ANESTHETIC In Action!!! - NDANA Heart Disease NDANA 10.12.11.pdfPhysiology In Action!!! Physiology 3 Anesthetic Management of Valvular Heart Disease ... • Connective tissue disorders

11

ANESTHETIC

MANAGEMENT OF THE

PATIENT WITH VALVULAR

HEART DISEASE

ANESTHETIC

MANAGEMENT OF THE

PATIENT WITH VALVULAR

HEART DISEASE

Peggy Contrera, MSN, CRNAPeggy Contrera, MSN, CRNA

CWRU/CC School of Nurse AnesthesiaCWRU/CC School of Nurse Anesthesia

Department of Cardiothoracic AnesthesiaDepartment of Cardiothoracic Anesthesia

Cleveland Clinic Health SystemCleveland Clinic Health System 22

Physiology

In Action!!!

Physiology

In Action!!!

33

Anesthetic Management of

Valvular Heart Disease

Anesthetic Management of

Valvular Heart Disease

�� Abnormal pressure and volume loadsAbnormal pressure and volume loads

�� Structural and functional mechanisms Structural and functional mechanisms

of compensationof compensation

�� Events that signal the limits of Events that signal the limits of

compensation (dysrhythmias, CHF)compensation (dysrhythmias, CHF)

�� Secondary complications (endocarditis Secondary complications (endocarditis

or emboli)or emboli)

44

Factors affecting blood flow

across the valve

Factors affecting blood flow

across the valve

1.1. Valve Area Valve Area �� Stenotic lesions Stenotic lesions �� ffixed ixed

�� Regurgitant lesions Regurgitant lesions �� vvariable based on loading conditions ariable based on loading conditions (preload and afterload)(preload and afterload)

2.2. Square root of the hydrostatic pressure gradient Square root of the hydrostatic pressure gradient across the valveacross the valve

3.3. Duration of flow whether systole or diastoleDuration of flow whether systole or diastole

GoalsGoals�� Stenotic lesions Stenotic lesions �� maximize or enhance transvalvular flowmaximize or enhance transvalvular flow

�� Regurgitant lesions Regurgitant lesions �� minimize regurgitant transvalvular minimize regurgitant transvalvular flowflow

55

Ventricular FunctionVentricular Function

Systolic FunctionSystolic Function

�� Ability to contract and generate a force against an afterload Ability to contract and generate a force against an afterload

�� Directly related to contractility which is Directly related to contractility which is independentindependent of of changes in preload and afterloadchanges in preload and afterload

�� Cardiac output however, does change based on preload and Cardiac output however, does change based on preload and afterloadafterload

�� ESV/ESPESV/ESP

Diastolic FunctionDiastolic Function

�� Ability to relax and accept preload Ability to relax and accept preload

�� EDP/EDVEDP/EDV

�� Directly related to complianceDirectly related to compliance

Both systolic and diastolic function require energy and can be Both systolic and diastolic function require energy and can be compromised by ischemia!compromised by ischemia!

66

Ventricular HypertrophyVentricular Hypertrophy

77

Ventricular HypertrophyVentricular Hypertrophy

Concentric Hypertrophy:Concentric Hypertrophy:

�� Occurs with pressure Occurs with pressure overload overload

�� Parallel replication of Parallel replication of sarcomeres sarcomeres

�� ↑↑ wall thickness (volume wall thickness (volume constant)constant)

�� Wall tension = P x R/2h. Wall tension = P x R/2h. Laplace's Law Laplace's Law

Eccentric HypertrophyEccentric Hypertrophy

�� Occurs with volume Occurs with volume overload overload

�� Results in an Results in an ↑↑ chamber chamber size (heart dilates)size (heart dilates)

88

The Cardiac Cycle and

The Pressure -Volume Loop

The Cardiac Cycle and

The Pressure -Volume Loop

Phase 1Phase 1: Diastolic Filling : Diastolic Filling

Phase 2Phase 2: Isovolumetric : Isovolumetric ContractionContraction

Phase 3Phase 3: Systolic Ejection: Systolic Ejection

Phase 4Phase 4: Isovolumetric : Isovolumetric RelaxationRelaxation

��Systole C Systole C →→ F (phases 2 & 3)F (phases 2 & 3)

��Diastole F Diastole F →→ C (phases 1 & 4)C (phases 1 & 4)�� ESVESV

�� EDVEDV

�� SVSV

99

Pressure -Volume

Relationships

Pressure -Volume

Relationships

��PreloadPreload

��AfterloadAfterload

��Compliance (EDPVR)Compliance (EDPVR)

��Contractility (ESPVR)Contractility (ESPVR)

