|Year : 2014 | Volume
| Issue : 3 | Page : 444-450
Jugular bulb oxygen saturation and the pyruvate lactate ratio are good signals for cerebral metabolism and oxygenation during hypothermia with altered target ventilation
R Tarek1, Zohry Gomaa1, Aamer Mahmod2, Farag Ehab2
1 Department of Anesthesia, Faculty of Medicine, Cairo University, Cairo, Egypt
2 Department of Anesthesia, Faculty of Medicine, Bani-suef University, Beni Suef, Egypt
|Date of Submission||18-Nov-2013|
|Date of Acceptance||27-Dec-2014|
|Date of Web Publication||27-Aug-2014|
Department of Anesthesia, Faculty of Medicine, Cairo University, Cairo
Source of Support: None, Conflict of Interest: None
The effect of deliberate hypothermia and hypocapnia on brain protection during neurosurgical procedures has been studied for many years, but in this study, the combination of deliberate hypothermia and hypocapnia was analyzed to detect their effects on cerebral oxygenation by the assessment of SjvO 2 and cerebral metabolism by the measurement of both jugular bulb lactate and pyruvate.
Patients and methods
Sixty patients scheduled for excision of supratentorial space-occupying lesions were randomly allocated into two groups. In group I, hypocapnia was induced combined with hypothermia, and in group II, normocapnia was maintained combined with hypothermia. Hypothermia was induced using a water blanket under the patient controlling the tympanic membrane temperature at 35°C. Jugular bulb venous and arterial blood gas analyses were performed before the induction of hypothermia ± hypocapnia (baseline), and then every 20 min till closure of the dura. The arterio-jugular venous oxygen content difference (AJDO 2 ) and the cerebral oxygen extraction ratio (COER) were calculated. Jugular bulb lactate and pyruvate levels were measured before the induction of hypothermia ± hypocapnia (baseline) and then every 30 min till closure of the dura.
There was a significant increase in pjH and significant decreases in both PjCO 2 and SjvO 2 in the hypocapnic group after the induction of hypocapnia. SjvO 2 reached 80.32 ± 4.59% in the normocapnic group, whereas it reached 75.3 ± 4.02% in the hypocapnic group. AJDO 2 and COER started to decrease after induced hypothermia in both groups compared with readings before induced hypothermia, but the hypocapnic group had a significantly higher AJDO 2 and COER than the normocapnic group during the period of induced hypothermia (AJDO 2 reached 3.98 ± 0.47 ml/dl and COER reached 25.93 ± 4.13% in comparison with the hypocapnic group, where AJDO 2 reached 4.58 ± 0.51 ml/dl and COER reached 31.96 ± 4.01%).Jugular bulb lactate and pyruvate levels were significantly higher during hypocapnia than during normocapnia.
Cerebral oxygenation and metabolism were better during hypothermia combined with normocapnia as reflected by relative ͽͽSjvO 2 and ͿͿAJDO 2 and COER as well as ͿͿjugular bulb lactate and pyruvate.
Keywords: cerebral metabolism, cerebral oxygenation, hypothermia, jugular saturation, lactate and pyruvate
|How to cite this article:|
Tarek R, Gomaa Z, Mahmod A, Ehab F. Jugular bulb oxygen saturation and the pyruvate lactate ratio are good signals for cerebral metabolism and oxygenation during hypothermia with altered target ventilation. Ain-Shams J Anaesthesiol 2014;7:444-50
|How to cite this URL:|
Tarek R, Gomaa Z, Mahmod A, Ehab F. Jugular bulb oxygen saturation and the pyruvate lactate ratio are good signals for cerebral metabolism and oxygenation during hypothermia with altered target ventilation. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 Oct 24];7:444-50. Available from: http://www.asja.eg.net/text.asp?2014/7/3/444/139594
| Introduction|| |
Intraoperative hypothermia and hypocapnia have been widely used for brain protection during neurosurgical procedures as both of them provide favorable effects on cerebral circulation and metabolism .
