Download Anaesthesia For Valvular Heart Diseases

Anaesthesia For Valvular Heart
Diseases
Made by: Dr. Meenal Aggarwal
Moderator: Dr. Aparna
Introduction
• Valvular ds: An increased burden on L or R ventricle
• Could be:
 Pressure overload (Stenotic lesions)
 Volume overload (Regurgitant lesions)
• Initially tolerated d/t compensatory mechanisms
Eventually cardiac muscle dysfunction
CHF ; even sudden death
Preoperative Assessment
• Aim: to know
 Severity of Disease
 Degree of impaired myocardial contractility
 Presence of assoc. organ system diseases
• O/H: Symptoms:
 Dyspnea, orthopnea, easy fatiguability
(Impaired myocardial contractility)
 Anxiety, diaphoresis, resting tachycardia
(Compensatory increase in sympathetic activity)
 Angina (d/t assoc CAD, or inc. myocardial O2 demand)
• Drug therapy:
 Beta Blockers
 Digitalis
Control HR (AS & MS: Allows diastolic filling)
 ACE inhibitors
 Vasodilators
Control BP and so dec. afterload (AR, MR)
 Diuretics
 Ionotropes
 Antiarrhythmic drugs
Control of CHF
• O/E: Signs:
 Inspection: Raised JVP
 Auscultation: Basilar chest rales, S3, Murmurs
Murmurs: D/t turbulent flow across the defective valve
o Note: character, location, intensity, direction of radiation
o Systolic murmurs: AS, PS or MR,TR
o Diastolic murmurs: MS, TS or AR, PR
 Dysrhythmias: AF (esp Mitral valve ds.) i.e. with enlarged Lt
atria
• Lab Investigations:
 CXR:
o Size & shape of heart & great vessels
o Pulmonary markings
o Enlarged LA (Elevated Lt main bronchus, calcified valve)
 ECG:
o Lt or Rt axis deviation (Lt or Rt ventricle hypertrophy)
o P mitrale (Broad notched P wave in Mitral valve ds.)
o Dysrhythmias
o Conduction abnormalities
o Evidence or active ischemia or previous MI
 Echo with doppler:
o Evaluating significance of murmurs
o Detection of antomical defects (Hypertrophy, chamber
size, valve area)
o Functional defects (Transvalvular pressure gradient,
magnitude of valvular regurgitation)
 Cardiac Catheterisation: Solves discrepancies b/w clinical
and echo findings
o Presence & severity of stenosis or regurgitation
o Intracardiac shunting
o CAD
•
Transvalvular pressure gradient (TVPG) (Severe MS when >
10mmHg, Severe AS when > 50 mm Hg)
•
Pulmonary artery pressures (Pulmn HT)
Assessment of Prosthetic Valve function:
•
Dysfunction (Change in intensity/ quality of clicks, new or
change in characteristics of murmurs)
 Tranthoracic Echo: To assess ring stability and leaflet motion
 Transesophageal Echo: Better resolution
 MRI: For prosthetic valve regurg, paravalvular leak
 Cardiac Catheterisation: For TVPG, Effective valve area
• Complications of prosthetic valves:
Risk of thromboembolism (Anticoagulation)
Subclinical intravascular hemolysis
Risk of endocarditis (AB)
• Management of anti coagulation:
Can be continued in minor surgery with min blood loss
For major surgery (Stop warfarin 3-5 days preop, UF
heparin or LMWH started & continued upto day/ day before
of surgery, restarted post op)
Avoid elective surgery with in 1 month after an acute
thromboembolic episode
 In pregnancy (TE prophylaxis to continue, S/C LMWH given +
low dose aspirin)
• Prophylaxis of Bacterial endocarditis:
 Infection likely from frequent exposure to bacteremia
 Weigh Risk to benefit ratio (AB resistance)
 Prophylaxis given to following pts:
1. Prosthetic material for cardiac valve repair
2. Previous IE
3. CHD: Unrepaired CHD, Completely repaired with prosthetic
material (during 1st 6 months after procedure), Repaired
defects with residual defect)
4. Cardiac transplant pt who develop valvulopathy
 AB prophylaxis not required for GU or GIT procedure
 Required for skin incision/ Biopsy or Resp tract invasive procedure
 For dental procedures (manipulation of gingiva, Mucosa)
MITRAL STENOSIS:
•
Most common cause RHD
•
Primarily affects females
•
Diffuse thickening of mitral leaflets & subvalvular apparatus,
Calcification
•
Gradual progression (over 20-30 yrs)
•
Other causes: Carcinoid syndrome, LA myxoma, Severe
mitral annular calcification, RA, thrombus formation, SLE,
congenital
Decreased mitral valve orifice
Mechanical obstruction to LV diastolic filling
Dec LV volume
Dec S.V.
