Mitral regurgiattion,MVP & Aortic regurgitation pathophysiology,preoperative assesement, risk indices,preparation,endocarditis prophylaxis,anaesthetic management , MR in pregnancy

1. Presenter: Dr.Naven kumar.S
PG IN Anaesthesiology
Moderator: Dr.Ravi Kumar
Professor ,
JJMMC,Davangere.
22-Apr-14
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2.  Introduction
 MR-pathophysiology
 AR-pathophysiology
 Preop. assessment
 Evaluation
 Guidelines for infective endocarditis
 Anaesthetic implications
 Conclusion
 References
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3.  Definition:- An acquired or congenital disorder of
cardiac valve characterised by stenosis(obstruction) or
regurgitation(backward flow) of blood.
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5. Leakage of blood from the left
ventricle, through the mitral valve, and
into the left atrium, when the left
ventricle contracts, i.e. there is regurgitation of blood back into
the left atrium.
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6.  Acute MR- ischemic heart disease, blunt chest wall trauma, infective
endocarditis, rupture of chordae tendineae.
 Chronic MR:
mitral valve prolapse( M/C cause)
mitral annular calcification
left ventricular hypertrophy,
cardiomyopathy,
myxomatous degeneration,
systemic lupus erythematosus,
rheumatoid arthritis,
ankylosing spondylitis, and
carcinoid syndrome
congenital lesions such as an endocardial cushion defect,
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7.  Acute phase
 Sudden volume overload of both LA and LV. The left ventricle now has to pump
out the forward stroke volume plus the regurgitant volume known as the total
stroke volume of the left ventricle.
 Increased ejection fraction initially contractile function deteriorates as disease
progressesdysfunctional LV and a decreased EF.
 Volume and pressure overload of the LA  pulmonary congestion- signs &
symptoms
 Regurgitant fraction >0.6 -Severe MR.
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8. Chronic phase:
Two phases-
a. Compensated:
 Develops slowly over months to years or if the acute phase
cannot be managed with medical therapy.
 Eccentric hypertrophy of the LV along with the increased
diastolic volume increase the stroke volume near
normalisation of CO.
 Volume overload of LADilatation of LA decrease in
filling pressure improves the drainage from the pulmonary
veins therefore signs & symptoms of pulmonary congestion
decrease.
 Thus the pt is asymptomatic & have normal exercise tolerances.
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9. Chronic phase:
b. Decompensated
 MR over years eventually develops left ventricular
dysfunction, the hallmark of this phase. characterized by
calcium overload within the cardiac myocytes.
 The stroke volume of the LV decreases decreased forward
CO & an increase in the end systolic volumeincreased filling
pressures of the LV and increased pulmonary venous
congestionsymptoms of CHF.
 LV dilatationdilatation of the mitral valve annulusworsens
the degree of MR & increases the stress on cardiac chamber
wall as well.
 EF decreases late in the course of disease.
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10.  The fraction of regurgitant volume depends on
(1) the size of the mitral valve orifice;
(2) heart rate, which determines the duration of ventricular
ejection;
(3) pressure gradients across the mitral valve.
 MR + MS -volume & pressure overload, resulting in a markedly
increased left atrial pressure.
 Atrial fibrillation, pulmonary edema, & pulmonary
hypertension develop much earlier in these patients
 Rheumatic fever induced MR causes marked left atrial
enlargement & AF.