��EF EF

��Systolic DysfunctionSystolic Dysfunction

��Diastolic DysfunctionDiastolic Dysfunction

1010

ESPVR Reflects ContractilityESPVR Reflects Contractility

1111

Alterations in

Preload and Afterload

Alterations in

Preload and Afterload

1212

Systolic (ESPVR) and

Diastolic Dysfunction (EDPVR)

Systolic (ESPVR) and

Diastolic Dysfunction (EDPVR)

1313

All Valvular DefectsAll Valvular Defects

1414

Each Valve DefectEach Valve Defect

EtiologyEtiology

Natural HistoryNatural History

AnatomyAnatomy

PathophysiologyPathophysiology

PressurePressure--Volume RelationshipVolume Relationship

MurmurMurmur

Anesthetic ConsiderationsAnesthetic Considerations�� Homodynamic GoalsHomodynamic Goals

�� MonitoringMonitoring

�� Anesthetic TechniqueAnesthetic Technique

�� Treatment of Untoward EventsTreatment of Untoward Events

Surgical OptionsSurgical Options

1515

Aortic StenosisAortic Stenosis

1616

Etiology of Aortic StenosisEtiology of Aortic Stenosis

Most serious valvular defectMost serious valvular defect

�� Carries the highest risk of sudden deathCarries the highest risk of sudden death

�� AS is present in 40% of pt w/ CADAS is present in 40% of pt w/ CAD

�� Independently Independently ↑↑ risk of MI 2.4 foldrisk of MI 2.4 fold�� Perioperative mortality is 11% w/ critical ASPerioperative mortality is 11% w/ critical AS

CongenitalCongenital�� Unicuspid (90% have AI)Unicuspid (90% have AI)

�� Bicuspid Bicuspid

�� TricuspidTricuspid

AcquiredAcquired�� Calcified (most common esp. w/Calcified (most common esp. w/↑↑↑↑↑↑↑↑ageageageageageageageage))�� RheumaticRheumatic

1717

Causes of AS as a

Function of Age

Causes of AS as a

Function of Age

From From PassikPassik CS, Ackermann DM, CS, Ackermann DM, PluthPluth JR, Edwards JR, Edwards

WD: Temporal changes in the causes of WD: Temporal changes in the causes of aoerticaoertic stenosisstenosis: :

A surgical A surgical patholologicpatholologic study of 645 cases. Mayo study of 645 cases. Mayo ClinClin

Proc 62;119, 1987Proc 62;119, 1987 1818


Long Asymptomatic PeriodLong Asymptomatic Period

Rx w/ statins and ACE inhibitorsRx w/ statins and ACE inhibitors

SurvivalSurvival

5 years after 5 years after

onset of onset of ANGINA*ANGINA*


onset of onset of SYCOPESYCOPE


onset of onset of CHF*CHF*

Sudden Death!Sudden Death!

***Caution when using nitrates to ***Caution when using nitrates to treat angina or CHF****treat angina or CHF****

1919

Anatomy of ASAnatomy of AS

VALVE AREA GRADIENTVALVE AREA GRADIENT(cm(cm22)) (mm Hg)(mm Hg)

Normal :Normal : 3 3 00

Mild (Stage 1)Mild (Stage 1) >1.5 >1.5 0 0 -- 20 20

Moderate (Stage 2)Moderate (Stage 2) 1.0 1.0 -- 1.5 1.5 20 20 –– 4040

Severe (Stage 2) Severe (Stage 2) < 1.0 < 1.0 >40>40

Critical (Stage 3)Critical (Stage 3) < 0.75< 0.75

Jet Flow > 4.5 m/sec or an Jet Flow > 4.5 m/sec or an ↑↑0.3 m/sec/year or 0.3 m/sec/year or

LV EF < 50%LV EF < 50%

2020

Pathophysiology of Aortic StenosisPathophysiology of Aortic Stenosis

Aortic Stenosis

Obstruction to LV Ejection

Chronic LV Pressure Overload�Parallel Replication of Sarcomeres

Concentric LV Hypertrophy

Pressure Gradient Created Across the Valve

2121

Pathophysiology of ASPathophysiology of AS

Concentric Hypertrophy (normal chamber size)Concentric Hypertrophy (normal chamber size)

Decreased ComplianceDecreased Compliance

�� ↑↑ LVEDPLVEDP

�� ↑↑ Reliance on atrial kick (40% of LVEDV)Reliance on atrial kick (40% of LVEDV)

CO and EF are initially normal (donCO and EF are initially normal (don’’t let this fool you!)t let this fool you!)

