Andreas Weyland

Bedside Assessment of Intravascular Volume Status in Patients Undergoing Coronary Bypass Surgery

BackgroundManagement of intravascular volume is crucial in patients after cardiopulmonary bypass as myocardial dysfunction is common. The purpose of this study was to validate a novel bedside technique for real-time assessment of Intravascular volumes. MethodsEleven patients undergoing cardiopulmonary bypass were studied. In addition to standard monitors, a fiberoptic thermistor catheter was placed in the descending aorta and central venous Injections of 10 ml ice-cold indocyanine green dye were performed. Total blood volume was measured by a standard in vitro technique. Circulating and central blood volume were calculated by using cardiac output, mean transit times, and a newly developed recursive convolution algorithm that models recirculation. Measurements were performed after Induction of anesthesia and at 1, 6, and 24 h after surgery. ResultsA two-compartment model of the circulation was required for adequate fit of the data. We found a significant correlation between total and circulating blood volumes (r = 0.87). One hour after surgery, central blood volume was decreased by 10% (P < 0.05). At 6 and 24 h after surgery, circulating blood volumes were significantly increased by 29% and 20%, respectively (P < 0.01), although central blood volume was similar to control values. Before surgery stroke volume index correlated with circulating blood volume (r = 0.87) but not with pulmonary capillary wedge and central venous pressures. ConclusionsThis study shows that bedside determinations of intravascular blood volumes are feasible and that these measurements are more Indicative of Intravascular volume status than are either pulmonary capillary wedge or central venous pressures in the post-cardiopulmonary bypass period. Our data also demonstrate that despite a normal central blood volume both circulating and total blood volume are significantly Increased in the immediate post-cardiopulmonary bypass period.

Comparison of cardiac output assessed by pulse-contour analysis and thermodilution in patients undergoing minimally invasive direct coronary artery bypass grafting

OBJECTIVE To investigate the precision and accuracy of continuous pulse contour cardiac output (PCCO) compared with intermittent transcardiopulmonary (TCPCO) and pulmonary artery thermodilution (TDCO) measurements in patients undergoing minimally invasive coronary bypass surgery (MIDCAB). DESIGN Prospective, controlled, clinical study. SETTING University hospital. PARTICIPANTS Twelve patients undergoing MIDCAB. INTERVENTIONS Thirty-six measurements of PCCO and thermodilution cardiac output (CO) were simultaneously performed after the start of surgery, during bypass grafting, and at the end of surgery. TCPCO and TDCO were simultaneously assessed by three injections of ice-cold saline randomly spread over the respiratory cycle. The pulse contour device was initially calibrated with an additional set of aortic thermodilution measurements. MEASUREMENTS AND MAIN RESULTS Absolute values of CO ranged between 1.6 and 9.2 L/min. A close agreement among the three techniques was observed at all measurements. Mean bias between PCCO and TDCO and TCPCO was 0.003 L/min (2 SD of differences between methods = 1.26 L/min) and 0.27 L/min (2 SD of differences between methods = 1.16 L/min), respectively. The correlation coefficients were r2 = 0.90 for TCPCO versus PCCO and r2 = 0.88 for TDCO versus PCCO. CONCLUSION The results of the present study show that compared with thermodilution CO, pulse contour analysis enables accurate measurement of continuous CO in patients undergoing MIDCAB.

Cerebrovascular tone rather than intracranial pressure determines the effective downstream pressure of the cerebral circulation in the absence of intracranial hypertension.

