Clinical questions

Q. What are other cardiac causes of chest pain?

A. Aortic stenosis, AS with AR, CAD

Q. What are non- ischaemic cardiac causes of chest pain?

A. Aortic dissection/ Severe RVH/ PA dilatation /Pericarditis/ MVP

Q. what does absence of ejection click suggest?

A. Absence of ejection click suggests ‘Calcific AS’

Q. What is the commonest age group of presentation in AS ?

A. 60 plus

Q. How to assess severity of AS clinically ?

A. Late peaking of murmur – The sign !

    Soft S2 and

    Pulses parvus et tardus. These are the signs indicative of severity of AS.

Q. Why it is valvular AS and not supravalvular or subvalvular AS ?

A. Presence of ejection click suggests valvular AS.

Q. What is Gallaverdin phenomenon?

A. In patients with severe calcific AS,a high velocity ejection produces a loud mid systolic murmur in aortic area and vibrations of the AV during systole create a soft apical musical murmur.This is called Gallaverdin dissociation of AS or phenomenon.

Q. What is the pathophysiology of AS ?

   The stenosis that occurs at the aortic valve leads to pressure gradient from LV to aorta.To overcome this stenosis, the intracavitary increase in systolic pressure increases myocardial wall tension as stated by Laplace’s law

     Wall tension = PR / 2h

•    This increase in wall tension is a direct stimulus or leads to parallel replication of sarcomere causing concentric hypertrophy.

•    The pressure gradient and the amount of cardiac output generated also is important as less pressure gradient may be generated when there is less cardiac output due to severe AS.This is explained by simplified Gorlin equation (Hakki equation) 

      AVA = CO / Square root of PG

Coronary perfusion 

•    The increase in LVEDP causes decrease in coronary perfusion as  CPP = ADP – LVEDP

•    Also, severe AS causes decrease in stroke volume which may compromise coronary perfusion.

•    Also, the coronary structural abnormalities, inadequate growth,increased systolic compression decrease the perfusion of hypertrophied myocardium.

Pressure Volume Loop

•    The PV loop in AS- main differences 

•    Peak pressure generated during systole is much greater because of high pressure gradient 

•    Slope of diastolic limb is steep because of decreased diastolic compliance due to LVH

•    This means small changes in diastolic in diastolic volume produce large increase in ventricular filling pressure 

•    Systolic limb shows preservation of pump function (SV & EF)

Atrial kick

o    This increase in chamber stiffness makes “atrial kick” very important in AS.It contributes 40 % of LVEDV

o    Also, the isovolumic relaxation time is increased ( due to abnormal diastolic filling and ventricular relaxation) which leads to less filling during early rapid filling phase so atrial kick becomes so important. The “preload reserve” and LVH are compensatory mechanisms to maintain cardiac output when they fail, LV dilatation occurs and CHF ensues.

Prone for Ischaemia

The hypertrophied LV is more prone for ischaemia because of 

•    Coronary abnormalities 

•    Subendocardialischaemia

•    Associated coronary artery disease

•    Decreased coronary perfusion pressure so decreased coronary supply

•    Increased MVO2

Q.What are the types of Bicuspid Aortic Valves ?

A. 3 morphologic types -

Type I BAV – 

•    Characterized by right-left lea?et fusion

•    70% of patients have this type of  BAV.   

•    Is associated coarctation of aorta, PDA, VSD and coronary variants.

Type II BAV-

•    Fusion of the right and noncoronary cusps, associated with more frequent valvular degeneration and greater rate of progression for both stenosis and regurgitation. 

Type III BAV-

•    Fusion of left and noncoronary cusps

 Approximately 40% of patients with coarctation of the aorta have an associated bicuspid valve.

Investigations in AS

Q) what are chest Xray findings in AS ?

•    Small heart

•    Dilated ascending aorta

•    Calcification at aortic valve

•    Calcification at aortic knuckle 

Q) what are the ECG findings in AS ?

•    LVH with strain pattern 

•    LBBB

•    Complete heart block if calcium extends on the conduction system 

•    Prolonged PR interval which can occur due to -digoxin toxicity,

calcification extending into AV node

and rheumatic carditis.

