Valvular Heart Disease & Anaesthetic Implications

This presentation is about valvular heart disease and anaesthetic implications..
Thankyou!

1. CHAIRPERSON: Dr.S.B.Gangadhar MODERATOR : Dr. Abhishek . M.S. PRESENTER : Dr. Daber Pareed VALVULAR HEART DISEASE

2. DEFINITION An acquired or congenital disorder of a cardiac valve characterized by stenosis (obstruction) or regurgitation (backward flow) of blood

3. All VHD are characterized by abnormalities of ventricular loading . The status of the ventricle changes over time as ventricular function and the valvular defect are influenced by the progression of volume or pressure overload. Valvular heart disease places a haemodynamic burden on the left ventricle and/or right ventricle Initially tolerated, as CVS compensates for overload. Haemodynamic overload 1)Cardiac muscle dysfunction 2)CHF 3)Sudden death

4. The most frequently encountered cardiac valve lesions produce PRESSURE OVERLOAD or VOLUME OVERLOAD on the LA/LV Perioperative management requires understanding of haemodynamic alterations that accompany valvular dysfunction.

5. Anaesthetic mgt during periop period is based on likely effects of drug induced changes in cardiac rhythm, heart rate, preload, afterload, myocardial contractility, systemic blood pressure, systemic vascular resistance & pulmonary vascular resistance related to pathophysiology of heart disease.

6. CARDIOLOGY-BASIC TERMS Systolic function – contract and eject blood Contractility – intrinsic ability of myocardium to contract and generate force Preload – load placed on myocardium before contraction – diastolic volume and filling pressure After load – load placed on myocardium during contraction – systolic volume and generated pressure

7. VALVULAR HEART DISEASE

8. Evaluation of patient Preoperative evaluation of patients with valvular heart disease includes assessment of (1) the severity of the cardiac disease, (2) the degree of impaired myocardial contractility, (3) the presence of associated major organ system disease

9. Current drug therapy Presence of secondary effects on pulmonary, renal, and hepatic function. The presence of concomitant coronary artery disease & other major organ system diseases

10. NEWYORK HEART ASSOCIATION functional classification Class I - No limitation of physical activity. Ordinary physical activity causes no undue fatigue, palpitations, dyspnea. Class II - Slight limitation of physical activity. Comfortable at rest, ordinary physical activity results in fatigue palpitations , or dyspnea. Class III - Marked limitation of physical activity. Comfortable at rest , less than ordinary activity causes fatigue, palpitations dyspnea. Class IV -Unable to carry out any physical activity without discomfort . Symptoms at rest .

11. Physical findings Signs of congestive heart Failure(CHF) S3 gallop Pulmonary rales Elevated JVP Hepatojugular reflux Hepatosplenomegaly Pedal edema Findings specific to individual valvular lesions (Murmur-character, systolic/diastolic , location , intensity,grade,radiation ) Neurologic deficits secondary to embolic phenomena

12. investigations Tailored to the patient and the procedure: ECG - LVH,RVH,arrythmias , ischaemia Chest X-ray - assess cardiac size and the presence of pulmonary vascular congestion. Echocardiography Cardiac catheterization to identify a)Coexisting CAD b)Severity of stenosis/regurgitation (transvalvular pressure gradients ) c)Intracardiac shunts d)Clinical & Echo discrepancies

13. Serum electrolytes Renal function tests Coagulation profile ABG- significant pulmonary symptoms

14. DOPPLER ECHO IN VHD-PURPOSE Determine significance of cardiac murmurs Determine transvalvular pressure gradient Determine valve area,cavity dimensions Determine ventricular ejection fraction Diagnose valvular regurgitation Evaluate prosthetic valve function

15. ENDOCARDITIS PROPHYLAXIS-AHA GUIDELINES

16. HIGH- AND MODERATE-RISK PATIENTS - PROPHYLAXIS RECOMMENDED(CLASS 1) Prosthetic valves / history of infective endocarditis Complex cyanotic congenital heart disease Surgically constructed systemic-pulmonary shunts or conduits Congenital cardiac valve malformations -bicuspid aortic valves A history of surgical valve repair Hypertrophic cardiomyopathy with resting/latent obstruction MVP with auscultatory evidence of valvular regurgitation and/or thickened leaflets on echocardiography