Very Vulnerable to IschemiaVery Vulnerable to Ischemia�� ↑↑ Demand d/t Demand d/t ↑↑ muscle mass and wall tensionmuscle mass and wall tension

�� ↓↓ Supply d/t Supply d/t ↓↓ diastolic time and diastolic time and ↑↑ LVEDPLVEDP�� ↑↑ HR can be disastrousHR can be disastrous

�� Maintaining diastolic BP is essentialMaintaining diastolic BP is essential

�� CPR is often ineffectiveCPR is often ineffective

2222

2323

Acute AS the Pressure -Volume LoopAcute AS the Pressure -Volume Loop

2424

Pressure Gradient

Across the Valve

Pressure Gradient

Across the Valve

2525

Physical FindingsPhysical Findings

�� Mid systolic Mid systolic

�� Ejection murmur Ejection murmur

�� RSB, 2nd ICSRSB, 2nd ICS

ECG ECG –– LVHLVH

2626

MonitoringMonitoring

ECG:ECG: LVHLVH

AA--Line:Line:

�� Slow upstroke Slow upstroke �� pulsuspulsustardustardus

�� Late peak w/ loss of the Late peak w/ loss of the dicroticdicrotic notch causing a notch causing a narrow pulse pressure narrow pulse pressure ��pulsuspulsus parvusparvus

PAPPAP waveformwaveform

�� Great beat to beat respiratory Great beat to beat respiratory variationvariation

Echo: Echo:

�� Narrowed orifice (causing jet)Narrowed orifice (causing jet)

�� LVHLVH

2727

Homodynamic GoalsHomodynamic Goals

PP-- Full: adequate intravascular volume to fill Full: adequate intravascular volume to fill noncompliant ventricular chambernoncompliant ventricular chamber

AA-- Already elevated, but relatively fixed; coronary Already elevated, but relatively fixed; coronary

perfusion pressure must be maintainedperfusion pressure must be maintained

CC-- Usually not a problem; inotropes may be helpful Usually not a problem; inotropes may be helpful

preinduction in endpreinduction in end--stage AS with hypotensionstage AS with hypotension

RR-- Not too slow (Not too slow (↓↓↓↓↓↓↓↓ CO), not too fast (ischemia)CO), not too fast (ischemia)

RhyRhy-- Sinus!! Cardioversion if hemodynamic crash fromSinus!! Cardioversion if hemodynamic crash from

supraventricular dysrhythmiasupraventricular dysrhythmia

MVO2MVO2-- Ischemia is an everIschemia is an ever--present risk; tachycardia andpresent risk; tachycardia and

hypotension must be avoidedhypotension must be avoided2828

HEMODYNAMIC GOALSHEMODYNAMIC GOALS

PA pressures remain relatively PA pressures remain relatively

normal until endnormal until end--stage aortic stage aortic

stenosis.stenosis.

MaintainMaintainPVRPVR

Afterload is elevated, but relatively Afterload is elevated, but relatively

fixed; coronary perfusion pressure fixed; coronary perfusion pressure

must be maintained. must be maintained.

Avoid hypotension.Avoid hypotension.

IncreasedIncreasedSVRSVR

Usually not a problem; Usually not a problem; inotropesinotropes may may

be helpful be helpful preinductionpreinduction in endin end--stage stage

aortic stenosis with hypotension.aortic stenosis with hypotension.

MaintainMaintainContractilityContractility

Avoid extremes of HR.Avoid extremes of HR. Decreased CO Decreased CO

with very slow HR, ischemia with with very slow HR, ischemia with

fast HR. Maintain Sinus Rhythm.fast HR. Maintain Sinus Rhythm.

Slow NormalSlow Normal

SinusSinusHeart RateHeart Rate

Need increased preload to fill Need increased preload to fill

noncompliant LV.noncompliant LV.IncreasedIncreasedPreloadPreload

2929

Anesthetic TechniqueAnesthetic Technique

RegionalRegional

�� Maintain filling pressureMaintain filling pressure

�� Keep diastolic BP upKeep diastolic BP up

�� Adequate pain control (avoid tachycardia)Adequate pain control (avoid tachycardia)

GeneralGeneral

�� Etomidate and primary narcotic techniqueEtomidate and primary narcotic technique

�� Low dose inhalation Low dose inhalation

�� Junctional rhythm is a distinct disadvantageJunctional rhythm is a distinct disadvantage

3030


Repair: rarely possibleRepair: rarely possible

Replacement:Replacement:

BioprosthesisBioprosthesis

Porcine( pig valve) orPorcine( pig valve) or

Bovine (cow pericardium sewn Bovine (cow pericardium sewn on frame)on frame)�� No anticoagulationNo anticoagulation

