Steady-state Cardiopulmonary Bypass Research Articles

Pulsatility does not change cerebral oxygenation during cardiopulmonary bypass.

To determine the effect of pulsatility during cardiopulmonary bypass (CPB) on cerebral oxygenation, we measured oxyhaemoglobin (HbO2), deoxyhaemoglobin (Hb) and oxidised cytochrome aa3 (CtO2) with near-infrared spectroscopy (NIRS) in 14 patients electively scheduled for cardiac surgery. Cerebral oxygenation was measured during steady state CPB at a core temperature of 32 degrees C. Non-pulsatile flow and pulsatile flow were performed for 10 min each. After 14 min of CPB, HbO2, Hb and CtO2 were significantly below prebypass values. HbO2 and CtO2 did not alter with changing flow patterns. Hb significantly increased both during the period of nonpulsatile (median: -0.7 vs. 0.25 micromol/l; P<0.05) and pulsatile flow (median: 0.25 vs. 0.5 micromol/l; P<0.001). This increase was independent of flow pattern. Neither oxygenated haemoglobin, nor intracellular oxygenation, represented by CtO2, indicated a beneficial effect of pulsatile perfusion during hypothermic CPB. These results, however, are only valid for short time effects within 10 min before rewarming from CPB and patients without flow-limiting stenoses of the carotid artery.

Effect of intraoperative angiotensin-converting enzyme inhibition by quinaprilat on hypertension after coronary artery surgery

Activation of the renin-angiotensin system during cardiopulmonary bypass (CPB) may be involved in early postoperative hypertension after coronary artery bypass grafting (CABG). As hypertensive episodes may be deleterious in the immediate postoperative period, we have assessed the effects of prophylactic treatment with the angiotensin-converting enzyme inhibitor quinaprilat in an open study. During steady state CPB, patients received quinaprilat 0.02 mg kg-1 (group A, n = 10), quinaprilat 0.04 mg kg-1 (group B, n = 10) or saline solution (group C, n = 10) as an i.v. bolus dose. Sodium nitroprusside (SNP) was given after operation when systolic arterial pressure was > 150 mm Hg. Requirements for SNP 1 h after arrival in the ICU were significantly less in groups A (two of 10) and B (two of 10) than in group C (eight of 10). Also, patients in group C had a greater systolic arterial pressure compared with groups A and B. There were no significant differences between groups in diastolic arterial pressure, heart rate, cardiac index or cardiac filling pressures. We conclude that quinaprilat can be used during CABG to reduce the incidence of postoperative hypertension. Further studies of the efficacy and safety of this technique are necessary.

Changes in cerebral hemodynamics and oxygenation during hypothermic cardiopulmonary bypass in neonates and infants.

Delay in development after open-heart surgery in infants has frequently been reported. Inadequate brain perfusion and oxygenation during deep hypothermic cardiopulmonary bypass (CPB) may play an important role. We investigated the effect of CPB on cerebral perfusion and oxygenation in 12 neonates and infants (age 0-11 months) undergoing open-heart surgery. Changes in cerebral blood volume (delta CBV; in ml/100 g brain tissue) and oxidation level of the intracerebral mitochondrial enzyme cytochrome aa3 (delta Cytaa3; in mumol/l) were measured with near infrared spectroscopy. Nasopharyngeal temperature (Tnas) for assessment of changes in brain temperature, and mean arterial blood pressure (MAP) were monitored continuously. CBV lowered during cooling and increased during rewarming. These changes were only related with changes in Tnas (p < 0.001; 0.07 ml.100 g-1/ degrees C). No relation was found with changes in MAP or pump flow rate of the heart-lung machine. During steady-state hypothermic CPB, changes in CBV were only related to changes in MAP (p < 0.001). The individual regression lines between delta CBV and MAP became steeper at lower absolute Tnas. Cytaa3 showed an increase shortly after the initiation of CPB in 9 patients, with a sustained decrease to baseline values in 8 patients towards the end of the CPB period. Two patients who had a circulatory arrest during CPB had a sharp decrease in delta cytaa3 after cessation of the heart-lung pump and showed no complete recovery of delta Cytaa3 to baseline at the end of the CPB period. We conclude that changes in CBV during CPB are related to changes in Tnas. During deep hypothermic steady-state CPB, changes in CBV and MAP were related to each other, suggesting lack of cerebral autoregulation. The large decrease in Cytaa3 in 2 patients with circulatory arrest suggests that this procedure compromises energy metabolism of the brain cell.