17. Isolated secundum ASD > 6 months after successful surgical or percutaneous repair of ASD , VSD, PDA MVP without MR or thickened leaflets on echocardiography Physiologic heart murmurs Echo e/o physiologic MR with absence of murmur with structurally normal valves Echo e/o physiologic TR and or PR with absence of a murmur and with structurally normal valves LOW-RISK PATIENTS - PROPHYLAXIS NOT RECOMMENDED(CLASS 111)

18. Antibiotic regimens

19. Prosthetic valves Bioprosthetic Mechanical Bioprosthetic valves Heterogeneous grafts made from animal tissue Low thrombogenic potential Do not need systemic anticoagulation Aspirin is recommended

20. Mechanical valves Longer lasting Need lifelong anticoagulation - Warfarin therapy. Aspirin is usually combined with warfarin in mechanical heart valves. Aspirin allergy – clopidogrel

21. PATIENTS WITH PROSTHETIC VALVES UNDERGOING SURGICAL PROCEDURES Complete history and physical examination. Type of valve inserted. Auscultation - high-pitched, crisp opening and closing sounds Bioprosthetic valves do not have special auscultatory characteristics. Onset of new murmurs / change in quality of murmurs - problem with the valve / endocarditis

22. AHA BRIDGING RECOMMENDATIONS FOR INTERRUPTION OF WARFARIN THERAPY FOR NON-CARDIAC SURGERY AND INVASIVE PROCEDURES ( i )Low risk of thrombosis - Eg :- Bileaflet mechanical aortic valve without risk factors Warfarin stopped 48 to 72 hour before surgery INR to fall to 1.5 Warfarin restarted within 24 hours after the procedure

23. ( ii)High risk for thrombosis – Eg :-Mechanical mitral valve or a mechanical aortic valve with any risk factor Warfarin stopped 48 to 72 hrs Unfractionated heparin(UFH) - INR falls < 2.0 , stopped 4 to 6 hours before. Warfarin restarted soon after Heparin continued until INR returns to therapeutic range with warfarin

24. MAJOR VALVULAR LESIONS LT SIDED RT SIDED

25. MITRAL VALVE DISEASE

26. Mitral stenosis ETIOLOGY Almost always rheumatic in origin Elderly - heavy calcification Rarely - Congenital mitral stenosis Rheumatoid arthritis

27. Mitral stenosis primarily affects females. Diffuse thickening of the mitral leaflets and subvalvular apparatus,commissural fusion, and calcification of the annulus and leaflets are typically present. This process occurs slowly,and many patients do not become symptomatic for 20 to 30 years after the initial episode of rheumatic fever. Over time, the mitral valve becomes stenotic , and CHF, pulmonary hypertension, and right ventricular failure may develop

28. CLINICAL FEATURES OF MITRAL STENOSIS Symptoms Breathlessness - pulmonary congestion Fatigue - low cardiac output Oedema , ascites - right heart failure Palpitation- atrial fibrillation Haemoptysis - pulmonary congestion, pulmonary embolism Cough - pulmonary congestion Chest pain - pulmonary hypertension Thromboembolic complication - stroke, ischaemic limb

29. Pathophysiology The normal mitral valve orifice area is 4 to 6 cm2. Mitral stenosis is characterized by mechanical obstruction to left ventricular diastolic filling secondary to a progressive decrease in the size of the mitral valve orifice. This valvular obstruction produces an increase in left atrial volume and pressure. With mild mitral stenosis, left ventricular filling and stroke volume are maintained at rest by an increase in left atrial pressure.

30. Symptoms usually develop when mitral valve area is less than 1.5 cm2 Symptoms usually develop when mitral valve area is less than 1.5 cm2. As the disease progresses the pulmonary venous pressure is increased in association with the increase in left atrial pressure. The result is transudation of fluid into the pulmonary interstitial space, decreased pulmonary compliance, and increased work of breathing, which leads to progressive dyspnea on exertion.

