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Valvular heart disease

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Presentation on theme: "Valvular heart disease"— Presentation transcript:

1 Valvular heart disease

2 CAD Vs VHD Unlike CAD the symptoms are not related to poor myocardial performance in VHD The ventricular function may be normal or even supranormal in VHD Symptoms are related to the alterations in the loading conditions in VHD: Volume overload Pressure overload

3 Anaesthetic management Patient is asleep Maintain haemodynamics Pathophysiology Haemodynamic effects of anaesthetic agents

4 Normal Everything goes in the right direction without impediment 7 25 / 7 12 120 / 12 RV RA LA LV PA 25 / 12 Ao 120 / 80

5 Your Basic Loop B C A D EDV ESV SV

6 Mitral Stenosis Fixed, chronic obstruction to LV filling 10 45 / 10 19 100 / 10 45 / 19100 / 65 LA, RV  LV 

7 Mitral Stenosis VOLUME PRESSURE

8 Left atrial pressure overload Diastolic inflow to LV: maintained by development of elevated pressure gradient across mitral valve Dilatation of LA Pressure Increase in PVR: pulmonary hypertension RV dilatation TR Biventricular failure with pulmonary congestion, peripheral edema and ascites



11 Changes in left ventricle Restriction of diastolic inflow: preload reserve is limited Intrinsic myocardial depression: rheumatic etiology Excess afterload: inadequate wall thickness, accounts for higher afterload at relatively normal end-systolic pressure

12 Assessment of severity Symptoms and Clinical examination X-ray chest Echo: Valve area: Normal: 4.5 cm 2 Mild: 1.5 to 2.5 cm 2 Moderate: 1 to 1.5 cm 2 Severe: < 1 cm 2 RVSP

13 Anaesthetic goals Mild disease: not to worry? Control the heart rate Restore and preserve sinus rhythm if possible Avoid hypovolemia Avoid systemic vasodilators Maintain normocarbia Nitroglycerin/nitroprusside

14 Effect of tachycardia Tachycardia shortens diastole proportionately more than systole Decreases the overall time available for transmitral flow In order to maintain CO, the flow rate per unit time must increase Pressure gradient increases by the square of the increase in flow rate


16 Tempe DK, et al: J Cardiothorac Vasc Anesth 1995;9:552-557

17 Mitral Regurgitation Chronic LV & LA volume overload  orifice size, time, pressure gradient 7 25 / 7 19 130/19 25 / 19 130/55 LA, LV 

18 Mitral regurgitation VOLUME PRESSURE



21 Pulmonary hypertension in mitral regurgitation Passive congestion of the pulmonary circulation Reactive pulmonary vasoconstriction Intrinsic LV dysfunction Combination of above

22 MR: assessment of the severity Symptoms and clinical examination X-ray chest Echo: Jet area RVSP LV dimensions: end-systolic > 4.5 cm LV ejection fraction

23 Anaesthetic goals In general, patients suffering from MR (except those with severe MR and severe PAH) tolerate anaesthesia well Faster, fuller, vasodilated

24 Aortic Insufficiency Chronic LV volume overload  orifice size, time, pressure gradient 7 25 / 7 15 150 / 17 25 / 15 150 / 55 LV 



27 AR: assessment of severity History and clinical examination X-ray chest Echo: Mild, moderate, severe LV dimensions: End-systolic >5.5 cm

28 AR: anaesthetic goals In general, patients tolerate surgery and anaesthesia well, unless CHF or LV dysfunction is present Aim: to decrease the regurgitant fraction Faster, fuller and vasodilated Monitor MAP

29 Aortic Stenosis Fixed, chronic obstruction to LV ejection at the level of the aortic valve LV  7 25 / 7 190 / 22 30 / 15110 / 65 17

30 Aortic Stenosis VOLUME PRESSURE


32 Low Compliance Ventricle

33 Aortic stenosis: pathophysiology Normal aortic valve area: 2.5 to 3.5 cm 2 Haemodynamically significant obstruction occurs at valve area of < 1 cm 2 Pressure overload causes concentric hypertrophy of LV