RETRACTED: DOES CORRECTION OF ACIDOSIS INFLUENCE MICROCIRCULATORY BLOOD FLOW DURING CARDIOPULMONARY BYPASS?

We studied 15 patients undergoing cardiopulmonary bypass (CPB) to examine the effect of response to correction of acidosis on microcirculatory blood flow. Acidosis was defined when base excess was less than -10.0 mmol litre-1 while carbon dioxide partial pressure was within the normal range. CPB was carried out at almost normothermic temperature (smallest rectal temperature 35.2 (SD) 0.4 degrees C). Sodium bicarbonate (NaHCO3) was given to correct acidosis during steady state CPB. Skin microcirculatory blood flow was assessed using a double-channel laser Doppler flow (LDF) monitor. LDF was measured on the patient's forehead and forearm before infusion of NaHCO3 (baseline) and 30 s, 1, 3, 5, 7, 10 and 15 min later. Skin, blood, rectal and nasopharyngeal temperatures did not change during the investigation. Plasma viscosity, haemoglobin and carbon dioxide partial pressure also remained unchanged. Mean arterial pressure (MAP) and systemic vascular resistance (SVR) decreased slightly after infusion of NaHCO3 (MAP -29%; SVR -32%). A total of NaHCO3 99.4 (4.4) mmol litre-1 was given for correction of acidosis. pH and HCO3- were within the normal range shortly after the infusion of NaHCO3. LDF measured on both the forehead (+49%) and the forearm (+29%) increased significantly after infusion of NaHCO3. Changes in pH correlated positively with changes in LDF (analyses of co-variance, P < 0.02), but haemodynamic and other laboratory values did not correlate with LDF. We conclude that the microcirculatory response to correction of acidosis with NaHCO3 during CPB can be monitored using skin laser Doppler flowmetry. Infusion of NaHCO3 resulted in a significant improvement in skin microcirculatory perfusion.

Cerebral blood flow pattern and autoregulation during open-heart surgery in infants and young children: a transcranial, Doppler ultrasound study.

To elucidate the effect of cardiopulmonary bypass on cerebral perfusion and on the autoregulatory ability of the cerebral vascular bed of infants and young children. Operating room. Prospective study. Thirteen newborn infants and young children undergoing open-heart surgery. Cerebral blood flow velocity was monitored in the patients undergoing open-heart surgery from just before the induction of anesthesia until the discontinuation of anesthesia after completion of the surgery. Cerebral blood flow velocity was assessed by semicontinuous measurement of temporal mean blood flow velocity in the middle cerebral artery using a range-gated, pulsed Doppler flowmeter with a transducer that was firmly attached to the left temporal region of the head. Mean arterial pressure (MAP) and nasopharyngeal temperature were continuously monitored. During hypothermic (18.4 degrees C to 31.9 degrees C) cardiopulmonary bypass, cerebral blood flow velocity decreased and showed a close relationship with nasopharyngeal temperature (p less than .0001). During steady-state cardiopulmonary bypass, cerebral blood flow velocity showed a correlation with MAP (p less than .01). The nasopharyngeal temperature influenced this relationship: at lower (absolute) nasopharyngeal temperatures, lack of cerebral autoregulation was more common. The finding suggests that cerebral blood flow decreases with decreasing nasopharyngeal temperature. During hypothermic cardiopulmonary bypass, cerebral autoregulation seems to be easily disturbed, especially at low nasopharyngeal temperatures.

Cerebral perfusion during major cardiac surgery in children.