Q) what data can be driven from cath in AS ?

•    Systolic gradient between LV and aorta

•    AR assessment 

•    Post stenotic dilatation of aorta

•    Coronaries 

Q) what is the operative mortality for AS ?

A) Overall 3-5 %

     Elderly >70 years 3-16 %

     Associated CAD and Age > 70years 21 %

Q) what is the operative mortality and MI for AVR in AS ?

A) <70>     AVR  3.3 % death and 2.6 % MI

AVR + CABG 5.2 % death and 4.4 % MI

Age > 70 years- 

  AVR 10% death and 1.6 % MI

AVR + CABG 12.3% death 

Q) what is Ross procedure,Ross 2 and Double Ross procedure ?

A) Use of autologous pulmonary valve for aortic position and use of homograft/ allograft for pulmonary position is called Ross procedure.

Ross 2 is pulmonary valve is used at mitral area

Double Ross is aortic valve to pulmonary valve and pulmonary valve to aortic valve is done.

Q.What are the problems with LV hypertrophy ?

A. LVH causes 

1. Altered diastolic compliance

2. Imbalance of oxygen supply and demand to myocardium 

3.decrease in intrinsic contractility of myocardium 

Q) What is stone heart ?

A)Irreversible ischaemic contracture that occurs post CPB after AVR is called stone heart.This occurs as the hypertrophied myocardium due to LVH is vulnerable for ischaemia ( See pathophysiology section for explanation)

Q) what are the anaesthetic goals in AS ?

A) Anaesthetic goals are determined according to the cardiac grid-

     Rate – maintained,no tachycardia,no bradycardia 

     Rhythm-sinus rhythm 

     Preload- increased

     After load-increased 

    Contractility- maintained 

Q) why each of this parameter is important?

A) Sinus rhythm- as atrial kick contributes to 40% LV filling

     Preload –Adequate intravascular volume as it is preload dependent 

     After load – avoidance of systemic hypotension as fixed low cardiac output state

And awareness of potential for myocardial ischaemia is very important 

Q) How will you induce this patient ?

A) I will induce AS patient with Surgeon scrubbed and Perfusionist ready with primed CPB.

     This is because if patient has bradycardia or severe hypotension AS being  a state of low and fixed cardiac output cannot compensate immediately by increasing CO.

Q) Which is your choice of induction agent ?

A) Inj Etomidate is of choice in AS 

Anaesthesia Management 

Q) How will you manage this patient posted for AVR ?

A) Firstly, ask investigations of this patient both Routine Investigations and Specific investigations 

Routine Investigations like -

•    Total Hemogram including Hb,CBC,Platelet count 

•    Liver Function Tests 

•    Kidney Function Tests 

•    Thyroid Function Tests 

•    Serum Electrolytes 

•    PT INR

•    Serology 

Specific Investigations like –

Chest Xray 

ECG

Echocardiography (Transthoracic)

Angiography 

Carotid Doppler

After seeing all the investigations give previous night medications like Sedative/Anxiolytic and Antacids 

After securing the wide bore IV line and Radial artery ( with monitors applied) Central venous cannulation under local anaesthesia in Right IJV done

Preoxygenation with 100% oxygen 

Induction with Inj Etomidate 0.2 mg/kg iv,Inj Fentanyl 3-5 micrograms/kg iv,Inj Midazolam 0.05mg/kg iv,Inj Vecuronium0.1mg/kg iv 

Inj Xylocard, Intubate with appropriate sized ETT

PAC,TEE and Foley’s catheter put

M/O – Inj Fentanyl and Inj Vecuronium intermittently at regular intervals 

Inj Heparin 400U/kg iv 

ACT >480 sec

On CPB- myocardial preservation is of particular importance 

While coming off CPB inotropes like Inj Dopamine and/or Inj Adrenaline are used

May be difficulty in coming off CPB due to stone heart (explained elsewhere) so high supports,pacing,IABP is a possibility 

TEE done

Protamine Reversal done.