Many cardiac malformations cause a mixture of venous blood and arterialised blood at ventricular ejection: tetralogy of Fallot, single ventricle, transposition of the great arteries, truncus arteriosus, etc. Although these heart diseases rarely allow survival into adulthood, they are nevertheless instructive from a pathophysiological perspective. In tetralogy of Fallot, the pulmonary vascular tree is protected by pulmonary stenosis. However, this is not the case in the other pathologies mentioned – here, pulmonary flow is proportional to the ratio of SVR to PVR. If SVR is increased, there is a risk of excessive pulmonary blood flow and pulmonary overload. Although SpO₂ increases, systemic blood flow may become insufficient, and the patient suffers from metabolic acidosis due to low blood flow [1]. The aim is therefore to establish equilibrium between the two circulations (Qp/Qs close to 1:1) and not the best possible SpO₂. SaO₂ of 80-85% without any acidosis is a highly satisfactory outcome. It may therefore be necessary to increase PVR during anaesthesia: low FiO₂ (0.3), hypercapnia by hypoventilation or adding CO₂ during CPB. 


 

Mixed cyanotic shunt

If the flows ejected by the ventricle(s) are not separated, the Qp/Qs ratio must remain close to 1:1, even if O2 saturation remains lowered.

© BETTEX D, CHASSOT PG, January 2008, last update May 2018



References 

1    LEYVI G, WASNICK JD. Single-ventricle patient: pathophysiology and anesthetic management. J Cardiothorac Vasc Anesth 2010; 24:121-30
 

 

 

 

 

 

Référence 
 

 

  1    LEYVI G, WASNICK JD. Single-ventricle patient: pathophysiology and anesthetic management. J Cardiothorac Vasc Anesth 2010; 24:121-30