Six children undergoing major cardiac surgery had extensive cerebral monitoring during cardiopulmonary bypass (CPB). The monitoring included continuous recording of arterial blood pressure (BP), central venous pressure (CVP), cerebral electrical activity by a cerebral function monitor (CFM), and middle cerebral artery (MCA) flow velocity by the transcranial pulsed Doppler (TCD) technique. Introduction of the precooled blood containing priming solution resulted in rapid fall in BP as well as MCA velocities in these children at the start of CPB. During steady-state CPB at 20 degrees C, MCA flow velocities were reduced in five of six children, range 45%-105% of pre-bypass value. These flow velocity values were recorded at cerebral perfusion pressures (CPP = BP - CVP) in the range of 14-26 mmHg. This reduced cerebral perfusion during steady-state CPB appears to be more than sufficient to meet the cerebral metabolic demands at the particular temperature. The reduced cerebral perfusion is in contrast to the enhanced perfusion found in adults during moderately hypothermic (28 degrees-30 degrees C) low-flow, low-pressure CPB previously reported. It was presumably due to the reduced temperature, reduced perfusion pressure, and less hemodilution. During periods of constant temperature, hematocrit, and partial pressure of carbon dioxide (PaCO2), MCA flow velocities varied passively with changes in CPP, demonstrating that cerebral autoregulation was not operative. Transcranial Doppler appears to be a suitable tool for investigating CPB techniques optimal with respect to cerebral circulation.

Augmentation of Venous Return by Adrenergic Agonists During Spinal Anesthesia

To test the effectiveness of adrenergic agonists in correcting the vascular sequelae of spinal anesthesia, we used venous reservoir volume (RV) and mean arterial pressure (MAP) as indices of the changes in venous capacitance and arterial resistance produced by adrenergic agonists in dogs anesthetized with pentobarbital and undergoing cardiopulmonary bypass (CPB). A CPB-based technique was chosen both to prevent drug and reflex effects on the heart from influencing the results and to provide a convenient means by which to monitor venous capacitance. Total spinal anesthesia significantly decreased both RV and MAP relative to steady-state CPB values. Return of these hemodynamic alterations to baseline was attempted using pure alpha- and beta-adrenergic agonists, and a mixed adrenergic agonist (phenylephrine, isoproterenol, and ephedrine, respectively). Isoproterenol increased RV, but further decreased MAP. Phenylephrine increased MAP but not RV. Ephedrine increased both MAP and RV. We conclude that a mixed adrenergic agonist such as ephedrine more ideally corrects the noncardiac circulatory sequelae of spinal anesthesia than does either a pure alpha- or beta-adrenergic agonist.

Augmentation of Venous Return by Adrenergic Agonists during Spinal Anesthesia

To test the effectiveness of adrenergic agonists in correcting the vascular sequelae of spinal anesthesia, we used venous reservoir volume (RV) and mean arterial pressure (MAP) as indices of the changes in venous capacitance and arterial resistance produced by adrenergic agonists in dogs anesthetized with pentobarbital and undergoing cardiopulmo-nary bypass (CPB). A CPB-based technique was chosen both to prevent drug and reflex effects on the heart from influencing the results and to provide a convenient means by which to monitor venous capacitance. Total spinal anesthesia significantly decreased both RV and MAP relative to steady-state CPB values. Return of these hemodynamic alterations to baseline was attempted using pure α-and β-adrenergic agonists, and a mixed adrenergic agonist (phenyl-ephrine, isoproterenol, and ephedrine, respectively). Isoproterenol increased RV, but further decreased MAP. Phenyl-ephrine increased MAP but not RV. Ephedrine increased both MAP and RV. We conclude that a mixed adrenergic agonist such as ephedrine more ideally corrects the noncardiac circulatory sequelae of spinal anesthesia than does either a pure α-or β-adrenergic agonist.