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11. Volume overload of LA
Volume overload of LV
Mitral regurgitation
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Early
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12. Volume overload of LA
Volume overload of LV
Mitral regurgitation
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Contractility
BP and CO
Early Late
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13. Volume overload of LA
Volume overload of LV
Mitral regurgitation
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Contractility
BP and CO
Reflexive arteriolar
constriction
SVR
LateEarly
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14. Volume overload of LA
Volume overload of LV
Mitral regurgitation
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Contractility
BP and CO
Reflexive arteriolar
constriction
SVR
Regurgitation
Early Late
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15. Volume overload of LA
Volume overload of LV
Mitral regurgitation
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Contractility
BP and CO
Reflexive arteriolar
constriction
SVR
Regurgitation
LA pressure Pulmonary
congestion
Early Late
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16. Volume overload of LA
Volume overload of LV
LA dilation
Normal LA
pressuresLV filling Fiber size
Stroke volume
Cardiac output and BP
maintained
Contractility
BP and CO
Reflexive arteriolar constriction
SVR
Forward flow Regurgitation
LA pressure Pulmonary
congestion
Early Late
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17.  MVP is the most common valvular abnormality
 Incidence of 0.6 – 2.4%, young females > males
 Benign course usually
 Occurs with heritable connective disorders like Marfan
syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta
and pseudoxanthoma elasticum
 90% of patients with Marfan syndrome have MVP
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18.  Most are asymptomatic, with a benign course
 Most common pathologic basis is “myxomatous proliferation”
 May result in complications like
Mitral regurgitation
Infective endocarditis
Thromboembolic episodes (if endothelium is disrupted)
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19.  TYPE I – leaflet edges do not co-apt
 TYPE II – billowing of mitral valve without regurgitation
 TYPE III – billowing and prolapsed mitral valve with
regurgitation
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20.  May reveal features of Marfan symdrome
 Classic auscultatory finding is mid-to-late systolic click (due to
leaflets prolapsing into LA)
 May be followed by high-pitched, mid-to-late systolic murmur at
the apex.
 Valsalva maneuver & standing – early click & prolonged murmur
 Supine position with legs raised – late click & shortened murmur
 ECG – usually normal, non-specific ST-segment and T wave
changes in leads II, III, aVF may be present
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23.  Acute AR:
Trauma, Rheumatic fever,infective Endocarditis,dissecting
aneurysm
 Chronic AR:
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25.  Volume overload → ↑End Diastolic gradient →Series
replication of sarcomeres → Chamber enlargement→ Eccentric
hypertrophy
 Acute AR- Sudden occurrence → Volume overload on LV
→Immediate compensatory sympathetic tone → Tachycardia &
↑ed contractile state
 Chronic AR
Stage-1: Mild AR-Asymptomatic with physiologic
compensation
Stage-2 moderate AR –symptomatic impairement
Stage-3 Severe AR –Terminal failure
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26. Why do we need guidelines for the anaesthetic management of valvular
heart disease patients?
 Still common in the developing world due to the prevalence of Rheumatic
Fever.
 In the past 2 decades, there have been major advances in understanding the
natural history and in improving cardiac function in patients with valvular
heart disease.
 Increases survival in this group of patients due to:-
Better noninvasive monitors of ventricular function
Improved prosthetic heart valves,
Better techniques for valve reconstruction
Development of guidelines for selecting the proper timing for surgical
intervention
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27.  Hemodynamic burden on the LV/RV initially tolerated by compensatory
mechanisms but eventually leads to cardiac muscle dysfunction, (CHF), or
even sudden death.
 Produce pressure overload (mitral stenosis, aortic stenosis) or
volume overload (mitral regurgitation, aortic regurgitation) on the left atrium
or left ventricle.
 Anaesthetic management during the perioperative period is based on
the likely effects of drug-induced changes in :-
Heart rate and rhythm,
Preload,
Afterload,
Myocardial contractility,
Systemic blood pressure,
Systemic and pulmonary vascular resistance relative
to the pathophysiology of the heart disease.
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28.  Includes assessment of
(1) the severity of the cardiac disease,
(2) the degree of impaired myocardial contractility, and
(3) the presence of associated major organ system disease.
(4) functional capacity of the patient
(5) surgical risk for cardiac index
 Recognition of compensatory mechanisms :Increased
sympathetic nervous system activity and cardiac hypertrophy
 Consideration of current drug therapy
 The presence of a prosthetic heart valve introduces special
considerations especially if noncardiac surgery is planned.
