Asian Cardiovasc Thorac Ann 2007;15:97-101
© 2007 Asia Publishing EXchange Ltd
Middle Cerebral Arterial Blood Flow Velocity and Hemodynamics in Heart Surgery
Abid Demirci, MD,
Süheyla Ünver, MD,
Ümit Karadeniz, MD,
Ye
im Çetinta, MD,
Dilek Kazanci, MD,
Özcan Erdemli, MD
Türkey Yüksek 
htisas Education and Research Hospital Ankara, Turkey
For reprint information contact: Ümit Karadeniz, MD Tel: 90 312 284 5154 Fax: 90 312 312 4120 Email: ukaradeniz2003{at}yahoo.com, Cukurambar Mahalle, 457. Sokak, 44.Cadde, 4/1, Ankara, Turkey.
 |
ABSTRACT
|
|---|
The aim of this study was to evaluate the effects of propofol, isoflurane, and sevoflurane on middle cerebral arterial blood flow velocity during open heart surgery, and the relationship between these effects and hemodynamic parameters. Fifty-two patients undergoing coronary artery bypass on cardiopulmonary bypass were divided randomly into 3 groups: the first group received 100 µg·kg–1·min–1 propofol, the other groups received one minimum alveolar concentration of sevoflurane or isoflurane for anesthesia maintenance. Middle cerebral arterial blood flow velocities were measured by transcranial Doppler, and hemodynamics were measured by the thermodilution technique. Middle cerebral arterial blood flow velocities decreased significantly after administration of isoflurane and propofol, but there was no significant difference between the groups. After weaning from cardiopulmonary bypass, cerebral blood flow increased and came close to the value after induction in all groups. The pulsatility index and resistivity index increased significantly only after the propofol infusion, but there was no significant difference between the groups.
|
INTRODUCTION
|
|---|
Neurological dysfunction is a frequent complication after cardiac surgery, and anesthetics have been proposed as potential cerebral protective agents.1 Evaluation of cerebral blood flow by transcranial Doppler ultrasonography during open heart surgery is gaining popularity. Generally, volatile anesthetics dilate cerebral blood vessels, increase cerebral blood volume and possibly intracranial pressure and vascular reactivity.2 Conversely, studies on the effects of propofol have demonstrated avoidance of these undesirable effects, with a reduction in cerebral blood volume and intracranial pressure.2 There are some studies addressing the relationship between hemodynamic variables and middle cerebral arterial blood flow velocity during cardiopulmonary bypass (CPB).3 However, the effects of various anesthetics on cerebral blood flow and hemodynamic variables during CPB have not been described. The aim of this study was to evaluate the effects of propofol, isoflurane, and sevoflurane on middle cerebral arterial blood flow velocity during various stages of open heart surgery. We also planned to evaluate the relationship between these changes and hemodynamic parameters.
|
PATIENTS AND METHODS
|
|---|
This clinical study was performed in our hospital with the approval of the Ethical Committee and the informed consent of the patients. Fifty-eight patients, aged 37 to 65 years, in American Society of Anesthesiologists physical status I or II undergoing coronary artery bypass surgery, were enrolled in the study. The exclusion criteria were: carotid artery lesions, valvular heart disease, diabetes mellitus, psychological disease, allergic reactions, and abnormal hepatic or renal function tests. Patients were randomized into one of 3 groups by drawing a number. As we did not hide the anesthetic vaporizer in the operating room, this was not a double-blind study.