Cerebral Carbon Dioxide Reactivity during Nonpulsatile Cardiopulmonary Bypass

Five patients undergoing extensive cerebral monitoring during cardiopulmonary bypass (CPB) procedures were subjected to studies on cerebral CO 2 reactivity during nonpulsatile CPB. The cerebral monitoring included recording of arterial blood pressure (BP), central venous pressure (CVP), epidural intracranial pressure (EDP), cerebral electrical activity by a cerebral function monitor (CFM), and middle cerebral artery (MCA) flow velocity by transcranial Doppler technique. The cerebral perfusion pressure (CPP) was thus continuously recorded (CPP = BP - EDP). During steady-state CPB with constant hematocrit, temperature, and arterial carbon dioxide tension (PaCO 2), MCA flow velocity varied with changing CPP in a pressure-passive manner, indicating that the cerebral autoregulation was not operative. During moderately hypothermic (28 to 32°C), nonpulsatile CPB, with steady-state hematocrit, temperature, and pump flow, we deliberately and rapidly changed PaCO 2 for periods of 1 or 2 minutes by increasing gas flow to the membrane oxygenator, thereby testing the cerebral CO 2 reactivity. Nineteen CO 2 reactivity tests, performed at CPP levels ranging from 17 to 75 mm Hg, disclosed that the cerebral CO 2 reactivity decreased with CPP, especially with CPP levels below 35 mm Hg. In these patients, concomitant changes in CPP during the CO 2 reactivity test could be compensated for by adjusting the observed change in MCA flow velocity. The corrected CO 2 reactivity values obtained in this way ranged from below 1.0 (observed at CPP levels below 20 mm Hg) to a 3.0 to 4.5% · mm Hg −1 change in PaCO 2 (observed at CPP levels above 35 mm Hg). Four CO 2 reactivity tests performed after rewarming was completed revealed corrected CO 2 reactivity values in the range from 1.3 to 1.9% · mm Hg −1 change in PaCO 2, observed at CPP in the range of 41 to 50 mm Hg. Cerebral CO 2 reactivity seems to be partially retained down to CPP levels of 20 mm Hg during moderately hypothermic, nonpulsatile CPB.

Dissociation between Cerebral Autoregulation and Carbon Dioxide Reactivity during Nonpulsatile Cardiopulmonary Bypass

Five patients undergoing cardiopulmonary bypass (CPB) procedures were extensively monitored because of anticipated high risk for neurological complications. Arterial blood pressure (BP), central venous pressure, and epidural intracranial pressure (EDP) were continuously recorded throughout CPB; thus, information on the cerebral perfusion pressure (CPP) was also continuously available (CPP = BP – EDP). Cerebral electrical activity was recorded by a cerebral function monitor. The flow velocity in the middle cerebral artery (MCA) was recorded using a transcranial Doppler technique. During steady-state CPB (constant hematocrit, constant temperature, and constant flow from the heart-lung machine) partial pressure of arterial carbon dioxide (PaCO 2) was repeatedly changed to study the effect of changes in this variable on MCA flow velocity during nonpulsatile bypass. During CPB with constant temperature, hematocrit, and PaCO 2, the effect of changes in CPP on MCA flow velocity was recorded and analyzed. During nonpulsatile, moderately hypothermic (28° to 32°C), low-flow (1.5 L/min/m 2) CPB, there was no evidence of cerebral autoregulation, with CPP levels ranging from 20 to 60 mm Hg. The CO 2 reactivity, however, was clearly present and in the range of 1.9 to 4.1%/mm Hg, indicating that there was a dissociation between cerebral autoregulation and CO 2 reactivity under these circumstances.

Cerebral Perfusion during Nonpulsatile Cardiopulmonary Bypass

The recording of middle cerebral artery (MCA) flow velocity by the transcranial Doppler method offers a new, noninvasive, continuous technique for studies of cerebral circulation. Comparative studies of electromagnetic internal carotid artery (ICA) flowmetry and MCA flow velocity by the transcranial Doppler technique have demonstrated that observed changes in MCA flow velocities reflect concomitant changes in cerebral circulation. Eleven high-risk patients undergoing cardiopulmonary bypass (CPB) procedures were included in a pilot study. Arterial blood pressure (BP), central venous pressure, and epidural intracranial pressure (EDP) were recorded during CPB. Cerebral electrical activity was recorded by a cerebral function monitor. Flow velocity in the MCA was increased during nonpulsatile CPB in 10 of the 11 patients. This increase was related to the degree of hemodilution, and the flow velocity during steady-state CPB was 80 to 300% of the prebypass value. The MCA flow velocity changed, however, in a pressure-passive manner with the cerebral perfusion pressure (CPP = BP – EDP) in the individual patient, which indicates that cerebral autoregulation was not operative. During the first 15 minutes after termination of bypass, the MCA flow velocity was reduced, but remained higher than the prebypass level, 110 to 210% of the level during the last 5 minutes preceding CPB.