Valvular Heart Disease 2 Flashcards Preview

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Flashcards in Valvular Heart Disease 2 Deck (31)
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1
Q

General model for thinking about valvular heart disease

A
  1. Valve dysfunction
  2. Pressure or volume stress on ventricle
  3. Hypertrophy and compensatory response
  4. Acute decompensation
2
Q

General model for mitral stenosis

A
  1. Mitral stenosis
  2. Impaired filling of LV
  3. LA pressure overload
  4. Pulmonary HTN
  5. Increased RV afterload
  6. Concentric RV hypertrophy
  7. Acute RV decompensation
3
Q

Two major contributors to acute pathologies in mitral stenosis

A
  1. Decompensation of RV resulting in right systolic heart failure
  2. Expansion of left atrium results in greatly increased risk of arrhythmias
4
Q

Common causes of mitral stenosis

A
  1. Rheumatic heart disease (25% of RHD patients develop mitral stenosis)
  2. Degenerative (w/ age, valve calcification. Patients w/ kidney failure on dialysis at much higher risk due to high Ca and PO4)
  3. Congenital mitral stenosis (generally rare, but often part of hypoplastic left heart syndrome)
5
Q

Mitral stenosis may cause both ___ and ___.

A

Mitral stenosis may cause both pulmonary arterial hypertension and pulmonary venous hypertension.

6
Q

At the atrioventricular valve, even small ___ can cause dysfunction

A

At the atrioventricular valve, even small resistance can cause dysfunction

The atria cannot generate much force, so even small pressure barriers like 10 mmHg can be a big deal. Meanwhile, 10 mmHg would be hardly noticeable as an aortic stenosis.

7
Q

Mitral stenosis murmur

A
  • Mid-diastolic opening click-decrescendo-crescendo
  • The small crescendo at the end is due to the atrial kick
  • Best heard at apex
  • Increase in intensity with passive leg raise
  • Decrease in intensity with valsalva
  • loud S1
  • Late stage: S3
8
Q

Treating Mitral Stenosis

A
  • Anticoagulants (required due to LA stasis)
  • Beta-blockers (increase the time of diastole to allow filling, decrease arrhythmias)
  • Diuresis
  • Ultimately, catheter-based or surgical intervention required
  • Balloon dilation is very useful for these patients and may substantially prolong time before surgery is necessary
9
Q

Unlike ventricles, atria do not tend to ___.

A

Unlike ventricles, atria do not tend to hypertrophy.

10
Q

General model for mitral regurgitation

A
  1. Mitral regurgitation
  2. Increased stroke volume to maintain CO
  3. Increased volume load on LV
  4. Eccentric hypetrophy of LV
  5. Acute decompensation
11
Q

Causes of mitral regurgitation

A
  • Annular dilation (as in dilated cardiomyopathy, calcification may also cause)
  • Leaflet dysfunction (myxomatous, endocarditis, rheumatic fever, valvulitis)
  • Chordae tendinae rupture (myxomatous, spontaneous, infective endocarditis)
  • Papillary muscle dysfunction (usually posterior papillary, which has less robust blood supply, due to large cardiac infarct)
12
Q

Acute mitral regurgitation

A
  • Usually due to large infarct including papillary muscle
  • Minutes-to-hours
  • No time for heart compensation
  • Often hard to hear murmur due to low flow
  • Sudden decrease in forward flow results in hypotension and syncopy
  • Sudden increase in left atrial pressure results in pulmonary hypertension
  • This needs immediate surgery
13
Q

Chronic mitral regurgitation

A
  • Happens over the course of years
  • Can be slowed, but not stopped, by medication
  • Allows time for compensation
    • Volume load on LV and LA results in dilation of both
    • Increases forward stroke volume, but decreases ejection fraction
  • Patients usually asymptomatic while compensated
  • Acute decompensation is a result of decreased contractility, usually from ischemia
14
Q

The vicious cycle of mitral regurgitation

A
  1. Ventricular dilation from volume load
  2. Annular dilation
  3. Increased mitral regurgitation
15
Q

Why can’t a ventricle dilate forever?

