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Ann Thorac Surg 2006;82:62-67
© 2006 The Society of Thoracic Surgeons
Dipartimento dell'Emergenza e Trapianti d'Organo, Azienda Ospedaliero-Universitaria Policlinico, Bari, Italy
Accepted for publication February 2, 2006.
* Address correspondence to Dr G Fiore, via A. De Ferraris 16, I-70124 Bari, Italy (Email: pinofiore{at}yahoo.it).
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Abstract |
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METHODS: In 19 patients undergoing multivessel elective off-pump coronary revascularization, systemic hemodynamics and superior mesenteric flow were assessed. Blood flow in the superior mesenteric artery was evaluated with duplex ultrasound using a transesophageal echo probe. Measurements were made four times: T0 (baseline), T1 (left anterior descendent anastomosis), T2 (heart displacement to expose the inferolateral and inferior walls), and T3 (closed chest, at the end of surgery).
RESULTS: Superior mesenteric blood flow significantly decreased at T2 (from 426.4 ± 83.1 mL to 212.9 ± 48.6 mL, p < 0.001), when also cardiac output was reduced. The percentage of the cardiac output directed toward the mesenteric arterial bed was also decreased at this time. At the end of surgery (T3), whereas cardiac output returned to the initial values, mesenteric flow was significantly increased compared with baseline, with a higher percentage of the systemic output flowing through the superior mesenteric artery.
CONCLUSIONS: Hemodynamic changes during off-pump coronary surgery induce a significant mesenteric hypoperfusion followed by a hyperemic response at the end of surgery. Transesophageal echo-Doppler allows the intraoperative measurement of blood flow distribution to splanchnic viscera.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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Duplex ultrasound, recognized as a valuable tool for the assessment of blood flow in many vascular territories, provides a noninvasive and accurate assessment of the mesenteric circulation. Blood flow derived from duplex ultrasound correlates with dye-elimination techniques and contrast angiography [9]. Transabdominal duplex ultrasound has been previously used to examine blood flow characteristics of the splanchnic vessels, and to assess blood flow modifications during various physiologic and pathologic conditions [10]. The anatomic proximity between stomach and the upper abdominal aortic branches permits a transgastric approach to these vessels. Recently, the visualization of major abdominal arteries by transesophageal echocardiography (TEE) has been reported [11], allowing intraoperative assessment of regional hemodynamics in different pathophysiologic conditions.
We hypothesized that, in off-pump patients, hemodynamic modifications at the time of heart displacement might induce a critical reduction of mesenteric arterial blood flow, with subsequent gastrointestinal hypoperfusion and ischemia. To test our hypothesis, we used TEE to assess, intraoperatively, the effects of heart displacement on superior mesenteric artery (SMA) blood flow during OPCABG.
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Patients and Methods |
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All patients were hemodynamically stable the morning of surgery, with no need for other intravenous pharmacologic support but nitroglycerin and heparin. Preoperative ß-blockers, nitrates, and (or) calcium-channel-blockers were continued until the morning of surgery. Patients received oral temazepam (1 to 2.5 mg) the evening before, and diazepam (0.015 mg/kg) 1 hour before surgery as premedication. After a supplemental dose of Diazepam (0.005 to 0.01 mg/kg intravenously) and fentanil (5 to 7 µg/kg e.v.), general anesthesia was induced with thiopental (1 to 4 mg/kg), and maintained with isoflurane (0.5% to 1%) and incremental doses of fentanil. Either vecuronium bromide boluses as needed or cisatracurium besilate continuous infusion (0.1 mg/kg per hour) were used for neuromuscular blockade. Patients were mechanically ventilated with an oxygen to air mixture (fraction of expired oxygen [FIO 2] = 0.4), setting a respiratory rate of 10 per minute and a minute volume adjusted to allow normocapnia.
The right radial artery was cannulated in all patients to monitor arterial blood pressure. A triple-lumen central venous catheter was inserted into the right internal jugular vein. The femoral artery was cannulated with a 4F thermistor-tipped catheter (Pulsion PV2014, Pulsion, Germany) connected to the PiCCO device (Pulsion Medical Systems, Munich, Germany) for transpulmonary thermodilution and continuous CO monitoring by the pulse-contour technique. Leads II and V5 were displayed for ischemia detection. Cautious volume expansion was used, as required, to normalize volemia before cardiac displacement. No patient was given intraoperative ß-blockers or calcium-channel-blocker infusion. We planned to use inotropic and (or) vasoconstrictor agents to treat significant hypotension (mean arterial pressure [MAP] < 60 mm Hg) or a low CO (confidence interval [CI] < 2 L/minute/m2) that outlasts the time of cardiac displacement.