�� Lasts 10Lasts 10--20 years20 years

MechanicalMechanical�� Require anticoagulationRequire anticoagulation

�� Careful antibiotic prophylaxisCareful antibiotic prophylaxis

�� Lasts a lifetimeLasts a lifetime

Other OptionsOther Options�� HomograftsHomografts (cadaver valves)(cadaver valves)

�� Ross Procedure (Pulmonary Valve placed in Aortic Position)Ross Procedure (Pulmonary Valve placed in Aortic Position)

�� PercutaneousPercutaneous AVRAVR

3131

Hypertrophic Cardiomyopathy

(HCM)

Hypertrophic Cardiomyopathy

(HCM)

AKA:AKA:

HOCM: HOCM:

Hypertrophic Obstructive Hypertrophic Obstructive

CardiomyopathyCardiomyopathy

IHSS: IHSS:

Idiopathic Hypertrophic Idiopathic Hypertrophic

SubaorticSubaortic StenosisStenosis

3232

HOCMHOCM

3333

HCMHCM

Etiology: Etiology: �� Genetic (mutation of the BGenetic (mutation of the B--myacinmyacin heavy chain)heavy chain)

�� Most common genetically transmitted CVDMost common genetically transmitted CVD

�� Leading Cause of Death in Athletes < 35Leading Cause of Death in Athletes < 35

Natural HistoryNatural History�� LVH in septum, apex and LVH in septum, apex and midventricalmidventrical (> 30 mm)(> 30 mm)

�� Not all patients are at equal risk, family Not all patients are at equal risk, family hxhx of sudden of sudden

death or documented obstruction are death or documented obstruction are ↑↑↑↑↑↑↑↑ riskriskriskriskriskriskriskrisk�� SxSx include: syncope, dyspnea, palpitations, PND, CHF, fatigueinclude: syncope, dyspnea, palpitations, PND, CHF, fatigue

�� MR causes LA enlargement making the patient prone to AMR causes LA enlargement making the patient prone to A--fibfib

�� SxSx worsen with worsen with ↑↑ HR, HR, ↓↓ preload, hypotension, PPV, and peeppreload, hypotension, PPV, and peep

�� Obstruction is worse with MR caused by SAM ( systolic Obstruction is worse with MR caused by SAM ( systolic anterior motion of the mitral valve)anterior motion of the mitral valve)

3434

HCM- Medical ManagementHCM- Medical Management

MedicationsMedications--�� Beta blockers to control HR and Beta blockers to control HR and ↓↓ outflow obstructionoutflow obstruction

�� Ca channel blockers to improve ventricular filling and Ca channel blockers to improve ventricular filling and ↓↓ ischemiaischemia

�� Disopyramide to Disopyramide to ↓↓ contractilitycontractility

�� Amiodarone for atrial dysrhythmiasAmiodarone for atrial dysrhythmias

ProceduresProcedures--�� Ethanol ablation of septal perforatorsEthanol ablation of septal perforators

�� AICDAICD

�� Asynchronous RV Asynchronous RV prexcitationprexcitation biventricular pacingbiventricular pacing

3535

Septal MyectomySeptal Myectomy

3636

Hemodynamic Goals in HOCMHemodynamic Goals in HOCM

3737

HOCM: HEMODYNAMIC GOALSHOCM: HEMODYNAMIC GOALS

Usually not a problem.Usually not a problem.MaintainMaintainPVRPVR

Increased afterload reduces the Increased afterload reduces the

gradient across LVOT.gradient across LVOT. Thickened Thickened

myocardium requires increased myocardium requires increased

diastolic BP.diastolic BP.

IncreasedIncreasedSVRSVR

Decreased contractility reduces Decreased contractility reduces

gradient across LVOT.gradient across LVOT. BetaBeta--

blockade is beneficial.blockade is beneficial.

DecreasedDecreasedContractilityContractility

Decreased HR reduces oxygen Decreased HR reduces oxygen

demand of thickened myocardium. demand of thickened myocardium.

May also allow time for adequate LV May also allow time for adequate LV

filling.filling.

DecreasedDecreasedHeart RateHeart Rate

Increased preload reduces the Increased preload reduces the

gradient across LVOT. Avoid gradient across LVOT. Avoid

hypovolemia.hypovolemia.

