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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.54 no.2 Campinas Mar./Apr. 2004

http://dx.doi.org/10.1590/S0034-70942004000200004 

SCIENTIFIC ARTICLE

 

Analysis of brain hemometabolism behavior during carotid endarterectomy with temporary clamping*

 

Análisis del comportamiento del hemometabolismo cerebral durante endarterectomia carotídea con pinzamiento transitorio

 

 

Gastão Fernandes Duval Neto, TSA, M.D.I; Augusto H. Niencheski, M.D.II

IProfessor Doutor Adjunto
IICirurgião Vascular Periférico

Correspondence

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: Carotid endarterectomy with temporary clamping changes cerebral blood flow and cerebral metabolic oxygen demand ratio with consequent oligemic hypoxia or hemometabolic uncoupling. This study aimed at identifying changes in brain hemometabolism, evaluated through changes in oxyhemoglobin saturation in internal jugular vein bulb (SvjO2) during carotid endarterectomy with clamping, and at correlating these changes with potentially interfering factors, mainly end tidal CO2 pressure (PETCO2) and cerebral perfusion pressure (CPP).
METHODS: Sixteen patients with unilateral carotid stenotic disease scheduled to carotid endarterectomy with carotid arterial clamping were enrolled in this study. Parameters including internal jugular bulb oxyhemoglobin saturation, stump pressure  and end tidal CO2 pressure were measured at the following moments: M1 - pre-clamping; M2 - 3 minutes after clamping; M3 - pre-unclamping; M4 - post-unclamping).
RESULTS: The comparison among SvjO2 (%, mean ± SD) in all studied periods has shown differences between those recorded in moments M1 (52.25 ± 7.87) and M2 (47.43 ± 9.19). This initial decrease stabilized during temporary clamping, showing decrease in the comparison between M2 and M3 (46.56 ± 9.25), without statistical significance (p = ns). At post-unclamping, M4 (47.68 ± 9.12), SvjO2 was increased as compared to M2 and M3 clamping stages, however it was still lower than that of pre-clamping stage M1.(M4 x M1 - p < 0.04) This SvjO2 decrease was followed by significant cerebral perfusion pressure (stump pressure) decrease. Factors influencing this brain hemometabolic uncoupling trend were correlated to PETCO2. The comparison between CPP and SvjO2 showed weak correlation devoid of statistical significance.
CONCLUSIONS: In the conditions of our study, SvjO2 measurement is a fast and effective way of clinically monitoring changes in CBF/CMRO2 ratio. Temporary carotid clamping implies in a trend towards brain hemometabolic uncoupling and, as a consequence, to oligemic ischemia; cerebral perfusion pressure does not assesses brain hemometabolic status (CBF and CMRO2 ratio); hypocapnia, may lead to brain hemometabolic uncoupling; PETCO2 monitoring is an innocuous and efficient way to indirectly monitor PaCO2  preventing inadvertent hypocapnia and its deleterious effects on CBF/CMRO2 ratio during temporary carotid clamping.

Key Words: MONITORING: jugular bulb oxyhemoglobin saturation, brain oximetry; SURGERY, Vascular: carotid endarterectomy


