11.9.6 Anesthesia principles

• Preload: this must remain high to compensate for the regurgitant volume and to keep the LV at the top of the Starling curve, but any excess will increase wall stress and, secondarily, protosystolic afterload. There is little room for manoeuvre as hypovolemia and hypervolemia are poorly tolerated.
• Afterload: the reduction in AI is doubly significant:
  • AI decreases as PAdiast decreases;
  • LV ejection is improved when PAsyst decreases.
    Systemic arterial vasodilatation is best achieved with isoflurane, an alpha-blocker (phentolamine, hydralazine) and/or nitroprusside; moreover, all three are tachycardic. Antagonists are not recommended (negative inotropic and chronotropic effects). In the case of systemic hypotension, ephedrine (effects α venous and β ) and volume (infusions) are sufficient, but phenylephrine is contraindicated as it has a pure alpha effect and causes reflex bradycardia. When reducing the SAR, avoid excessive diastolic hypotension that would compromise coronary perfusion, especially if there is evidence of ischaemia; empirically find the best compromise for each individual case.
• Contractility: must be maintained or improved. The agents of choice are amines with pure β effects (dobutamine, isoprenaline) and inodilators such as anti-phosphodiesterase-3 (milrinone) or levosimendan. β-blockade is contraindicated intraoperatively and in acute situations, but is often prescribed at low doses in the chronic management of AI associated with ascending aortic aneurysm. EF does not reflect true systolic function because of the very specific loading constraints; the telesystolic dimension of the LV is a better criterion: the LV is dysfunctional when its telesystolic diameter is > 2.5 cm/m² .
• Rate: tachycardia shortens diastole and therefore reduces regurgitant time, regurgitant volume per diastole, Vtd and LV Ptd; coronary perfusion is improved. The ideal rate is around 80 beats/minute and bradycardia must be avoided. Recommended agents: isoflurane, pancuronium, ephedrine.
• Pulmonary resistance: normal in the absence of mitral insufficiency or left-sided decompensation.
• Positive pressure ventilation: generally well tolerated (lower LV afterload) provided venous return is maintained. If PAP is normal, hyperventilation should be avoided as hypocapnia induces systemic vasoconstriction.

 Anaesthesia technique for AVR in aortic insufficiency

• Induction technique depends on the degree of LV compensation/decompensation.
  • Etomidate: the only agent that does not alter preload, afterload or contractility, it is recommended if there is LV dysfunction or dilation.
  • Midazolam: adequate, the decrease in central sympathetic tone leads to a reduction in SAR; risk of slight bradycardia.
  • Propofol: reduces preload more than afterload; can be used in appropriate doses and slowly in stable patients, compensating with volume; should be avoided in LV failure.
  • Fentanils: slow administration due to bradycardia; fentanyl and sufentanil OK, but remifentanil not recommended.
  • Thiopental, ketamine: their tachycardia would be beneficial, but the reduction in contractility (thiopental) and increase in SAR (ketamine) are prohibitive.
  • Topical anaesthesia of the larynx and trachea should be used to prevent hypertension during intubation.
  • Curare: pancuronium.
  • Bradycardia is the most dangerous risk.
• Maintain anaesthesia: look for a decrease in SAR and avoid bradycardia.
  • Isoflurane: agent of choice ( ↓ SAR and tachycardia); sevoflurane: little effect on SAR.
  • Perfusion of propofol or midazolam: adjust doses to ensure haemodynamic stability.
  • Desflurane: not recommended ( ↑ SAR and PAR).
  • IPPV ± PEEP (< 8 cm H₂O): beneficial for the LV as long as venous return is maintained.
  • Systemic hypotension: ↑ volume (infusions), ephedrine; no α vasopressor .
• Avoid bradycardia, which is the most dangerous risk.
• Reduce SAR ( ↓ IA) but avoid diastolic hypotension which would compromise coronary prefusion, especially if there is evidence of ischaemia.
• Support contractile function.
  • Dobutamine.
  • Inodilator: milrinone (± adrenaline), levosimendan.
• TEE monitoring.
  • LV size and function, degree of dilation, segmental kinetics, RV function.
  • Assessment of blood volume.
  • Aortic valve: type of lesion, dilatation of the aortic root, possibility of valve preservation, feasibility of surgery.
  • If MI: mechanism.
  • Post-CEC: prosthesis function, paravalvular leak, prosthesis control, residual AI, MI.
• Pulmonary artery catheter: useful to assess PCWP and effective SV.
  • PCWP: reflects pulmonary capillary pressure (stasis), but underestimates LV diastolic pressure (high) in the event of premature mitral valve closure due to aortic regurgitation; very useful for assessing CAP in ischaemia (CAP = MAP - PCWP).
  • Measurement of anterograde VS, systemic DC and SvO₂ (adequacy to metabolic needs).
  • Measurement of PAP in PHT or right-sided failure.
• ScO₂ : Assessment of peripheral perfusion.
• PiCCO™: calibration of transpulmonary thermodilution is biased by AI.

These principles can be summarised as follows

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