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Right arrow Cerebral protection

Ann Thorac Surg 2004;77:72-79
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Cerebral autoregulation after hypothermic circulatory arrest in operations on the aortic arch

Eugenio Neri, MDa*, Carlo Sassi, MDa, Lucio Barabesi, DrPhb, Massimo Massetti, MDe, Giorgio Pula, MDc, Dimitrios Buklas, MDa,e, Rossana Tassi, MDd, Pierpaolo Giomarelli, MDc

a Department of Surgery, University of Siena, Siena, Italy
b Units of Thoracic Aorta Surgery and Vascular Surgery, University of Siena, Siena, Italy
c Institute of Quantitative Methods, University of Siena, Siena, Italy
d Department of Neurological Sciences, Neurophysiology Unit, University of Siena, Siena, Italy
e Department of Thoracic and Cardiovascular Surgery, University of Caen, Caen, France

Accepted for publication July 17, 2003.

* Address reprint requests to Dr Neri, Dipartimento di Chirurgia Universita' agli Studi di Siena, Policlinico le Scotte, Viale M. Bracci, 53100 Siena, Italy
e-mail: euxneri{at}tin.it


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: The purpose of this study was to determine whether patients who undergo thoracic aorta repairs with the aid of hypothermic circulatory arrest experience impairments in cerebral autoregulation, and to ascertain the influence of three different techniques of cerebral protection on autoregulatory function.

METHODS: Sixty-seven patients undergoing elective aortic arch procedures with hypothermic circulatory arrest were tested for cerebral dynamic autoregulation using continuous transcranial Doppler velocity and blood pressure recordings. Twenty-three patients were treated using hypothermic circulatory arrest without adjuncts (group 1), 25 using antegrade cerebral perfusion (group 2), and 19 using retrograde cerebral perfusion (group 3).

RESULTS: There were no hospital deaths. Two major strokes occurred in this series; 9 patients experienced temporary neurologic dysfunction: in all these patients severe impairment of cerebral autoregulation was observed. Cerebral autoregulation in the immediate postoperative period was preserved only in patients treated with antegrade cerebral perfusion. Severe impairments were observed in the other two groups in which the degree of autoregulatory response was inversely correlated to the duration of the cerebral protection time during hypothermic circulatory arrest. Postoperative improvement of autoregulatory function was observed in the majority of patients. Our data suggest the exposure to brain damage in the presence of autoregulation impairment, thus indicating that postoperative hypotensive phases may further contribute to neurologic impairment.

CONCLUSIONS: The status of cerebral autoregulation in the postoperative period after hypothermic circulatory arrest procedures is profoundly altered. The degree of impairment is influenced by the cerebral protection technique. This study indicates the beneficial role of antegrade perfusion during hypothermic circulatory arrest for the preservation of this function and suggests that postoperative cerebral autoregulation impairment can be regarded as an expression of central nervous system injury.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Cerebral autoregulation (CA) refers to the inherent ability of the cerebral blood vessels to keep cerebral blood flow constant for a wide range of systemic blood pressure levels; it is usually observed at a mean arterial blood pressure of between approximately 50 and 150 mm Hg [1]. Cerebral autoregulatory response is impaired in a variety of disease states and during extreme cardiopulmonary bypass (CPB) conditions such deep hypothermia and circulatory arrest [2].

There is not much information available about CA in the postoperative period after CPB procedures and in particular after hypothermic circulatory arrest (HCA) operations. The purpose of this study was to assess the status and the time course of postoperative CA response in these patients as well as to determine the effects of different perfusion techniques on this function.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
Study participants
Sixty-seven elective patients who had undergone operations on the thoracic aorta with the HCA technique during a 49-month period between January 1999 and March 2003 were included in the study. Written informed consent was obtained from each participant. Twenty-three patients were treated using HCA without adjuncts (group 1), 25 using antegrade cerebral perfusion (group 2), and 19 using retrograde cerebral perfusion (group 3). The three groups were not randomized, and the choice of protection method was individualized during the institutional surgical indications conferences on the basis of patients' disease and surgeons' preferences. The clinical and demographic characteristics of the patients are illustrated in the Table 1. The age range was between 46 and 75 years. Before being entered into the study, all patients were screened for extracranial carotid artery disease by Doppler ultrasonography and for intracranial vascular disease by transcranial Doppler ultrasonography; moreover, they all underwent preliminary dynamic CA testing, using noninvasive methods for pressure recordings and end-tidal carbon dioxide measurements [3]; all patients had an intact dynamic CA response before surgery and no significant differences in autoregulatory function were found among the groups (Table 1). None of the patients included in the study presented any of following conditions: emergency surgical interventions, known carotid artery or intracranial stenosis, preoperative stroke or other cerebrovascular complications (recent or remote), preoperative CA impairment, or the absence of a temporal bone window.


