Cardiac Valve Issues Flashcards
What is the normal Aortic Valve Area?
2.5 - 6.0 cm2
-Normally has 3 cusps
What are the causes of Aortic Stenosis?
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
What are the S/Sx of Aortic Stenosis?
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
Why does Angina Pectoris occur with AS?
-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
Describe the PV loop for AS.
Elevated peak SBP
EDP elevated with steeper diastolic slope
Decreased SV
Describe HD management for Aortic Stenosis.
Slow (HR), Tight (SVR), Full (PL)
What do you want to do to HR for Aortic Stenosis?
-Slow and Sinus
-High = dec coronary perfusion
-Low allows for systolic ejection across stenotic valve, need atrial kick
-Long diastole perfuses coronaries
What do you do for Preload with AS?
PL augmentation is necessary to maintain normal SV (decreased LV compliance and increased LVEDP & LVEDV)
What do you do for Contractility with AS?
Keep them where they live. Avoid BBs
What do you do for Afterload with AS?
-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.
Describe anesthetic management of Aortic Stenosis.
-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
What is the valve area for Severe Aortic Stenosis?
< 1 cm2
What is the normal valve area for the Mitral Valve?
4.0 - 5.0 cm2
What is the valve area for Severe Mitral Stenosis?
< 1.0 cm2
MVA 0.3-0.4 cm^2 smallest area compatible with life
What is the usual cause of Mitral Stenosis?
Usually r/t Rheumatic HD -> scarring and fibrosis of edges of leaflets
What are the S/Sx of Mitral Stenosis?
-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
Why are MS patients predisposed to afib?
Increased LAP leads to LA enlargement→ predisposes these patients to AFib
What are the pulmonary effects of Mitral Stenosis?
-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
Describe the PV Loop for Mitral Stenosis
-Decreased SV
-Decreased ESV
What is the HD management for MS?
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
What is the anesthetic management for MS?
-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
What are indications for TAVR?
Patients high risk or inoperable d/t age & comorbidities
Patients have severe AS
Why do we pace with TAVRs?
-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
What are complications with TAVRs?
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