Cerebral perfusion pressure is commonly calculated from the difference between mean arterial pressure and intracranial pressure because intracranial pressure is known to represent the effective downstream pressure of the cerebral circulation. Studies of other organs, however, have shown that effective downstream pressure is determined by a critical closing pressure located at the arteriolar level. This study was designed to investigate the effects of PCO2-induced variations in cerebrovascular tone on the effective downstream pressure of the cerebral circulation. Sixteen patients recovering from head injury were studied. Intracranial pressure was assessed by epidural pressure transducers. Blood flow velocity in the middle cerebral artery was monitored by transcranial Doppler sonography. Effective downstream pressure was derived from the zero flow pressure as extrapolated by regression analysis of instantaneous arterial pressure/middle cerebral artery flow velocity relationships. PaCO2 was varied between 30 and 47 mm Hg in randomized sequence. Intracranial pressure decreased from 18.5 ± 5.2 mm Hg during hypercapnia to 9.9 ± 3.1 mm Hg during hypocapnia. In contrast, effective downstream pressure increased from 13.7 ± 9.6 mm Hg to 23.4 ± 8.6 mm Hg and exceeded intracranial pressure at hypocapnic PaCO2 levels. Our results demonstrate that, in the absence of intracranial hypertension, intracranial pressure does not necessarily represent the effective downstream pressure of the cerebral circulation. Instead, the tone of cerebral resistance vessels seems to determine effective downstream pressure. This suggests a modified model of the cerebral circulation based on the existence of two Starling resistors in a series connection.

Flow velocity measurements as an index of cerebral blood flow. Validity of transcranial Doppler sonographic monitoring during cardiac surgery.

Background:Transcranial Doppler sonography is increasingly used to monitor changes in cerebral perfusion intraoperatively. However, little information is available about the validity of velocity measurements as an index of cerebral blood flow (CBF). The purpose of this study was to compare invasive and Doppler-derived measurements of cerebral hemodynamic variables during coronary artery bypass graft surgery. Methods:In 15 male patients, measurements of CBF and middle cerebral artery flow velocity (VMCA) were performed before and after induction of fentanyl-midazolam anesthesia, during hypothermic cardiopulmonary bypass (CPB), and at the end of the surgical procedure. Transcranial Doppler sonography recordings of systolic, diastolic, and mean VMCA, and derived parameters such as pulsatility (PI) and resistance (RI) indexes were recorded from the proximal segment of the right middle cerebral artery. CBF was measured by the Kety-Schmidt inert gas saturation method with argon as a tracer. To facilitate comparisons of CBF and VMCA measurements, changes between consecutive measurements were expressed as percentage values. Calculations of cerebral perfusion pressure and cerebral vascular resistance (CVR) were based on jugular bulb pressure. The cerebral metabolic rate for oxygen was calculated from CBF and the arterial — cerebral venous oxygen content difference. Results:Changes In mean VMCA paralleled changes in mean CBF except for hemodynamic changes associated with hypothermic CPB. At this stage of surgery, mean VMCA increased while actual CBF decreased. Separate analysis of the periods before and after CPB revealed a poor association between percentage changes In CBF and VMCA (r=0.26, P=0.36; r=0.51, P=0.06, respectively). Mean values of CVR, PI, and RI showed consistent changes after induction of anesthesia. After termination of CPB, mean CVR significantly decreased, whereas mean PI and RI remained virtually unchanged. Neither before nor after CPB was a clinically useful correlation found between percentage changes in PI, RI, and CVR (PI r=0.28, P=0.34; r=-0.47, P=0.09, respectively; RI r=0.16, P=0.59; r=-0.53, P=0.06, respectively). Conclusions:Hypothermic CPB seems to alter the relation between global CBF and flow velocity in basal cerebral arteries. Inconsistency in directional changes in CBF and VMCA at this stage of surgery might be attributable to changes in middle cerebral artery diameter, red blood cell velocity spectra, and regional flow distribution. Although changes in mean VMCA before and after CPB appear to parallel changes In mean CBF, individual responses of VMCA cannot reliably predict percentage changes in CBF. Furthermore, Doppler sonographic PI and RI cannot provide an approximation of changes in CVR during cardiac surgery.

Effects of one minimum alveolar anesthetic concentration sevoflurane on cerebral metabolism, blood flow, and CO2 reactivity in cardiac patients.