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: La endarterectomia carotídea con pinzamiento transitorio altera la relación entre el flujo sanguíneo cerebral y la demanda metabólica cerebral de oxígeno, con consecuente generación de una tendencia a hipóxia oliguemica o desacoplamiento hemometabólico. El objetivo del presente estudio fue identificar las alteraciones del hemometabolismo cerebral, evaluados por medio de las alteraciones de la saturación de la oxihemoglobina en el bulbo de la vena yugular interna (SjO2), durante endarterectomia carotídea con pinzamiento, correlacionando esas alteraciones con factores con potencialidad de interferir con las mismas, principalmente la presión de CO2 expirada (PETCO2) y la presión de perfusión cerebral (PPC).
MÉTODO: Participaron del estudio 16 pacientes con enfermedad estenosante unilateral y sometidos al pinzamiento arterial transitorio durante endarterectomia carotídea. Los parámetros monitorizados (saturación de la oxihemoglobina en el bulbo de la vena yugular interna, stump pressure y la presión de CO2 expirado) fueron analizados en los siguientes momentos: M1 - pre-pinzamiento; M2 - 3 minutos pos-pinzamiento; M3 - pre-despinzamiento; M4 - pos-despinzamiento.
RESULTADOS: La comparación entre la SjO2 (%, Media ± DP) en los períodos estudiados evidenció una diferencia entre la registrada en los momentos M1 (52,25 ± 7,87) y M2 (47,43 ± 9,19). Esa reducción inicial estabilizó durante el pinzamiento transitorio, con disminución en la comparación entre M2 y M3 (46,56 ± 9,25), sin significado estadístico (p = ns). En la fase pos despinzamiento, M4 (47,68 ± 9,12), la media de la SjO2 presentó una elevación, cuando comparada con los momentos de pinzamiento M2 e M3, más inferior al momento pre-pinzamiento M1 (M4 x M1 - p < 0,04). Esa disminución de la SjO2 fue acompañada de disminución significante de la presión de perfusión cerebral (stump pressure). Los factores que influencian esa tendencia al desacoplamiento hemometabólico cerebral presentaron correlación con la PETCO2. La comparación entre la PPC y la SjO2 presentó un bajo índice de correlación, sin significación estadística.
CONCLUSIONES: En las condiciones de este estudio la aferición de la SjO2 es un modo de monitorización clínico efectivo y de rápida respuesta en la evidenciación de las alteraciones de la relación FSC/CCO2; el pinzamiento carotídeo transitorio implica en una tendencia al desacoplamiento hemometabólico cerebral y consecuentemente, hipóxia oliguemica; la PPC de forma aislada, no evalúa la situación hemometabólica cerebral (relación entre FSC y el CCO2); la hipocapnia puede llevar a situaciones de desacoplamiento hemometabólico; la monitorización de la PETCO2 es forma inocua y eficiente de monitorizar la PaCO2, evitando situaciones de hipocapnia inadvertidas, con sus efectos deletéreos sobre la relación FSC/CCO2, durante pinzamiento carotídeo transitorio.


 

 

INTRODUCTION

Carotid endarterectomy has been considered superior for severe and symptomatic carotid stenotic disease when compared to clinical treatment 1,2, but this benefit is significantly lower in asymptomatic carotid stenosis 3.

Ischemic brain injuries are factors significantly contributing for increased perioperative morbidity and mortality in carotid endarterectomy with temporary intraoperative clamping. In theory, the pathophysiology of such complications is explained by thromboembolic processes 4-6, hemodynamic changes 7 or both.

Global blood flow and brain metabolic oxygen demand ratio characterizes the so-called brain hemometabolism, which may be evaluated by the measurement of oxyhemoglobin saturation of venous blood samples drawn from the internal jugular vein bulb ipsilaterally to the surgically intervened carotid artery. On the other hand, regional changes between flow and brain O2 demand, secondary to thromboembolic episodes, are not detectable with this type of monitoring 8,9.

Anesthesiologists may significantly influence brain hemometabolism during carotid endarterectomy, especially through intraoperative mechanical ventilation control (CO2 arterial pressure) and/or hemodynamic control (cerebral perfusion pressure) during temporary common carotid artery clamping.

This study aimed at identifying brain hemometabolism changes evaluated through oxyhemoglobin changes in jugular bulb venous oxygen saturation (SvjO2) during carotid endarterectomy with temporary intraoperative arterial clamping, and at correlating such changes to factors potentially interfering with them, especially end-tidal CO2 pressure (PETCO2) and cerebral perfusion pressure (CPP).