34 Thickened LV wall compliance of LV Ventricular filling depends upon adequate intravascular volume and atrial contraction NSR is very important: atrial contraction can contribute up to 40% of LV filling

35 Decreased compliance Increased LVEDP Pulmonary congestion CPP CHFIschaemia

36 Myocardial contractility is usually well preserved with normal ejection fraction until very late in the course of the disease

37 Aortic stenosis: anaesthetic goals Mild disease: not to worry Sinus rhythm is important Bradycardia is dangerous Maintain adequate preload Avoid ischaemia (Hypertension/Hypotension) PA catheter?


39 Open heart surgery Induction of anaesthesia Monitoring Heparinisation Establishing the bypass Termination of bypass Protamine administration Transfer to ICU Postoperative management Ventilation Management of pain and sedation

40 Anaesthetic management Opioids should form a “base” Hypnotics and / or benzodiazepines in small doses used as supplemental agents during induction of anaesthesia

41 Muscle relaxants Succinylcholine : 1 to 1.5 mg/ Kg Pancuronium : 0.08 to 0.15 mg/Kg Vecuronium : 0.08 to 0.2 mg/Kg Atracurium :0.5 to 1 mg/Kg rocuronium :0.6 mg/Kg

42 Pt arrives in the OT venous access additional morphine/midazolam if premed. inadequate arterial cannulation (lt radial) good LV: induction bad LV: PAC, CVC and wide bore venous access

43 Induction Morphine: 0.5 to 0.75 mg/Kg OR Fentanyl: 5 to 10 µg/Kg Hypnosis with: diazepam or midazolam (2-5 mg) :thiopental (50-100 mg)

44 Maintenance of anaesthesia Opioid Nitrous oxide Volatile agents Halothane Isoflurane Isoflurane: The clinical evidence suggests that isoflurane is safe in patients with CAD and if hypotention is avoided, it is safe even in patients with steal prone anatomy

45 Maintenance of anaesthesia (contd.) On bypass Opioid + relaxant + benzodiazepine in the prime Repeat half dose every hour Propofol Inhalational agent

46 Haemodynamic monitoring ECG Arterial pressure CVP PA catheter LA pressure Trans-oesophageal echo (TOE)














60 Mehta N, Lochab S, Tempe DK, Cath Cardiovasc Diag 1998;43:87











71 Heparinisation 3-4 mg/Kg of heparin is administered 3-5 min before aortic cannulation ACT monitoring >300 sec is safe as no clot formation has been reported below this limit Generally acceptable figure is >400 sec Dose response curve








79 Cardiopulmonary bypass Partial bypass Total bypass Aortic cross clamping Infusion of cardioplegia Into the root of aorta Directly in to the coronaries Retrograde: coronary sinus Release the aortic clamp Come off CPB

80 Cardiovascular support Inotropes EpinephrineMilrinone DobutamineAmrinone DopamineEnoximone Dopexamine Norepinephrine Isoprenaline Dilators NTG SNP Ca blockers, Beta blockers

81 Changing trends in anaesthetic management Based on the objective of facilitating early extubation General anaesthesia Lower or no doses of opioids Propofol Isoflurane, sevoflurane vecuronium

82 Problems of such anaesthetic technique Awareness Postoperative pain relief Haemodynamic instability?

83 Patients can be reversed with neostigmine at the end of the surgery Extubation can be managed in the ICU

84 Postoperative pain relief Thoracic epidural (bupivacaine 0.5%, 0.05-0.1 mL/Kg) with general anaesthesia Intrathecal morphine (5-10 µg/Kg) by lumbar approach with general anaesthesia Intrapleural analgesia Intercostal block


86 Conclusions Opioids in variable doses still form the basis of cardiac anaesthesia With the availability of newer anaesthetic agents, the safety has improved Early extubation in valvular heart surgery is being practiced at few centres, but care should be exercised in sicker patients.

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