Monitoring of cerebral oxygenation during hypothermia with or without hypocapnia during neurosurgical procedures using jugular bulb oxygen saturation allows the detection of cerebral hypoperfusion and ischemia. Also, monitoring of cerebral metabolism by measuring jugular bulb lactate and pyruvate as proper indices of anaerobic metabolism during neurosurgery allows the detection and prevention of cerebral ischemia and also ensures cerebral protection during this critical time .
| Patients and methods|| |
After approval of the local Ethics Committee and after obtaining written informed consent, 60 patients, ASA (American Society of Anesthesiologists) physical status I or II, scheduled for excision of supratentorial space-occupying lesions less than 30 mm on MRI, and with GCS more than 14, were included in our comparative study, which was conducted in the El-Kasr El-Einy Hospital. Patients were randomly allocated using computer-generated random tables into two groups (30 patients in each group). In group I, hypocapnia was induced combined with hypothermia, and in group II, normocapnia was maintained combined with hypothermia. Patients with a history of previous surgery, drug allergy, or severe coexisting diseases such as hypertension, diabetes, or ischemic heart disease were excluded from the study. All patients were cannulated with 18-G wide-bore cannula after lidocaine infiltration, and were then given intravenous midazolam (0.05 mg/kg) together with ranitidine (50 mg) and phenytoin at a loading dose of 15 mg/kg. Also, the radial artery of the nondominant hand was cannulated with a 20-G arterial cannula after lidocaine infiltration (after performing a modified Allen's test) to monitor the arterial blood pressure and for analysis of arterial blood gases. Intraoperative monitoring included five-lead ECG, pulse oximetry, noninvasive and invasive blood pressure, core temperature probe, capnography, peripheral nerve stimulator applied to the ulnar nerve and urinary catheter for urine output monitoring. Anesthesia was induced using propofol (2 mg/kg) and fentanyl (2 μg/kg); intubation was facilitated after the disappearance of a train of four on peripheral nerve stimulator using atracurium (0.5 mg/kg). The lungs were mechanically ventilated using 100% O 2 . Anesthesia was maintained using isoflurane (1%), and the atracurium infusion was maintained at a rate of 0.5 mg/kg/h. Fentanyl (1 μg/kg) was given at the time of skin incision and once again at the time of bone drilling. Surgery was performed while patients were placed in the supine position with a head elevation of 30°. Hypothermia was induced using a water blanket under the patient controlling the tympanic membrane temperature at 35°C. Mechanical ventilation was maintained to ensure target normocapnia (EtCO 2 30-35 mmHg) in group II and target hypocapnia (EtCO 2 25-30 mmHg) in group I, after the induction of hypothermia. The depth of anesthesia was adjusted to maintain the hemodynamics around 20% of the baseline readings. Brain dehydrating measures in the form of mannitol (0.5 g/kg), frusemide (0.2 mg/kg), and dexamethasone (0.2 mg/kg) were given according to the intracranial tension. Fluids were given at a rate of 3 ml/kg/h in the form of Ringer's solution; fluid losses were replaced accordingly together with blood loss, keeping the CVP at 5-8 cmH 2 O. If there was excessive blood loss of more than 20% of the blood volume or if the hematocrit was less than 30%, the patient received blood transfusion and was excluded from the study.
A retrograde internal jugular catheter was inserted after the induction of anesthesia, on the same side of the lesion with the patient placed in the horizontal position with the neck in the neutral position or slightly turned to the contralateral side. If difficulty in localizing the vein was encountered, the patient was tilted 15° head down. The junction between the sternal and the clavicular heads of the sternocleidomastoid muscle was identified, and the skin was punctured with a 16-G needle mounted with a 5-ml syringe. During gentle aspiration, the needle was passed in a cranial direction for 1-2 cm at an angle of 15-20° in the sagittal plane. Once the vein was entered, the catheter was advanced over the needle until a slight elastic resistance was felt, or when the tip of the catheter was estimated to be just behind the mastoid process. A guide wire (Seldinger's technique) might be used. The position of the catheter tip [certofix 7Fx8(20 cm] was checked with a plain radiograph of the neck. This tip should lie at the level of and just medial to the mastoid bone and curved slightly in the medial direction.