31. signs Mitral facies Atrial fibrillation - irregularly irregular pulse, pulse deficit Signs of pulmonary hypertension Auscultation Loud first heart sound, opening snap Loud P2- pulmonary htn Low-pitched rough rumbling mid-diastolic murmur with presystolic accentuation best heard at the apex with bell of steth in left lateral decubitus position,breath held in expiration Signs of raised pulmonary capillary pressure Crepitations, pulmonary oedema, effusions

32. ECG-Tall peaked P wave in lead 2,upright in V1 RAD,RVH-Severe PAH CXR- Straightening of upper left cardiac border Prominence of main pulmonary arteries Dilatation of upper lobe pulmonary veins Postr displacement of esophagus by enlarged LA Kerley -B lines-Fine, dense, opaque, horizontal lines most prominent in lower&mid zones

33. ECHO Echocardiography is used to assess the anatomy of the mitral valve, including the degree of leaflet thickening, calcification, changes in mobility, and extent of involvement of the subvalvular apparatus. The severity of mitral stenosis is assessed by calculation of mitral valve area and measurement of the transvalvular pressure gradient. Echocardiography also allows evaluation of cardiac chamber dimensions, pulmonary hypertension, left and right ventricular function, and other valvular disease, and examination of the left atrial appendage for the presence or absence of thrombus

34. Mitral Stenosis Severity     Mild Moderate Severe Pulmonary artery systolic pressure (mm Hg) Normal – 18-25mmHg Less than 30 30–50 Greater than 50 Valve area (cm 2 ) Greater than 1.5 1.0–1.5 Less than 1.0

35. Management Minor symptoms – medical treatment Diuretics - ↓ pulmonary congestion Digoxin , β-blockers , CCB - control ventricular rate in AF A nticoagulants - ↓ risk of embolism A ntibiotic prophylaxis - infective endocarditis Definitive treatment – Surgical Severe symptoms(NYHA III/IV) Symptomatic despite medical treatment Pulmonary hypertension)(PA systolic pressure>50mm of Hg) balloon valvuloplasty, mitral valvotomy , mitral valve replacement

36. Anaesthetic goals Maintenance of adequate diastolic filling time (prevent tachycardia & treat promptly in periop period ) Preservation of adequate preload with out overload/ pulm vascular congestion. Avoid hypovolemia Avoidance of factors that precipitate pulmonary vasoconstriction & impair RV function Maintenance of the contractile state and systemic and coronary artery perfusion pressure. Maintain sinus rhythm Maintain afterload

37. ANAESTHETIC GRID IN MS LV PRELOAD HR RHYTHM CONTRACTILITY SVR PVR MS ↑ ↓ Controlled ventricular response Maintain constant Maintain ↓

38. Preoperative Medication Decrease anxiety and associated tachycardia- low dose Opioids and benzodiazepines ( Avoid oversedation !!!....sensitive to small doses of narcotics& hypnotics) Drugs for HR control- continued till time of surgery Diuretic-induced hypokalemia detected and treated preoperatively Continue anticoagulant therapy for minor surgery Major surgery with significant blood loss – regional techniques - discontinue anticoagulants

39. Induction of Anesthesia Avoid ketamine - increase the heart rate Intubation & muscle relaxation by cardiostable muscle relaxant - VECURONIUM Avoid relaxants with histamine release. Short acting β blocker for rate control(Esmolol)

40. Maintenance of Anesthesia Nitrous oxide/ low conc volatile anesthetic/ Opioid Nitrous oxide - pulmonary vasoconstriction = no clinical significance unless pul HTN present. Cardiostable muscle relaxants Reversal - slowly to prevent drug-induced tachycardia caused by anticholinergic drug Intraoperative fluids – careful titration – avoid fluid overload

41. Monitoring Monitoring asymptomatic patients without evidence of pulmonary congestion - routine monitors Symptomatic mitral stenosis undergoing major surgery * Central venous pressure(CVP) * Transesophageal echocardiography (TEE) *Intra-arterial pressure(IBP) *Pulmonary artery pressure(Caution in pulm htn….PA rupture from wedging catheter) *Left atrial pressure *ABG-adjust ventilatory parameters

42. Postoperative Management Risk of pulmonary edema and RV failure continues into postop period Cardiovascular monitoring continued Relief of postoperative pain ( pain  hypoventiln resp acidosis & hypoxemiaincr in HR & PVR) Opioids I/V or NEURAXIAL Decreased pulmonary compliance and increased work of breathing - mechanical ventilation maybe required

43. INTERACTION WITH PREGNANCY Expanded blood volume of pregnancy increases the risk of pulmonary congestion and edema Physiologic tachycardia of pregnancy ↓ left ventricular filling time ↑ left atrial and pulmonary arterial pressures.

