Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.     

Effect of induced hypotension on arterial blood-gases

Arterial blood-gases were evaluated before, during and after the vasodilator induced hypotension in patients undergoing mastectomy. Forty-two patients studied were anesthetized with halothane and nitrous oxide in oxygen. They were divided into following four groups according to vasodilators used: trimetaphan (TMP), nitroglycerin (TNG), adenosine triphosphate (ATP), and prostaglandin E1 (PGE1). Significant reduction in PaO2 was observed during induced hypotension in all groups. However, there was no difference in the degree of PaO2 decrease among four groups. A small but significant increase in PaCO2 and a decrease in pH were observed during and/or after hypotension with TNG and PGE1. These findings suggest that induced hypotension may impair the pulmonary gas exchange by decreased cardiac output and/or change in ventilation-perfusion ratio regardless of vasodilators used. Therefore, continuous arterial blood-gas monitoring should be desirable under these conditions.     

The effect of hypocapnia on arterial oxygenation in thoracotomized dogs

The effect of hypocapnia on arterial oxygenation was investigated in unilaterally thoracotomized patients (N = 11) and dogs (N = 9) anesthetized with N2O-O2-enflurane. In patients, a change in PaCO2 from 39.7 +/- 1.4 to 28.2 +/- 1.7 mmHg produced a significant fall in PaO2 from 146 +/- 32 to 126 +/- 27 mmHg. In dogs, the change in PaCO2 from 38.7 +/- 0.8 mmHg (normocapnia) to 22.4 +/- 0.9 mmHg (hypocapnia) produced a significant decrease in PaO2 from 94 +/- 6 to 77 +/- 5 mmHg and a significant increase in pulmonary shunt (Qs/Qt) from 13.5 +/- 1.6 to 19.4 +/- 1.7%. Hypocapnia induced significant decreases in cardiac output and pulmonary arterial pressure; from 3.6 +/- 0.4 to 3.1 +/- 0.3 l.min-1, and from 20.8 +/- 1.3 to 17.5 +/- 1.0 mmHg, respectively. After the thoracotomy, the end-expiratory volume of the lung of the thoracotomized side became smaller. Therefore, a large fraction of low VA/Q regions might have existed in the lung of the studied patients and animals. Since hypocapnia induces an attenuation of hypoxic pulmonary vasoconstriction (HPV), an attenuation of HPV by hypocapnia might have occurred in the present study, which in turn produced a disproportionate increase in perfusion to low VA/Q regions, leading to the increase in Qs/Qt as observed in the present study.     

Cerebral vascular responses to hypocapnia during nitroglycerin-induced hypotension

For many neurosurgical procedures, elective hypotension is used to reduce the risk of cerebral vessel rupture and hypocapnia is used to constrict cerebral vessels, thereby reducing cerebral blood volume. Although nitroglycerin (NTG) often is used to produce hypotension during neurological surgery, it is not known whether NTG-induced cerebral vasodilation interferes with the cerebral vasoconstrictor response to hypocapnia. This study examined cerebral vascular responses to hypocapnia during NTG-induced hypotension in eight dogs that were lightly anesthetized with halothane and had an open cranium. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg and at PaCO2 = 20 mm Hg were examined first at normal mean arterial pressure (MAP) and then at MAP = 50 mm Hg. CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP but absent during hypotension. These results suggest that the cerebral vasodilation that accompanies NTG-induced hypotension exerts a greater influence on cerebral vessels than the cerebral vasoconstricting influence of hypocapnia. It is concluded that, during NTG-induced hypotension and craniotomy, hypocapnia will not reduce cerebral blood volume or further decrease CBF to cause ischemia.     

呼气末正压通气对二氧化碳气腹病人动脉血氧合的影响

目的观察腹腔镜手术期间呼气末正压通气(PEEP)对二氧化碳气腹病人动脉血氧合及血液动力学的影响。方法20例ASAⅠ～Ⅱ级经腹腔镜肾上腺肿块、输尿管上段结石及肾切除的病人,随机均分为P组和C组。50%氧气混合空气机械通气,P组予以5cmH2O的PEEP,C组无PEEP。观察建立二氧化碳气腹前(T0)、气腹后10min(T1)、30min(T2)、1h(T3)和2h(T4)的PaO2、PaCO2、HR及MAP。结果P组气腹期间PaO2有上升趋势,而C组呈下降趋势,气腹后1hC组显著低于P组(P<0.05)。两组MAP和HR波动均未超过11%。结论腹腔镜手术期间PEEP能促进动脉血氧合,对循环影响较小。     

Cerebral metabolism and the electroencephalogram during hypocapnia plus hypotension induced by sodium nitroprusside or trimethaphan in dogs

