Cardiac Valve Issues Flashcards

1
Q

What is the normal Aortic Valve Area?

A

2.5 - 6.0 cm2
-Normally has 3 cusps

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2
Q

What are the causes of Aortic Stenosis?

A

AS may result from congenital or acquired valvular heart disease:
-Congenitally bicuspid AV occurs in 1-2% of general population: most common congenital valvular malformation
-Calcification of bicuspid AV results in early onset AS: most common cause of AS in patients <70 yo
-Acquired AS: senile degeneration most common cause in developed world
-Calcification associated with senile degeneration appears to have inflammatory component as well, similar to that observed with CAD

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3
Q

What are the S/Sx of Aortic Stenosis?

A

Onset of any one of the triad (SAD) indicates life expectancy < 5 years.
1) Syncope (dec in SVR)
2) Angina Pectoris
3) Dyspnea (usually DOE)

If they develop CHF, life expectancy is 1-2 years

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4
Q

Why does Angina Pectoris occur with AS?

A

-May occur in absence of CAD d/t increase in myocardial O2 requirements as concentric LV hypertrophy develops and myocardial work increases to overcome afterload produced by stenotic valve
-Myocardial O2 delivery also likely to be decreased d/t compression of subendocardial blood vessels by increased LV pressure

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5
Q

Describe the PV loop for AS.

A

Elevated peak SBP
EDP elevated with steeper diastolic slope
Decreased SV

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6
Q

Describe HD management for Aortic Stenosis.

A

Slow (HR), Tight (SVR), Full (PL)

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7
Q

What do you want to do to HR for Aortic Stenosis?

A

-Slow and Sinus
-High = dec coronary perfusion
-Low allows for systolic ejection across stenotic valve, need atrial kick
-Long diastole perfuses coronaries

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8
Q

What do you do for Preload with AS?

A

PL augmentation is necessary to maintain normal SV (decreased LV compliance and increased LVEDP & LVEDV)

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9
Q

What do you do for Contractility with AS?

A

Keep them where they live. Avoid BBs

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10
Q

What do you do for Afterload with AS?

A

-High SVR is needed to avoid hypotension.
-Coronary steal can happen with these patients. If you decrease pressure on the other side of the stenotic lesion, won’t have enough pressure to perfuse coronaries.
-Alpha agonists (neo) used a lot
-CPR can be ineffective - not enough pressure in the ventricle to get blood to eject through a stenotic aortic valve.

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11
Q

Describe anesthetic management of Aortic Stenosis.

A

-Light premedication (Avoid tachycardia)
-Preinduction A-Line
-NTG used cautiously if ischemic
-PCWP may overestimate preload of non-compliant LV
-TEE used to monitor intraop LV function, PL, and AL
-In presence of myocardial hypertrophy, antegrade and retrograde cardioplegia may be used (extra cardioplegia due to rly thick hearts)
-In absence of preop ventricular dysfunction and CAD, inotropic support not often required as weaning from CPB→ valve replacement itself decreases ventricular afterload

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12
Q

What is the valve area for Severe Aortic Stenosis?

A

< 1 cm2

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13
Q

What is the normal valve area for the Mitral Valve?

A

4.0 - 5.0 cm2

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14
Q

What is the valve area for Severe Mitral Stenosis?

A

< 1.0 cm2

MVA 0.3-0.4 cm^2 smallest area compatible with life

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15
Q

What is the usual cause of Mitral Stenosis?

A

Usually r/t Rheumatic HD -> scarring and fibrosis of edges of leaflets

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16
Q

What are the S/Sx of Mitral Stenosis?

A

-Symptoms first associated with exercise or high CO states
-Slow, progressive decline with repeated episodes of fatigue, chest pain, palpitations, SOB, paroxysmal nocturnal dyspnea, pulmonary edema, and hemoptysis
-Hoarseness d/t recurrent laryngeal nerve compression by distended LA and enlarged PA
-Clinically, MS recognized by early diastolic opening snap + rumbling diastolic murmur best heard at apex or in left axilla
-Broad, notched P waves on ECG (p-mitrale) suggest LA enlargement
-Afib present in ~1/3 of patients with severe MS

17
Q

Why are MS patients predisposed to afib?

A

Increased LAP leads to LA enlargement→ predisposes these patients to AFib

18
Q

What are the pulmonary effects of Mitral Stenosis?

A

-MS results in increased Left Atrial Pressure (LAP)
-LAP reflects back into the pulmonary vasculature
-Inc in PVR in response to inc LAP can eventually lead to RV dilation and failure
-PA constriction, Pulmonary HTN eventually

19
Q

Describe the PV Loop for Mitral Stenosis

A

-Decreased SV
-Decreased ESV

20
Q

What is the HD management for MS?

A

Slow (HR), Tight (SVR), Full ish (PL)
-Basically same as AS, but don’t want to over do it on fluid/PL due to risk of pulmonary issues

21
Q

What is the anesthetic management for MS?

A

-Light premed to avoid acute decrease in preload or oversedation (which would lead to hypoxemia and hypercapnia)
-Avoid ketamine for induction d/t propensity to increase HR
-Short-acting beta blocker may be necessary to treat episodes of tachycardia during induction
-PA catheters: PA’s dilated→ especially CAREFUL floating SGC d/t increased risk of PA rupture
-TEE to assess repair, paravalvular regurg, SAM of anterior mitral leaflet, and RV/LV loading conditions
-Muscle relaxant reversal should be administered slowly to ameliorate tachycardia associated with anticholinergic administration

22
Q

What are indications for TAVR?

A

Patients high risk or inoperable d/t age & comorbidities
Patients have severe AS

23
Q

Why do we pace with TAVRs?

A

-Rapid pacing: aortic valve stays open
-Anesthesia will rapid pace at 180 bpm when cardiologist instructs us to do so
-Cadence: “pacing on, inject, deploy, pacing off”
-CRITICAL that rapid pacing continues throughout deployment

24
Q

What are complications with TAVRs?

A

Big 3: Blood (bleeding), Brain (stroke), and Brady (need PPM)

-Stroke
-Cognitive dysfunction
-Aortic dissection
-Bleeding
-Mediastinal hematoma
femoral/iliac artery injury
-Valve size mismatch
-Conduction system issues
-Perivalvular leaks