 

METHODS

After Ethics Committee approval and informed consent, 16 patients of both genders, 65 ± 10.3 year-old, with symptomatic carotid stenotic disease scheduled to unilateral carotid endarterectomy were enrolled in the study. All obstructive lesions were symptomatic and unilateral with diameter equal to or above 70%, and diagnosed by Doppler ultrasound (Sonos 2000 - Hewlett Packard with 7.5 MHz transducer) and/or arteriography with digital subtraction of carotid and vertebral vascular beds. Carotid and vertebral arteries opposite to the stenotic vessels had no critical lesions.

Patients on drugs with cerebro-vascular actions as well as diabetic patients were excluded from the study. No patient had hemoglobin or hematocrit abnormalities that could impair oxygen transportation. Anesthesia was induced with propofol (2 mg.kg-1) and sufentanil (0.15 µg.kg-1) and was maintained with inhaled isoflurane associated with sufentanil boluses, in order to maintain stable anesthetic depth based on hemodynamic parameters. Muscle relaxation was achieved with atracurium (0.5 mg.kg-1) and neuromuscular block intensity was assessed with peripheral nerve stimulator, in order to obtain no muscle responses at TOF stimulation. Patients were mechanically ventilated with tidal volumes of 8 mL.kg-1 at 10 cycles per minute. PETCO2 was used to adjust the ventilatory regimen.

Retrograde ipsilateral internal jugular vein catheterization was performed under direct vision with 17G 5.1 cm length needle (1.5 mm) through which a 19G (1.1 mm) 30 cm length radio-opaque catheter (Intracath® and Vialon® wire guide - Becton-Dickinson, USA) was inserted. Cephalad catheter progression was slowly and carefully performed until elastic resistance corresponding to upper internal jugular vein bulb wall was perceived. When this occurred, catheter was removed approximately 5 mm maintaining smooth and continuous aspiration until continuous venous flow was obtained, a maneuver that indicates catheter detachment from bulb wall. The jugular bulb catheter was connected to the 3-way stop-cock and continuously flushed with heparinized saline solution (2500 U in 250 ml saline solution), at 1 mL.h-1.

Sampling consisted of gentle aspiration of 3 ml jugular bulb venous blood in 90 s in order to prevent contamination with extra-cranial venous blood. Samples were collected at pre-established observation moments.

Common carotid artery catheterization distally to clamping site (common and external carotid) was performed under direct vision with a 5-French Swan-Ganz catheter (BIOMEDICA® USA) to measure mean arterial blood pressure, which was considered cerebral perfusion pressure (CPP), which was measured by a BIOMONITOR 7® (Bese - Bio Engenharia de Sistema e Equipamentos S.A. - Belo Horizonte, MG), zeroed at the mid-axillary line. For measuring distal (cranial) mean blood pressure, the catheter cuff was inflated. Stump pressures lesser than 25 mmHg from baseline were considered indication for temporary shunt, and patients were excluded from the study.

Radial artery was catheterized with 18G catheter for continuous mean blood pressure monitoring (Biomonitor 7® - Bese - Bio Engenharia de Sistema e Equipamento S.A. - Belo Horizonte, MG) and blood sampling for gas analysis (PaCO2).

Arterial (radial artery) and venous (internal jugular vein bulb) blood samples were simultaneously collected at the ratio of 2 mL of arterial to 1 mL venous blood, at the observation moments. One ml of venous sample was used to measure SvjO2 in a hemoximeter (Hemoximeter™ OMS3® - Radiometer® - NV, Denmark 1991), and the 2-mL arterial sample was sent to arterial blood gases analysis (178 pH/Blood Gas Analyzer - Corning Glass Works® - Corning Limited, Halstead, Essex, England). Arterial hemoglobin saturation was kept stable throughout the procedure.

Measurements were performed at the following moments: M1 - previously to carotid clamping, M2 - 3 minutes after carotid clamping, M3 - immediately before carotid unclamping, and M4 - 3 minutes after carotid unclamping.