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  		Table 1. Clinical Characteristics and Results of One-Way Analysis of Variance for Differences Among Groups

 
Surgery and cardiopulmonary bypass management
Patients were treated using standard surgical techniques; operations are listed in the Table 2. Axillary cannulation was routinely used for the CPB arterial return. The methods of profound hypothermia, circulatory arrest, and cerebral protection have been described in detail in previous studies [4, 5]. All patients were cooled using the {alpha}-stat method of pH control until nasopharyngeal temperature reached 20°C. During the period of circulatory arrest the head was packed in ice to prevent warming of the central nervous system, and standard doses of steroids and barbiturates (thiopental at 5 mg/kg) were given before circulatory arrest as an adjunct for cerebral protection. Antegrade cerebral perfusion (group 2) was obtained using the right axillary cannulation [5, 6], supplemented by endoluminal common carotid cannulation in patients with inadequate intracranial bihemispheric perfusion as assessed by transcranial Doppler [7]. Pump flow indexes of 10 to 15 mL · kg-1 · min-1, with pump perfusion pressures not exceeding 80 mm Hg, were used to perfuse the brain while maintaining perfusion temperatures less than 12°C.


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  		Table 2. Operations

 
In patients on whom retrograde cerebral perfusion was used (group 3), the superior vena cava flow was adjusted to maintain a central venous pressure of 25 to 30 mm Hg, which corresponded to a rate of between 150 and 350 mL/min; perfusate temperature was less than 12°C. Patients were rewarmed with a maximal gradient of 10°C between nasopharyngeal and heat exchanger water temperature.

Myocardial protection was obtained with cold blood cardioplegia delivered antegradely and retrogradely from the coronary sinus.

Neurologic evaluation
All patients were neurologically assessed before the operation. Postoperative neurologic events were evaluated by a consulting neurologist, and the outcome was classified in accordance with Ergin and associates [8]. In the presence of neurologic complications, a brain computed tomographic or magnetic resonance imaging scan was performed immediately and repeated during the hospital course when appropriate.

Cerebral autoregulation measurements
Dynamic CA was evaluated perioperatively using bilateral transcranial Doppler sonography and the thigh cuff method to alter arterial blood pressure [9, 10].

In each participant, both middle cerebral arteries were identified by transcranial Doppler ultrasonography according to standard criteria [11]. The transducers were then fixed in place by a headband, and cerebral mean blood flow velocities, together with arterial blood pressure, were continuously monitored and recorded by the computer connected to the Doppler unit (Multidop X; DWL Corp, Sipplingen, Germany). To allow for optimal test conditions, the minute ventilation was adjusted to maintain arterial blood carbon dioxide concentration at 35 mm Hg; moreover, to avoid any interference on CA by volatile anesthetic agents [12], sedation was obtained with propofol (180 to 200 µg/kg per minute).

Large blood pressure cuffs were placed around both thighs and inflated to 20 to 40 mm Hg above the systolic blood pressure for 3 minutes. Releasing the cuffs caused a sharp but moderate transient drop in systemic blood pressure. Drops in mean arterial blood pressure of more than 12 mm Hg were considered a sufficient autoregulatory stimulus.

The dynamic autoregulatory response was assessed using this rapid step-decrease in mean arterial blood pressure according to the technique proposed by Aaslid and associates [9].

The sharp drop in mean arterial blood pressure that is usually observed lasts approximately 10 seconds before returning to its original level. A simultaneous drop in cerebral blood flow velocity accompanies the fall in mean arterial blood pressure. The rate of regulation, which reflects the phase with the maximal change in cerebrovascular resistance and tone, was calculated using the measurements of the arterial blood pressure and the flow velocities as a function of time [13]. With normal autoregulation, the recovery of cerebral blood flow velocity to its resting level will tend to precede that of arterial blood pressure. This typical response can be quantified with a mathematical model proposed by Tiecks and colleagues [3]. The Doppler device software transfers this rate of regulation into the autoregulatory index (ARI) [3]. A value of zero signifies a total loss of autoregulation, 1 to 3 indicates a severe impairment of autoregulation, 3 to 6 is a fairly preserved autoregulation, whereas values more than 6 to 9 reflect an intact autoregulation.