IncreasedIncreasedPreloadPreload

3838

SAMSAMIntraoperative

transesophageal

echocardiography

images

demonstrating systolic anterior

motion of the

anterior mitral

valve leaflet (upper

right panel) and an interleaflet gap

(lower left panel)

through which a jet

of mitral

regurgitation (lower

right panel) is centrally directed

into the left atrium

3939

Aortic InsufficiencyAortic Insufficiency

4040

Etiology of AIEtiology of AI

Congenital: (rarely an isolated lesion)Congenital: (rarely an isolated lesion)

Acquired:Acquired:�� AcuteAcute

•• Infective endocarditisInfective endocarditis

•• Dissections of the thoracic aorta d/t Dissections of the thoracic aorta d/t MarfanMarfan’’ss or thoracic or thoracic traumatrauma

�� ChronicChronic

•• RHD is the most common causeRHD is the most common cause

•• Aortic root Aortic root annuloaortectasiaannuloaortectasia from from

•• AgingAging

•• Chronic HTN Chronic HTN

•• Connective tissue disorders Connective tissue disorders

•• Appetite suppressant meds (Appetite suppressant meds (fenfluraminefenfluramine))

4141

Natural History of AINatural History of AI

AcuteAcute�� Sudden LV failureSudden LV failure

�� Pulmonary congestionPulmonary congestion

�� Systemic hypotensionSystemic hypotension

ChronicChronic�� Long asymptomatic period (20 years) Long asymptomatic period (20 years)

�� Regurgitant flow Regurgitant flow �� volume overload. volume overload.

•• Volume overload Volume overload �� ↑↑ SV SV �� HTN HTN ��PPressure Overload.ressure Overload.

�� Progressive eccentric hypertrophy of LVProgressive eccentric hypertrophy of LV

�� When failure finally occurs, When failure finally occurs, damage is irreversibledamage is irreversible

�� LV function is both an early and late predictor of LV function is both an early and late predictor of mortality after AVRmortality after AVR

�� Survival after Survival after sxsx begin is 5begin is 5--10 years10 years

4242

Anatomy: AV Incompetence Anatomy: AV Incompetence

Angina, CHF,Angina, CHF,

Irreversible LV Irreversible LV

dysfunctiondysfunction

>60%>60%4+4+Severe Severe

(wide open)(wide open)

Dyspnea & Dyspnea &

CHFCHF4040--60%60%2+ 2+

3+3+

ModerateModerate

MinimalMinimal< 40%< 40%1+1+MildMild

SymptomsSymptomsRegurgitantRegurgitant

FractionFraction

GradeGradeClassificationClassification

4343 4444

Pathophysiology of Aortic RegurgitationPathophysiology of Aortic Regurgitation

Backward flow of blood from aorta into LV (Diastolic)

Increased LV volume

and pressure

Increased SV (Frank-Starling Mechanism)

Peak systolic pressure increased because of

increased SV ejected into aorta

Increased diastolic wall-tension produces eccentric hypertrophy

Rapid fall of aortic pressure during diastole

Increased pulse pressure

Increased LA pressure

Increased pulmonary

venous pressure

Pulmonary edema

4545

Pressure Volume RelationshipPressure Volume Relationship

4646

Classic Murmur of AI Classic Murmur of AI

Decrescendo diastolic @ 2Decrescendo diastolic @ 2ndnd ICS RSB ICS RSB

4747

Homodynamic GoalsHomodynamic Goals

PP-- Normal Normal -- Full: adequate intravascular volume to fill Full: adequate intravascular volume to fill compliant ventriclecompliant ventricle

AA-- Reduction beneficial with vasodilators or anesthetics;Reduction beneficial with vasodilators or anesthetics;

Increases augment regurgitant flowIncreases augment regurgitant flow

CC-- Usually adequateUsually adequate

RR-- Modest tachycardia reduces ventricular volume, Modest tachycardia reduces ventricular volume, raises aortic diastolic pressureraises aortic diastolic pressure

RhyRhy-- Usually sinusUsually sinus

MVO2MVO2-- Not usually a problemNot usually a problem

4848

AORTIC REGURGITATION:

HEMODYNAMIC GOALS

AORTIC REGURGITATION:

HEMODYNAMIC GOALS

PA pressures remain relatively PA pressures remain relatively

normal except in patients with endnormal except in patients with end--

stage disease.stage disease.

MaintainMaintainPVRPVR

Afterload reduction is helpful in Afterload reduction is helpful in

improving forward flow.improving forward flow.DecreasedDecreasedSVRSVR

Must be maintained.Must be maintained.MaintainMaintainContractilityContractility

Increased HR reduces diastolic time Increased HR reduces diastolic time

and reduces and reduces regurgitantregurgitant fraction.fraction.

Also raises diastolic BP and Also raises diastolic BP and

decreases LVEDP.decreases LVEDP.