Exposure and stabilization of the target coronary vessels were achieved by a modified Lima stitch [12] and a suction type stabilizer (Octopus III Tissue Stabilizer, Medtronic Inc, Minneapolis, MN). The strategy was always to graft first the left anterior descending coronary artery to restore blood flow to the anterior wall as soon as possible, with minimal displacement of the heart.
Measurements were performed according to the following timing: (1) T0 (baseline, during left internal mammary artery starvation); (2) T1 (anastomosis on the left anterior descending artery); (3) T2 (cardiac displacement during the anastomosis on inferolateral and inferior walls); (4) T3 (end of surgery, chest closed).
The following hemodynamic parameters were recorded: MAP, central venous pressure (CVP), heart rate, CO, stroke volume, systemic vascular resistance, time-averaged mean velocity (TAMV) in the SMA, SMA diameter. Both hemodynamic and mesenteric blood flow measurements were taken at each time. Cardiac output was measured by arterial thermodilution.
All echographic measurements were performed with an Omniplanar transesophageal probe connected to an HP Sonos 4500 (Hewlett-Packard, Andover, MA). The same sonologist (FG) performed all the Doppler examinations. To measure the SMA blood flow, the TEE probe was advanced into the stomach, with an appropriate rotation and upward flexion applied to keep the image of the aorta on the screen. The SMA was then visualized in two scanning planes. (1) transversal plane (Fig 1): transducer at 0 degrees; the first tract of the SMA appeared at the 1 to 3 o'clock position of the aorta. (2) Longitudinal plane (Fig 2): transducer at about 110 degrees to140 degrees; SMA appeared in long axis, with both the first tract, directed anteriorly, and the second tract, directed caudally. Doppler power, gain, and scale control were adjusted to provide a clear spectral recording with no noise. Doppler measurements were taken just beyond the point at which the vessel changes its course from an anterior to a caudal direction (longitudinal plane), or alternatively at least 1 cm from its origin (transverse plane). In each patient, the same scanning plane was used at all times to minimize the effects of changing the insonation angle. B-mode imaging was used to identify the exact location of the SMA, allowing accurate determination of the vessel diameter and placement of the Doppler sample volume gates in the arterial lumen.
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d)2 · TAMV · 60. The inner diameter of the SMA was determined on the real-time B-mode image, displaying the artery at long axis, at the same point of Doppler sampling, with the calipers positioned at the internal surfaces of the vessel wall. At each time, three estimates of diameter were made and the mean calculated. Following other papers [13], no attempt was made to standardize the measurements of diameter to a given phase of the cardiac cycle; this seemed more appropriate, as a single value of diameter is used together with the TAMV to estimate volume flow. The TAMV was determined by off-line planimetry, on a spectrum of five heart cycles, in order to minimize the variability due to the respiratory cycle phase [14]. The position of the pulsed-wave Doppler transducer was adjusted to give an angle of less than 60 degrees between the ultrasound beam and the long axis of the vessel, with the sample volume including the entire inner vascular diameter. In all instances, this angle was kept constant between time points in each patient. The vascular resistance of the SMA, in mm Hg · minutes per liter, was calculated by dividing the MAP by flow volume [15]. The mesenteric perfusion pressure was calculated as the difference between MAP and CVP.
All continuous data are presented as mean ± standard deviation. Normal distribution of variables was verified with the Kolmogorov-Smirnov test. One-way analysis of variance for repeated measures with post-hoc Tukey testing for multiple comparisons was used to analyze the hemodynamic changes. Percentage changes of CO and SMA blood flow were compared with the Student's t-test for independent samples. The linear regression analysis was used to assess the correlations between CO and SMA blood flow, and between CVP and mesenteric vascular resistance. A p value of less than 0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The hemodynamic and mesenteric blood flow modifications are shown in Table 2.
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During heart displacement (T2), major hemodynamic derangements were coupled to a significant decrease of SMA blood flow and an increase of SMA vascular resistance. Both CO and stroke volume diminished (–34.8%, p< 0.001 and –38.6%, p < 0.001, respectively), with a slight increase in heart rate (HR) (+5.7%, p < 0.05). Systemic vascular resistance also increased (+23.8%, p < 0.001), limiting the reduction of MAP (–7.7%, p < 0.01). The CVP nearly doubled compared with T0 (+91.3%, p < 0.001). The SMA blood flow decreased by 52.7% (p < 0.001) due to a reduction in both TAMV (–37.7%, p < 0.001) and arterial diameter (–13.1%, p < 0.01), with a twofold increase of the SMA resistance (+100.8%, p < 0.001) and a significant reduction of mesenteric perfusion pressure (–19.6%, p < 0.01). The ratio between SMA blood flow and CO reduced from 8.1 ± 1.0% at T0 to 5.9 ± 1.2% at T2 (p< 0.001; Fig 3).