Statistical analysis included Student's t, Fisher and Pearson's r correlation coefficients as appropriate. Significance level was 5% (p < 0.05).

 

RESULTS

Mean patients' age was 65 ± 10.3 years. No patient had procedure-related neurological complications in the 48-hour postoperative period of observation in the intensive care unit).

MBP and SvjO2 were maintained stable as shown in table I.

Jugular oxyhemoglobin saturation (SvjO2) - comparisons of SvjO2 (% mean ± SD) detected in studied periods showed statistically significant differences between M1 (52.25 ± 7.87) and M2 (47.43 ± 9.19) (p < 0.02). This decrease stabilized during temporary clamping with mild non-significant decrease in the comparison between M2 and M3 (46.56 ± 9.25). At M4 mean SvjO2 was increased as compared to M2 and M3 (47.68 ± 9.12), but still lower than M1 (M4 x M1 - p < 0.04) (Figure 1).

Cerebral perfusion pressure - comparisons of CPP (mmHg, mean and SD) showed statistically significant differences between M1 (70.31 ± 12.46) and M2 (39.00 ± 6.68) (p < 0.001). This decrease stabilized during temporary carotid clamping, while keeping statistically significant difference when M2 was compared to M3 (50.75 ± 10.66) (p < 0.01). At M4 (63.50 ± 10.49), CPP has significantly increased (p < 0.03), however remaining below M1 (p < 0.05), that is, not reaching pre-clamping pressures (Figure 2).

Correlation between SvjO2 (%) and CPP (mmHg) - figure 3 shows linear regression between studied variables, with a weak correlation coefficient and without statistical significance (r = 0.089; p = ns).

Correlation between PaCO2 and PETCO2 - figure 4 shows linear regression with strong positive and statistically significant correlation (r = 0.94; p < 0.0001) between PaCO2 and PETCO2. No changes were seen in such parameters in the opposite direction, that is increased PaCO2 has always corresponded to increased PETCO2.

Correlation between SvjO2 and PaCO2 - linear regression illustrated in figure 5 shows a moderate correlation between PaCO2 and SvjO2 (r = 0.69; p < 0.0001).

Correlation between SvjO2 and PETCO2 - linear regression shown in figure 6 shows a moderate correlation between PETCO2 and SvjO2 (r = 0.72; p < 0.0001), which is consistent with previous correlation (Figure 6).

 

DISCUSSION

Patients submitted to carotid endarterectomy are at risk of developing perioperative brain complications, which are very often clinically evidenced during the anesthetic recovery period. These complications may be attributed to two major pathophysiological mechanisms: hemodynamic, by changing cerebral blood flow as a consequence of temporary carotid clamping, or by thromboembolic phenomena secondary to surgical handling of arterial vascular system, resulting in atheromatous plaque displacement and, eventually, brain microembolism 4-7.

The brain is dependent on glucose mitochondrial aerobic oxidation to produce the necessary energy for its normal cellular functioning. Approximately 50% of this energy is used in maintaining and restoring ionic gradients necessary for depolarization and repolarization of neuronal membranes and the remaining 40% are spent in maintaining cell integrity. On the other hand, the brain has little glucose reserve and low adenosine triphosphate concentration (ATP). For this reason, the maintenance of adequate cerebral blood flow (CBF) to supply tissue metabolic demands (brain oxygen consumption - CMRO2) is critical for the anatomicofunctional integrity of central nervous system neurons.

Although brain represents only 2% of body weight, its high metabolic index requires 15% of cardiac output to maintain a perfect brain oxygen supply/consumption ratio (CBF/CMRO2).

CBF/CMRO2 ratio, that is, the hybrid association between hemodynamic and metabolic phenomena is clinically evaluated as a whole, and called brain hemometabolism. Although varying CBF and CMRO2, the ratio between these two variables is maintained within narrow limits. In fact, tissue CMRO2 participates in brain vascular resistance control through CO2 production, thus regulating CBF. This phenomenon is called brain hemometabolic coupling (BHMC) 10.