The heart rate and the arterial blood pressure (systolic, diastolic, and mean) were recorded before the induction of anesthesia (baseline), 1 min after the induction of hypothermia ± hypocapnia, 10 min after induction, at dural incision, and then every 20 min till closure of the dura. Jugular bulb venous and arterial blood gas analysis were obtained before the induction of hypothermia ± hypocapnia (baseline), and then every 20 min till closure of the dura.
(1) The arterio-jugular venous oxygen content difference (AJDO 2 ) and the cerebral oxygen extraction ratio (COER) were calculated from the arterial and the jugular bulb venous oxygen partial pressure and saturation using the following equations:
CaO 2 = (SaO 2 Hb 1.39) + 0.0031 PaO 2 ,
CjO 2 = (SjO 2 Hb 1.39) + 0.0031 PjO 2 ,
AJDO 2 = CaO 2 -CjvO 2 ,
where CaO 2 and CjO 2 are the arterial and the jugular bulb venous oxygen contents, respectively.
Global hypoperfusion was defined as jugular blood oxygen saturation (SjvO 2 ) less than 50%. Ischemia was defined as SjvO 2 less than 40% and AJDO 2 greater than 9 ml/dl .
AJDO 2 and COER were calculated every 20 min till closure of the dura.
(2) Jugular bulb lactate and pyruvate levels were measured before the induction of hypothermia ± hypocapnia (baseline) and every 30 min till closure of the dura.
A comparison of the measured variables such as hemodynamics and blood gas data was performed using two-way analysis of variance with repeated measures followed by the Student-Newman-Keuls test for multiple comparisons. Data were expressed as mean ± SD. Differences were considered to be statistically significant at P value less than 0.05.
| Results|| |
Sixty patients were included in the study; there were no significant differences between the two groups with regard to age, weight, sex, height, the duration of surgery and the duration of hypothermia [Table 1].
There was no statistically significant difference between both groups with regard to their hemodynamics [Table 2] and [Table 3].
Blood pressure measurement followed a similar course for systolic, diastolic, and mean blood pressure in the two groups. There was a transient decrease in the blood pressure relative to the baseline after the induction of anesthesia. However, it increased again with dural closure [Table 3], but there was no significant difference between the two groups.
Arterial blood gas analysis showed no statistically significant differences between the two studied groups with regard to pHa, PaCO 2 , PaO 2 , and SaO 2 before the induction of hypothermia and hypocapnia. However, after the induction of hypocapnia, there was a significant increase in pHa and a significant decrease in PaCO 2 in group I [Table 4].
Jugular blood gas analysis showed no statistically significant differences before the induction of hypothermia and hypocapnia. However, after the induction of hypocapnia, there was a statistically significant difference in pjH, PjCO 2 , and SjvO 2 between the two groups [Figure 1], [Figure 2], [Figure 3], [Figure 4]. There was a significant increase in pjH and significant decreases in both PjCO 2 and SjvO 2 in the hypocapnic group after the induction of hypocapnia.
|Figure 1: Jugular pjH at 20, 40, 60, 80, 100, 120 min after induced hypothermia (mean pjH).|
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|Figure 2: Mean jugular PjCO2 at 20, 40, 60, 80, 100 and 120 min after induced hypothermia [mean PjCO2 (mmHg)].|
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|Figure 3: Mean jugular PjCO2 at 20, 40, 60, 80, 100 and 120 min after induced hypothermia [mean PjCO2 (mmHg)].|
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|Figure 4: Jugular SjvO2 at 20, 40, 60, 80, 100 and 120 min after induced hypothermia [mean SjvO2 (%)].|
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The arterio-jugular venous oxygen content difference (AJDO 2 ) and the COER started to decrease significantly after induced hypothermia in both groups compared with readings before induced hypothermia, but the hypocapnic group had significantly higher AJDO 2 and COER than the normocapnic group during the period of induced hypothermia, as shown in [Table 5] and [Table 6].