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The linear regression analysis showed a significant correlation between CO and SMA blood flow (r = 0.79; p < 0.001: Fig 4). There was also a strong linear correlation between CVP and mesenteric vascular resistance, but only at CVP values greater than 12 mm Hg (r = 0.85;p < 0.0001; Fig 5).
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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In our patients SMA blood flow changed significantly, first decreasing, at the time of heart displacement, and then increasing in comparison with the baseline after completion of the surgical procedure. During surgery mesenteric arterial flow variations were consistent with the systemic cardiovascular changes, as suggested by the strong linear correlation between CO and SMA blood flow (Fig 4). Therefore, at the time of the anastomosis on the left anterior descending artery (T1), when minimal hemodynamic effects were apparent, SMA blood flow remained substantially unchanged. On the contrary, when the heart was displaced to perform the anastomoses on the inferolateral and inferior walls (T2), a noticeable reduction was seen in both CO and SMA blood flow.
The effects of low CO on the splanchnic blood flow are well known from both experimental and clinical studies. The fraction of CO directed toward the splanchnic vascular bed decreases early in the course of both hypovolemic and cardiogenic shock [16], with a greater reduction of visceral perfusion compared with CO [17], so that blood flow to the heart and the central nervous system is maintained at the expense of gastrointestinal microcirculation [18]. The splanchnic hypoperfusion is due to a regional vasoconstriction in response to catecholamine, sympathetic and renin-angiotensin stimulation [16], which involves also the mesenteric arterial trunk. In fact, the mesenteric artery is provided by adrenergic innervation [19] and behaves as a resistance vessel, with a pressure drop of 40% to 60% from the abdominal aorta to the mesenteric border of the intestine [20]. Accordingly, in our patients SMA blood flow reduced to a greater extent than the CO (–52,7% vs –34,8%, p < 0.001), with a decrease in the fractional output flowing through the SMA from 8.1% at T0 to 5.8% at T2 (p < 0.001; Fig 3). Along with the blood flow reduction, mesenteric vascular resistance increased strikingly at T2 (+100.8%, p < 0.001), with a concomitant decrease in mesenteric arterial diameter (–13.1%, p < 0.01). This latter finding agrees with several papers reporting changes in the mesenteric artery diameter, measured by ultrasonography, in different functional states of the intestinal vascular bed, with increases during the postprandial hyperemia and decreases in the low flow states [15].
The reduction of SMA blood flow at T2 was coupled with a significant decrease of splanchnic perfusion pressure (–19.6%, p < 0.01), resulting from a slight reduction of MAP and a striking increase in CVP. Moreover, the linear regression analysis revealed that, in our patients, there was a significant positive correlation between CVP and mesenteric vascular resistance only at the higher CVP values, greater than 12 mm Hg (r = 0.85; p < 0.0001; Fig 5). Central venous pressure is the downstream pressure for the venous return from the splanchnic vascular bed, and any increase in CVP must be followed by an increase in portal venous pressure to maintain the antegrade flow through the liver. Thus, in the presence of a normal or reduced MAP, a high CVP hinders mesenteric blood flow reducing the pressure gradient for gut perfusion. Moreover, the elevated CVP, raising portal pressure, induces a mesenteric vasoconstriction, the commonly named venoarterial response [21], which might further increase mesenteric vascular resistance while decreasing the fraction of CO flowing through the mesenteric vascular bed. The potential role of venous hypertension is further highlighted by the finding that hepatosplanchnic hypoperfusion due to low CO seems to induce ischemia only if CVP is increased [22].