44. Vaginal delivery : Early admission/invasive blood pressure monitoring/ Small top-ups for epidural/avoid fluid overload . Caesarean delivery - Spinal anaesthesia avoided. Careful epidural anaesthesia in NYHA class 1 and 2 patients General anaesthesia NYHA class 3 and 4 patients Bolus oxytocin contraindicated - risk of systemic hypotension and pulmonary hypertension. Brief period of postoperative ventilation may be required in some cases.

45. Mitral regurgitation Acute Endocarditis Papillary muscle rupture (post-MI) Trauma Chordal rupture leaflet flail ( MVP) Chronic Myxomatous (MVP) Rheumatic fever Endocarditis (healed) Mitral annular calcification Congenital (cleft, AV canal) Ischemic (LV remodeling) Dilated cardiomyopathy

46. MR-PATHOPHYSIOLOGY The basic hemodynamic derangement in mitral regurgitation is a decrease in forward left ventricular stroke volume and cardiac output. A portion of every stroke volume is regurgitated through the incompetent mitral valve back into the left atrium, which results in left atrial volume overload and pulmonary congestion. Patients with a regurgitant fraction of more than 0.6 are considered to have severe mitral regurgitation.

47. The fraction of left ventricular stroke volume that regurgitates into the left atrium depends on the size of the mitral valve orifice heart rate, which determines the duration of ventricular ejection pressure gradients across the mitral valve. Such gradients are related to left ventricle compliance and impedance to left ventricular ejection into the aorta. Pharmacologic interventions that increase or decrease systemic vascular resistance have a major impact on the regurgitant fraction in patients with mitral regurgitation.

48. CLINICAL FEATURES OF MITRAL REGURGITATION Symptoms Dyspnoea - pulmonary venous congestion Fatigue - low cardiac output Palpitation Oedema , ascites - right heart failure Signs Atrial fibrillation/flutter Cardiomegaly Apical pansystolic murmur ± thrill Soft S1, apical S3 Signs of pulmonary venous congestion- Crepitations , pulmonary oedema , effusions Signs of pulmonary hypertension and right heart failure

49. SEVERITY OF MR Method MILD Moderate Severe Regurgitant volume 30-40 mL 40-60 mL >60 mL Regurgitant fraction 10%-30% 30%-50% >55% Regurgitant orifice area <0.2 cm 2 0.3-0.4 cm 2 >0.4 cm 2

50. MANAGEMENT Diuretics Vasodilators . ACE inhibitors Digoxin - AF Anticoagulants – AF Antibiotic prophylaxis - IE Surgical valvuloplasty with moderate to severe symptoms regurgitant volume 30-60%

51. ANAESTHETIC MANAGEMENT Primary goal - maintaining forward systemic flow & reduction regurgitant fraction HR - high-normal range -80 to 100 beats/min Avoid bradycardia - ↑ duration of systole prolongs regurgitation Rhythm- maintain sinus rhythm Preload - Maintain or slightly increase- elevated preload cause an ↑regurgitant flow- low preload inadequate cardiac output Afterload - Decrease to improve forward cardiac output-avoid sudden increases in SVR Contractility - Maintain or increase to decrease left ventricular volume

52. ANAESTHETIC GRID IN MR LV PRELOAD HR RHYTHM CONTRACTILITY SVR PVR Maintain higher rate Maintain sinus rhythm Maintain ↓ ↓

53. Induction of Anesthesia With an intravenous induction drug. Dosing adjusted to prevent ↑SVR & ↓HR muscle relaxant - Pancuronium modest ↑ in heart rate

54. Maintenance of Anesthesia Volatile anesthetics- isoflurane, desflurane & sevoflurane - choices for maintenance of anesthesia. Severely compromised myocardium - opioid-based anesthetic is preferred - minimal myocardial depression. Mechanical ventilation - adjusted to maintain near-normal acid-base and respiratory parameters. The pattern of ventilation - provide sufficient time between breaths for venous return. .

55. Pregnancy Considerations No specific recommendations for management of MR during labour and delivery. Prior to labour- symptoms - managed with diuretics & vasodilators. Labour & CS - regional anaesthesia well tolerated. NYHA class 3-4- GA may be required.

