Valvular heart disease CIS (Darrow) Flashcards

1
Q

A 35 y/o female from South Africa presents with a history of rheumatic heart disease. She presents with fever, fatigue and neck throbbing. She complains of abdominal fullness. Examination shows peripheral edema and ascites. There is a 1/6 systolic blowing murmur at the lower left sternal border with a 3/6 diastolic rumble (tricuspid stenosis). Both murmurs are increased with inspiration . A split first heart sound is present.
This patient would also be expected to exhibit which abnormality in the jugular venous tracing?

Prominent  A wave
Prominent C wave
Sharp Y descent
Minimal V wave
Prominent CV wave
1. What valve gradient is considered 
significant in this case? 
2. What is the most common cause 
of this in the US? 
3. What is the sign related to the increased 
intensity with inspiration?
A

Prominent A wave (cannon a wave) with blunted y descent
when right atrium contracts and there is a stenotic tricuspid valve, the a wave will increase.
Blunted y descent- very tiny b/c valve won’t let blood leave efficiently

  1. What valve gradient is considered
    significant in this case?
    Valve–> tricuspid stenosis
    Valve gradient > 5 mmHg
  2. What is the most common cause
    of this in the US?
    Carcinoid (rarely rheumatic) - develops on tricuspid leaflets. see picture on slide 3
  3. What is the sign related to the increased
    intensity with inspiration?
    Carvallo sign
    (blood goes into the right atrium–> right ventricle, so the murmurs get louder with inspiration- Carvallo sign)
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2
Q

what is the treatment of tricuspid stenosis?

A

Diuretics – especially torsemide –better absorbed from the gut *** Spironolactone for ascites.
-reduce volume coming back to the heart

Balloon valvotomy, open commissurotomy, or bioprosthetic valve (because of low flow velocity and tendency to clot with mechanical valves).

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3
Q

A 55 y/o female with history of a prior right ventricular MI presents with fatigue and abdominal fullness. Examination shows peripheral edema and ascites. There is a 3/6 systolic blowing murmur at the lower left sternal border with an audible S3 (when the AV valves open, and blood rushes in, but there is already old blood in there, and it creates vibratory sound). The murmur is increased with inspiration (Carvallo sign)
This patient would also be expected to exhibit?

Q wave in V6
Small RV diameter
Kerley B lines
Pulmonary valve regurgitation
Prominent “cV wave”
A

This is most likely a tricuspid regurgitation

Prominent “cV wave”***
large amount of regurgitated blood
there is a huge filling wave

Q wave in V6- NO, this is lateral wall MI

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4
Q

what is the treatment of tricuspid regurg?

A

Treat the primary issue, ie LV failure or pulmonary hypertension.

If a true valvular defect, then use a bioprosthetic*** valve since mechanical valves will clot with the low flow state at the tricuspid valve.

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5
Q

What else causes this valvular defect (tricuspid regurg) to exist?

A

Any RV dilation as in pulmonary hypertension, pulmonic regurgitation, or LV failure where PA or RV systolic pressure is above 40 mmHG.

Or more rarely an inherent valvular problem as in Ebstein’s anomaly, pacemaker catheter injury, endocarditis, MI, sarcoid, RV dysplasia, or even fenfluramine/phenteramine (“FenPhen”) which causes low pressure TR.

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6
Q

A 55 y/o male with COPD and pulmonary hypertension presents with a split P2 and a diastolic 2/6 murmur at the left 2nd intercostal space (pulmonic valve) that increases with a deep breath.
what does he have ?

A

he has high pressure pulmonary insufficiency/regurg

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7
Q

What is the difference between low and high pressure Pulmonary Insufficieny?

A

Pulmonic regurgitation – high pressure PI - Prolonged RV systole with split S2, from pulmonary hypertension as from mitral stenosis, ie Graham-Steell murmur. (due to COPD or mitral stenosis)

Low pressure PI - very little murmur - for example, trauma with a dilated pulmonary annulus, carcinoid plaque, bicuspid valve, repaired tetralogy, etc. (Due to some event that involved the pulmonic valve)

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8
Q

what is the treatment of pulmonic regurgitation

A

High pressure – treat pulmonary hypertension.
(ex. treat COPD)

Low pressure – watchful expectancy.

