe stepwise approach for diagnosing severe AS:
- Low Gradient
- Normal LVEF
Describe the treatment algorithm:
- Moderate AR
Describe the treatment algorithm:
- Severe AR
Describe imaging interval for BAV
Describe TR treatment algorithm:
- Progressive TR
Describe the treatment algorithm
- Severe TR
- Asymptomatic
Describe the prosthetic valve treatment algorithm:
- Valve thrombosis/suspected thrombosis or
- TE event
Describe the treatment algorithm
- Severe TR
- Symptomatic
Describe the treatment algorithm
- Progressive TR
Describe the treatment algorithm
- Severe TR
- Right Heart Failure
Describe Echo criteria for severe TR
- VC ≥ 0.7 cm
- RVol ≥ 45 mL
- EROA ≥ 0.4 cm2
Surgical correction of which valvular abnormality would result in the following change in the PV loop?
Mitral Regurgitation
- decrease preload
- fixing the valvular abnormality
- decreased SV
- increased afterload after removing low pressure atrial offloading
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- increased afterload after removing low pressure atrial offloading
What is the major pathophysiologic abnormality?
Increased afterload, normal preload
- severe AS
Describe the findings and effect on LV filling pressure?
- Valsalva maneuver performed
High Filling Pressures - Square wave response
- Valsalva initiated (normal filling pressured)
- Preload drops (beats 4, 5, 6, 7) → SV drops → PP drops → BP drops
- Valsalva initiated (elevated filling pressure) = flat starling curve
- Preload drops ( beats 4, 5, 6, 7) →
- negligible drop in SV, PP, BP
Describe the phases of the Valsalva maneuver
- Phase I - Early phase - Bearing down
- increase in intrathoracic pressure
- Preload to LV not affected
- Pressure increases
- Phase 2 - Strain phase
- continuous decrease in preload to the LV →
- SV and PP decreases
- Reflex tachycardia
- continuous decrease in preload to the LV →
- Phase 3 - Release phase
- intrathoracic pressure drops
- LV pressure drops
- Phase 4
- Overshoot
- Preload returns to LV - SV, PP returns to normal
Describe the management:
- Prosthetic heart valve
- Thromboembolic event
Describe the management:
- Prosthetic heart valve
- Suspected mechanical valve thrombosis
- Urgent TTE, TEE, Fluoro and/or CT imaging
- Left-sided mechanical obstruction
-
TPA
- urgent slow-infusion
- Emergency surgery
-
TPA
Describe the management:
- Prosthetic heart valve
- Suspected bioprosthetic valve thrombosis
- 3D TEE or 4D CT imaging
- VKA treatment
****2a recommendations
Differentia factors favoring each in prosthetic valve thrombosis
- TPA
- Surgery