11.8.6 Anaesthesia principles in cardiac surgery

 Aortic stenosis imposes a very restrictive limit on cardiac output, because the systolic volume ejected depends on the duration of systole and the LV power ; the latter hypertrophies, but its contractile force per unit of mass does not increase; in the long term, it eventually fails in the face of excessive afterload. From these pathophysiological data, we can derive some basic rules for anaesthesia. 
 
  • Preload: as LV compliance is impaired by concentric hypertrophy, end-diastolic pressure is high. Stroke volume is highly dependent on filling as the Starling curve is straightened; hypovolaemia causes profound hypotension, especially as compensatory tachycardia is limited by the slow flow through the stenosis. Curarisation and the initiation of controlled ventilation cause significant drops in pressure due to the restriction of systemic venous return. CVP or PCWP underestimate filling because of diastolic dysfunction: for the same end-diastolic volume, PtdLV is higher; a patient may be hypovolemic with a normal PCWP. Preload must be maintained by adequate blood volume.
  • Afterload: An increase in SBP hardly changes the workload of the LV because the upstream obstacle represented by the stenosis is greater and fixed. On the other hand, arterial hypotension (low SAR) reduces coronary perfusion and increases the transvalvular pressure gradient. As cardiac output is relatively fixed, blood pressure depends solely on the SAR. Alpha vasoconstrictors (phenylephrine, noradrenaline) are the first choice in hypotension.
  • Contractility: generally preserved, it is reduced only in the phase of myocardial decompensation and congestive failure. It must then be maintained within the limits imposed by the supply of O2 (associated ischaemia) with an inotropic agent.
  • Frequency: Ejection and filling times are necessarily slowed to maintain stroke volume; tachycardia reduces flow and simultaneously increases mVO2. However, bradycardia cannot be compensated for by an increase in stroke volume because the ventricular chamber is too small (concentric LVH) or the myocardium is insufficient (dilatation and decompensation phase). Loss of sinus rhythm due to atrial and/or junctional tachyarrhythmias reduces output by 40-50%; this risk is present with halogenated agents that depress sinus node function. VESs may rapidly progress to VT and ventricular fibrillation.
  • Ischaemic risk: Not only is the association with coronary artery disease common, but coronary perfusion of healthy vessels is limited by high intramyocardial and intracavitary pressures. Aortic diastolic pressure, represented by mean arterial pressure (MAP), must be strictly maintained above 80 mmHg. Coronary perfusion pressure (CPP) is the difference between MAP and PtdLV; any decrease in MAP will decrease CPP by the same amount, because PtdLV is related to the fixed obstruction of aortic stenosis and will not decrease in the presence of hypotension.
  • Positive Pressure Ventilation: Curarisation and initiation of PPV reduce venous return and preload, and are responsible for a significant decrease in stroke volume and arterial hypotension. Equilibration is achieved by increasing preload (elevation of the lower limbs, 500 mL perfusate) and SAR (phenylephrine, noradrenaline); ephedrine is a poor choice because it is tachycardic. 
 On the basis of these data, the choice of technique is guided by clinical considerations, since neither the surface area of the valve nor its pressure gradient are major determinants of the severity of the case, since only tight stenoses are operated on in cardiac surgery. 
 
  • A patient under 65 years of age in good general health with healthy coronary arteries and preserved ventricular function is a candidate for simple management and a fast track: moderate doses of opioids, equipment with arterial catheter, central venous line and TEE, and rapid extubation.
  • The advanced age of some patients (> 75 years) makes them high-risk patients, whether or not they have associated pathologies. However, once they have completed the surgical phase, their prognosis is excellent.
  • The presence of extensive coronary artery disease is always a major risk; combined AVR + CABG carries a mortality rate three times higher than simple AVR. However, there are two possible scenarios
    • Tight aortic stenosis during investigations where a significant, asymptomatic and isolated coronary stenosis is discovered; AVR + simple CABG remains a low-risk procedure that can follow a fast track.
    • Symptomatic triple-vessel coronary artery disease and symptomatic or asymptomatic aortic stenosis. Here, ischaemic disease dominates and prevention is a priority. The combination of multi-CABG + AVR makes these patients "heavy" cases requiring invasive management; prevention of ischaemia and intraoperative haemodynamic stability are the priority, while recovery time is secondary.
  • The presence of congestive heart failure requires invasive monitoring (Swan-Ganz pulmonary catheter, PiCCO™) and a technique adapted to the systolic dysfunction. The best preoperative criterion to assess LV adequacy is its cavity size: in concentric LVH, it should be small; an LV with normal or enlarged dimensions (short-axis Dtd > 4 cm/m2 ) indicates severe dysfunction and/or associated volume overload (aortic or mitral regurgitation).

