Anesthesia for Valvular Heart Surgery
Charles E. Smith, MD
Professor of Anesthesia
Director, Cardiothoracic Anesthesia
MetroHealth Medical Center
Case Western Reserve University
Objectives
• Pathophysiology
– Aortic valve: AS, AI
– Mitral valve: MS, MR
– Tricuspid valve: TR
• Hemodynamic Goals
• Anesthetic management
Aortic Stenosis
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May occur at 3 levels:
1. Valvular
2. Subvalvular
3. Supravalvular
Valvular Aortic Stenosis
1. Calcification + fibrosis of normal tricuspid
valve- very common
2. Calcification + fibrosis of congenital
bicuspid AV
3. Rheumatic- uncommon since antibiotics
Aortic Stenosis
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Normal AVA: 2-4 cm2
Severe AS: AVA < 1cm2
If normal LV- mean PG > 50 mmHg
If poor LV function- mean PG may be low!
Pathophysiology of Aortic Stenosis
• Chronic LV pressure overload
• Concentric LVH to ↓ wall stress
• LVH → ↓ diastolic compliance, ↓ coronary
blood flow + imbalance of MVO2 supplydemand
• ↓ diastolic compliance → ↑LVEDP + LVEDV
• Myocardial ischemia bc LVH, ↑ wall stress,
↓ diastolic coronary perfusion + ↓ coronary
flow reserve
Hemodynamic Goals: AS
• SR is crucial. Cardiovert SVTs promptly
• Optimal HR 60-80. Tachycardia → ischemia +
ectopy. Bradycardia → low CO due to fixed SV
• Adequate preload essential but difficult to predict
bc diastolic dysfunction [TEE useful]
• Maintain contractility. Avoid myocardial
depressants
• Treat hypotension promptly- phenylephrine,
volume, Trendelenburg
AS: Considerations
• Drugs to maintain CPP:
– Phenylephrine
– Norepinephrine
• Atrial kick – crucial. HR 60-80 preferred
• Spinal + epidural anesthesia poorly tolerated if
 preload or  HR
AS: Management
• Premed: young+ anxious get benzos.
Frail + elderly  dose (or avoid)
• Intraop: std monitoring + preinduction
art line.
• Resting HR 60-80. Avoid myocardial
depressants
• CVP, PAC, TEE- routine for optimal
management
AS: Weaning from Bypass
• Thick, hypertrophied heart may be difficult
to protect- stone heart still occurs (rare)
• Noncompliant LV dependent on stable
rhythm
• Inotropes if preop LV dysfunction
• Dynamic subaortic or cavitary obstruction
after AVR if septal LVH
• Tx w volume, β-blockers. Rarely need
myomectomy [inotropes worsen obstruction]
Septal LVH with SAM. Tx= volume + beta-blockers
Aortic Regurgitation: Etiology
1. Aortic root dilatation- HTN, ascending
aorta dissection, cystic medial necrosis,
Marfans, syphilitic aortitis, ankylosing
spondylitis, osteogenesis imperfecta
2. Deformed + thickened cusps- rheumatic,
IE, bicuspid valve
3. Cusp prolapse- dissection
Horse kick to upper chest with severe AI.
The RCC was torn from the STJ
Pathophysiology: Chronic AR
• Asymptomatic for many years
• LV volume + pressure overload occurs
• LV maintains systolic fct by dilation +
↑ compliance
• LV decompensates at later stages w
↑ LVEDP + LVEDV→ CHF, arrhythmias,
sudden death
Pathophysiology: Acute AR
• LV unable to dilate acutely
• LV volume overload occurs
• ↑ LVEDP + LVEDV→ acute pulmonary
edema
• Emergency surgery often needed
Hemodynamic Goals: AR
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Optimal HR= 90.
