Anaesthetic management of valvular heart disease for non cardiac surge

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Anaesthetic Management of Valvular Regurgitation coming for noncardaic surgery:

Anaesthetic Management of Valvular Regurgitation coming for noncardaic surgery Presenter: Dr.Naven kumar.S PG IN Anaesthesiology Moderator: Dr.Ravi Kumar Professor , JJMMC,Davangere . 23-Apr-14 1

Synopsis :

Introduction MR-pathophysiology AR-pathophysiology Preop . assessment Evaluation Guidelines for infective endocarditis Anaesthetic implications Conclusion References 23-Apr-14 2 Synopsis

Valvular Heart Disease:

Definition:- An acquired or congenital disorder of cardiac valve characterised by stenosis (obstruction) or regurgitation(backward flow) of blood . Valvular Heart Disease 23-Apr-14 3




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 . MITRAL REGURGITATION 23-Apr-14 5

Etiology :

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, Etiology 23-Apr-14 6


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. PATHOPHYSIOLOGY 23-Apr-14 7


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. PATHOPHYSIOLOGY 23-Apr-14 8


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. PATHOPHYSIOLOGY 23-Apr-14 9


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. PATHOPHYSIOLOGY 23-Apr-14 10

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Volume overload of LA Volume overload of LV Mitral regurgitation LA dilation Normal LA pressures LV filling Fiber size Stroke volume Cardiac output and BP maintained Early 23-Apr-14 11

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Volume overload of LA Volume overload of LV Mitral regurgitation LA dilation Normal LA pressures LV filling Fiber size Stroke volume Cardiac output and BP maintained Contractility BP and CO Early Late 23-Apr-14 12

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Volume overload of LA Volume overload of LV Mitral regurgitation LA dilation Normal LA pressures LV filling Fiber size Stroke volume Cardiac output and BP maintained Contractility BP and CO Reflexive arteriolar constriction SVR Late Early 23-Apr-14 13

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Volume overload of LA Volume overload of LV Mitral regurgitation LA dilation Normal LA pressures LV filling Fiber size Stroke volume Cardiac output and BP maintained Contractility BP and CO Reflexive arteriolar constriction SVR Regurgitation Early Late 23-Apr-14 14

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Volume overload of LA Volume overload of LV Mitral regurgitation LA dilation Normal LA pressures LV 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 23-Apr-14 15

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Volume overload of LA Volume overload of LV LA dilation Normal LA pressures LV 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 23-Apr-14 16


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 23-Apr-14 17 MITRAL VALVE PROLAPSE


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) 23-Apr-14 18 PATHOPHYSIOLOGY


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 23-Apr-14 19 MVP- TYPES

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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 23-Apr-14 20



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Acute AR: Trauma, Rheumatic fever,infective Endocarditis,dissecting aneurysm Chronic AR : 23-Apr-14 23

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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 23-Apr-14 25

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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 23-Apr-14 26


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 . INTRODUCTION 23-Apr-14 27


I ncludes 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 . PREOPERATIVE ASSESSMENT 23-Apr-14 28 Perioperative carrdiac assesment for non cardiac suregry –AHA2013


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. D yspnea , orthopnea,PND & easy fatigability- impaired myocardial contractility A nxiety , 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. PREOPERATIVE ASSESSMENT 23-Apr-14 29

Assesment of functional capacity:

1 MET = oxygen consumption of 3.5ml/kg/min at rest Peri -operative risk increases greatly if patient is unable to meet 4 MET 23-Apr-14 30 Assesment of functional capacity


P hysical 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) PREOPERATIVE ASSESSMENT 23-Apr-14 31


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 23-Apr-14 32 MR


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 23-Apr-14 33 AR-Signs


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 23-Apr-14 34 AR

Preoperative pharmacological optimisation :

Preoperative pharmacological optimisation 23-Apr-14 35


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 23-Apr-14 36 PREOPERATIVE EVALUATION

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Effects of drug therapy PT, aPTT , BT , CT Serum electrolytes Serum digoxin levels Assess rheumatic activity ESR ASO titre 23-Apr-14 37


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) 23-Apr-14 38 PREOPERATIVE EVALUATION

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Increase size of Left atrium Left ventricle Pulmonary vascular markings 23-Apr-14 40

AR- Hall mark findings:

23-Apr-14 41 AR- Hall mark findings

ECG- L eft ventricular hypertrophy:

23-Apr-14 42 ECG- L eft ventricular hypertrophy

Ecg- p mitrale, AF:

23-Apr-14 43 Ecg - p mitrale , AF

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23-Apr-14 45 ECG- LVH IN AR

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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 23-Apr-14 46


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 . 23-Apr-14 47


23-Apr-14 48 MR


23-Apr-14 49 MR

Echo- qualitative measurements in MR:

23-Apr-14 50 Echo- qualitative measurements in MR

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AR: Cause of AR Severity of AR Assessing LV performance Rapid high frequency fluttering of ant. mitral leaflet by impact of 23-Apr-14 52

Echo- AR:

23-Apr-14 53 Echo- AR


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 . PREOPERATIVE EVALUATION 23-Apr-14 54

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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. 23-Apr-14 57

Infective endocarditis propylaxis:

23-Apr-14 58 Infective endocarditis propylaxis JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY,2009

Infective endocarditis propylaxis:

23-Apr-14 59 Infective endocarditis propylaxis

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P rogress 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. MR -TREATMENT PLANS 23-Apr-14 61

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Monitoring ASA recommended Pulse- oximetry ECG End-tidal CO2 NIBP Temperature 23-Apr-14 64

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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. 23-Apr-14 65


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) ANAESTHETIC MANAGEMENT 23-Apr-14 66

Role of regional anaesthesia:

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 . Role of regional anaesthesia 23-Apr-14 67

Epidural :

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 23-Apr-14 68 Epidural

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 Antibiotic prophylaxis for bacterial endocarditis Continue medications like digoxin, ACE inhibitors 23-Apr-14 69 General anaesthesia

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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 23-Apr-14 70

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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. 23-Apr-14 71

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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 23-Apr-14 72


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. 23-Apr-14 73 MITRAL REGURGITATION IN PREGNANCY

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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 23-Apr-14 74

Cardiovascular changes during labour::

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 23-Apr-14 75 Cardiovascular changes during labour :

Cardiovascular changes during puerperium :

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 23-Apr-14 76 Cardiovascular changes during puerperium

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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 23-Apr-14 77


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. 23-Apr-14 78 ANESTHETIC MANAGEMENT

Continuous epidural anesthesia is preferred for labor and vaginal or cesarean delivery:

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 . 23-Apr-14 79 Continuous epidural anesthesia is preferred for labor and vaginal or cesarean delivery

If GA is required:

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 . 23-Apr-14 80 If GA is required


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. 23-Apr-14 81 ANAESTHETIC IMPLICATIONS IN MVP

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Aortic Insufficiency :

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 23-Apr-14 83 Aortic Insufficiency

Treatment: :

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) 23-Apr-14 84 Treatment:

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CHOICE OF ANAESTHETIC Regional Anaesthesia General Anaesthesia REGIONAL Spinal Epidural Used in mild & moderate cases     23-Apr-14 86

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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 23-Apr-14 87

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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 23-Apr-14 88

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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. 23-Apr-14 89


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- 5 th edition Harrisons Internal medicine- 17 th ed A practical approach to anaesthesia for Emergency Surgery Miller’s Anaesthesia – 7 th edition Kaplan’s Cardiac Anaesthesia – 5 th edition References 23-Apr-14 90

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23-Apr-14 91 Thank Q

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