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9
Q

A 35 y/o pregnant female from Iran presents with exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea. Auscultation with the patient in the left lateral decubitus position reveals a loud M1 and an early diastolic sound at the mitral area. EKG, chest xray and ECHO are shown. see slide 16

A

patient has mitral stenosis

straightening of the left heart border

hockey stick sign

more findings?? see slide

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10
Q

what are the ausculatory findings with mitral stenosis

4 signs!!

A

Thickened immobile leaflets (RF) versus annular calcium deposits (degenerative). Symptoms with pregnancy or AF.

Loud M1 (unless calcified).

Opening snap (unless calcified)- earlier after S2 with worsening LA pressure.

Rumbling diastolic murmur – bell lightly.

Presystolic accentuation of diastolic rumble (as the atrium contracts)

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11
Q

what are 2 syndromes associated with mitral stenosis and how do they present?

A

Two syndromes:
A. Mild to moderate (valve surface area of 1.5 cm2) with early pulmonary edema.

B. Severe (< 1 cm2 ) with pulmonary HTN (“2ndary pulmonary vasculature stenosis”) and right sided CHF, AFib and low CO. (vessels are clamping down) this patient doesn’t have pulmonary edema, but rather right sided heart failure, can go into A-fib, etc.

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12
Q

what is graham steell murmur

A

Graham Steell murmur at left sternal border from relative PI.

mitral stenosis leads to pulmonary regurg/insufficiency (why? listen)

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13
Q

what are the ECG findings in mitral stenosis?

A

Neg P wave in V1

Right Axis Deviation.

right atrial hypertrophy

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14
Q

mitral stenosis treatment?

A

Based on ECHO evaluation with a scoring system which grades various mitral parameters to decide time for intervention with mitral valvuloplasty.

Score of 8 or less try valvuloplasty;
> 8-10 needs mechanical (INR 2.5 - 3.0) or bioprosthetic valve (last 10-15 years).

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15
Q

A 55 y/o male with long standing mitral regurgitation presents with new onset palpitations, orthopnea and PND. There is a high pitched pan systolic murmur with an S3* at the apex (VSD can also cause this). The patient is on a beta blocker and an ACE inhibitor. Chest xray, EKG and color doppler ECHO are shown.
* = marker for severe MR

What is the diagnosis and what are the dynamics in regard to preload,
afterload and EF? What eventually happens with LV failure?

A

MItral regurg–> The mitral valve can be defective at the papillary muscles (dilated cardiomyopathy, MI), chordae (too long, too short or ruptured as in MVP), leaflets (redundant, perforation in endocarditis) or annulus (calcified or cardiomyopathy).

In MR there is a volume load on the heart = increased preload and decreased afterload.
The increased preload = enlarged LV ***= increased EF.
But eventually the LV fails and EF drops with increased end systolic volume.

MR–> CV wave in left atrium *** listen to slide 31 again

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16
Q

IN mitral regurg…

  1. What lab test might have revealed the onset of CHF in this patient?
  2. What is the effect of handgrip and squatting on this murmur?
  3. What ECG changes are expected?
A
  1. Increased BNP (especially > 105 pg/mL) indicates LV dysfunction. if the BNP is increasing, it indicates the left ventricle is starting to fail
  2. Increased intensity. Decreased with amyl nitrate and valsalva. No change with ectopic beat.

Hand grip–> afterload increases, blows more blood back into the atrium and makes the murmur louder.
Squatting- increases periphearla resistance and back pressure, make the murmur louder b/c it increases afterload and preload

Differs from mitral valve prolapse!

  1. ECG with LVH, LAH/or AF
    once the atria gets beyond 40 mm? you get a-fib
17
Q

how do you differentiate sudden onset MR from chronic MR?