Brain O2 release (BRO2) may be described by the following equation:

BRO2 = CBF x CaO2

Where

CaO2 - arterial oxygen content

On the other hand, CMRO2 may be calculated by the following equation:

CMRO2 = CBF x (CaO2 - CvjO2)

Where

CvjO2 - jugular bulb venous oxygen content

The difference between arterial and jugular bulb venous oxygen content is expressed as (CaO2 - CvjO2) or DajvO2. Thus, the above equation may be modified as follows:

DajvO2 = CMRO2 / CBF

It is possible to calculate DajvO2 through CBF and CMRO2 or, in a more practical and clinical manner, through the arterial and jugular oxygen content.

DajO2 = CaO2 - CjO2

Blood (arterial or venous) oxygen content results from the addition of volumes of oxygen bound to hemoglobin and dissolved in plasma.

CaO2 = Hba x1.39 x SaO2 + PaO2 . 0.003

CjO2 = Hbjv x 1.39 x SvjvO2 + PjvO2 . 0.003

PaO2 - O2 arterial pressure
PjvO2 - jugular bulb venous O2 pressure
Hba - arterial hemoglobin concentration
Hbjv - jugular venous hemoglobin concentration
0.003 - O2 solubility coefficient

O2 content (CaO2 - CjvO2) is the total amount of this gas carried by a certain blood volume and resulting in the following formula:

DajO2 = [(SaO2.Hba) - (SvjO2.Hjj)],1.39 - [PaO2 - PjO2].0.003
                                             100

Considering the low O2 plasma solubility (solubility coefficient = 0.003) it is acceptable to disregard the participation of O2 dissolved in plasma in calculating blood oxygen content. Arterial hemoglobin is similar to venous hemoglobin allowing the consideration of just one value. Thus:

DajvO2 = (SaO2 -SvjO2) x Hb x 1.39

DajvO2 has been used to establish the presence or absence of an auto-regulation system of the functioning CBF/CMRO2 ratio.

As previously presented, provided Hb is kept stable and SaO2 is the highest (close to 100%), DajvO2 becomes a direct reflex of SvjO2 (since SaO2, Hb and 1.39 are constant). SvjO2 and DajvO2 may also represent the amount of O2 extracted from CBF in a time unit. In fact, brain O2 extraction (ECO2) is a function of the difference of arterio-jugular content over arterial content.

ECO2 = (CaO2 - CjO2)
                CaO2

If the same previously considered simplifications are applied, we have:

ECO2 = (SaO2 - SvjO2)
                SaO2

When maximum arterial blood Hb (100%) is almost reached, as it was the case in this study (Figure 1), extraction is directly represented by jugular blood hemoglobin saturation, that is, by SvjO2.

ECO2 = 1 - SvjO2

It is clear from the above that SvjO2 is a function of CBF and CMRO2 ratio. So, continuous or intermittent SvjO2 monitoring is a fast and simple way to monitor brain hemometabolic status during carotid clamping in endarterctomies.

In such conditions, direct SvjO2 analysis identifies and quantifies brain hemometabolic status (global brain oxygenation) in a certain moment. This monitoring does not evaluate regional ischemic or perfusional hemometabolic changes 8,9.

In general, DajvO2 is stable around 4 to 8 ml of O2 per 100 mL of CBF. If CMRO2 remains constant, DajvO2 changes may reflect CBF changes. On one hand, DajvO2 < 4 mL of O2 per 100 mL-1 CBF confirms that O2 supply is higher than demand (luxuriant CBF); on the other hand, DajvO2 > 8 mL of O2 per 100 mL-1 CBF suggests demand greater than flow, which characterizes a clinical situation of oligemic brain ischemia 11-14.