The effects on cerebral metabolism and the electroencephalogram (EEG) of combining hypocapnia with hypotension have been only incompletely examined. The present study examined the possibility that hypocapnia may worsen the cerebral metabolic and EEG disturbances caused by hypotension. Cerebral metabolism and the EEG were studied at three levels of hypotension during hypocapnia (PaCO2 = 20 mm Hg) in dogs under light halothane anesthesia. A sequential decrease of the mean arterial pressure (MAP) to 60, 50, and 40 mm Hg (30 minutes at each level) was achieved with sodium nitroprusside (SNP) (n = 12) or trimethaphan (TMP) (n = 12). With SNP-induced hypotension plus hypocapnia, the power of the alpha and beta 2 spectra of the EEG decreased at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 or 50 mm Hg. Brain tissue phosphocreatine and the cerebral energy charge decreased, and the lactate/pyruvate ratio increased at a MAP of 40 mm Hg. With TMP-induced hypotension plus hypocapnia, power decreased in the alpha and beta 2 spectra of the EEG at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 mm Hg. At MAP less than or equal to 50 mm Hg, power in the beta 1 spectrum, brain tissue phosphocreatine, and the cerebral energy charge all decreased. At a MAP of 40 mm Hg, the cerebral glucose value decreased and the lactate/pyruvate ratio increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of induced hypotension on arterial blood ketone body ratio (AKBR)

Arterial blood ketone body ratio (AKBR; acetoacetate/beta-hydroxybutyrate) is known as a parameter to indicate the function of the liver cells. We evaluated the effects of induced hypotension with prostaglandin E1 (PGE1) or trimetaphan (TMP) on AKBR in patients without liver disease undergoing mastectomy. Almost no change was observed in AKBR before, during and after hypotension with PGE1, but slight diminution was observed during hypotension with TMP. No hepatic dysfunction, however, developed in these patients postoperatively. These findings suggest that usual hypotension with TMP may provoke no postoperative hepatic dysfunction in patients without liver disease. For the patient who required either hypotension of long duration or hypotension with other factors affecting function of liver (surgical procedures, drugs and others), we prefer PGE1 to TMP as a hypotensive drug. We should also adopt PGE1 when cardiovascular control with hypotensive drug is necessary in patients with liver disease.     

Attenuation of arterial baroreceptor reflex response to acute hypovolemia during induced hypotension

Preservation of the arterial baroreflex response is important to restore cardiac output and blood pressure by reflex sympathetic nerve activation in the event of sudden hypotension caused by acute blood loss during surgery. However, the arterial baroreflex may be significantly attenuated by both anesthetics and hypotensive agents. In isoflurane-anesthetized dogs, the authors investigated the arterial baroreflex response 1) to bolus injections of sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM); and 2) to rapid blood loss (5 ml/kg) before and during induced hypotension with SNP, PGE1, and TM by measuring mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Hypotension produced by both SNP and PGE1 was accompanied by an increase in RSNA and HR. The increase in RSNA and HR following the SNP bolus injection was significantly greater than that following injection of PGE1 (P less than 0.05). Trimethaphan was associated with a decrease in RSNA and HR. Rapid blood loss resulted in the same degree of MAP reduction (20 +/- 2 mmHg) before and during induced hypotension. Sensitivities of baroreflex, as evaluated by ratios of maximum changes in RSNA or HR to MAP (delta RSNA/delta MAP, delta HR/delta MAP), in response to rapid blood loss, were significantly suppressed during continuously induced hypotension, as compared with responses before induced hypotension. Despite the same degree of induced hypotension (70 +/- 5 mmHg of MAP), delta RSNA/delta MAP and delta HR/delta MAP in response to rapid blood loss were significantly greater with PGE1 than those with SNP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of spontaneous sighs on arterial oxygenation during isoflurane anesthesia in humans

The presence, frequency, and volume of spontaneous sighs was evaluated in 21 (ASA 1-2) supine patients aged 44 +/- 15.2 (SD) yr, during isoflurane-nitrous oxide anesthesia. Before induction the inspiratory capacity of each patient was determined. After induction of anesthesia and tracheal intubation patients breathed spontaneously except for three manual inflations to each patient's predetermined inspiratory capacity at the beginning and end of surgery. Arterial blood gas tensions were measured before and 5 min after each set of mechanical deep breaths and each hour during surgery, the mean duration of which was 2 +/- 0.09 hr. Spontaneous sighs occurred in 13 of 21 patients. The average frequency was 6 +/- 4 sighs/hr. At FIO2 = 0.5, nonsighing patients had an initial PaO2 of 229 +/- 59 mm Hg and sighers had an initial PaO2 of 162 +/- 57 mm Hg (P less than 0.05). Arterial oxygen did not change in sighing patients during the course of surgery, while in nonsighing patients the PaO2 decreased from the initial value of 229 +/- 60 mm Hg to 170 +/- 63 mm Hg (P less than 0.05). Mechanical deep breaths administered at the end of surgery produced no improvement in oxygenation in either sighers or nonsighers. The presence or absence of sighs did not correlate with PaO2 or PACO2. Though the results suggest that spontaneous sighs in some patients may function to help maintain arterial oxygenation, all patients maintained their PaO2 while breathing spontaneously under general anesthesia in the supine position.     