Inc LA volume & pressure
Inc Pulmn Venous Pressure
RV Hypertrophy & failure
Overt Pulmn Edema
Pathophysiology of Mitral Stenosis
• Diagnosis:
Clinical signs: opening snap (in early diastole), rumbling
diastolic heart murmur
Venous thrombosis (stasis, decreased activity)
CXR:
-LA enlargement (straightening of left heart border,
elevation of left main stem bronchus, double density of LA)
-Mitral calcification
-Evidence of pulmn congestion
ECG: Broad notched P wave (P mitrale), AF
Echo: (Anatomical details: Leaflet thickening, calcification,
changes in mobility, chamber dimension, thrombus)
Severity assessed by:
- Mitral valve area, TVPG
Also for Pulmn HT, Ventricular function
• Treatment:
 Mild MS: Diuretics
 In AF: Beta blockers, Ca #, Digitalis (H.R. control)
Anticoagulants (Warfarin to get INR of 2.5 to 3)
 Surgical correction:
• Percutaneous valvotomy
• Valve reconstruction
• Valve replacement, surgical commisurotomy
• Management of Anaesthesia:
Avoid tachycardia (prevents filling)
Avoid decrease in SVR (use vasopressors which avoid
Tachycardia)
Do no permit volume overload (can ppt CHF)
Prevent hypercarbia & hypoxemia, lung hyperinflation
(Worsen Pulmn HT)
If RVF : Requires ionotropic support & pulmonary
vasodilators
• Premedication: decrease anxiety (watch for resp depression),
Continue drugs for HR control, Treat diuretic induced hypoK+
Anticoagulant therapy (acc to minor or major procedure),
coagulation tests for regional anaesthesia
• Induction: I/V agents (except ketamine), MR (which doesn’t Inc
HR or Dec BP d/t histamine release)
• Maintenance: Min effect on HR, SVR & PVR, contractility (N2O+
opioid+ Low conc Volatile agents)
Reversal achieved slowly (to avoid tachycardia d/t glyco/atropine)
Prevent light plane of anaesthesia (symp stimulation)
Pulmonary vasodilator may be required
Careful fluid replacement intraop (risk of Pulmn edema)
• Monitoring: In asymptomatic (routine)
Symptomatic/ major surgery (Intraarterial pressure
monitoring, Pulmonary artery pressure, LA pressure: at
higher risk of rupture of pulmn A so done carefully and less
frquently, TEE)
• Post operative management:
Prevent fluid overload
Manage pain (to prevent tachycardia, hypoventilation so
hypoxia), neuraxial opioids
May require mechanical ventilation (thoracic surgery)
MITRAL REGURGITATION:
•
In RHD, usually assoc with MS
•
Other causes: Papillary muscle dysfxn, mitral annular dilatation,
rupture of chordae tendinae, endocarditis, MVP, Congenital
•
Pathophysiology:
Regurgitation into LA
Dec LV stroke volume
LA volume overload
Pulmn congestion
LA enlargement & AF
•
Regurgitant fraction depends on:
 Size of valve orifice
 Heart rate
 Pressure gradient across MV (SVR)
•
When MR develops gradually: LV becomes more compliant
•
When acute MR: No compensation, sudden sever Dec in S.V. l/t
cardiogenic shock, with pulmn congestion
•
When MR+ MS : both volume and pressure overload
Diagnosis:
•
O/E: holosystolic apical murmur, radiation to axilla
•
CXR: Cardiomegaly (LA & LV hypertrophy)
Diagnosis cont…
•
ECG: Lt axis deviation
•
Echo: Confirms MR, Anatomy (LA size, LV wall thickness, cavity
dimension), S.V., LA appendage for thrombus
•
Doppler: Severity assessment (Calculation of regurgitant
volume and fraction), area of regurgitant jet
•
Pulmn A. Occ. Pressure: Shows a ‘V’ wave in the waveform
signifies regurgitation
•
Cardiac catheterisation: If surgery planned or severity doubtful
•
Coronary angiography: In elderly patients
Treatment:
•
Surgical:
 Mitral valve repair (preferred as apparatus preserved)
 Mitral valve replacement
Survival increased by surgery of performed before LVEF < 60%, or
before End systolic LV dimension >= 45mm
Patients who do not improve with surgery:
* LVEF < 30% * LV end systolic dimension > 55mm
•
Medical :
 Vasodilators (Acute MR)
 Beta #, ACE inhibitors
 Biventricular pacing
Management of Anaesthesia:
•
Prevent events which Dec C.O.