In the event of inadvertent transition to tachycardia or ventricular fibrillation, resuscitation by external cardiac massage is illusory; only defibrillation can restore cardiac output. When a Swan-Ganz catheter is inserted, there is a significant risk of complete block if there is a previous left bundle branch block. In these circumstances, it is recommended that the catheter is not floated into the PA until the pericardium has been opened and direct resuscitation or rapid transfer to ECC is possible.

 Anaesthesia technique for AVR in case of aortic stenosis

  • As the risk of arrhythmia is high, you must be prepared to defibrillate or cardiovert the patient very quickly. As it is impossible to ensure cardiac output through the stenosis during resuscitation, a surgeon and a perfusionist must be present in the operating theatre from the moment of induction. The induction technique depends on the ischaemic risk and ventricular function.
    • Etomidate: the only agent that does not alter preload, afterload or contractility, it is recommended in all high-risk cases or in cases of LV dysfunction.
    • Midazolam: adequate but reduced central sympathetic tone results in hypotension due to reduced preload and afterload. Prolonged wakefulness.
    • Propofol: reduces preload more than afterload; can be used at appropriate doses and slowly in stable patients, compensated by volume and a vasoconstrictor.
    • Fentanils: beneficial (bradycardia).
    • Thiopental, ketamine: not recommended because of their tachycardia; thiopental has a significant negative inotropic effect.
    • Local anaesthesia of the larynx and trachea should be used to avoid tachycardia or arrhythmia during intubation.
    • Hypotension is much more dangerous than hypertension; proactively administer an alpha vasopressor (phenylephrine) as soon as the blood pressure falls by a few mmHg to avoid a period of coronary hypoperfusion. Induction in aortic stenosis should be performed with a syringe of phenylephrine in the hand!
    • In the event of electromechanical arrest or dissociation, cardiac massage is illusory; the only solution is to put the patient on bypass as soon as possible (femoral cannulation).
  • Maintenance of anaesthesia: avoid a fall in SAR and an increase in mVO2.
    • Sevoflurane: the agent of choice.
    • Propofol perfusion: adjust doses to ensure haemodynamics remain stable.
    • Isoflurane: not recommended (↓ SAR and tachycardia).
    • Desflurane: not recommended (↑ frequency and PAP).
    • IPPV ± PEEP (< 8 cm H2O): tolerated once haemodynamics have adapted by increasing preload and SBP; keep mean inspiratory pressure (mean Pit) as low as possible.
    • Systemic hypotension: ↑ SAR with an alpha vasopressor (phenylephrine, noradrenaline), maintain blood volume.
  • Avoid tachycardia and loss of sinus rhythm.
    • Contraindicated are thiopental, ketamine and pancuronium.
    • No ephedrine; for hypotension: phenylephrine (CF ↓ ), noradrenaline.
    • Do not use atropine in cases of excessive bradycardia (unpredictable response); prefer ephedrine.
    • After AVR, tachycardia is less dangerous.
  • If necessary, maintain contractility.
    • Dopamine adequate if dose < 5 mcg/kg/min.
    • If higher: dobutamine + noradrenaline.
  • TEE monitoring.
    • LV size and function, degree of LVH, LV function.
    • Assessment of blood volume.
    • Aortic valve: calcification, atheroma in the aorta, measurements of the annulus and the aorta, possible AI (monitoring of the LV to avoid dilatation during cardioplegia).
    • Measurement of LVOT: diameter, septal spur, Vmax.
    • If IM: mechanism; possibility of combined operation (MVR or associated MVP).
    • After ECC: prosthesis function, paravalvular leakage, MI, HOCM effect.
  • Pulmonary artery catheter.
    • Not indicated in simple AVR.
    • Measurement of PAP in PHT or right-sided failure.
    • PCWP: reflects pulmonary capillary pressure and LV diastolic pressure; useful to assess CPP in ischaemia (CPP = MAP - PCWP) but misleading in hypovolaemia.
    • There is a high risk of serious arrhythmias when crossing the RV (ventricular tachycardia, complete block if LBB is already present); it is advisable to leave the Swan-Ganz in RA (protective cover unrolled) until the pericardium is opened; it is positioned when the surgeon is ready to insert the cannulas, so that ECC can be started in the event of an uncontrollable arrhythmia.
  • ScO2 : assessment of peripheral perfusion.