The patients were premedicated with 10 mg diazepam orally the night before surgery, and with 0.1–0.15 mg·kg–1 morphine intramuscularly on the day of surgery. Preoperatively, they underwent routine electrocardiograms, pulse oximetry, and invasive arterial pressure monitoring. A right internal jugular venous catheter with a 110 cm 4-lumen 7F thermodilution catheter (Abbott Critical Care Systems; North Chicago, IL, USA) was inserted under local anesthesia, and cardiac output measurements were performed with an Abbott cardiac output computer. Measurements of mean arterial pressure (MAP), central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, heart rate, cardiac output (CO), cardiac index, pulmonary vascular resistance [(pulmonary arterial pressure-pulmonary capillary wedge pressure) x 80/cardiac output], and systemic vascular resistance (SVR) [(mean arterial pressure-central venous pressure) x 80/cardiac output] were recorded. Cerebral blood flow velocity measurements were performed with a Doppler sonograph (Hewlett Packard, Sonos 1000, Palo Alto, CA, USA) with 2-MHz probes. Measurements were made on the temporal bone on the left side over the zygomatic arch, on the line from eye to ear, where the best image was found. From the Doppler flow curves, maximum velocity (Vmax), velocity at end-diastole (Vmin), and mean velocity (Vmean) were calculated. Pulsatility index (PI = Vmax – Vmin/Vmean) and resistivity index (RI = Vmax – Vmin/Vmax) were calculated by the software of the sonograph.
All patients received the same anesthetic induction with 10 µg·kg–1 fentanyl, 0.1 mg·kg–1 midazolam, and 0.1 mg·kg–1 pancuronium. After induction of anesthesia and the second set of measurements, one group received an infusion of 100 µg·kg–1·min–1 propofol, another group received 1 minimum alveolar concentration (MAC) of sevoflurane, and the third group had 1 MAC of isoflurane. Before sternotomy, an additional 2.5 µg·kg–1 fentanyl and 0.025 mg·kg–1 pancuronium were given to all patients. After the initiation of CPB, the group-specific anesthetic drugs were ceased because we did not have a suitable anesthetic vaporizer on the pump. During CPB, 2.5 µg·kg–1 fentanyl and 0.025 µg·kg–1 pancuronium were added. After perfusion, the group-specific drugs were started again.
Measurements and derived parameters were recorded at 6 time points: (I) before anesthetic induction, (II) 5 min after induction, (III) 10 min after administration of the specific drugs, (IV) after aortic cannulation, (V) on reaching 34°C during the cooling period of CPB, and (VI) after skin closure. Prior to cannulation for the institution of CPB, 300–400 U·kg–1 heparin sulphate was administered to raise the activated clotting time to at least 450 sec. The CPB circuit consisted of a roller pump, cardiotomy reservoir, arterial filter, and a Hilite 7000 membrane oxygenator (Medos, Stolberg, Germany) with an integrated heat exchanger. The circuit was primed with 700 mL of Ringer’s lactate solution containing 1 mol·L–1 sodium bicarbonate and 5,000 IU heparin. During hypothermic CPB, non-pulsatile pump flow was kept at 1.2–2.4 L·m–2·min–1 with a roller pump (Cobe; Sarns/3M, Ann Arbor, MI, USA). Blood electrolytes, glucose, and osmolality were monitored and maintained within normal ranges. Alpha-stat strategy was used for pH management, and patients were kept at normocapnia (PaCO2 35–45 mm Hg). Concentrated erythrocyte suspensions were added to the pump prime if the hematocrit dropped below 20% during CPB. Mean arterial pressure during CPB was stabilized at 50–70 mm Hg. Mild hypothermia (32°C) was applied in all patients. Nasopharyngeal temperature was continuously monitored as the indicator of cerebral temperature. For myocardial protection, cold (4°C) crystalloid cardioplegia (Plegisol; Abbott) was rapidly infused into the aortic root after aortic cross clamping for the induction of cardioplegic arrest. Maintenance of cardioplegic arrest was achieved with antegrade or retrograde (via coronary sinus) administration of blood cardioplegia (5 mL·kg–1). After aortic declamping, patients were re-warmed to 36.5°C, and CPB was terminated. Fluid management before and after CPB was determined by hemodynamic (arterial pressure and central venous pressure) and hematological requirements. Ringer’s lactate was used as a priming fluid. Although there are conflicting data, most studies suggest that the observed increases in tissue edema, extravascular lung water, and pulmonary shunt fraction are due to low colloid oncotic pressure. There is no evidence that low oncotic pressure adversely affects cardiac performance or hemodynamic variables.4
The data were recorded on a computer with SPSS for Windows 10.0.1 statistical software (SPSS Inc., Chicago, IL, USA). Parameters were evaluated with the Kolmogorov-Smirnov test for distribution and Leven’s test for homogeneity. The differences between the means of the 3 groups were tested by analysis of variance (ANOVA) if the data were parametric, or the Kruskal-Wallis test if the data were nonparametric. Means of 5 or 6 measurements at each time point within the same group were compared with ANOVA with repeated measures if the data were parametric, and with the Friedman test if the data were nonparametric. The comparisons of parametric data between groups, which were gathered by measurements, were evaluated with Pearson’s test, and nonparametric data with the Spearman correlation test. After ANOVA, Kruskal-Wallis, ANOVA with repeated measures, Friedman tests, and posthoc tests were performed to find the pair causing the difference between the groups or within the group. In all tests, the differences were accepted as significant when p values were less than 0.05.