•
Maintain N to slightly higher H.R.
•
Vasodilators to dec afterload
•
Ionotropes to improve LV contraction
Induction:
•
I/V agent used
•
MR (pancuronium beneficial- raises HR)
Maintainence:
•
Inhalational agents (Dec rise in BP & SVR caused by surgical
stimulation) iso, des, sevo
•
Opioids (when severely compromised myocardial function)
•
Mechanical ventilation (allow venous return)
•
Maintain I/V volume
Monitoring:
•
Asymptomatic / minor surgery (no invasive monitoring)
•
Severe MR (Pulmn A. Catherisation V wave)
MITRAL VALVE PROLAPSE:
•
Prolapsed one/ both mitral leaflets into LA during systole
•
M.C. form of valvular ds. (young women)
•
With or Without MR
•
Causes: Marfan’s, RHD, Myocarditis, thyrotoxicosis, SLE
Diagnosis:
•
Usually benign, but can l/t IE, cerebral embolisation, Severe
MR, Severe dysrrhythmias, sudden death
•
C/F: Palpitation, anxiety, orthostatic symptoms, dysnea, fatigue,
atypical chest pain
•
Echo: valve prolapse of 2mm or more above mitral annulus
With/ without leaflet thickening (elderly/connective ts. ds)
Functional form (mild bowing)
Management of Anaesthesia:
•
Influenced by degree of MR
•
Basis: Larger LV will have lesser prolapse
•
Inc sympathetic activity
•
Dec SVR
•
Upright posture
•
hypovolemia
Increase MR
•
Inc LV vol will Dec MVP (HTN/ Vasoconst, drug induced
myocardial depression, volume resuscitation)
Preoperative Evaluation:
•
Differentiate functional MVP from significant MR
•
Usually< 45 y, female
•
Beta blocker for arrhythmias (continued)
•
If H/O Transient neurological event with sinus rhythm, no atrial
thrombi (pt usually on aspirin 81-325mg/d)
•
Pt with AF &/or with atrial thrombi or previous stroke (usually on
warfarin)
•
ECG changes (PVC’s, QT prolongation) no implication
•
Pt may have systolic clicks, murmur even without symptoms (no
need of cardio consultation)
•
In older men (MVP can present with CHF) pt on diuretics, ACE inh
Anaesthesia technique:
•
When LV function normal, tolerates both GA & regional
Induction:
•
I/V agent (assess need to avoid dec in SVR)
•
Etomidate (min Myocardial depression)
•
Ketamine not to be used (Enhances LV emptying so inc MR)
Maintenance:
•
Minimize sympathetic nervous system activity d/t surgical stimuli
•
Volatile anaesthetics with N2O +/- Opioids
•
Low dose: 0.5 MAC (iso, des, sevo) in significant MR
•
Any MR (keep in mind vagolytic/ histamine induced effects)
•
Unexpected ventricular arrhythmias can occur intra op (Beta
blocker or lignocaine)
•
Proper fluid balance
•
Vasopressors may be required
•
Avoid controlled hypertension technique (increases MVP)
Monitoring:
•
Routine
•
Significant MR/ LV dysfunction (Pulmn A. catheter)
AORTIC STENOSIS:
•
Degeneration & calcification of leaflets (ageing), then stenosis
•
Causes : Elderly, Bicuspid Aortic Valve
•
N valve area: 2.5-3.5 cm2
•
Almost always assoc with some AR
•
Angina may occur despite absence of CAD (Inc myocardial
demand, dec supply)
•
Syncope (fall in SVR can’t be compensated by inc C.O.)