Avoid bradycardia- ↑ regurg
Avoid high afterload
SNP preferred
Acute AR- often need inotropes +
vasodilator [epi+ SNP/milrinone]
• IABP- contraindicated
Anesthetic Management: AR
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Premed w benzos
Routine monitoring: art line, CVP, PAC
TEE beneficial
Narcotic based technique if impaired LV
If acute AR: RSI w ketaminesuccinylcholine
• Inotropes if acute AR or preop LV
dysfunction
Mitral Stenosis
• Usually rheumatic- thickening, calcification
+ fusion of MV leaflets + commissures
• May be combined w MR + AR
• Surgery if MVA < 1 cm2 w NYHA class III
or IV dyspnea [or embolus- LAA clot]
MS- Pathophysiology
• Pressure gradient between LA + LVprevents LV filling
• Pulmonary HTN w ↑ LAP
• ↑ LAP → LAE, atrial arrhythmias (Afib)
• Pulm HTN → RV dysfct, RVE, TR [may
need TV repair]
• LV dysfct uncommon unless CAD
MS: Hemodynamic Goals
• Preserve SR, if present
• Avoid tachycardia which ↓ diastolic filling
of LV + worsens MS
• Avoid factors which worsen pulmonary
HTN- hypercarbia, acidosis, hypothermia,
sympathetic nervous system activation,
hypoxia
Anesthetic Management: MS
• Premed: benzos to avoid tachycardia
• If pulm HTN- supplemental O2
• Control of HR- β blockers, digoxin, CEB,
amiodarone
Intraop Management: MS
• Std monitors + CVP, PAC, TEE
• PAP underestimates LVEDP + LVEDV
• Esmolol:
– single most useful drug with severe MS, even
if CHF + pulmonary edema
– 10-20 mg bolus; 50-100 mcg/kg/min
• N2O avoided bc effects on pulm HTN
• Panc avoided bc tachycardia
Weaning from Bypass: MS
• MV replacement- hemodynamics usually
improved bc obstruction to LV filling
resolved
• If preop pulm HTN + RV dysfctmay need milrinone or nitric oxide
Mitral Regurgitation: Etiology
1. Myxomatous degeneration
(most common)
2. Ischemic (functional)- papillary muscle
dysfunction, annular dilatation,
LV dysfct + tethering
3. Infective endocarditis
4. Trauma
Papillary muscle rupture after blunt trauma
MR- Pathophysiology
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Volume overload of LV→ LVE, LAE
LA can massively dilate
Atrial arrhythmias with LAE
Dilated LV decompensates at later stages
w  LVEDV
Chronic MR. Dilated LA w normal LAP
Chronic MR. Dilated LA
w normal LAP
Acute MR. Small LA with ↑ ↑ LAP+ pulmonary edema
Severity of MR
1. Pressure gradient between LA + LV
2. Size of regurgitant orifice (ERO)
3. Duration of ventricular systole
Hemodynamic Goals- MR:
• Vasodilators: NTG, SNP - ↓ afterload +
regurgitant fraction + ↑ forward flow
• High normal HR to ↑ time of ventricular
systole
• Maintain contractility
Anesthetic Management MR:
• MV repair (v. replacement)
– preserved papillary muscle + chordae
– enhanced LV function
– requires TEE to assess repair
• LV dysfct unmasked after MV surgery bc
LV cannot offload into LA
• May need inotropes + vasodilators
Tricuspid Regurgitation
• Primary: rheumatic, IE, carcinoid,
Ebstein’s, trauma
• Secondary: chronic RV dilatation, often w
MV disease
Flail TV after blunt trauma
TR- Pathophysiology
• RV + RA overloaded + dilated
• RA v compliant so RAP rises only w end
stage disease
• Pulm HTN due to MV disease↑ RV afterload + worsens TR
• RVE → paradoxical motion LV septum w
imapired LV filling + compliance
• Right heart failure: hepatomegaly, ascites
TR- Hemodynamic Goals
• If secondary to MV- treat left heart lesion
• Avoid pulm HTN + high PVR
• Normal to high preload for RV stroke
volume
• Hypotension treated w inotropes + volume
bc vasoconstrictors may worsen pulm
HTN
TR- Anesthetic Management
• Premed- benzos
• Std monitors + art line, CVP, TEE
• PAC if pulm HTN + MV pathology; but CO
overestimated w severe TR. May be
impossible to float Swan
• Weaning from CPB: if preop RV
dysfunction/ dilation- inotropes, inodilators,
vasodilators, nitric oxide
Summary- I
• Knowledge of patient + extent of valvular
heart disease
• Functional + hemodynamic status
• Co-morbidities
• Planned surgery: cannulation sites, repair
vs replacement, minimally invasive vs full
bypass.
• Inotropes, vasodilators, vasopressors,
infusion pumps
Summary- II
• Understand pathophysiology of lesions +
hemodynamic goals: AS, AR, MS, MR, TR
• Monitoring: standard + invasive +TEE
• Anesthetic technique: most can be used
safely.
• Adjustment of dosages more important
than adhering to a rigid anesthetic
technique.