Cardiopulmonary bypass (CBP) is used to temporarily perform the functions of the heart (circulation of blood) and lungs (gas exchange) during surgical procedures on the heart and great vessels. It involves a pump and oxygenator connected through an extracorporeal circuit that provides oxygenated blood flow to the systemic circulation, bypassing the heart and lungs.

1. Components of circuit
   1. Venous blood is drained from the venous cannula (inserted into the right atrium) to a venous reservoir. Maintaining an adequate fluid level in the venous reservoir is critical to prevent air entrainment.
   2. A pump (roller or centrifugal) propels the venous blood forward. Unlike roller pumps, centrifugal pumps are afterload sensitive and will decrease flow if resistance increases (eg, with outflow obstruction). Centrifugal pumps are less traumatic to blood and do not pump air.
   3. Venous blood enters a heat exchanger and an oxygenator that adds oxygen and removes carbon dioxide by adjusting the FiO₂ and sweep rate. A volatile anesthetic (eg, isoflurane) is added to the oxygenator gas mixture. The arterialized blood enters the systemic circulation via an aortic cannula, which is usually inserted in the ascending aorta. The femoral artery is sometimes used for aortic cannulation for emergency or redo sternotomy situations.
   4. Cardioplegic solution containing high potassium is infused into the coronary circulation to induce and maintain cardiac arrest. Cardioplegia can be infused via the aortic root or coronary ostia (antegrade) or through the coronary sinus (retrograde).
   5. Left ventricular (LV) vent removes blood that accumulates in the LV to decrease wall tension by suctioning on the same catheter placed for antegrade cardioplegia or one inserted into the LV via the right pulmonary vein across the mitral valve (MV).
2. CPB pathophysiology. Contact of blood with the CPB circuit can lead to an intense systemic inflammatory response via the complement, kallikrein and coagulation cascades. A prolonged CPB time is associated with multisystem compromise including neurologic dysfunction, acute respiratory distress syndrome, coagulopathy, hepatic insufficiency, and acute kidney injury. A number of approaches have been tested to decrease inflammation in CPB including leukocyte depletion, hemofiltration, administration of monoclonal antibodies against inflammatory mediators, and the coating of circuitry with heparin. None have shown definitive clinical benefit in humans.
3. CPB effects on pharmacokinetics. CPB results in increased volume of distribution and decreased protein binding. Acid-base shifts can affect the ionized and unionized concentrations of drugs. Decreased perfusion pressures during CPB can lead to reduced hepatic and renal clearance. Hypothermia further decreases hepatic enzyme function.