In the present study the measurements were performed after induction of anesthesia (test 0) and after surgery, within 90 minutes after intensive care unit admission (test 1), as soon as ventilatory, hemodynamic, and body temperature stabilization of patients was achieved. Table 3 summarizes the physiologic and clinical measurements recorded at the moment of the postoperative test (test 1). To assess postoperative CA recovery during the first week after the operation, we further evaluated the patients with dynamic CA tests; measurements were performed on postoperative days 3 and 7 (follow-up tests 1 and 2).


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  		Table 3. Relevant Physiologic and Clinical Variables Recorded in the Immediate Postoperative Period at the Moment of Cerebral Autoregulation Testsa

 
Statistical analysis
The normality of data distribution was tested by the Kolmogorov-Smirnov test. Normally distributed data were treated with parametric tests, otherwise with nonparametric tests. Values are expressed as means ± standard deviation if normally distributed, otherwise as median and 25th and 75th percentiles. The data were analyzed using the following statistical methods where appropriate: Fisher's exact test, Student's t test, Mann-Whitney U test, one-way analysis of variance, and regression analysis. The data collection and analysis group were blinded from the therapeutic group.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Mortality and morbidity
There were no hospital deaths. No significant differences were observed among the groups with regard to the length of stay in the intensive care unit and hospitalization time (Table 1). Two patients (2.9%) experienced major strokes with permanent hemiplegia; both patients belonged to group 1. Nine patients (13.4%) experienced temporary neurologic dysfunction characterized by agitation (6 patients) or obtundation (3 patients); these patients belonged respectively to group 1 (5 patients) and group 3 (4 patients). Neurologic symptoms were resolved in all these cases within a week of operation, and control computed tomographic and magnetic resonance imaging scans remained negative. There was a significant association observed between neurologic complication and ARI (p < 0.0001), as illustrated in Table 4. These patients with neurologic complications experienced more prolonged or severe hypotensive phases compared with the other patients, as indicated by a significantly higher hypotension index (p < 0.0001; Table 4); postoperative hypertension index was not statistically significant. These data suggest that postoperative hypotensive phases may further contribute, in the absence of autoregulation, to neurologic impairment.


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  		Table 4. Differences of Perioperative Variables Between Patients With or Without Neurologic Complications

 
Cerebral autoregulation
There was no significant difference in dynamic autoregulation values observed by the two-tailed paired Student's t test between the right and left middle cerebral arteries (p = 0.98). The regression analysis also indicated close correlations between the ARI values in the right and left hemispheres in all patients (y = 0.01 + 1.00x; r2 = 0.99; p < 0.0001). We therefore assigned one ARI value, the mean ARI, to each participant.

Table 1 illustrates the differences among groups with regard to preoperative variables as assessed by one-way analysis of variance (continuous variables) and the exact contingency analysis (proportions); Table 3 summarizes the relevant physiologic and clinical variables recorded at the time of the first postoperative measurements in the three groups.

There were no significant differences (Table 3) with regard to baseline mean arterial blood pressure and mean arterial blood pressure immediately after the release of the blood pressure cuffs. The blood pressure drop was significantly less pronounced in group 1 than in group 3 patients; however, this should not significantly affect the results because the ARI calculation takes into account the magnitude of the blood pressure drop.

The decrease in ARI from preoperative to immediate postoperative tests (t0 versus t1; Fig 1) was highly significant, either in the overall population, or in patients operated on with antegrade cerebral perfusion, with simple HCA or retrograde cerebral perfusion. Significant differences between preoperative and postoperative ARI were observed among groups; in particular group 2, which had a lower decrease in ARI, differed significantly from groups 1 and 3, whereas no significant differences were observed between groups 1 and 3. It should be said that the between-groups differences with regard to hematocrit values, before and after the operation (to versus t1), were not significant at one-way analysis of variance (Table 3).