UNLABELLED We investigated the cerebral hemodynamic effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane anesthesia in nine male patients scheduled for elective coronary bypass grafting. For measurement of cerebral blood flow (CBF), a modified Kety-Schmidt saturation technique was used with argon as an inert tracer gas. Measurements of CBF were performed before the induction of anesthesia and 30 min after induction under normocapnic, hypocapnic, and hypercapnic conditions. Compared with the awake state under normocapnic conditions, sevoflurane reduced the mean cerebral metabolic rate of oxygen by 47% and the mean cerebral metabolic rate of glucose by 39%. Concomitantly, CBF was reduced by 38%, although mean arterial pressure was kept constant. Significant changes in jugular venous oxygen saturation were absent. Hypocapnia and hypercapnia caused a 51% decrease and a 58% increase in CBF, respectively. These changes in CBF caused by variation of Paco2 indicate that cerebrovascular CO2 reactivity persists during 1 MAC sevoflurane anesthesia. IMPLICATIONS We used a modified Kety-Schmidt saturation technique to investigate the effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane on cerebral blood flow, metabolism, and CO2 reactivity in cardiac patients. We found that the global cerebral blood flow and global cerebral metabolic rate of oxygen remained coupled and that cerebrovascular CO2 reactivity is not impaired by the administration of 1 MAC sevoflurane.

Relationship between Intracranial Pressure and Critical Closing Pressure in Patients with Neurotrauma

Background The driving pressure gradient for cerebral perfusion is the difference between mean arterial pressure (MAP) and critical closing pressure (CCP = zero flow pressure). Therefore, determination of the difference between MAP and CCP should provide an appropriate monitoring of the effective cerebral perfusion pressure (CPPeff). Based on this concept, the authors compared conventional measurements of cerebral perfusion pressure by MAP and intracranial pressure (CPPICP) with CPPeff. Methods Simultaneous synchronized recordings of pressure waveforms of the radial artery and blood flow velocities of the middle cerebral artery were performed in 70 head trauma patients. CCP was calculated from pressure–flow velocity plots by linear extrapolation to zero flow. Results Intracranial pressure measured by intraventricular probes and CCP ranged from 3 to 71 and 4 to 70 mmHg, respectively. Linear correlation between ICP and CCP was r = 0.91. CPPICP was 77 ± 20 mmHg and did not differ from CPPeff; linear correlation was r = 0.92. However, limits of agreement were only ± 16.2 mmHg. Therefore, in 51.4% of the patients, CPPICP overestimated CPPeff by 19.8 mmHg at most. Conclusion Assuming that CPPeff (MAP − CCP) takes into account more determinants of cerebral downstream pressure, in individual cases, the actual gold standard of CPP determination (MAP − ICP) might overestimate the CPPeff of therapeutic significance.

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease

Background Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO (2) on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. Methods In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety‐Schmidt technique with argon as a tracer. End‐diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer‐tipped catheter. Results The cardiac index significantly changed with varying PaCO (2) levels (hypocapnia, ‐ 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying Pa (CO)2 levels. Conclusions In anesthetized patients with coronary artery disease, short‐term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

Haemodynamic changes during minimally invasive coronary artery bypass surgery using high-dose esmolol.

UNLABELLED We aimed to investigate the effects of high-dose esmolol on haemodynamics and oxygen extraction in minimally invasive direct coronary artery bypass (MIDCAB) surgery patients. METHODS In 18 patients, heart rate (HR), mean arterial (MAP), central venous (CVP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and mixed venous oxygen saturation (Sv0(2)) were prospectively measured after induction of anaesthesia (T1), start of surgery (T2), during bypass grafting with beta-blockade (T3), and at the end of surgery (T4). RESULTS Mean esmolol dose at T3 was 0.44+/-0.2mgkg(-1)min(-1). HR was unchanged, whereas significant decreases in mean CO (3.1+/-0. 8 vs 4.8+/-1.0lmin(-1)m(-2), pre-esmolol), MAP (53+/-10 vs 89+/-14mmHg), and SvO(2) (65+/-10 vs 81+/-4%) were observed during esmolol administration. All haemodynamic parameters normalized immediately after termination of esmolol (T4). CONCLUSIONS Despite unchanged HR esmolol reduced CO and MAP suggesting a favorable reduction of myocardial oxygen consumption. Mean Sv0(2) during esmolol administration reflects an acceptable ratio of whole-body oxygen delivery and consumption. Haemodynamic changes with high-dose esmolol during MIDCAB surgery remain within safety margins.

