Anesthesia for Valvular Heart Surgery

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Anesthesia for Valvular Heart Surgery

• Charles E. Smith, MD
• Professor of Anesthesia
• Director, Cardiothoracic Anesthesia
• MetroHealth Medical Center
• Case Western Reserve University

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Objectives

• Pathophysiology
• Aortic valve AS, AI
• Mitral valve MS, MR
• Tricuspid valve TR
• Hemodynamic Goals
• Anesthetic management

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Aortic Stenosis

• May occur at 3 levels
• Valvular
• Subvalvular
• Supravalvular

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Valvular Aortic Stenosis

• Calcification fibrosis of normal tricuspid
  valve- very common
• Calcification fibrosis of congenital bicuspid
  AV
• Rheumatic- uncommon since antibiotics

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Aortic Stenosis

• Normal AVA 2-4 cm2
• Severe AS AVA lt 1cm2
• If normal LV- mean PG gt 50 mmHg
• If poor LV function- mean PG may be low!

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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

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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

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AS Considerations

• Drugs to maintain CPP
• Phenylephrine
• Norepinephrine
• Atrial kick crucial. HR 60-80 preferred
• Spinal epidural anesthesia poorly tolerated if
  ? preload or ? HR

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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

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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, ß-blockers. Rarely need myomectomy
  inotropes worsen obstruction

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Septal LVH with SAM. Tx volume beta-blockers
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Aortic Regurgitation Etiology

• Aortic root dilatation- HTN, ascending aorta
  dissection, cystic medial necrosis, Marfans,
  syphilitic aortitis, ankylosing spondylitis,
  osteogenesis imperfecta
• Deformed thickened cusps- rheumatic, IE,
  bicuspid valve
• Cusp prolapse- dissection

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Horse kick to upper chest with severe AI. The
RCC was torn from the STJ
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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

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Pathophysiology Acute AR

• LV unable to dilate acutely
• LV volume overload occurs
• ? LVEDP LVEDV? acute pulmonary edema
• Emergency surgery often needed

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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

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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

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Mitral Stenosis

• Usually rheumatic- thickening, calcification
  fusion of MV leaflets commissures
• May be combined w MR AR
• Surgery if MVA lt 1 cm2 w NYHA class III or IV
  dyspnea or embolus- LAA clot

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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

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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

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Anesthetic Management MS

• Premed benzos to avoid tachycardia
• If pulm HTN- supplemental O2
• Control of HR- ß blockers, digoxin, CEB,
  amiodarone

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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

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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

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Mitral Regurgitation Etiology

• Myxomatous degeneration (most
  common)
• Ischemic (functional)- papillary muscle
  dysfunction, annular dilatation, LV
  dysfct tethering
• Infective endocarditis
• Trauma

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Papillary muscle rupture after blunt trauma
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MR- Pathophysiology

• Volume overload of LV? LVE, LAE
• LA can massively dilate
• Atrial arrhythmias with LAE
• Dilated LV decompensates at later stages w ? LVEDV

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Chronic MR. Dilated LA w normal LAP
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• Chronic MR. Dilated LA w normal LAP

Acute MR. Small LA with ? ? LAP pulmonary edema
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Severity of MR

• Pressure gradient between LA LV
• Size of regurgitant orifice (ERO)
• Duration of ventricular systole

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Hemodynamic Goals- MR

• Vasodilators NTG, SNP - ? afterload
  regurgitant fraction ? forward flow
• High normal HR to ? time of ventricular systole
• Maintain contractility

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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

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Tricuspid Regurgitation

• Primary rheumatic, IE, carcinoid, Ebsteins,
  trauma
• Secondary chronic RV dilatation, often w MV
  disease

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Flail TV after blunt trauma
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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

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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

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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

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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

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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.