A

Acute–> high LA pressure

Sudden as in IHD with papillary muscle dysfunction, MVP with ruptured chordae, or infective endocarditis with valve perforation = pulmonary edema, tall cV wave in LA (no LA enlargement) and low CO.

Chronic–> dilated LA with normal pressure

Chronic MR leads to LA and LV enlargement as seen on chest Xray.

18
Q

treatment of mitral regurg?

A

With time the failing heart yields a decreased EF (< 60%) with increased end systolic dimension(> 40 mm) = needs surgery even when asymptomatic.

Asymptomatic patients with severe MR, tend to have effective regurgitant orifice (ERO) > 40 mm2.

In the sedentary patient, severe MR may show as exercise inducible pulmonary hypertension on ECHO.

decreased EF to 60% –> time to replace the valve

End systolic dimension dropped to 40 —> replace valve

know the 60 and 40 values for test

Treatment is REPAIR if there is no calcification in the annulus or valve, ERO > 40 mm2, and chordae can be maintained.

If chordae can’t be maintained or are destroyed then REPLACEMENT can be attempted. ***

19
Q

An anxious 32 y/o female presents with complaints of chest pain and palpitations. Exam reveals a mid systolic click with a late systolic murmur which shortens with lying down, handgrip and squatting. The patient has joint laxity and skin changes as shown. ECHO reveals:

-Valve is prolapsed

What maneuvers make the murmur louder and longer?

A

The patient has Mitral valve prolapse

Maneuvers help differentiate b/w standar MR and mitral valve prolapse.

Maneuvers that make the mitral valve prolapse murmur longer and louder:

Standing

  • prolapsed valve, lots of blood makes the valves approximate and there isn’t much regurg, so its quieter
  • with standing–> there is less blood, and the leaflets don’t approximate together so its LOUDER. Less blood, louder murmur. and this is OPPOSITE from standard regurg.

Valsalva
-increases afterload, increases venous return ? how ???

Amyl Nitrate

20
Q

Mitral valve prolapse

A

Associated with aortic root disease.

Maybe part of a hyperadrenergic syndrome in young females.
Myxomatous degeneration of the mitral valve – Marfans, Ehlers Danlos syndrome – associated with aortic regurgitation – skeletal changes (straight back, pectus, etc).
Mid-systolic clicks with late systolic murmurs which worsen with a smaller ventricle, ie murmur earlier (lengthens) with standing, valsalva and amyl nitrate.
Atrial and ventricular arrhythmias.

21
Q

how do you treat mitral valve prolapse?

A

Beta blockers (hyperadrenergic state?)

Mitral valve repair (wedge resection, chordae shortening, mitral annular ring insertion)

Mitral replacement

22
Q

A 45 y/o male presents with syncope. History is positive for a “murmur” since childhood. He reports recent onset of PND and exertional dyspnea and chest pain. There is an ejection sound with a diamond shaped harsh systolic murmur at the base and a high pitched systolic murmur at the apex. The former murmur increases after an ectopic beat and decreases with squatting.

What phenomenon is present at the apex?
What type of aortic problem is present?
What accounts for the syncope?
Characterize the pulse? EKG?

A

Congenital bicuspid aortic valve

What phenomenon is present at the apex?
Gallaverdin phenomenon.
high pitched component is referred to the apex (can sound like Mitral regurg)

What type of aortic problem is present?
Biscuspid valve or degenerative (calcific as is atherosclerosis). (Vit D and Notch1 may be involved in cell-cell communication for valve development).

What accounts for the syncope?
Peripheral vasodilation from high ventricular pressures stimulating baroreceptors in the LV. The reduced afterload calls for increased stroke volume which can’t occur due to the aortic stenosis, thus BP falls and the patient “passes out”
the ventricle has to contract harder

Characterize the pulse? EKG?
Carotid palpitation reveals a “parvus et tardus”- late and slow. Aortic stenosis is limiting flow of blood. EKG shows LVH and LAH.

23
Q

in a patient with Bicuspid valve or degenerative (Aorta) ….