IncreasedIncreasedHeart RateHeart Rate

Because of increased LV volumes, Because of increased LV volumes,

need increased preloadneed increased preload to maintain to maintain

forward flow. Avoid hypovolemia.forward flow. Avoid hypovolemia.

IncreasedIncreasedPreloadPreload

4949


��ECGECG

��AA--line: line:

•• Rapid upstroke with low Rapid upstroke with low dicrotic notchdicrotic notch

•• Wide pulse pressure (80Wide pulse pressure (80--100 mmHg)100 mmHg)

•• Double peaked (Double peaked (biferiensbiferiens))

•• BoundingBounding

��CVPCVP

��PA Catheter (giant V wave PA Catheter (giant V wave on wedge trace)on wedge trace)

��TEETEE

•• Grade regurgitant Grade regurgitant fxfx

•• Assess adequacy of repair Assess adequacy of repair or replacementor replacement

5050

Anesthetic ManagementAnesthetic Management

Regional AnesthesiaRegional Anesthesia

�� Afterload reduction reduces regurgitant Afterload reduction reduces regurgitant fxfxand enhances forward flowand enhances forward flow

�� Maintain intravascular volumeMaintain intravascular volume

General AnesthesiaGeneral Anesthesia

�� Use agents that maintain or elevate HRUse agents that maintain or elevate HR

�� Potent agents are OKPotent agents are OK

�� Etomidate/Narcotic technique good for poor Etomidate/Narcotic technique good for poor LVFLVF


5151


Indications:Indications:

�� All symptomatic patientsAll symptomatic patients

�� Asymptomatic patients with Asymptomatic patients with �� LV LV fxfx

Options:Options:

�� Repair with annuloplasty ring or valvular Repair with annuloplasty ring or valvular plicationplication

�� Replace with mechanical or biologic valveReplace with mechanical or biologic valve

�� Experimental Experimental percutaneouspercutaneous AV AV replacementreplacement

5252

Mitral StenosisMitral Stenosis

5353

EtiologyEtiology

CongenitalCongenital

AcquiredAcquired

�� Rheumatic FeverRheumatic Fever (2 (2 xx’’ss as frequent in as frequent in women)women)

�� Sometimes after radiation of the chest Sometimes after radiation of the chest from breast or other CAfrom breast or other CA

�� Rheumatoid Arthritis, lupus or Rheumatoid Arthritis, lupus or carcinoidcarcinoid syndromesyndrome

5454


��Stenosis begins 2 yrs Stenosis begins 2 yrs after RHDafter RHD

��20 yr asymptomatic20 yr asymptomatic

��SxSx begin in 40begin in 40’’ss-- 5050’’ss

��Heart failure is most Heart failure is most common presentationcommon presentation

��40% develop a40% develop a--fibfib

��SxSx develop w/pregnancy, develop w/pregnancy, anemia, infectionanemia, infection

5555

Anatomy of MSAnatomy of MS

VALVE AREA VALVE AREA SYMPTOMSSYMPTOMS(cm(cm22))

Normal :Normal : 44--6 6

Mild (Stage 1)Mild (Stage 1) 1.51.5--2.5 2.5 with exercisewith exercise

Moderate (Stage 2)Moderate (Stage 2) 1.0 1.0 -- 1.5 1.5 mild exertion mild exertion

onset of aonset of a--fibfib

Severe (Stage 3) Severe (Stage 3) < 1.0 < 1.0 at restat rest

5656

Pathophysiology of MSPathophysiology of MS

�� LV LV fxfx usually maintained (15% LV dysfunction)usually maintained (15% LV dysfunction)

�� PG = PG = (Cardiac Output)(Cardiac Output)22

Diastolic Filling TimeDiastolic Filling Time

�� AA--fib fib →→ ��PG (2PG (2o rapid HR) → pulmonary edema

� Pulmonary HTN (80%)

� 5-15 x’s ↑ In PVR

� V/Q mismatches (reversal in normal apex to base perfusion gradient)

5757

Pathophysiology of Mitral StenosisPathophysiology of Mitral Stenosis

Obstruction to LA emptying

Increased LA pressure

Increased LA size

Atrial fibrillation

Increased pulmonary artery pressure

Decreased LV filling

RV overload

Increased pulmonary venous pressure

Pulmonaryedema

5858

5959

Pressure Volume RelationshipsPressure Volume Relationships

6060

Pressure Volume LoopPressure Volume Loop

6161

Murmur MSMurmur MS

Diastolic rumbling murmur Diastolic rumbling murmur

Heard best at the apexHeard best at the apex

6262

Hemodynamic Goals MSHemodynamic Goals MS

PP-- Enough to maintain flow across stenosisEnough to maintain flow across stenosis