When CMRO2 is increased without simultaneous CBF increase, brain increases arterial blood O2 extraction resulting in decreased O2 content or effluent brain venous blood oxyhemoglobin saturation (internal jugular vein bulb), that is widening of DajvO2 or narrowing of SvjO2. Normal SvjO2 range between 55% and 75% is lower than systemic venous blood saturation 14,15.

Since SvjO2 is a global measure, its monitoring is highly specific but poorly sensitive for ischemia, that is, normal SvjO2 may not reflect areas of focal brain ischemia, but low SvjO2 is indicative of low global cerebral blood flow 15.

A study 16 suggests that minimum SvjO2 level to promote neurological injuries is bellow 50%. When lower SvjO2 levels are detected, therapeutic interventions to increase CBF or decrease CMRO2 are indicated.

There are clinical situations, among them temporary carotid clamping, potentially able to generate brain hemometabolism uncoupling, which are clinically characterized by SvjO2 decrease due to relative increase in oxygen extraction by brain tissues. This phenomenon, as previously seen, may be called oligemic ischemia.

In our study, figure 1 represents an analysis of SvjO2 behavior of the whole population of studied patients (n = 16) in pre-established observation moments. This analysis has shown that in comparing SvjO2 values (%, Mean ± SD) found in M1 (pre clamping) and M2 (3 minutes after clamping), there has been a statistically significant decrease.

The period between M2 and M3 (clamping period) has shown a mild trend to SvjO2 decrease, without statistical significance. These findings represent clinically changes in CBF:CMRO2 ratio, which tends to stabilize during the total clamping period. This phenomenon is evidenced by comparing moments M2 and M3, suggesting that stabilization may be attributed to the interference of CBF auto-regulation mechanisms.

In comparing SvjO2 in moments M3 (previously to unclamping) and M4 (after unclamping) a significant increase was found there, showing improvement in CBF:CMRO2 ratio with reestablishment of carotid blood flow, although this increase does not reach normal values even when M4 is compared to M1 (p < 0.04).

Results in figure 1 suggest that carotid clamping during endarterectomy results in a trend to significantly change CBF:CMRO2 ratio, that is, brain metabolism, with the possibility of generating a situation of hemometabolic uncoupling or oligemic ischemia. The downward trend of SvjO2 during this procedure suggests that collateral or retrograde cerebral blood flow through contralateral carotid and/or vertebral arteries, may not be sufficient to keep stable the ratio. Several factors may potentiate this change in CBF:CMRO2 ratio, among them cerebral perfusion pressure and CO2 arterial pressure.

In our study, the short period between carotid clamping and/or unclamping and SvjO2 changes demonstrates its sensitivity to global brain perfusion changes when MBP, Hb concentration and SaO2 are kept stable and within the normal range. Therefore, SvjO2 may help in detecting brain ischemic episodes during carotid endarterectomy with carotid clamping and may be included among evaluation parameters for the installation of shunts during clamping, especially in some special situations where there is previous difficulty in maintaining CBF auto-regulation, such as diabetes.

In continuing this study, some clinical parameters, cerebral perfusion pressure (CPP) and end tidal CO2 pressure (PETCO2) were evaluated, which may potentially influence brain hemometabolism changes during temporary carotid clamping.

Stump pressure (carotid stump pressure) represents mean blood pressure measured in the internal carotid artery, distally to the common and the external carotid clamping sites. This measurement represents the pressure retrogradely transmitted along the ipsilateral carotid artery, by ipsilateral vertebral artery and/or by contralateral carotid artery 17.

Cerebral perfusion pressure (CPP) may be calculated by the following equation:

CPP = MBP - ICP (or CVP)

Where

MBP - mean blood pressure
ICP - intracranial pressure
CVP - central venous pressure.

Considering that in our patients ICP was normal and stump pressure has been measured directly in the internal carotid artery, it was considered representative of cerebral perfusion pressure (CPP).