Evaluation of arterial oxygenation during anaesthesia

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - The clinical or physiological signs of hypoxaemia have limited value during anaesthesia. In the absence of surgical bleeding,...     

Partial preservation of cerebral vascular responsiveness to hypocapnia during isoflurane-induced hypotension in dogs

This study was undertaken to determine whether the cerebral vascular response to hypocapnia is preserved during isoflurane-induced hypotension. In six dogs (group 1) cerebral vascular resistance and cerebral blood flow were determined at normocapnia (PaCO2 40 mm Hg) and at hypocapnia (PaCO2 20 mm Hg) while mean arterial pressure was normal, and then again during isoflurane-induced hypotension to a mean arterial pressure of 50 mm Hg. Hypocapnia increased cerebral vascular resistance and decreased cerebral blood flow during both normotension and isoflurane-induced hypotension. However, the magnitude of these responses was greater when mean arterial pressure was normal. In another six dogs (group 2), CO2 responsiveness was examined during isoflurane-induced hypotension without prior determination of CO2 responsiveness at normal mean arterial pressure and during sodium nitroprusside-induced hypotension to a mean arterial pressure of 50 mm Hg. As in group 1, partial preservation of CO2 responsiveness was observed during isoflurane-induced hypotension; the magnitude of the response in group 2 during isoflurane-induced hypotension was similar to that in group 1. In contrast, in group 2 during sodium nitroprusside-induced hypotension, hypocapnia caused no significant change of cerebral vascular resistance or cerebral blood flow. It is concluded that cerebral vessels respond to changes in PaCO2 differently during isoflurane-induced hypotension than during hypotension with other commonly used hypotensive treatments. Hypocapnia decreases cerebral blood flow during isoflurane-induced hypotension and, therefore, may also decrease cerebral blood volume, brain bulk, and intracranial pressure.     

Cerebral metabolism and EEG during combination of hypocapnia and isoflurane-induced hypotension in dogs

Isoflurane (ISF)-induced hypotension causes equal reductions of cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) so that no disturbance of cerebral energy stores or metabolites occurs. While hypocapnia during ISF-induced hypotension causes a further reduction of CBF, the effects on cerebral energy stores and metabolites produced by combining hypocapnia with ISF-induced hypotension are not known. This study examined the effect of hypocapnia (PaCO2 = 20 mmHg) on CMRO2, the electroencephalogram (EEG), and levels of adenine nucleotides, phosphocreatine, lactate, pyruvate, and glucose in brain tissue in 12 dogs during ISF-induced hypotension. All dogs were examined at: normocapnia with normotension; hypocapnia with normotension; hypocapnia combined with ISF-induced hypotension to cerebral perfusion pressures of 60, 50, and 40 mmHg; and restoration of normocapnia with normotension. In six dogs CMRO2 was determined, and the EEG was evaluated using compressed spectral analysis. In the other six dogs brain tissue metabolites were determined. Hypocapnia combined with ISF-induced hypotension (all levels) caused a decrease of the power of the beta-2 spectra, an increase of the power of the alpha and beta-1 spectra, but no change in total power of the EEG. There was no change in cerebral energy stores or brain tissue metabolites. CMRO2 was reduced by approximately 27%. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites remained unchanged and CMRO2, and the power of the alpha, beta-1, and beta-2 spectra of the EEG returned to control values. These results suggest no adverse effect on cerebral metabolism or function during hypocapnia combined with ISF-induced hypotension.     

Predicting arterial oxygenation during one-lung anaesthesia

Eighty patients undergoing elective thoracotomy were studied to assess the possibility of predicting arterial oxygenation (PaO2) during one-lung anaesthesia (OLA). The first 50 patients were studied retrospectively. The method of multiple linear regression was used to construct a predictive equation for PaO2 during OLA. Potential predictors of PaO2 during OLA which were considered were: age, side of operation, preoperative pulmonary flow rates, preoperative and intraoperative PaO2 during two-lung ventilation. The three most significant predictors for PaO2 during OLA were: side right of operation (P < 0.05), preoperative FEV1% (P < 0.01) and intraoperative PaO2 during two-lung ventilation (P = 0.0001). The predictive equation for PaO2 after ten minutes of OLA was: PaO2 = 100 - 72 (side) - 1.86 (FEV1%) + 0.75 (two-lung) PaO2; (for side insert 0 for left-sided thoracotomy and 1 for right-sided thoracotomy). The remaining 30 patients were studied prospectively and the predicted PaO2 correlated with the observed PaO2 after ten minutes of OLA (r = 0.73, P < 0.01). Four of 30 patients had a predicted PaO2 at ten minutes of OLA < 150 mmHg. Of these, 2/4 subsequently required abandonment of OLA for pulse oximetric saturation < 85%. We conclude that although it is not possible to predict an individual patient's PaO2 during OLA with a high degree of accuracy, it is possible, before the initiation of OLA, to identify those patients whose arterial oxygenation is likely to decrease to low levels during OLA.