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Valvular heart disease www.anaesthesia.co.in [email protected] om

Valvular heart disease [email protected]

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Valvular heart disease

www.anaesthesia.co.in

[email protected]

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

Anaesthetic management

Patient is asleep Maintain haemodynamics

Pathophysiology Haemodynamic effects of anaesthetic agents

NormalEverything goes in the right direction without impediment

7

25 / 7

12

120 / 12RV

RA LA

LV

PA25 / 12

Ao120 / 80

Your Basic Loop

B

C

A

D

EDV

ESVSV

Mitral StenosisFixed, chronic obstruction to LV filling

10

45 / 10

19

100 / 10

45 / 19 100 / 65

LA, RV

LV

Mitral Stenosis

VOLUME

PR

ES

SU

RE

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

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

Assessment of severity Symptoms and Clinical examination X-ray chest Echo:

Valve area: Normal: 4.5 cm2

Mild: 1.5 to 2.5 cm2

Moderate: 1 to 1.5 cm2

Severe: < 1 cm2

RVSP

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

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

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

Mitral Regurgitation

Chronic LV & LA volume overload orifice size, time, pressure gradient

7

25 / 7

19

130/19

25 / 19130/55

LA, LV

Mitral regurgitation

VOLUME

PR

ES

SU

RE

Pulmonary hypertension in mitral regurgitation Passive congestion of the

pulmonary circulation Reactive pulmonary

vasoconstriction Intrinsic LV dysfunction Combination of above

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

Anaesthetic goals

In general, patients suffering from MR (except those with severe MR and severe PAH) tolerate anaesthesia well

Faster, fuller, vasodilated

Aortic Insufficiency

Chronic LV volume overload orifice size, time, pressure gradient

7

25 / 7

15

150 / 17

25 / 15 150 / 55

LV

Aortic Insufficiency

VOLUME

PR

ES

SU

RE

ACUTE

CHRONIC

AR: assessment of severity History and clinical examination X-ray chest Echo:

Mild, moderate, severe LV dimensions: End-systolic >5.5 cm

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

Aortic Stenosis Fixed , chronic obstruction to LV ejection at the level of the aortic valve

LV

7

25 / 7 190 / 22

30 / 15 110 / 65

17

Aortic Stenosis

VOLUME

PR

ES

SU

RE

Pre

ssur

e

Volume

Low Compliance Ventricle

Aortic stenosis: pathophysiology Normal aortic valve area: 2.5 to

3.5 cm2

Haemodynamically significant obstruction occurs at valve area of < 1 cm2

Pressure overload causes concentric hypertrophy of LV

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

Decreased compliance

Increased LVEDP

Pulmonary congestion CPP

CHF Ischaemia

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

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?

OPEN HEART SURGERY

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

Anaesthetic management

Opioids should form a “base” Hypnotics and / or

benzodiazepines in small doses used as supplemental agents during induction of anaesthesia

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

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

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)

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

Maintenance of anaesthesia (contd.)

On bypass Opioid + relaxant + benzodiazepine

in the prime Repeat half dose every hour

Propofol Inhalational agent

Haemodynamic monitoring

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

Mehta N, Lochab S, Tempe DK, Cath Cardiovasc Diag1998;43:87

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

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

Cardiovascular support

Inotropes Epinephrine Milrinone Dobutamine Amrinone Dopamine Enoximone Dopexamine Norepinephrine IsoprenalineDilators NTG SNPCa blockers, Beta blockers

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

Problems of such anaesthetic technique

Awareness Postoperative pain relief Haemodynamic instability?

Patients can be reversed with neostigmine at the end of the surgery

Extubation can be managed in the ICU

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

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.

www.anaesthesia.co.in [email protected]