|
RESULTS
|
|---|
Of the 58 patients enrolled in the study, 6 had to be excluded because of inotropic drug administration and inappropriate images. There were no significant differences in demographic data among the groups (Table 1
). The MAP, CO, and SVR measurements are shown on Table 2. After administration of propofol, sevoflurane, or isoflurane, MAP increased in the propofol and sevoflurane groups, while it decreased in the isoflurane group. Mean arterial pressure after administration of group-specific drugs was significantly lower in the isoflurane group than the propofol and sevoflurane groups ( p < 0.05). Cardiac output decreased significantly in the isoflurane group only. Systemic vascular resistance did not increase significantly and did not differ among the groups (Table 2).
Middle cerebral artery Vmax, Vmean, PI, and RI can be seen on Table 3. Vmax decreased after administration of all group-specific drugs, but the change was significant only in the propofol and isoflurane groups ( p < 0.05). Vmean decreased significantly after administration of isoflurane and propofol only. Resistivity index and PI increased in all groups, but this increase was significant only in the propofol group. In the propofol group, a correlation was found between: MAP and PI at time VI ( p = 0.001); MAP and RI at time VI ( p = 0.001); CO and Vmax at time I, II, and III ( p = 0.001, p = 0.004, p = 0.015); CO and Vmean at time I, II, III ( p = 0.002, p = 0.02, p = 0.006); SVR and Vmax at time I, II, III ( p = 0.001, p = 0.05, p = 0.001); SVR and Vmean at time I, II, III ( p = 0.05, p = 0.05, p = 0.05). In the sevoflurane group, a correlation was found between: MAP and Vmax at time VI ( p = 0.04); CO and Vmax at time VI ( p = 0.01); CO and Vmean at time VI ( p = 0.001); SVR and Vmax at time IV, VI ( p = 0.01, p = 0.001); SVR and Vmean at time IV, VI ( p = 0.05, p = 0.001). In the isoflurane group, a correlation existed between: MAP and PI at time III, VI ( p = 0.02, p = 0.005); MAP and RI at time III, VI ( p = 0.01, p = 0.005); CO and RI at time VI ( p = 0.03); and SVR and Vmax at time III ( p = 0.03).
|
DISCUSSION
|
|---|
Volatile anesthetics are often used as well as intravenous anesthetics during open heart surgery. The effects of both groups of drugs on the cardiovascular system, cerebral vascular structure, and cerebral blood flow have been well defined in clinical studies.5–8 The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent’s intrinsic vasodilatory action.9 In another study, halothane was found on transcranial Doppler ultrasonography to significantly increase the time-averaged mean velocity in the middle cerebral artery in a dose-dependent manner (0.5, 1, 1.5 MAC), whereas isoflurane and sevoflurane produced no significant dose-related changes.10 Similarly, Lundar and colleagues11 showed that isoflurane at 2 MAC did not affect cerebral blood flow. Cho and colleagues12 found that sevoflurane at 1 and 2 MAC reduced cerebral blood flow, but if nitrous oxide was added, it increased cerebral blood flow. Conversely, Matta and colleagues9 in a comparative study showed that sevoflurane and isoflurane increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC; the increase was less with sevoflurane. In a study that compared the effects of isoflurane and sevoflurane at 0.5 and 1.5 MAC, volatile anesthetics increased cerebral blood flow, but this effect was more pronounced with isoflurane.6 We found a decrease in cerebral blood flow after administration of isoflurane but not with sevoflurane at 1 MAC, which indicates that sevoflurane preserves cerebral blood flow better than isoflurane. After CPB, cerebral blood flow increased and came close to values after induction with both agents.