AA-- Avoid Avoid ↑↑↑↑↑↑↑↑ RV afterload (pulmonary vasoconstrictors)RV afterload (pulmonary vasoconstrictors)

? ? inotropesinotropes for systemic hypotensionfor systemic hypotension

CC-- LV usually OK until after CPB; right ventricle may beLV usually OK until after CPB; right ventricle may be

impaired if there is longimpaired if there is long--standing pulmonary standing pulmonary hypertensionhypertension

RR-- Slow to allow time for ventricular fillingSlow to allow time for ventricular filling

RhyRhy-- Often atrial fibrillation; control ventricular responseOften atrial fibrillation; control ventricular response

MVO2MVO2-- Not a problemNot a problem

CPBCPB-- Vasodilators may help post CPB RV failure; control ofVasodilators may help post CPB RV failure; control of

ventricular response may be difficultventricular response may be difficult

6363

Hemodynamic GoalsHemodynamic Goals

Avoid TachycardiaAvoid Tachycardia

�� Continue/Administer meds that control HRContinue/Administer meds that control HR

�� Treat new onset A fib aggressively (control ventricular rate)Treat new onset A fib aggressively (control ventricular rate)

Avoid Exacerbations of PHTAvoid Exacerbations of PHT

�� Avoid hypoxia, Avoid hypoxia, hypercarbiahypercarbia and acidosisand acidosis

�� Avoid NAvoid N22OO

�� Avoid trendelenburg positionAvoid trendelenburg position

�� Rx PHT w/ hypocapnia, NTG, and Nitric OxideRx PHT w/ hypocapnia, NTG, and Nitric Oxide

�� Watch for RV failure and consider Watch for RV failure and consider MilrinoneMilrinone

Maintain adequate intravascular volumeMaintain adequate intravascular volume

Treat hypotension with volumeTreat hypotension with volume (vasoconstrictors can worsen (vasoconstrictors can worsen PHT)PHT)

Early use of inotropes if neededEarly use of inotropes if needed

6464


EKGEKG

AA--lineline

Pa Pa CathCath

�� PCWP or LAP will be > LVEDPPCWP or LAP will be > LVEDP

�� With tachycardia, LAP With tachycardia, LAP �� while LVEDP while LVEDP ��

TEETEE

�� Check adequacy of repairCheck adequacy of repair

�� Check for leaksCheck for leaks

�� Check for regurgitation after Check for regurgitation after commissurotomycommissurotomy

6565


RegionalRegional

�� Caution d/t residual anticoagulationCaution d/t residual anticoagulation

�� Avoid hypotension. Avoid hypotension.

�� Position for adequate ventilationPosition for adequate ventilation


GeneralGeneral

�� Consider Etomidate/narcotic technique for PHT or Consider Etomidate/narcotic technique for PHT or severe LVsevere LV

�� Inhalation agents OK Inhalation agents OK except Nexcept N22OO

�� Avoid agents that Avoid agents that �� HRHR


6666


CommissurotomyCommissurotomy--fused leaflets are separatedfused leaflets are separated

DecalcificationDecalcification

Replacement with bioprosthetic or mechanical valveReplacement with bioprosthetic or mechanical valve

If full sternotomyIf full sternotomy-- Maze or Pulmonary Vein Isolation Maze or Pulmonary Vein Isolation to treat Ato treat A--fibfib

Left atrial appendage ligation or resectionLeft atrial appendage ligation or resection

AA--fib treated with radiofrequency (heat) ablation or fib treated with radiofrequency (heat) ablation or cryotherapycryotherapy (freeze) ablation(freeze) ablation

6767

Mitral Insufficiency

or Regurgitation

Mitral Insufficiency

or Regurgitation

6868

Etiology of MREtiology of MR

CongenitalCongenital--rarerare

AcquiredAcquired-- both acute and chronicboth acute and chronic

�� RHDRHD-- rarerare

�� Most commonly encountered valve lesionMost commonly encountered valve lesion

�� Mitral Valve Prolapse (MVP)Mitral Valve Prolapse (MVP)•• Most common causeMost common cause

•• 15% will develop chronic MR15% will develop chronic MR

�� ChronicChronic•• LVH w/ annular dilation (eccentric hypertrophy)LVH w/ annular dilation (eccentric hypertrophy)

•• MVPMVP

•• MyxomatousMyxomatous degenerationdegeneration

•• FenfluramineFenfluramine appetite suppression appetite suppression

�� AcuteAcute•• Papillary muscle dysfunctionPapillary muscle dysfunction

•• Ruptured chordea Ruptured chordea tendineatendinea (most often (most often d/td/t ischemia)ischemia)