56. MITRAL VALVE PROLAPSE Prolapse of one or both mitral leaflets into left atrium during systole with or without mitral regurgitation Most common form of valvular heart disease Common in young women Associated with Marfan syndrome Rheumatic carditis Myocarditis Thyrotoxicosis Systemic lupus erythematosus

57. Maybe anatomical or functional Anatomical -Redundant & thickened leaflets Connective tissue diseases , elderly men Functional Normal appearing leaflets/mild bowing only

58. CLINICAL FEATURES Anxiety orthostatic symptoms Palpitations Dyspnea Fatigue atypical chest pain Cardiac dysrhythmias Older men with anatomical MVP can p/w mild to moderate CHF(exercise intolerance, DOE, orthopnoea)

59. Midsystolic click+/- systolic murmur(in absence of symptoms doesn’t warrant a cardio consultation) S3 gallop,Midsystolic/holosystolic murmur,basal creps -CHF

60. complications cerebral embolic events infective endocarditis severe mitral regurgitation requiring surgery Dysrhythmias sudden death

61. Preoperative evaluation Functional disease from those with significant mitral regurgitation β-blockers to control dysrhythmias continued throughout the periop period Anticoagulants

62. Management of anaesthesia-principles Periop factors which ↑ LV emptying& ↓ filling avoided: 1) ↑ sympathetic activity 2) ↓ SVR 3)Upright posture 4) Hypovolemia ( ↓ LV filling)

63. Selection of Anesthetic Technique Most MVP have normal left ventricular function Tolerate all forms of general and regional anesthesia. General-volatile anaesthetic induced myocardial depression beneficial Regional- maintain adequate intravascular volume to prevent fall in SVR

64. Induction of Anesthesia Intravenous induction drug- avoid significant & prolonged ↓ SVR Etomidate - choice for induction in hemodynamically significant MVP Ketamine avoided - ↑ sympathetic NS activity- ↑ MVP and MR

65. Maintenance of Anesthesia Volatile anesthetics /nitrous oxide / opioids-titrate doses to maintain SVR 0.5 MAC of isoflurane, desflurane, and sevoflurane can decrease the regurgitant fraction Muscle relaxants- Vecuronim/Pancuronium Proper fluid balance Vasopressors - α-agonist - phenylephrine acceptable.

66. Invasive monitoring –in haemodynamically significant MVP only (MR/LV dysfunction) COMPLICATIONS Ventricular dysrhythmias - cause of death in young adults with undiagnosed MVP- Rx -beta blockers , Lidocaine

67. Aortic Stenosis Two factors are associated with development of aortic stenosis. Degeneration and calcification of the aortic leaflets and subsequent stenosis. This is a process of aging. Presence of a bicuspid rather that a tricuspid aortic valve.

68. CAUSES OF AORTIC STENOSIS Infants, children, adolescents Congenital aortic stenosis Congenital subvalvular aortic stenosis Congenital supravalvular aortic stenosis Young adults to middle-aged Calcification and fibrosis of congenitally bicuspid aortic valve Rheumatic aortic stenosis Elderly Degeneration & calcification with ageing

69. AS-PATHOPHYSIOLOGY Obstruction to ejection of blood into the aorta caused by a decrease in the aortic valve area necessitates an increase in left ventricular pressure to maintain stroke volume. The normal aortic valve area is 2.5 to 3.5 cm2. Transvalvular pressure gradients higher than 50 mm Hg and an aortic valve area of less than 0.8 cm2 are characteristic of severe aortic stenosis. Aortic stenosis is almost always associated with some degree of aortic regurgitation

70. Angina pectoris may occur in patients with aortic stenosis despite the absence of coronary disease. Goldman and colleagues in 1977 showing that patients with aortic stenosis had an increased risk of perioperative cardiac complications, many studies have demonstrated that patients with aortic stenosis have an increased risk of perioperative mortality and of nonfatal myocardial infarction regardless of the presence or absence of risk factors for coronary artery disease

71. CLINICAL FEATURES OF AORTIC STENOSIS Symptoms(develop when preload reserve exhausted) Angina Exertional syncope Exertional dyspnoea Sudden death Episodes of acute pulmonary oedema Signs Slow-rising carotid pulse Narrow pulse pressure Heaving apex beat (LV pressure overload) Ejection systolic murmur aortic area Signs of pulmonary venous congestion (crepitations)