Ederberg and colleagues13 examined the effects of propofol on cerebral blood flow after anesthetic induction with 10 µg·kg–1 fentanyl, 2–3 mg·kg–1 thiopental sodium, and 0.1 mg·kg–1 pancuronium, and with institution of CPB at 32°C. They found that at high doses (such as 10 mg·kg–1·hr–1), propofol decreased cerebral blood flow by 35% on transcranial Doppler. Cho and colleagues12 found that lower doses of propofol (1.2 mg·kg–1·hr–1, after 2 mg·kg–1 bolus) reduced cerebral blood flow by 51%. Strebel and colleagues1 showed that 100 µg·kg–1·min–1 propofol did not compromise cerebral autoregulation. In our study, 100 µg·kg–1·min–1 propofol decreased cerebral blood flow less (18%) than in previous reports. After CPB, we found no change in cerebral blood flow rates.
There is no consensus on drug dosages and their effects in previous studies. This is probably because cerebral blood flow is affected by multiple factors. Gupta and colleagues14 found no significant change in mean velocity in the middle cerebral artery with an increase in MAP while awake or during 0.5 and 1.5 MAC sevoflurane anesthesia, and concluded that cerebral pressure autoregulation remained intact during sevoflurane anesthesia in humans. Cerebral autoregulation maintains constant cerebral blood flow during changes in cerebral perfusion pressure between 50 and 170 mm Hg. Inhaled anesthetics impair both the ability to autoregulate (static autoregulation) and the rate of autoregulation (dynamic autoregulation) in a dose-dependent manner. Summors and colleagues15 investigated the effect of sevoflurane and isoflurane on dynamic cerebral pressure autoregulation using transcranial Doppler, and concluded that dynamic cerebral autoregulation is better preserved during sevoflurane than isoflurane anesthesia in humans. In another study at 1.5 MAC, isoflurane and desflurane impaired autoregulation, whereas propofol preserved it.14
In our study, middle cerebral arterial blood flow velocity decreased significantly after isoflurane and propofol but not sevoflurane. During cannulation and CPB, cerebral arterial blood flow velocity continued to decrease in all groups; during cannulation and CPB hemodilution, hypothermia and decreased metabolic demand may change the cerebral regulation dynamics. After CPB, we found no difference in cerebral arterial blood flow velocity in all groups compared to initiation of these agents. Only after propofol infusion, were PI and RI increased. According to Strebel and colleagues,1 all volatile anesthetics have the same cerebral vasodilating properties, in contrast to intravenous anesthetics that generally have vasoconstrictive capabilities (with the exception of ketamine); this difference in vasomotor tone might explain the effect of propofol on PI and RI. After anesthetic induction, MAP and CO decreased in all groups, while there were increases in SVR. After starting the specific drugs, SVR increased, while CO decreased (significantly only in the isoflurane group). Mean arterial pressure also decreased in all groups but this decrease was greater in the isoflurane group compared to the sevoflurane and propofol groups ( p < 0.05). At the end of CPB, the decrease in MAP in the isoflurane group continued.