Brain perfusion pressure is a monitor often used as indicator of brain perfusion quality during carotid clamping and, according to some vascular surgeons and anesthesiologists, it may be taken into consideration for the indication of intraoperative carotid shunt. However, the literature 18-20 is controversial about its usefulness as a sole method to assess the quality of brain perfusion during this type of surgical procedure, based on the following assumptions:

  1. Lack of conclusive data evidencing the relationship between CPP and the incidence of perioperative morbidity/mortality;
  2. Controversy about normal pressure level;
  3. Evidence of major influence of anesthetic techniques on this type of monitor.

A study 21 has shown that stump pressure does not correlate well with CBF because significant EEG changes, suggestive of brain ischemia generated by critical regional CBF levels, may be detected with pressures above 50 mmHg. On the other hand, there may be situations of absence of EEG signals suggestive of brain ischemia, with stump pressures below 50 mmHg.

The major objective of CBF auto-regulation system is to maintain a stable CBF/CMRO2 ratio during variations of their component factors, maintaining optimal conditions for normal neuronal function performance.

CBF is a function of CPP and cerebro-vascular resistance (CVR) ratio, that is:

CBF = CPP - CVR

Where

CVR - cerebro-vascular resistance

It is important to stress that CVR is dependent on two variables - blood viscosity and brain arterial vascular diameter.

Based on the above-mentioned equation, one may conclude that CPP alone does not reflect CBF; so, it does not represent CBF/CMRO2 ratio.

In a recent study 22 that compared CPP monitoring to SvjO2 and consequent brain perfusion control and prophylaxis during carotid endarterectomy with temporary clamping, the latter parameter was considered superior.

Table I and figure 2 represent, respectively, MBP and CPP evolution during the study period. It is note-wise that even with stable MBP, CPP has significantly changed after carotid clamping. CPP decrease after clamping suggests the possibility of CBF/CMRO2 ratio changes with consequent brain hemometabolism change.

Figure 3 shows a linear regression between CPP to SvjO2. A weak non-significant correlation coefficient can be observed between them. Thus, considering SvjO2 as a sensitive method for CBF/CMRO2 ratio evaluation, one may conclude that isolated mean arterial pressure measurement at the vascular stump distal to clamping is not a safe monitor to evaluate the stability of the CBF/CMRO2 ratio. As a consequence, it should not be considered, by itself, a major parameter for the indication of temporary carotid shunt.

The second evaluated factor was the interference of PETCO2 on brain hemometabolism.

CBF changes secondary to PaCO2 variations without simultaneous changes in tissue pH seem to be a way to maintain brain hemometabolic coupling. Increased PaCO2 increases CBF, allowing an effective washout of the metabolically produced CO2, the opposite being true during hypocapnia 23.

Hypocapnia results in vasoconstriction that may reach the threshold for brain tissue hypoxia and anaerobic metabolism, causing adverse effects on brain cell activity. Additionally, hypocapnia causes left-shift of the Hb dissociation curve, exacerbating brain tissue hypoxia by impairing O2 release. These phenomena result in increased H+ ions and consequent decrease in brain tissue pH 24.

Brain vascular reactivity to CO2 is mediated by pH changes in the CSF surrounding the arteriolar bed, where pH depends on arterial blood pressure of free CO2, which crosses the blood-brain barrier, and on the concentration of bicarbonate in CSF. The understanding of the double-nature of CBF chemical control (arterial CO2 and CSF bicarbonate) is important to justify the pathophysiology of brain vasoplegia during brain metabolic acidosis followed by hemometabolic uncoupling. Some authors suggest that intracellular pH in vascular smooth muscles influences brain vascular tone, by the activation of NMDA (N-methyl-D-aspartate) receptors, which causes changes in intracellular ionic calcium concentrations 25,26.

