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

• 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

• 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 supply-demand

• ↓ 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

• 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

• Premed w benzos• Routine monitoring: art line, CVP, PAC• TEE beneficial• Narcotic based technique if impaired LV• If acute AR: RSI w ketamine-

succinylcholine• 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 + LV- prevents 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 dysfct- may 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

• 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.