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  		Fig 1. Autoregulation index (ARI) measurements of the three groups at the different time points of the study. Significant differences were found between preoperative and immediate postoperative time points (t0 vs t1): 5.0 ± 0.4 versus 2.4 ± 1.3; p < 0.0001 (paired-sample Student's t test). Significant differences were found also for each group: group 1 (white boxes; simple hypothermic circulatory arrest): 5.1 ± 0.4 versus 1.3 ± 0.6, p < 0.0001; group 2 (light gray boxes; patients operated on with antegrade cerebral perfusion): 5.0 ± 0.4 versus 4.0 ± 0.4, p < 0.0001; or group 3 (dark gray boxes; retrograde cerebral perfusion): 5.0 ± 0.5 versus 1.4 ± 0.3, p < 0.0001. Despite a dramatic recovery, the autoregulation index at the end of the study still differed significantly from the preoperative values, both in the overall population (5.0 ± 0.4 vs 3.7 ± 0.9; p < 0.0001, paired-sample Student's t test) and in each group (group 1: 5.0 ± 0.4 vs 3.1 ± 0.7, p < 0.0001; group 2: 5.0 ± 0.4 vs 4.7 ± 0.3, p = 0.005; group 3: 5.0 ± 0.5 vs 3.1 ± 0.5, p < 0.0001).

 
One-way analysis of variance was conducted to evaluate the relationships between the three different perfusion methods and the ARI in the immediate postoperative period (Table 3). There were significant differences in the means between the group that received antegrade cerebral perfusion (group 2) and those who received HCA alone or retrograde cerebral perfusion (group 3). No significant difference was observed between patients treated with HCA alone (group 1) and patients treated with retrograde cerebral perfusion (group 3).

Using an ARI cutoff value of 3 [14], we divided patients into two categories, those with intact autoregulation and those with impaired autoregulation, to detect possible differences in the test conditions or physiologic variables that could account for the differences found in the ARI values (Table 5).


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  		Table 5. Differences of Clinical and Physiologic Perioperative Variables Between Patients With Impaired and Preserved Cerebral Dynamic Autoregulationa

 
All group 2 patients (n = 25) had an adequate ARI (ARI >= 3) whereas all patients in group 3 (n = 19) and 22 patients in group 1 (n = 23) had an ARI less than 3 (p < 0.001). At univariate analysis (Table 5) we found no significant differences with regard to the majority of physiologic and clinical variables between patients who had severely impaired CA and those who did not. However, the perfusion method was significantly associated with ARI impairment; in particular, the nonuse of antegrade cerebral perfusion influenced the CA status.

To uncouple the effects of CPB time and cerebral protection time during HCA from those attributable to the type of cerebral protection, we performed separate correlation analyses both in the whole patient population and within each group.

In the entire patient population we found no significant correlation between ARI and CPB time or total cerebral protection time (Table 6), whereas marked differences were observed in each group. The patients treated with simple circulatory arrest and those treated with retrograde cerebral perfusion exhibited an inverse correlation between CA capacity and cerebral protection time; conversely in group 2 patients, who received antegrade perfusion, we found the ARI to be independent of cerebral protection time.


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  		Table 6. Results of the Correlation Analysis Between the Autoregulatory Index and Cardiopulmonary Bypass Time and Hypothermic Circulatory Arrest Duration in the Overall Population and in Each of the Three Groups

 
With regard to CPB duration, a significant inverse correlation was found for group 1 but not for group 2 and 3 patients.

To evaluate the time course of the degree of CA recovery, we analyzed the follow-up measurements (postoperative days 3 and 7).

On the third postoperative day only 12 patients among the 42 (29.2%) who had a postoperative ARI less than 3 recovered an adequate (ARI >= 3) autoregulatory function.

Remarkably, on the seventh postoperative day, the majority of patients (52 of 67; 77.6%) had an ARI of 3 or more; in particular 26 of the 41 patients (63.4%) with severe postoperative CA impairment (ARI < 3) recovered an adequate autoregulatory function at the end of the study. Despite this dramatic recovery, at the end of the study the ARI was still significantly different from the preoperative values, both in the overall population and in each group.

Figure 1 summarizes the ARI measurements of the three groups at the different time points of the study.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Study limitations
The study is a prospective nonrandomized design undertaken to appraise the modifications of a function, CA, in the clinical setting of HCA operation. The observational nature of the study performed on the three nonrandomized groups, with regard to the choice of protection method, may represent a relative source of bias in the comparisons and consequently limit the information provided by the study.