We found a relationship between CO, SVR, and middle cerebral arterial blood flow velocities in the same group. In a similar study, Diamant and colleagues3 performed simultaneous noninvasive monitoring of blood pressure, systemic hemodynamic parameters, and blood flow velocity in the middle cerebral artery in healthy subjects during a 24 hr period. They concluded that changes in stroke volume and cardiac output and to a lesser extent blood pressure variations, affected middle cerebral arterial velocity throughout 24 hours. In contrast, we did not find a significant relationship between SVR and PI or RI. We acknowledge that the experimental protocol used in this study had some limitations. We could not exclude the effect of agents used in induction (fentanyl, midazolam, and pancuronium) and the short time between starting the specific drugs and CPB onset might be insufficient for the appearance of effects of specific agents.
It was concluded that there was no differences between the drugs in their effects on middle cerebral arterial blood flow rates, although there was a trend for better preservation with sevoflurane than isoflurane and propofol at the doses used.
|
REFERENCES
|
|---|
- Strebel S, Lam AM, Matta B, Mayberg TS, Aaslid R, Newell DW. Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology 1995;83:66–76.[Medline]
- Marval PD, Perrin ME, Hancock SM, Mahajan RP. The effects of propofol or sevoflurane on the estimated cerebral perfusion pressure and zero flow pressure. Anesth Analg 2005;100:835–40.[Abstract/Free Full Text]
- Diamant M, Harms MP, Immink RV, Van Lieshout JJ, Van Montfrans GA. Twenty-four-hour non-invasive monitoring of systemic haemodynamics and cerebral blood flow velocity in healthy humans. Acta Physiol Scand 2002;175:1–9.[Medline]
- Hall TS. The pathophysiology of cardiopulmonary bypass. The risks and benefits of hemodilution. Chest 1995;107:1125–33.
- Drummond JC, Patel PM. Cerebral physiology: effects of anesthetics and technics. In: Miller RD, editor. Scientific principles. 5th ed. New York: Churchill Livingstone, 2000:695–735.
- Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation during sevoflurane anesthesia: a comparison with isoflurane. Anesth Analg 1999;88:341–5.[Abstract/Free Full Text]
- Bedforth NM, Girling KJ, Harrison JM, Mahajan RP. The effects of sevoflurane and nitrous oxide on middle cerebral artery blood flow velocity and transient hyperemic response. Anesth Analg 1999;89:170–4.[Abstract/Free Full Text]
- Bedforth NM, Hardman JG, Nathanson MH. Cerebral hemodynamic response to the introduction of desflurane: a comparison with sevoflurane. Anesth Analg 2000;91:152–5.[Abstract/Free Full Text]
- Matta BF, Heath KJ, Tipping K, Summors AC. Direct cerebral vasodilatory effects of sevoflurane and isoflurane. Anesthesiology 1999;91:677–80.[Medline]
- Kuroda Y, Murakami M, Tsuruta J, Murakawa T, Sakabe T. Blood flow velocity of middle cerebral artery during prolonged anesthesia with halothane, isoflurane, and sevoflurane in humans. Anesthesiology 1997;87:527–32.[Medline]
- Lundar T, Lindegaard KF, Refsum L, Rian R, Nornes H. Cerebrovascular effects of isoflurane in man. Intracranial pressure and middle cerebral artery flow velocity. Br J Anaesth 1987;59:1208–13.[Abstract/Free Full Text]
- Cho S, Fujigaki T, Uchiyama Y, Fukusaki M, Shibata O, Sumikawa K. Effect of sevoflurane with and without nitrous oxide on human cerebral circulation. Transcranial Doppler study. Anesthesiology 1996;85:755–60.[Medline]
- Ederberg S, Westerlind A, Houltz E, Svensson SE, Elam M, Ricksten SE. The effects of propofol on cerebral blood flow velocity and cerebral oxygen extraction during cardiopulmonary bypass. Anesth Analg 1998;86:1201–6.[Abstract]
- Gupta S, Heath K, Matta BF. Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans. Br J Anaesth 1997;79:469–72.[Abstract/Free Full Text]
- Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation during sevoflurane anesthesia: a comparison with isoflurane. Anesth Analg 1999;88:341–5.[Abstract/Free Full Text]
TOP
ABSTRACT
INTRODUCTION