  1. How is the pressure gradient across the aortic valve measured in this patient? What is the critical valve area?
  2. What are the dangers in heart cathertization
    and the treatment of AS?
A

1.Peak doppler gradient = measurement of the flow velocity through the valve orifice squared x 4. Thus a 4 m/s flow = 64 mm Hg peak gradient. (42 x 4). LV failure, angina or syncope occur when the peak valvular gradient reaches 64 mmHg * (or mean gradient of 40 mmHg*) Valve area replace

  1. Crossing the aortic valve at heart cath for CAD can induce cardiogenic shock, pulmonary edema, stroke or death.
    Nitrates are also dangerous b/c the patient will pass out, nitrates dilate aorta
24
Q

How is it possible for a patient with severe aortic stenosis to present
with a valve gradient of < 30 mmHg?

A

This is called low gradient, low flow aortic stenosis*** with reduced EF (there is a paradoxical normal EF). The patient either has failure as a result of the increased afterload or another cardiac contractility problem as from ischemic heart disease, MI, fibrosis or some other cardiomyopathy.

Diagnose with a dobutamine ECHO: < 20% increase in SV = no muscle reserve and you don’t replace the valve, the heart is shot

BNP may be used in this situation of poor LV function and aortic stenosis, ie if > 550 pg/mL = poor prognosis regardless of result of dobutamine.

25
Q

what is the treatment of Aortic stenosis.

A

make sure to check the coronary arteries!!!

Often needs CABG as well.

Young: percutaneous valvuloplasty.

Elderly: bovine valve.

Middle age : mechanical plus anticoagulation (INR 2.0-2.5).

May need aortic root replacement, especially with bicuspid valve, and aortic root diameter > 50 mm.

Trancutaneous Aortic Valve Replacement (TAVR) is in vogue for comorbid patients, but is associated with strokes.

26
Q

A 50 y/o male with history of a biscuspid aortic valve and hypertension presents with new onset PND. Upon exam he has a 2/6 systolic murmur at the base with a 3/6 descrendo diastolic murmur at the base and a 1/6 late diastolic low pitched murmur at the apex.

What will be the response of the basal diastolic murmur to squatting and handgrip?

What is characteristic of the patient’s pulse and what else can produce this problem?

A

Patient has aortic regurg/insufficiency

What will be the response of the basal diastolic murmur to squatting and handgrip?
1. Increased.
Decreased with standing or valsalva.

What is characteristic of the patient’s pulse and what else can produce this problem?
2. Wide pulse pressure*** ( ie. 140/50) -
Corrigan’s and Quincke’s (nailbed) pulse- can see flashes of blood,
De Musset sign : Atherosclerosis, AV fistula, thyrotoxicosis, anemia, fever, heart block.

aortic insufficiency creates very LARGE hearts.

large, bounding pulse with aortic insufficiency

27
Q

Patient with aortic insufficiency

The patient’s EKG and chest xray are shown- very large heart. The patient subsequently
becomes more dyspneic and orthopneic with increased basilar crackles.
Further evaluation reveals an absent M1 (see above) with a only a grade 1/6 diastolic murmur and disappearance of the wide pulse pressure.

Upon what would you base the need for surgery?

What other type of acute aortic insufficiency might present with an
absent M1, Austin Flint murmur, 1/6 aortic diastolic murmur and
acute CHF?

A

1a. Symptoms of exertional dyspnea , orthopnea and PND.
1b. LV dysfunction with contractility failure (EF 50 ***mm) (AR = 55/50)
1c. BNP > 130 pg/mL = progression to surgery.

  1. Aortic dissection (marfan’s, Ehlers Danlos), endocarditis , hypertension, inflammatory disease (syphilis, giant cell arteritis, Takayasu’s), seronegative spondyloarthropathies.
28
Q

how do you treat aortic insufficiency

A

Afterload reduction: Beta blockade versus ARBs (the latter reduce aortic stiffness by blocking TGF beta). These are not to be used in the absence of hypertension.

BNP evaluation as surgical indication.

Root replacement with valve replacement.