Methodology and measurements
Cerebral autoregulation occurs with a substantial degree of temporal heterogeneity in that physiologic adjustments of cerebral blood flow occur both quickly and slowly. Static CA refers to cerebral blood flow adjustments in response to more prolonged blood pressure changes and is a measure of the overall efficiency of the system. Dynamic CA refers to the ability to maintain cerebral blood flow in the face of blood pressure changes occurring during a matter of seconds and reflects the latency of the cerebral vasoregulatory system. The method used to assess autoregulation in this study was the dynamic autoregulatory response of the relative blood flow changes in both middle cerebral arteries measured using transcranial Doppler ultrasonography. This method was first described by Aaslid and coworkers [9] and Larsen and associates [15], and its validity has subsequently been confirmed by multiple studies [16, 17].

Although our initial study design included a parallel measurement of static autoregulation, the decision from the ethics committees to not allow the use of static autoregulation tests (which entails the administration of vasopressor drugs) made it impossible to assess actual differences between the two responses. However, it has been shown [3] that the impairment of CA affects first the latency of the autoregulatory response (measured by dynamic tests) and then the efficiency (static tests); therefore, the exclusive use of dynamic tests does not impair the sensitivity of the study.

Although the analysis of the differences between preoperative and postoperative ARI reflected the general divergence between the groups, we chose to center our inferences on only the postoperative ARI values because of the significant drop in hematocrit level observed between preoperative and postoperative measurements.

Cerebral autoregulation and central nervous system injury
A loss of CA has already been observed in other conditions including post–head injury disorders, neonatal hypoxic damage, focal ischemia, acute ischemic stroke, and carotid artery disease [18–22]. Furthermore several animal and human studies have indicated that during CBP cerebral pressure-flow autoregulation is preserved under most bypass conditions except for those in which pH-stat blood gas management, deep hypothermia (<22°C), and circulatory arrest are used [2, 23].

In the present study we found that after surgery a significant number of patients who had undergone HCA operations had severely impaired or absent CA function. We also documented that the impairment of CA continued beyond the immediate postoperative period, and our data strongly suggest that patients who have poorly functioning autoregulation are vulnerable to brain damage during the time in which their autoregulation was impaired, in particular in the presence of postoperative hypotensive phases. These observations, together with the demonstration that postoperative autoregulatory function is not attributable to a low cerebral perfusion pressure at the time of measurement, indicate that the status of CA is greatly influenced by the perfusion technique used in these procedures.

We found that simple HCA, at least in our current protocol, and also retrograde cerebral perfusion provided inadequate protection against postoperative CA impairment. More importantly we demonstrated that CA loss could be effectively prevented by the use of antegrade cerebral perfusion, indicating that a reduction in this function may represent expression of central nervous system injury. On the other hand our findings strongly suggest that the status of CA may represent a marker of cerebral damage inasmuch as the more complex cases, requiring the more prolonged cerebral protection times, were treated using antegrade perfusion with a better preservation of autoregulatory function.

Further studies are needed to determine the causes of impaired autoregulation in these patients; we hypothesize an ischemic microvascular damage occurs. With respect to this hypothesis, the demonstration by Langley and coworkers [24] of the cerebral microvascular injury that develops during HCA may represent the ultrastructural substrate of this supposition.

Beside this we should take into account the effects of CPB time, which is inversely correlated to ARI in patients treated without cerebral protection but does not influence the autoregulation in patients treated with the use of antegrade cerebral perfusion and also in patients treated with retrograde cerebral perfusion (Table 6). This indicates that maintaining a cerebral arterial perfusion counteracts the detrimental effects of prolonged CPB times [25–28].

Conclusions
This study, although far from exhaustive on these important issues, indicates that the status of CA, in the postoperative period after HCA procedures, is profoundly altered and demonstrates that only cerebral antegrade perfusion has a beneficial role for the preservation of the CA function. Moreover, our findings suggest a potential role of dynamic autoregulation measurement in the clinical practice, either as an indicator of central nervous system injury or a measure of cerebral protection in HCA patients.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
The authors thank Mr Massimo Gistri del Nicchio for his help with the Doppler studies. We also thank all the patients who participated in the study.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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Right arrow Cerebral protection

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