•• Bacterial endocarditisBacterial endocarditis

6969


��VariableVariable

��Long asymptomatic period Long asymptomatic period

w/ eccentric hypertrophy of w/ eccentric hypertrophy of

LA and LVLA and LV

��SxSx of forward heart failure of forward heart failure

develop (fatigue, weakness)develop (fatigue, weakness)

��Dysfunction is significant if Dysfunction is significant if

EF is EF is ≤≤ 50%50%

7070

Anatomy: MV Incompetence Anatomy: MV Incompetence

CHF,CHF,

Irreversible LV Irreversible LV

dysfunctiondysfunction

>60%>60%4+4+Severe Severe

(stage 3)(stage 3)

Fatigue, Fatigue,

weakness, CHFweakness, CHF3030--60%60%2+2+--3+3+Moderate Moderate

(stage 2)(stage 2)

MinimalMinimal< 30%< 30%1+1+Mild Mild

(stage 1)(stage 1)

SymptomsSymptomsRegurgitantRegurgitant

FractionFraction

GradeGradeClassificationClassification

7171

PathophysiologyPathophysiology

Chronic MRChronic MR

�� LV volume load LV volume load →→ eccentric hypertrophyeccentric hypertrophy

�� Regurgitant volume determined by Regurgitant volume determined by atrial/ventricular pressure gradientatrial/ventricular pressure gradient

�� Ventricular size directly correlates with annulus Ventricular size directly correlates with annulus sizesize

�� Vasodilators may improve hemodynamics (Vasodilators may improve hemodynamics (�� LV LV size)size)

�� Patients with Patients with sxsx have underlying LV dysfunctionhave underlying LV dysfunction

Acute MRAcute MR

�� LAP and PAP LAP and PAP �� →→ pulmonary edema and RHFpulmonary edema and RHF

�� In Acute MI w/ MR In Acute MI w/ MR →→ ischemia is usually present ischemia is usually present and survival is poorand survival is poor

7272

7373

Pathophysiology of Mitral RegurgitationPathophysiology of Mitral Regurgitation

Backward flow of blood from LV to LA (Systolic)

Increased LA volume and

pressure

Increased LV filling(Increased LVEDV)

Increased SV

Blood ejected into aorta

Left atrial enlargement

Increased pulmonary

venous pressures

Pulmonaryedema

7474

Pressure Volume RelationshipPressure Volume Relationship

7575

Pressure Volume Loop in Chronic MRPressure Volume Loop in Chronic MR

7676

Murmur (Pansystolic or Holosystolic)Murmur (Pansystolic or Holosystolic)

7777

Hemodynamic Goals In MRHemodynamic Goals In MR

7878

Hemodynamic ConsiderationsHemodynamic Considerations

�� Mild TachycardiaMild Tachycardia

�� Low SVR (peripheral venodilation)Low SVR (peripheral venodilation)

�� ExceptionException: in patients with MVP who : in patients with MVP who

have redundant leaflets because have redundant leaflets because

higher HR and Low SVR will cause higher HR and Low SVR will cause

more obstruction to flowmore obstruction to flow

7979


��EKGEKG

��AA--lineline

��CVPCVP

��PA PA CathCath-- classic classic

giant V wavegiant V wave

��TEETEE

8080


RegionalRegional-- benefits from benefits from �� afterloadafterload

GeneralGeneral

�� Inhalation/STP is OK for normal LVInhalation/STP is OK for normal LV

�� Etomidate/Narcotic for impaired LVEtomidate/Narcotic for impaired LV

8181


““Mini Mitral Valve RepairMini Mitral Valve Repair”” (Cosgrove Ring for (Cosgrove Ring for AnnuloplastyAnnuloplasty))

Robotically Assisted MV repair or Robotically Assisted MV repair or replacementreplacement

PercutaneousPercutaneous mitral valve repair (Emitral valve repair (E-- Valve)Valve)

Repair flail leaflet, Chordae or papillary Repair flail leaflet, Chordae or papillary musclemuscle

Replacement with biologic or mechanical Replacement with biologic or mechanical valvevalve

If Full Sternotomy: Maze or PV Isolation for If Full Sternotomy: Maze or PV Isolation for AA--fibfib

8282

8383

Thanks for Your AttentionThanks for Your Attention

A Pleasure and a Privilege!A Pleasure and a Privilege!

Documents

ANESTHETIC In Action!!! - NDANA Heart Disease NDANA 10.12.11.pdfPhysiology In Action!!! Physiology 3 Anesthetic Management of Valvular Heart Disease ... • Connective tissue disorders