Effect of ketanserin on global cerebral blood flow and middle cerebral artery flow velocity

The aim of this study was to examine the influence of ketanserin, a 5-hydroxytryptamine antagonist antihypertensive agent, on the relationship between cerebral blood flow (CBF) and middle cerebral artery flow velocity (Vmean MCA) and to compare Doppler-sonographic indices of downstream resistance (pulsatility index, PI; resistance index, RI) with calculations of cerebrovascular resistance (CVR) in 17 male patients under fentanyl/midazolam anesthesia. CBF was measured with the Kety-Schmidt technique using argon as a tracer. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and jugular bulb pressure. Measurements of Vmean MCA and determinations of PI and RI were performed by use of a 2-MHz transcranial Doppler ultrasound device. All variables were measured at normo- and moderate hypocapnia before and after intravenous (IV) bolus administration of 0.3 mg/kg ketanserin followed by an infusion of 0.06 mg centered dot kg-1 centered dot h-1. Ketanserin changed neither average CBF nor Vmean MCA. The CO2 reactivity of Vmean MCA was significantly lower than the CO2 reactivity of CBF (P < 0.01); however, ketanserin did not change the relationship between CBF and Vmean MCA. During hypocapnia, CVR as well as PI and RI significantly increased (P <or=to 0.01), indicating consistent directional changes in arteriolar resistance and flow velocity pulsatility. In contrast, after IV administration of ketanserin, CVR decreased (P < 0.05), whereas both Doppler-derived indices increased (P < 0.01). These results suggest that ketanserin in a clinically relevant dose does not alter the validity of serial Vmean MCA measurements as an index of global CBF and that ketanserin does not change the diameter of middle cerebral arteries (MCAs). Doppler-derived indices of pulsatility and resistance, which are supposed to estimate changes in downstream resistance, reflect changes, after administration of ketanserin, in systemic hemodynamics rather than changes in CVR. (Anesth Analg 1995;80:64-70)

Moderate hyperventilation during intravenous anesthesia increases net cerebral lactate efflux

Background:Hyperventilation is known to decrease cerebral blood flow (CBF) and to impair cerebral metabolism, but the threshold in patients undergoing intravenous anesthesia is unknown. The authors hypothesized that reduced CBF associated with moderate hyperventilation might impair cerebral aerobic metabolism in patients undergoing intravenous anesthesia. Methods:Thirty male patients scheduled for coronary surgery were included in a prospective, controlled crossover trial. Measurements were performed under fentanyl-midazolam anesthesia in a randomized sequence aiming at partial pressures of carbon dioxide of 30 and 50 mmHg. Endpoints were CBF, blood flow velocity in the middle cerebral artery, and cerebral metabolic rates for oxygen, glucose, and lactate. Global CBF was measured using a modified Kety–Schmidt technique with argon as inert gas tracer. CBF velocity of the middle cerebral artery was recorded by transcranial Doppler sonography. Data were presented as mean (SD). Two-sided paired t tests and one-way ANOVA for repeated measures were used for statistical analysis. Results:Moderate hyperventilation significantly decreased CBF by 60%, blood flow velocity by 41%, cerebral oxygen delivery by 58%, and partial pressure of oxygen of the jugular venous bulb by 45%. Cerebral metabolic rates for oxygen and glucose remained unchanged; however, net cerebral lactate efflux significantly increased from −0.38 (2.18) to −2.41(2.43) µmol min−1 100 g−1. Conclusions:Moderate hyperventilation, when compared with moderate hypoventilation, in patients with cardiovascular disease undergoing intravenous anesthesia increased net cerebral lactate efflux and markedly reduced CBF and partial pressure of oxygen of the jugular venous bulb, suggesting partial impairment of cerebral aerobic metabolism at clinically relevant levels of hypocapnia.