Brain arteriolar tone regulated by MBP modulates the effects of PaCO2 on CBF. For example: moderate arterial hypotension blocks the ability of cerebral circulation to respond to PaCO2 changes, while severe arterial hypotension totally abolishes this mechanism. On the other hand, PaCO2 changes MBP-dependent CBF auto-regulation mechanism, that is, starting from a situation of hypercapnia toward hypocapnia, there is a widening of the plateau of the auto-regulation curve 27,28.

Some studies 29,30 have considered PETCO2 measurement as a valid estimate of PaCO2 during anesthesia, in situation of no clinical intra-cardiac shunt, pathological increase of the alveolar dead space or compensation of metabolic acid-base abnormalities. In addition, PETCO2 values are 2 to 5 mmHg lower than PaCO2.

A study aiming at comparing PaCO2 and PETCO2 during neurosurgical anesthesia has presented some contradictory results as compared to what has been stated above. Although results show a strong and statistically significant correlation between both parameters (r = 0.81; slope = 0.76; r2 = 0.22), 17 out of 35 correlations observed had no statistical significance and in 18% of them, parametric changes went in opposite directions. These findings led the authors to conclude that PETCO2 does not stably reflect PaCO2 during craniotomies 31.

In spite of controversial data, this study has validated the correlation between PaCO2 and PETCO2, as shown in figure 4, through the strong and significant correlation coefficients observed at all moments of study (r = 0.94; p < 0.001). So, our study contradicts the above-mentioned study and preconizes PETCO2 monitoring as a clinical, practical continuous and noninvasive method to control PaCO2.

CO2 is the most effective modulator of brain vascular resistance being considered the coupling factor between CBF and CMRO2, that is, brain hemometabolism. Increased brain metabolic index results in increased CO2 production, which generates a local dilatation process. Fast CO2 spread through blood-brain barrier allows it to modulate extracellular CSF pH, thus affecting arteriolar resistance.

Decreased CBF secondary to carotid clamping suggests that during this period the auto-regulation mechanisms are at their maximal vasodilatory capacity. During this period, hyperventilation with consequent hypocapnia may result in changes or elimination of the referred mechanism, increasing the possibility of clinical brain hypoperfusion or oligemic hypoxia.

It is important to stress that the anesthetic technique used in this study, that is, the association of propofol and sevoflurane, does not significantly interfere with brain vascular reactivity to CO2 although hyperventilation may potentiate CBF decrease secondary to propofol administration 32.

Figure 6 shows a moderate and statistically significant correlation index between PETCO2 and SvjO2. Based on these findings, we could conclude that during carotid endarterectomy with temporary clamping, hyperventilation should be avoided through continuous monitoring of CO2 expired concentration - noninvasive method which truly represents PaCO2, as shown in figure 5.

Based on the method and the population evaluated, we could conclude that during carotid endartererctomy with temporary clamping:

  1. SvjO2 measurement is and effective monitoring method with fast response in representing CBF/CMRO2 ratio changes, once not contaminated by extra-cranial venous blood;
  2. Stump pressure does not effectively evaluate brain hemometabolic situation during this type of surgical procedure;
  3. The presence of even moderate hypocapnia (PETCO2 25 - 30 mmHg) may lead to hemometabolic uncoupling situations, that is, oligemic ischemia;
  4. PETCO2 monitoring is an innocuous and efficient method to indirectly monitor PaCO2, thus preventing inadvertent hypocapnia with its noxious effects on CBF/CMRO2 ratio.

 

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Correspondence to
Dr. Gastão Fernandes Duval Neto
Rua Dom Pedro II, 801/301
96010-300 Pelotas, RS
E-mail: gduval@terra.com.br

Apresentado (Submitted) em 22 de maio de 2003
Aceito (Accepted) para publicação em 30 de julho de 2003

 

 

* Recebido da (Received from) Disciplina de Anestesiologia Faculdade de Medicina da Universidade Federal de Pelotas, RS