Jugular bulb lactate and pyruvate levels during induced hypothermia followed the same course in the two groups; they decreased significantly relative to the preinduction of hypothermia, but the hypocapnic group had significantly higher jugular bulb lactate and pyruvate levels than the normocapnic group during induced hypothermia [Table 7] and [Table 8]
| Discussion|| |
The results obtained in the present study showed that in the preinduction of hypothermia, SjvO 2 was slightly higher in the normocapnic group than in the hypocapnic group; then, with induced hypothermia, SjvO 2 started to increase in both groups, but it was significantly higher in the normocapnic group than in the hypocapnic group; this means that cerebral oxygenation is better in the normocapnic group compared with the hypocapnic group under the same conditions of induced hypothermia. This means that the risk of cerebral hypoperfusion is higher in the hypocapnic group when compared with the normocapnic group under the same conditions of induced hypothermia.
Also, the arterial to jugular oxygen difference (AJDO 2 ) and the COER, which reflect the oxygen supply/demand ratio, were decreased in the present study in both groups during induced hypothermia, but the decrease in both values was significantly higher in the normocapnic group; this indicated a maintained balance of CBF/CMRO 2 ratio in the normocapnic group. Jugular bulb lactate and pyruvate concentrations are thought to reflect anaerobic and aerobic metabolism, respectively, with the lactate/pyruvate ratio being considered an important marker of the tissue perfusion and cellular metabolism. In the present study, it was noted that during normocapnia, the incidence of decreased jugular bulb lactate and pyruvate was higher than during hypocapnia under the same conditions and time of induced hypothermia; the previous results reflected that the incidence of anaerobic metabolism and tissue hypoperfusion is higher in the hypocapnic group compared with the normocapnic group.
There have been several reports on the effect of hypothermia and hypocapnia on brain protection, cerebral oxygenation and metabolism.
Marion et al.  studied the effect of 30 min of hyperventilation (mean PaCO 2 , 24.6 mmHg) on extracellular metabolites associated with ischemia and on the local cerebral blood flow (CBF) using microdialysis and local cerebral blood flow techniques. Normal-appearing brain adjacent to evacuated hemorrhagic contusions or underlying evacuated subdural hematomas was studied. Hyperventilation trials were performed 24-36 h after injury and again 3-4 days after injury. Dialysate concentrations of glutamate, lactate, and pyruvate were measured before and for 4 h after the hyperventilation trials. They found that in the brain tissue adjacent to cerebral contusions or underlying subdural hematomas, even brief periods of hyperventilation can significantly increase extracellular concentrations of mediators of secondary brain injury. These hyperventilation-induced changes are much more common during the first 24-36 h after injury than at 3-4 days; this was consistent with the present study. Gelb et al.  found that if it is deemed necessary for acute control of increased ICP or brain bulge, mild degrees of hypocapnia (30-35 mmHg) are recommended. Where available, the use of monitors of cerebral ischemia may be a further guide to the safe use of hyperventilation; examination of the evidence does not reveal a strong case for the use of hyperventilation in most neurosurgical scenarios. Indeed, there are numerous studies that indicate the potential for hypocapnia to be detrimental to the patient. Previous results were consistent with the results of the present study, which was conducted under induced hypocapnia, which carries the risk of cerebral hypoperfusion, and showed an increased incidence of lower SjvO 2 during hypothermia combined with hypocapnia. Artru et al.  have studied the levels of jugular blood oxygen saturation (SjvO 2 ) and lactate as indicators of cerebral ischemia and prognosis. However, the sensitivity and the specificity of these markers remain unknown. They retrospectively analyzed records of a series of 43 comatose patients at risk for cerebral ischemia, mainly after head injuries or subarachnoidal hemorrhage. Their SjvO 2 , jugulo-arterial lactate difference (VADLactate), and lactate-oxygen index (LOI) were determined every 8 h. An increase in VADLactate and LOI was found, indicating ischemia on computed tomographic scan, with threshold values of 0.30 and 0.15 mmol/l, respectively. The