72. DIAGNOSIS ECG:LVH CXR-Ascending aorta dilatation(post- stenotic ) Echo+Doppler -Assess severity of AS: Aortic valve area Transvalvular pressure gradient LVH Other points noted in Echo- Valve thickening/calcification Mobility of leaflets Bicuspid valve Systolic/diastolic dysfunction

73. C- Xray – Ascending aorta dilation

74. SEVERITY OF AS Grade Mean Pressure Gradient (mm Hg) Valve Area (cm 2 ) Mild <25 ≥1.5 Moderate 25-40 1.0-1.5 Severe 40-50 0.7-1.0 Critical >50 <0.7 The normal valve area is 2.5 to 3.5 cm 2

75. Treatment Asymptomatic - medical management Symptomatic - Aortic valve replacement Coronary revascularization - pts with both aortic stenosis and CAD Percutaneous aortic balloon valvotomy - adolescents & young adults with congenital /rheumatic etiology

76. Indications for aortic valve replacement Severe AS with any of the classic symptoms(angina/syncope/dyspnoea) Severe AS undergoing CABG Severe AS undergoing surgeries on aorta or other heart valves Operative mortality is high in pts with severe LV dysfunction & low transvalvular pressure gradient but improves fnctionl status.

77. Management of Anesthesia Principle : AS is a fixed cardiac output state & hypertrophied LV is sensitive to ischemia Prevention of hypotension & hemodynamic changes that ↓cardiac output Anesthetic Considerations    Maintain normal sinus rhythm  /Avoid bradycardia or tachycardia   Avoid hypotension    Optimize intravascular fluid volume to maintain venous return and left ventricular filling

78. ANAESTHETIC GRID IN AS LV PRELOAD HR RHYTHM CONTRACTILITY SVR PVR ↑ Avoid ↓ or↑ Maintain sinus rhythm Maintain constant ↑ Maintain constant

79. Key pts in intraop BP management Rx intraop hypotension with directly acting alpha agonists( phenylephrine )…. Rapid transfusion to correct hypovolemia / cardioversion shouldn’t delay administration of direct acting vasopressors Inotropes -if signs of myo ischemia persist despite above Rx Avoid vasodilators to Rx intraop HTN

80. Induction of Anesthesia General anesthesia selected in preference to neuraxial block – HYPOTENSION Induction of anesthesia Etomidate, opioids, midazolam Ketamine - avoid Thiopentone - decreases preload Propofol – hypotension

81. Maintenance of Anesthesia Nitrous oxide / volatile anesthetic and opioids or by opioids alone. Marked LV dysfunction - nitrous oxide + opioids or high dose opioids alone - recommended Fentanyl (10–25μg/kg) OR Sufentanil (2–5μg/kg) primary anesthetic for maintenance

82. MAINTENANCE Neuromuscular blocking drugs with minimal hemodynamic effects

83. PREGNANCY CONSIDERATIONS CS GA with invasive haemodynamic monitoring Spinal anaesthesia contraindicated vaginal delivery careful epidural analgesia maintenance of BP with vasopressors – phenylephrine

84. AORTIC REGURGITATION ETIOLOGY Congenital Bicuspid valve or disproportionate cusps Acquired Rheumatic disease Infective endocarditis Trauma Aortic dilatation - Marfan's syndrome, aneurysm, dissection, syphilis, ankylosing spondylitis

85. PATHOPHYSIOLOGY The basic hemodynamic derangement in aortic regurgitation is a decrease in cardiac output because of regurgitation of a part of the ejected stroke volume from the aorta back into the left ventricle during diastole. Combined pressure and volume overload on the left ventricle

86. The magnitude of the regurgitant volume depends on (1) the time available for the regurgitant flow to occur, which is determined by the heart rate (2) the pressure gradient across the aortic valve, which is dependent on the systemic vascular resistance. The magnitude of aortic regurgitation is decreased by tachycardia and peripheral vasodilation . With aortic regurgitation, the entire stroke volume is ejected into the aorta. Because the pulse pressure is proportional to the stroke volume and aortic elastance , the increased stroke volume increases systolic pressure, and systolic hypertension increases afterload .

87. The left ventricle compensates by developing hypertrophy and enlarging to accommodate the volume overload. Because of the increased oxygen requirements necessitated by left ventricular hypertrophy and the decrease in aortic diastolic pressure, which reduces coronary blood flow, angina pectoris may occur in the absence of coronary artery disease.