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Perioperative carrdiac assesment for non cardiac suregry –AHA2013

29. History:
Questions designed to define exercise tolerance are necessary to
evaluate cardiac reserve in the presence of valvular heart disease
and to provide a functional classification according to the criteria
established by the NYHA.
 Dyspnea, orthopnea,PND & easy fatigability- impaired
myocardial contractility
 Anxiety, diaphoresis, palpitations & resting tachycardia-
compensatory increase in sympathetic nervous system activity
 CHF- frequent in chronic valvular heart disease, Basilar chest
rales, jugular venous distention, S3 and dependant edema elective
surgery is deferred until CHF can be treated and myocardial contractility
optimized.
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30. 1 MET = oxygen consumption of 3.5ml/kg/min at rest
Peri-operative risk increases greatly if patient is unable to
meet 4 MET
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31. Physical examination:
Depend in the severity and duration of MR:
 Inspection
- Features of CHF ( pt propped up and dyspneic,
edema, raised JVP etc)
-Precordial bulge
 Palpation
-Pulse- regular, normal pressure usually.
May show a sharp upstroke in chronic severe MR
narrow pulse pressure in acute severe MR
-Systolic thrill at the apex (best in left lateral position at the
height of expiration) , hyperdynamic and laterally displaced
apex ,palpable rapid filling S3 (chronic severe MR)
-Left parasternal heave and epigastric pulsations (RVH)
-Palpable P2 I pulmonary area (PAH)
-Bipedal pitting edema (CHF)
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32.  Auscultation
-S1 –usually absent,soft or buried in the
murmur.
-S2-audible. Wide physiological splitting in
severe MR (aortic valve closes early)
-S3 –low pitched 0.12-0.17s after A2 may be
followed by rumbling MDM
-S4- in acute severe MR
 Murmur- High pitched soft blowing holosystolic apical
murmur atleast grade III/IV in left lateral position at the
height of expiration with radiation to the left axilla and
inferior angle of scapula. Intensified by isometric exercise but
reduced during Valsalva.
 Pulmonary area- Ejection systolic murmur with loud P2
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33.  Quincke’s sign: capillary
pulsation
 Corrigan’s sign: water
hammer pulse
 Bisferiens pulse (AS/AR
> AR)
 De Musset’s sign: systolic
head bobbing
 Mueller’s sign: systolic
pulsation of uvula
 Durosier’s sign: femoral
retrograde bruits
 Traube’s sign: pistol shot
femorals
 Hill’s sign:BP Lower
extremity >BP Upper
extremity by
◦ > 20 mm Hg - mild AR
◦ > 40 mm Hg – mod AR
◦ > 60 mm Hg – severe AR
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34.  Widened pulse pressure
◦ Systolic – diastolic = pulse pressure
 Apex: Enlarged, Displaced,Hyper-dynamic,Palpable S3
 High pitched, blowing, decrescendo diastolic murmur at LSB
Best heard at end-expiration & leaning forward
Hands & Knee position
 Austin-Flint murmur
 Aortic diastolic murmur
◦ length correlates with severity (chronic AR)
◦ in acute AR murmur shortens as Aortic DP=LVEDP
◦ in acute AR - mitral pre-closure
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36. ROUTINE INVESTIGATIONS
 Blood investigations – Hb, TC, DC.
 Urine – albumin, sugar , micro.