At the end of surgery (T3), whereas the systemic hemodynamics returned to baseline values, SMA blood flow was significantly higher compared with T0, both as an absolute value and as a fraction of the overall CO (Fig 3), with a concurrent decrease of mesenteric vascular resistance. Several studies report a hyperemic response after a transient reduction of blood flow to the gastrointestinal tract. Experimentally, a pronounced reactive hyperemia was regularly seen after a sustained reduction of mesenteric arterial flow due to either a stimulation of constrictor fibers to the mesenteric vessels [23] or a mechanical occlusion of the SMA [24]. Such findings agree with ours, showing a significant increase of blood flow to the gastrointestinal tract after a transient hypoperfusion. This hyperemic response does not represent, per se, "good" tissue perfusion. At least one study [6] reports a progressive worsening of gastric mucosal acidosis in the immediate postoperative period in patients undergoing OPCABG. Moreover, Gerrittsen and colleagues [25] found that markers of ischemia-reperfusion were also present during and after surgery in off-pump patients, although with a trend toward lower values compared with CPB, suggesting that, among several factors, the effects of Trendelenburg and hemodynamic deterioration on distal perfusion to abdominal organs can be of importance.
Usually the hemodynamic changes during OPCABG are regarded as benign. However, our findings show that SMA blood flow modifications last well beyond the transient decrease of CO and MAP. Because of the potential risks of gut ischemia, the clinician has to make every effort to minimize mesenteric hypoperfusion. Some suggestions can be drawn from our data. The use of vasoconstrictive agents to maintain perfusion pressure seems less than optimal from the point of view of splanchnic perfusion. Also, the Trendelenburg position, frequently recommended to increase venous return during heart displacement, should be applied cautiously because it raises CVP, which can reduce splanchnic perfusion pressure and increase mesenteric vascular resistance. On the contrary, after preload optimization, low dose dobutamine could be the best way to maintain CO while preserving gastrointestinal flow.
Our data show that the transesophageal approach allows intraoperative noninvasive assessment of blood flow changes in the abdominal arteries by duplex ultrasound. This method is simple and reproducible in the hands of the same (experienced) operator [15] and the combination of Doppler interrogation with the two-dimensional image, along with accurate estimates of the vessel diameter, allows correct determination of the Doppler angle, permitting accurate velocity measurements. However, technical limitations have to be taken into account. Any inaccuracy in the measurement of vessel diameter might induce significant errors in blood flow calculation. The angle of the incident Doppler beam to the direction of blood flow must be kept below 60 degrees, and it must be constant between measurements in the same subject. Moreover, in some patients the SMA cannot be visualized by the transesophageal approach, and in others the angle of insonation may be inadequate. In the present study only patients with satisfactory SMA visualization were included, and the same insonation angle was kept in each patient at all of the four experimental times. The attention paid to technical details allowed us to keep the mean intraexamination coefficient of variation of Doppler SMA blood flow measurements below 5%.
The present study has some limitations. First, we did not include a control CPB group. However, our aim was to describe SMA flow modifications during OPCABG, evaluating at the same time the reliability of TEE to assess, intraoperatively, blood flow through the mesenteric artery. Second, we assessed blood flow only in the SMA. Although other branches of the abdominal aorta can be visualized by TEE, we chose to focus on the SMA because it supplies only one vascular bed (the intestinal), providing most of the arterial flow to the gut. On the contrary, the celiac trunk supplies several vascular beds (gastric, hepatic, pancreatic), whose behavior in low flow states is heterogeneous, and the inferior mesenteric artery is not easily visualized by TEE. Third, we did not assess mucosal microcirculation. Mucosal ischemia is clinically very relevant and gastrointestinal mucosal hypoperfusion during and after OPCABG has already been shown by Velissaris [6]. However, large heterogeneity exists in blood flow distribution inside the mesenteric vascular bed [18] due to an uneven distribution across the different intestinal wall layers. Accordingly, after cardiac surgery, blood flow in large conductance vessels has been reported to behave differently to microcirculation, so that gastric mucosal pH does not always reflect changes in splanchnic blood flow in cardiac surgical patients [26]. Therefore, we have chosen to focus on blood flow modifications in the conductance artery to evaluate this side of organ perfusion as well.
In conclusion, OPCABG causes significant modifications in the amount of blood flowing through the superior mesenteric artery, with a decreased blood flow during heart displacement followed by a hyperemic response at the end of surgery. The hypoperfusion, although transient, may induce a subclinical ischemic injury accounting for a gastrointestinal complication rate not dissimilar to on-pump surgery. Future studies are needed to compare mesenteric arterial flow changes in off-pump and CPB patients, and to understand better if any therapeutic intervention could reduce-attenuate mesenteric hypoperfusion.
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References |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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This article has been cited by other articles:
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  J. M. Albes Invited commentary. Ann. Thorac. Surg., July 1, 2006; 82(1): 68 - 68. [Full Text] [PDF]
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= SMA vs CO correlation points.
= CVP 
12 mm Hg;