Published on 13/02/2015 by admin
Filed under Anesthesiology
Last modified 22/04/2025
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David J. Cook, MD and Eduardo S. Rodrigues, MD
Cardiopulmonary bypass (CPB) replaces heart and lung function during cardiopulmonary arrest. The basic features of the circuit are a pump, an oxygenator, and venous return and arterial inflow lines. A heat exchanger and a blood reservoir are also essential elements.
A right atrial or bicaval cannula is the source for drainage of blood into the venous reservoir. Blood exits the reservoir, goes to a pump (roller or centrifugal), and is pumped through an oxygenator (typically hollow fiber), most of which have integrated heat exchangers. For hollow-fiber oxygenators, the PaO2 is determined by the FIO2 of the fresh-gas flow passing countercurrent through the hollow fibers; the PaCO2 is determined by the total gas flow rate though the oxygenator. The pressurized oxygenated blood then typically passes through an arterial line filter before entering the aortic cannula (usually placed in the proximal aorta).
Additional features of the CPB circuit include several monitors of temperature and oxygenation, a cardioplegia delivery system, and a means for cardiotomy suctioning and ventricular venting.
The factors that control systemic oxygenation during non-CPB conditions also control oxygenation during CPB. Oxygen requirements are most profoundly affected by body temperature, whereas O2 delivery is determined by pump flow and hematocrit.
< ?xml:namespace prefix = "mml" />Arterial O2 content (Cao2)= 1 .34 (hemoglo bin) (O2sat%)+ 0.003 (Pao2)
Systemic D˙O2= cardiac output or CPB pump flow× Cao2
The temperature coefficient (Q10) describes the ratio of metabolic rates at two temperatures separated by 10° C. In humans, the Q10 is approximately 2 (i.e., when a patient’s temperature rises from 27° C to 37° C, the metabolic rate doubles. Conversely, every 10° C decrease in body temperature decreases theO2 by about 50%.
Nonpulsatile flow (2.0-2.5 L·min−1·m−2) is based on the cardiac index under anesthesia in non-CPB conditions. The flow rate may also be expressed as mL·kg−1·min−1. The most recent literature suggests that mild to moderate hypothermia more close to the normal range (i.e., 28° C-35° C) reduces the incidence of low cardiac output syndromes without an attendant increase in neurologic complications.
Moderate normovolemic hemodilution should be maintained. The literature, comprising primarily retrospective data, suggests that increased complication rates (neurologic, cardiovascular, and renal) occur when the hematocrit is less than 20% to 23%. However, other data suggest that “treating” this anemia with transfusion of red blood cells may worsen outcomes. It is likely that CPB-related anemia is a function of the prebypass period and, therefore, primarily a marker of greater comorbidity instead of being an independent determinant of adverse outcome.
A mean arterial pressure (MAP) of 60 to 80 mm Hg should be maintained. Even with moderate hypothermia, cerebral autoregulation begins to fail below a cerebral perfusion pressure of 50 to 55 mm Hg. In patients with a history of hypertension or peripheral vascular disease, keeping the MAP at a minimum of 70 mm Hg reduces the incidence of adverse cardiac and neurologic outcomes. A practical way to calculate the goal MAP during CPB is to use the patient’s age as a goal for MAP in patients older than 60 years of age.
Under non-CPB conditions, moderate hemodilution decreases CaO2 but may not decrease because hemodilution is associated with increases in cardiac output. However, during CPB, pump flow is typically less than the cardiac output that would be seen with equivalent hemodilution under non-CPB conditions, resulting in a decrease in whole body during CPB, which is approximately equivalent to the degree of hemodilution. Additionally, in the absence of increases in compensatory flow, MAP during CPB is typically reduced because the lower blood viscosity associated with hemodilution reduces systemic vascular resistance (SVR).
Hypothermia to 27°C reduces systemic O2 requirements by approximately 60%. Because O2 demand decreases so dramatically with hypothermia, adequate oxygenation can be maintained with reduced flows, greater degrees of hemodilution, or a combination thereof. However, during the early and late CPB period, when patients approximate normothermia, the margin between systemic O2 supply and demand is narrowed. A beneficial effect of hypothermia is that the associated increases in SVR may offset the reductions in SVR associated with hemodilution alone.
Anesthetic depth has less influence than does hypothermia on O2 during CPB. However, anesthetic depth is of greater relative importance at body temperatures above 32°C. Plasma levels of anesthetic agents decrease with the onset of CPB secondary to dilution from an increased circulatory volume. Therefore, intravenous infusion techniques or the use of inhalation agents during CPB helps ensure adequate anesthesia.
Mixed venous O2 saturation (SO2) reflects venous O2 content, i.e., the amount of O2 left in the venous blood after systemic O2 requirements are met. Although SO2 does not measure either O2 or , it does provide an index of the adequacy of their matching. As such, SO2 monitoring conveys extremely valuable information as to the interaction among systemic O2 requirements, pump flow, arterial O2 content, hematocrit level, and temperature. An SO2 above 65% generally indicates a satisfactory margin of safety for systemic oxygenation. A higher saturation is indicated during hypothermia given that hypothermia increases the O2 affinity of hemoglobin.
In-line hemoglobin or hematocrit monitors are available and are usually coupled to the SO2 detector. Temperature monitoring is performed in three areas: the venous line (reflecting the adequacy of whole body cooling or warming), the arterial inflow line, and the heat exchanger, where temperature should not exceed 38.5°C. Optional arterial in-flow line-monitoring devices are available to monitor gases (PaO2, pH, PaCO2, base deficit, and temperature).
During stable hypothermia, systemic oxygenation is easy to maintain, but the transitions to and from hypothermia can be a problem. Initiation of CPB is associated with nearly instantaneous hemodilution and decreased SVR. In the absence of increased flow, hypotension commonly occurs until cooling is initiated, SVR is increased pharmacologically, or volume resuscitation occurs.
During rewarming from CPB, SVR and MAP will fall as vasodilation occurs and blood viscosity decreases. This occurs at a time when systemic O2 demand may double (27° C-37° C).
Cardioplegia with a high-K+ solution results in depolarization and diastolic arrest. This induces electromechanical silence and reduces myocardial O2 demand by more than 80%. The use of cardioplegia is indicated when the aortic cross-clamp is in place because there is no coronary blood flow at this time. Cardioplegia may consist of an oxygenated blood–high-K+ mixture (blood cardioplegia) or high-K+ solution alone (crystalloid cardioplegia). Cardioplegia is usually given intermittently into the aorta proximal to the cross-clamp (antegrade) or directly into the coronary ostia. Retrograde cardioplegia via the coronary sinus is also used. Left ventricular hypertrophy and coronary artery disease make myocardial protection more difficult to achieve.
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is determined by pump flow and hematocrit.
because hemodilution is associated with increases in cardiac output. However, during CPB, pump flow is typically less than the cardiac output that would be seen with equivalent hemodilution under non-CPB conditions, resulting in a decrease in whole body 
during CPB, which is approximately equivalent to the degree of hemodilution. Additionally, in the absence of increases in compensatory flow, MAP during CPB is typically reduced because the lower blood viscosity associated with hemodilution reduces systemic vascular resistance (SVR).
, it does provide an index of the adequacy of their matching. As such, S