sensitivity and the specificity were 100 and 64%, respectively, for the VADLactate threshold, and 90 and 55%, respectively, for the LOI threshold. Regarding the prediction of a poor outcome, only an increase in VADLactate had a predictive value with a sensitivity of 100% and a specificity of 67%. No threshold value with sufficient sensitivity and specificity was found for SjvO 2 as an indicator of either ischemia or outcome. During progression to brain death, VADLactate and LOI reached abnormal levels earlier than cerebral perfusion pressure or SjvO 2 . They reacted markedly to focal ischemia due to vasospasm. Hyperlactacidemia rendered VADLactate and LOI uninterpretable by causing a brain lactate influx. These data, if confirmed by a prospective study, would justify the inclusion of intermittent VADLactate and LOI determinations in the multimodal cerebral monitoring. Moritz et al.  investigated the accuracy of jugular bulb venous monitoring in detecting cerebral ischemia: they performed ipsilateral jugular bulb venous monitoring in 48 patients undergoing carotid surgery under regional anesthesia. Cerebral ischemia was assumed when neurologic deterioration occurred. During carotid clamping, the maximal arterial-jugular venous oxygen content difference [AJDO 2 (max], the minimal jugular venous oxygen saturation [SjO 2 (min], the maximal arterial-jugular venous lactate content difference [AJDL (max], the maximal lactate-oxygen index [LOI (max], and the maximal modified LOI [mLOI (max] were determined. To quantify the selectivity of each parameter, they performed receiver operating characteristic analysis and determined the area under the curve. The cutoff points providing the highest accuracy and the corresponding sensitivity (Se) and specificity (Spec) were determined. Neurologic deterioration occurred in 12 patients. All parameters, except AJDO 2 (max), showed significant ability to distinguish between ischemic and nonischemic patients. In conclusion, that investigation showed that AJDL, SjO 2 , LOI, and mLOI provide the ability to detect cerebral hypoperfusion. The highest accuracy was found with AJDL. The calculation of neither LOI nor mLOI showed improved results. Nordmark and colleagues found that after resuscitation from cardiac arrest, there was a risk of cerebral secondary energy failure (reflected as an increased lactate/pyruvate ratio), but hypothermia treatment seemed to counteract this effect. Cerebral oxygen extraction, measured by SjvO 2 , was increased in the hypothermic group probably due to reduced metabolism. Rewarming did not reveal any obvious harmful events . Kadoi and colleagues showed that the SjvO 2 value was well maintained during mild hypothermic (32°C) CPB in elderly patients. In contrast, cerebral desaturation (SjvO 2 <50%) occurred more often in the normothermic group than in the hypothermic group of elderly patients. These studies are consistent with the present study as they showed a better effect of mild hypothermia on cerebral oxygenation by monitoring SjvO 2 although they did that during CPB and after cardiopulmonary resuscitation . The effect of hypothermia on brain metabolism was studied a long time ago as evidenced by Busto et al. , who demonstrated that hypothermia to 33°C resulted in a significant decrease in histologic neuronal damage as in excitatory neurotransmitter release in a rat model of global ischemia. Also, Leonov et al.  demonstrated both an improved neurologic outcome and decreased neuronal histologic damage in a dog model of global ischemia at 34°C. The same was shown by Chopp et al. , who observed a reduction in histologic damage for global ischemia in a rat model when mild hypothermia (to 34°C) was instituted immediately after an ischemic insult. Kader et al.  documented a reduction in histologic damage in a rat model of permanent focal ischemia in animals maintained at 34.5°C during ischemia. Sano and colleagues showed marked improvement in the histologic outcome after decreasing the temperature to 35°C when comparing halothane-anesthetized and isoflurane-anesthetized normothermic control animals. Infact a modest temperature reduction may be more important than the choice of anesthesia as a determinant of the outcome from cerebral ischemia .
| Conclusion|| |
The combination of hypothermia with hypocapnia might carry a risk on cerebral oxygenation and metabolism; hence, normocapnia may be a better choice when hypothermia is induced in neurosurgical practice.
| Acknowledgements|| |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]