 Anaesthesia technique according to approach

AVR is usually performed via a median sternotomy with cannulation of the ostia oblongata and ascending aorta, aortic clamping and cardioplegia via the root of the aorta, supplemented by direct cannulation of the coronary ostia. ECC time is typically less than one hour. Competition from percutaneous aortic prosthesis implantation has stimulated the development of minimally invasive surgery. This allows a fast-track anaesthetic circuit with reduced opiate doses, early extubation and reduced immediate post-operative morbidity (see Chapter 4, Fast-track). The minimally invasive route has several features for the anaesthetist [2].

  • High median sternotomy approach over the ascending aorta (10-12 cm incision) or anterior right mini-thoracotomy in the 3rd or 4th intercostal space; pulmonary exclusion is not necessary, so standard intubation is performed.
  • These routes do not provide access to the ventricles or pericardial space. Cannulation must be modified accordingly.
    • ECC arterial cannulation via the femoral or right subclavian route; TEE verifies the presence of the spike in the descending aorta. It is a good idea to place a pulsoximeter on a toe or finger on the side of the cannulation to monitor the peripheral circulation of the limb.
    • Venous cannulation via the femoral route; the guidewire is visualised on TEE in bi-caval view (100°) when entering the RA and should enter the superior vena cava. In the case of a PFO, it may enter the LA.
    • The left vent, usually placed in the LV via the right superior pulmonary vein, is replaced by a pulmonary suction catheter (EndoVent™) placed via the right internal jugular vein.
    • For retrograde cardioplegia, the coronary sinus cannula is inserted via the right internal jugular vein and manipulated under TEE control.
  • External defibrillator plates placed anteroposteriorly.
  • Anaesthetic technique aimed at early extubation: propofol or sevoflurane, no midazolam, restrictive doses of fentanyl, dexmedetomidine, normothermia, analgesia by local anaesthetic infiltration, etc.

This approach tends to reduce morbidity (transfusion, mechanical ventilation, pain) compared with conventional surgery, particularly in elderly patients at risk; mortality is identical or slightly lower than with the usual approach (2.3% versus 3.0%) [1].

The general recommendations for anaesthesia during AVR for aortic stenosis can be summarised simply:

 

Hemodynamic sought in case of aortic stenosis 
 High preload

Systemic vasoconstriction (MAP ≥ 80 mmHg)

Normal frequency, sinus rhythm

Inotropic support if ventricular dysfunction (Dtd > 4 cm/m2 )

Low blood pressure is more dangerous than high blood pressure

Positive pressure ventilation: Low pit

Full - Regular - Closed  

 

 

 © CHASSOT PG, BETTEX D, August 2011, last update November 2019

 

References

 

  1. LIM JY, DEO SV, ALTARABSHEH SE, et al. Conventional versus minimally invasive aortic valve replacement: pooled analysis of propensity-matched data. J Card Surg 2015; 30:125-34
  2. RAMAKRISHNA H, PATEL PA, GUTSCHE JT, et al. Surgical valve replacement - Clinical update on recent advances in the contemporary era. J Cardiothorac Vasc Anesth 2016; 30:1733-41