88. CLINICAL FEATURES Symptoms Mild to moderate AR Often asymptomatic palpitations Severe AR Breathlessness Angina

89. CLINICAL FEATURES Signs Pulse - collapsing' pulse increased pulse pressure Bounding peripheral pulse Capillary pulsation in nail beds Femoral bruit Murmurs Early diastolic murmur Systolic murmur (increased stroke volume) Austin Flint murmur (soft mid-diastolic) Other signs Displaced, heaving apex beat (volume overload) Fourth heart sound Pulmonary venous congestion ( crepitations )

90.   Severity of Aortic Regurgitation by Echocardiography   Mild Moderate Severe Regurgitant jet width as percentage of LVOT width 25–46 47–64 >65 Regurgitant jet area as percentage of LVOT area   4–24 25–59 >60

91. Treatment Medical Therapy Asymptomatic Patients with Normal Left Ventricular Function Afterload reduction Vasodilators Nifedipine ACE inhibitors Hydralazine Surgical Therapy Acute Aortic Regurgitation 1) Vasodilators – Nitroprusside 2)course of antibiotics 3) Valve replacement /repair Chronic Aortic Regurgitation Aortic valve repair Aortic valve prosthesis

92. ANAESTHETIC GOALS Normal heart rate - Avoid bradycardia Maintain sinus rhythm Adequate volume loading High normal systemic vascular resistance Minimize myocardial depression

93. ANAESTHETIC GRID IN AR LV PRELOAD HR RHYTHM CONTRACTILITY SVR PVR ↑ ↑ Maintain sinus rhythm Maintain ↓ Maintain constant

94. Induction of Anesthesia In stable patients - sodium thiopental / Etomidate Alternatively - high dose narcotic and benzodiazepine induction critically ill with acute AR - require inotropic and vasodilatory support prior to induction of anesthesia.

95. Maintenance of Anesthesia Severe LV dysfunction- nitrous oxide plus a volatile anesthetic and/or opioid. Isoflurane, desflurane & sevoflurane Severe LV dysfunction - high dose opioid Bradycardia and myocardial depression – N2O / BZD high-dose narcotic

96. Increase in heart rate associated with PANCURONIUM administration could be helpful. Bradycardia with hemodynamic compromise treated promptly. Atropine 0.4–0.8mg Ephedrine - poor choice because ↑ in afterload Hypotension not treated routinely with vasopressors Spinal/Epidural well tolerated.

97. Pregnancy considerations Avoidance of aortocaval compression Epidural analgesia and anesthesia ↓ afterload and is preferred for vaginal / cesarean delivery During labor early administration of epidural analgesia prevents the pain-associated ↑ SVR –prevent acute LV volume overload Bradycardia not tolerated - treated promptly.

98. Right-sided valvular lesions TRICUSPID STENOSIS Rare & usually coexists with MS Back pressure into the right atrium Upper-extremity venous congestion, hepatic enlargement, and ascites Medical: Salt restriction, digitalization, diuretics Surgical therapy- valvuloplasty / valve replacement Anaesthetic goal: Maintain preload & control HR

99. Tricuspid regurgitation It is usually functional Caused by tricuspid annular dilation secondary to RV enlargement or pulmonary hypertension OTHER CAUSES OF TR infective endocarditis , rheumatic fever chest trauma Ebstein’s anomaly

100. TR is well tolerated by most patients in the absence of pulmonary hypertension. In moderate to severe TR, tricuspid annuloplasty may be considered N2O can increase TR Inotropes like dobutamine , isoproterenol dilate pulmonary vasculature

101. THE PULMONIC VALVE I solated from the other three heart valves by the infundibulum . Pulmonary valvular disease is usually congenital Stenosis > regurgitation Congenital pulmonary stenosis is usually treated with balloon valvuloplasty.

102. Mild pulmonary regurgitation occurs in cardiac surgical patients with a PAC Significant PR rare & well tolerated RV dysfunction secondary to pulmonary regurgitation should be surgically corrected.

103. REFERENCES Stoelting’s Textbook of Coexisting diseases Miller’s Textbook of Anaesthesia Kaplan’s Textbook of Cardiac anaesthesia Practical Approach to Cardiac Anaesthesia( Henseley & Martin ) Harrison’s Textbook of Internal Medicine Davidson’s Textbook Of Medicine

104. THANK YOU