A

It becomes impossible to perfuse

Ischemia, necrosis, and reduced contractility, resulting in decompensated heart failure

16
Q

Electrical properties of the pulmonary vein - left atrial junction

A

For whatever reason, when this junction is stretched (as in mitral regurgitation), its electrical properties are such that it can cause substantial atrial fibrillation on its own

17
Q

Clinical manifestations of chronic MR

A

The time from diagnosis to first symptoms aside from murmur is often more than 15 years.

Eventually, there will be a decline in systolic function and increased arrhythmias.

18
Q

Both forms of mitral valve disease predipose to ___.

A

Both forms of mitral valve disease predipose to arrhythmias.

19
Q

Mitral regurgitation murmur

A
  • At the apex, radiating to axilla
  • Increases with handgrip
  • Decreases with standing and valsalva
  • Soft S1
  • Widely split S2
  • S3 (note, S3 does not always mean active decompensated heart failure, it just means there is a lot of volume in the ventricle)
  • PMI laterally displaced
  • PMI hyperdynamic (due to increased total EF)
20
Q

“Severe” mitral regurgitation

A

MR that is seen to regurgitate all the way into the pulmonary vein on echocardiography

21
Q

Treating mitral regurgitation

A

The only cure is surgery. But, since MR is often a chronic disease, one can increase the time before they will eventually need that surgery:

  • Decreased the preload with diuresis and nitrates
  • Maintain sinus rhythm with antiarrhythmics
  • Prevent thrombosis due to hemostasis with anticoagulants

Paradoxically, decreasing afterload has not been shown to be clinically effective. This is likely because this is a pathology of pure volume load, not pressure load. So, decreasing blood pressure is unlikely to have much of an effect.

22
Q

When it comes to mitral regurgitation, and total EF below ___ is concerning.

A

When it comes to mitral regurgitation, and total EF below 60% is concerning.

Recall that a healthy EF is usually less than 55%. That is how high these mitral regurg EFs are.

23
Q

Indications for surgery in mitral regurgitation

A

Symptoms of heart failure

Pre-op end systolic diameter (as it increases, there is worse contraction, so this is an indication that heart failure is likely to happen soon)

24
Q

Marfan cardiac symptoms

A
  • Over 90% of Marfan patients will develop mitral regurgitation
  • Prevalence or Marfan is 1/500. VERY high
  • Dissection risk for Marfan patients is greater if aorta >4.5 cm, a much lower metric than for the general population, since its ability to deal with increased wall stress is so low
25
Q

Risk for aortic dissection in an otherwise healthy patient with aortic regurgitation

A

Low until the diameter of the adult ascending aorta approaches ~5-6 cm

This may be used as a risk asssessment factor for asymptomatic patients to guide when they might consider surgery to mitigate risks

26
Q

Acute and chronic aortic valve regurgitation on a PV plot

A
27
Q

Bicuspid aortic valve is associated with . . .

A

. . . both stenosis and regurgitation

28
Q

Major symptoms of acute MR

A

Patients generally develop signs and symptoms of left-sided heart failure such as dyspnea and orthopnea

there is not time for the left atrium to dilate, so the increased volume seen by the LA is transmitted back to the pulmonary veins and then to the pulmonary capillaries, leading to pulmonary edema / “left-sided heart failure”.

29
Q

Vasodilators in acute MR

A

Vasodilators are often used in acute severe MR to relieve left-sided heart failure by lowering SVR and thereby “encouraging” more blood ejected by the LV to exit through the AV and out to the body, rather than regurgitating across the open MV into the lower pressure LA.

30
Q

Marfan syndrome is associated with. . .

A
  • Mitral valve prolapse
  • Joint hypermobility
  • Aortic aneurysm
  • Aortic dissection
  • Spontaneous pneumothorax
31
Q

What mediates Eisenmenger syndrome?

A
  • High pulm artery pressure
  • Sheer stress
  • Increased resistance in pulmonary circuit
  • RVH
  • Decreased RV compliance
  • Shunt reversal