 Blood grouping and matching
SPECIFIC INVESTIGATIONS
1.Assessment of severity and organ damage
 Chest X-ray
 ECG
 ECHO
 LFT, Renal function tests
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37. 2. Effects of drug therapy
 PT, aPTT, BT , CT
 Serum electrolytes
 Serum digoxin levels
3. Assess rheumatic activity
 ESR
 ASO titre
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38. X RAY findings:
 MR:
- Enlarged LA and LV
-Signs of pulmonary
venous hypertension
-Signs of pulmonary
edema (acute severe
MR)
-RVH
-Mitral calcification (in
co existing MS)
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40.  Increase size of
Left atrium
Left ventricle
Pulmonary vascular markings
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46.  ECG- AR:
-LV hypertrophy
-ST segment depression, T wave inversion in lead
1,Avl,V3,V4,V5&V6
rtrophy
-ST segment depression, T wave inversion in lead 1,Avl,V5&V6
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47. ECHO-
Qualitative measurements:
Color flow jet
Density of continous wave doppler signal
Pulmonary vein flow pattern
Quantitative measurements:
EROA(effective regurgitation orifice area)
Regurgitation volume
Regurgitation pattern
 Assesment of ventricular size,atrial size &chamber
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52. AR:
 Cause of AR
 Severity of AR
 Assessing LV performance
 Rapid high frequency fluttering of ant. mitral leaflet by impact of
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54. Laboratory Data
 CARDIAC CATHETERISATION:
-Presence and severity of valvular stenosis and/or regurgitation,
coronary artery disease, and intracardiac shunting.
-Resolve discrepancies between clinical and echocardiographic
findings.
-MS/MR: measurement of pulmonary artery pressure and right
ventricular filling pressure may provide evidence of pulmonary
hypertension and right ventricular failure.
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57.  In asymptomatic pts with severe AR & MR & preserved LV
function,non cardiac surgery can be performed without
additional risk.
 Symptomatic pts & those who are asymptomatic with severly
impaired LVEF (<30%)are at high risk of cvs complications &
non cardiac surgery should be performed only if necessary.
 Pts with severe MR & AR may benefit from optimization of
pharmacological therapy to produce maximal haemodynamic
stabilization.
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JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY,2009

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61.  Progress insidiously, causing left ventricular damage & remodeling before
symptoms have developed.
Survival may be prolonged if surgery is performed before the ejection
fraction is less than 60%.
 Surgery-
-Mitral annuloplasty/valvuloplasty-preferred because restores valve
competence, maintains the functional aspects of the mitral valve apparatus, &
avoids insertion of a prosthesis.
-Mitral valve replacement
 Pts with an EF <30% or left ventricular end-systolic dimension more than 55
mm do not improve with mitral valve surgery.
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64. Monitoring
ASA recommended
Pulse-oximetry
ECG
End-tidal CO2
NIBP
Temperature
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65. In case of severe MR With left ventricular dysfunction
 Invasive monitoring- ( CVP, PAC)
Not required in Minor surgery with asymptomatic MR
Useful in severe MR- detecting the adequacy of CO and the
hemodynamic response to anesthetic and vasodilator drugs
and facilitating intravenous fluid replacement.
 Pulmonary artery occlusion pressure –
-V waveform to assess severity of MR
-May be a poor measure of left ventricular end-diastolic
volume in patients with chronic mitral regurgitation.
-With acute mitral regurgitation, the left atrium is less
compliant, and PAOP does correlate with LA and LV EDP.
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66. GOALS:
 Prevention & treatment of events that decrease CO.
 Improve forward LV Stroke Volume & decrease regurgitant
fraction.
Vasodilatation can improve forward flow- NTG/ nitroprusside
infusions. Useful in PAH as well but not once RVF sets in.
 Maintain adequate preload
 Modest or increase HR- Avoid bradycardia
 Decrease in afterload is beneficial
 Minimize drug-induced myocardial depression
 Avoid hypoxia,hypercarbia & acidosis (all increase PAH)
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67.  Basic principles:
Afterload support
Maintainence of sinus rhythm
Careful volume management
Avoidance of bradycardia
 Can be safely employed in a case of mild to moderate MR
 Care should be taken regarding sudden hypotension &
bradycardia associated with sub-arachnoid block.
 Epidural using opiods- supplement to GA
Avoid adrenaline in test dose while inserting catheter.
Optimise fluid status & achieve sensory level with titrated doses
of Local anaesthetic until adequate for surgery.