Diagnosis:
•
C/F: angina, syncope, dyspnea on exertion
•
O/E: Systolic murmur best heard in aortic area (be careful as
mostly patients undiagnosed)
•
CXR: Prominent ascending aorta
•
ECG: LV hypertrophy
•
Echo with doppler: Bileaflet aortic valve, thickening/ calcification
of aortic valve, decreased mobility, LV hypertrophy
•
Echo cont…
Valve area, TVPG
•
Cardiac Catheterisation
•
Coronary Angiography
•
Exercise stress testing for Asymptomatic patients
Treatment:
•
Asymptomatic: Continue medical therapy (delay Surgery untill s/s
appear)
•
Aortic Valve replacement
•
Coronary revascularisation (if co-existant CAD)
•
Percutaneous aortic balloon valvuloplasty
Management of Anaesthesia:
•
Maintain N sinus rhythm
•
Avoid bradycardia/ tachycardia
•
Avoid hypotension (if occurs aggressive Tt required)
•
Optimise I/V fluid volume
CPR is generally ineffective in AS (Not enough CO generated)
Induction:
•
GA preferred (regional causes Hypotension)
•
I/V agents used (ones which do not dec SVR)
•
If LV function compromised opioid induction
Maintenance:
•
Avoid drugs which suppress S.A.node (if occurs give atropine/
glyco/ ephedrine)
•
If persistent tachycardia use esmolol
•
In supravent. tachycardias cardioversion to be done
•
Chanced of VT present (Lidocaine & defib)
•
If LV dyfxn (avoid drugs depressing myocardial contractility)
•
NM blocker with min hemodynamic effects
•
I/V fluid vol to be maintained
Monitoring:
•
ECG, Intraarterial cath, P.A. cath, TEE
AORTIC REGURGITATION:
•
Causes: IE, RF, Bicuspid aortic valve, ds of root of aorta
•
Magnitude of regurgitation depends on:
 Time available for regurgitation (H.R. dependent)
 Pressure gradient across the valve (SVR dependent)
Diagnosis:
•
C/F: Dysnea, orthopnea, fatigue, coronary ischemia
•
O/E: Diastolic murmur (Lt sternal border), bounding pulses, wide
pulse pressure, Austin Flint murmur (low pitched diastolic
murmur)
•
CXR & ECG: LV enlargement & hypertrophy
•
Echo: LVEF & ESV, Severity of regurgitation (on doppler)
•
Cardiac cath & MRI
Treatment:
•
Surgical:
 Replacement (even in asymptomatic) Immediate surgery in
acute AR (as l/t sudden heart failure)
 Ross procedure (Pulmonic valve autograft)
 Valve reconstruction
•
Medical:
 Vasodilators (Nitroprusside)
 Ionotropes (Dobutamine)
 Long term Nifedipine/ Hydralazine
Management of Anaesthesia:
•
Avoid bradycardia (HR above 80/min), use atropine
•
Avoid inc in SVR
•
Minimize myocardial depression
•
If LV failure (vasodilators and ionotropes)
•
GA chosen
Induction: I/V agent which doesn’t inc SVR or dec HR
Maintenance: N2O + volatile agent &/or opioid
•
Iso, Des, Sevo good (inc HR, dec SVR, min myo depression)
•
If severe LV dysfunction high dose opioid (caution: bradycardia)
•
NM blocker: Pancuronium useful, modest tachycardia
Monitoring:
•
Minor surgery with asymptomatic ds. (routine)
•
Severe AR:
 Pulmonary A catheter
 TEE
Useful for guiding I/V volume replacement, detecting myocardial
depression, measuring response to vasodilators
TRICUSPID REGURGITATION:
•
Usually functional (d/t RV enlargement or Pulmn HT)
•
IE, Carcinoid, RHD, Ebstein anomaly
•
Mild TR in highly trained athletes
Pathophysiology:
•
Regurgitation through TV  RA vol Overload (but minimal
rise in RA pressure)
O/E: Raised JVP, Hepatomegaly, ascites, edema
Tt: Tt the cause (improve lung fxn, relieve LV failure, dec PHT)
Surgery (rarely for TR alone), Tricuspid annuloplasty/
valvuloplasty/ replacement
Management of Anaesthesia:
•
Keep CVP to high Normal
•
IPPV may decrease venous return
•
Avoid hypoxemia & hypercarbia (to prevent inc Pulmn A.
pressure)
•
N2O: weak Pulmn A. vasoconst (may inc TR)
•
Intra op measurement of RA pressure to guide fluid therapy
•
Very high LA pressure can l/t R L shunt (patent foramen ovale)
TRICUSPID STENOSIS:
•
M.C.cause: RHD (coexiztant TR, Mitral n aortic valve ds)
•
Inc RA pressure & pressure gradient b/w RA & RV
PULMONARY REGURGITATION:
•
Secondary to Pulmn HT
•
Rarely symptomatic
PULMONARY STENOSIS:
•
Usually congenital (detected and treated in early childhood)
•
C/F: Syncope, angina, RV Failure
•
Tt: surgical valvotomy
Thank You