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68.  Advantages:
Reduced stress response
Decreased blood loss
Early ambulation
Early detection of
complications in awake
patient
Superior post-operative
analgesia
Lower incidence of PONV
 Disadvantages:
Pt on anticoagulation therapy
CI to epidural anaesthesia
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69. PREMEDICATION
 Anxiolysis – Midazolam 0.05 mg/kg IV
 Analgesia – Fentanyl 2µg/kg IV
 Anti-emetic – Ondansetron 4 mg IV
 Anti-sialagogue – Glycopyrolate 0.01 mg/kg IV
 Antibiotic prophylaxis for bacterial endocarditis
 Continue medications like digoxin, ACE inhibitors
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70.  INDUCTION:
 Avoid bradycardia
 In absence of LV dysfunction – Inj propofol 2mg/kg IV or
Inj Thiopentone 3-5mg/kg IV or
 In presence of LV dysfunction - Inj Midazolam 0.2 - 0.3 mg/kg
IV + Inj Fentanyl 0.01 mg/kg IV
 Muscle relaxation with Inj pancuronium 0.01mg/kg (prefered)
or Vecuronium 0.1 mg/kg IV
 Avoid scoline
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71.  When myocardial function is severely compromised, use of an
opioid-based anesthetic is another option
 Mechanical ventilation should be adjusted to maintain near-
normal acid-base and respiratory parameters.
 The pattern of ventilation must provide sufficient time
between breaths for venous return.
 Maintenance of intravascular fluid volume is very important
for maintaining left ventricular volume and CO in these
patients.
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72. MAINTAINENCE
 Maintained with oxygen+ N2O + Inj Fentanyl + Inj Pancuronium 0.01
mg/kg
 Nitrous oxide avoided in severe PAH.
 Maintain heart rate between 80 – 100/min
 Maintain preload
 Hypotension – small dose of Inj ephedrine 5mg bolus IV,
if unresponsive then titrated doses of Inj Dobutamine or low dose
epinephrine are desirable
 Reversed with Inj Neostigmine 0.05mg/kg + Inj Glycopyrolate 0.01
mg/kg
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73.  Pregnant women with rheumatic mitral MR well tolerate the
increased blood volume & heart rate of pregnancy, if sinus
rhythm is maintained.
 Valve repair is usually feasible for non-rheumatic causes of
MR, & women with severe MR should have the repair before
conception.
 There is an increased risk of AF during pregnancy in women
with MR.
 Some physicians recommend prophylactic digoxin therapy to
decrease the risk of a rapid ventricular response, if AF occur.
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74.  The hypercoagulability of pregnancy increases the risk of
systemic embolization.
 Systemic embolization may occur in 20% of pregnant women
with MR.
 Anticoagulation may be indicated if
(1) cardioversion is planned,
(2) there is a h/o of embolic phenomena, or
(3) a new onset of AF occurs
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75. parameter Stage of labour Percentage of change
(increase)
Cardiac output Latent phase 10%
Active phase 25%
Expulsive phase 40%
Immediate post-partum 75-80%
Heart rate All stages Increase
CVP All stages Increase
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76. parameter Stage of labour Percentage of change
(increase)
Cardiac output <1hr 30% above prelabor
values
24-48hrs Just below prelabor
values
2 weeks 10% above pre-
pregnant values
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77.  During labor, SVR is increased by pain, expulsive efforts &
aortic compression by the uterus.
 Increased SVR is poorly tolerated by parturients with
regurgitant valvular lesions.
 These women are at increased risk for infective endocarditis,
and antibiotic prophylaxis is indicated
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78.  The goals of anesthetic management for patients with MR are
as follows:
1. Prevent an increase in SVR.
2. Maintain HR - normal or slightly increased.
3. Maintain sinus rhythm, if present. Aggressively treat acute AF.
4. Avoid aortocaval compression & maintain venous return, but
prevent an increase in central vascular volume.
5. Avoid myocardial depression during GA.
6. Prevent pain, hypoxemia, hypercarbia & acidosis, which may
increase pulmonary vascular resistance.
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79.  Epidural anesthesia(EA) prevents the increase in SVR that is
a/w with pain.
 It may result in decrease in SVR, promotes the forward flow of
blood & helps prevent pulmonary congestion.
 However, it also may result in decreased venous return (VR).
 Careful administration of Iv crystalloid & left uterine
displacement are necessary to maintain VR & left ventricular
filling.
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80.  Anesthesiologist should give attention to the maintenance of
adequate HR & decreased afterload.
 The increased HR a/w with ketamine & pancuronium may be
desirable in these pts.
 Aviod Myocardial depression.
 Hypoxemia, hypercarbia, acidosis & hypothermia produce an
undesirable increase in PVR .
 Acute AF must be treated promptly & aggressively.
Hemodynamic instability warrants the immediate performance
of cardioversion.
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81.  Prophylactic antibiotics indicated in the presence of murmur
with mid-systolic click
 Avoid hypovolemia, hypotension & tachycardia.
 Reduction in LV volume worsens the amount of MR
 Adequate preloading is a must.
 GA using volatile agents with careful volume
replacement, vasoconstrictors to support BP & B-blockers to
control HR are recommended.
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83.  Characterized by:
◦ Volume overload
◦ Ventricular dilatation
◦ Eccentric hypertrophy
◦ Forward stroke volume higher than normal causing increased
systolic pressure
◦ Regurgitation across the valve causes diastolic pressure to be
lower than normal
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84. ◦ Once symptomatic, death can occur within 5 years unless
lesion is surgically repaired.
◦ Digitalis, diuretics and afterload reduction (ACE inhibitors) for
chronic (eventual surgical repair)
◦ Inotropes (dopamine, dobutamine) and vasodilator for
severe, chronic AR (requires surgery)
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86. CHOICE OF ANAESTHETIC
 Regional Anaesthesia
 General Anaesthesia
REGIONAL
 Spinal
 Epidural
 Used in mild & moderate cases
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87. GENERAL ANAESTHESIA:
Premedication:
 Anxiolysis – Midazolam 0.05 mg/kg IV
 Analgesia – Fentanyl 2µg/kg IV
 Anti-emetic – Ondansetron 4 mg IV
 Anti-sialagogue – Glycopyrolate 0.01 mg/kg IV
Induction
 Inj Thiopentone 3-5 mg/kg or
 Inj Propofol 1-2 mg/kg or
 Inj Etomidate 0.2-0.5mg/kg
Maintenance
 O2+N2o +Fentanyl 1-2µg/kg +IPPV
 O2+N2o +desflurane/sevoflurane+IPPV
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88. Relaxation
Inj vecoronium 0.05mg/kg
Reversal
Inj neostigmine 0.05mg/kg + inj glycopyolate 0.02mg/kg
POST OPERATIVE MANAGEMENT
 Analgesia
 Post op nausea and vomiting
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89. CONCLUSION:
 Management of a patient with significant valvular heart
disease is very challenging
 Knowledge of patho-physiology of each lesion is a
prerequisite to understanding hemodynamic goals in
these patients
 These aims can then be combined with knowledge of
effects of anaesthetic agents to choose the safest
anaesthetic course.
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90.  JACC,ACC/AHA 2006,2008 Update on VHD- Focused update on
infective endocarditis.
 Guidelines for pre-operartive cardiac risk assesment &
management in non cardiac surgery,ESC 2009 guidelines
 Uptodate2013,estimation of cardiac risk prior to non cardiac
surgery
 Perioperative cardiac assesment for non cardiac surgery,AHA-
2013
 Preoperartive evaulation of adult undergoing non cardiac
surgery,ESA guidelines
 Stoeltings Anaesthesia and co existing disease- 5th edition
 Harrisons Internal medicine- 17th ed
 A practical approach to anaesthesia for Emergency Surgery
 Miller’s Anaesthesia – 7th edition
 Kaplan’s Cardiac Anaesthesia – 5th edition
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Thank Q