Cardiovascular effects of epidural local anaesthetics

The cardiovascular effects of 20 ml 0.75% bupivacaine with adrenaline 5 micrograms/ml injected epidurally were compared with those of 20 ml 0.75% ropivacaine with adrenaline. Cardiovascular measurements were performed with a transthoracic electrical bioimpedance monitor. The maximum mean arterial blood pressure decreased significantly from baseline values after both solutions, but the decrease after 20 minutes was more pronounced with bupivacaine (21%) than with ropivacaine (9.6%). Stroke volume increased significantly in both groups (52% for bupivacaine and 29% for ropivacaine). Cardiac output increased significantly from baseline values 2 minutes after epidural administration; the mean of the maximum increase was 64% for bupivacaine and 53% for ropivacaine (NS). The mean of the maximum increase of the ejection fraction was 13% in the bupivacaine group and 9% in the ropivacaine group, but was only significantly different from baseline values following bupivacaine. There was no difference in the onset time or height of the sensory block between the groups. The cardiovascular changes can be ascribed to sympathetic blockade and to systemic absorption of the local anaesthetics and adrenaline.     

INCREMENTAL SPINAL ANAESTHESIA FOR ELECTIVE CAESAREAN SECTION: MATERNAL AND FETAL HAEMODYNAMIC EFFECTS

We have performed serial haemodynamic investigations in 20 womenundergoing elective Caesarean section under continuous spinalanaesthesia with a 32-gauge catheter with 0.5% heavy bupivacaine.Cardiac output was measured by Doppler and cross-sectional echocardiographyat the aortic valve. Doppler flow velocity waveforms were recordedalso from the umbilical artery. A block to 74 or above was achievedin all patients. The median dose of 0.5% bupivacaine administeredwas 2.0 ml (range 1.5–4.5 ml). Mean cardiac output increasedfrom 7 to 8 litre min^-1 after preloading with Ringer lactatesolution 1.5 litre and then remained unchanged after injectionof bupivacaine. Two subjects developed hypotension, althoughmean values of arterial pressure and umbilical artery pulsatilityindex did not change. The median umbilical artery pH was 7.27(range 6.98–7.32) and there was a significant correlationbetween pH and the maximum percentage decrease in cardiac output.The results suggest that continuous spinal anaesthesia is associatedwith greater haemodynamic stability than single bolus spinalinjection. (Br. J. Anaesth. 1993; 70: 634–638)     

The effects of 20% saline solution on the circulatory dynamics during the hemorrhagic shock state]

This experiment was performed to study the effects of administration of 20% saline solution 1.5 ml.kg-1 on the circulatory dynamics during the hemorrhagic shock state. Administration of 20% saline solution 1.5 ml.kg-1 during the hemorrhagic shock produced twofold increase of the mean arterial blood pressure for one hour, 2.5 fold increase of the cardiac output, increasing tendency in the mean pulmonary arterial pressure, central venous pressure, and the heart rate, accompanied by decrease in total peripheral resistance and the pulmonary blood vessel resistance. There were no improvements in acidosis and hematocrit. These data suggest that the circulatory improvements after the administration of 20% saline solution depend on an increase in cardiac output as the result of improvements in both pre- and after-load, but not of plasma volume expansion. The results also suggest that the administration of 20% saline solution 1.5 ml.kg-1 is useful for an emergency case with acute circulatory insufficiency or for emergency resuscitation.     

Nitroprusside-Hypotension: Cerebral Blood Flow and Cerebral Oxygen Consumption in Neurosurgical Patients

The effects of nitroprusside-induced hypotension on cerebral blood flow and cerebral oxygen consumption were investigated in nine patients scheduled for cerebral arterial aneurysm surgery. Anesthesia was maintained with nitrous oxide/oxygen and fentanyl; muscle relaxation was achieved with pancuronium; Paco₂ was maintained at 4.79-5.32 kPa. Mean arterial pressure was reduced to 50 mm Hg by nitroprusside infusion after opening of the dura. Measurements were recorded and blood samples were taken 15 min before induction of hypotension, during stable hypotension and 15 min after termination of nitroprusside infusion. Measurements included: cerebral blood flow, using the argon-washin technique, cardiac output (thermodilution), mean arterial pressure and heart rate. Cerebral blood flow averaged 56 ± 6 ml/min. 100 g before hypotension. Nitroprusside produced hypotension but did not significantly alter cerebral blood flow (61 ± 7 ml/min · 100 g). Cerebral blood flow remained virtually at preinfusion values upon cessation of infusion (53 ± 6 ml/min · 100 g). Cerebral oxygen uptake averaged 3 ± 0.2 ml/min · 100 g before hypotension and did not change significantly during hypotension (3.3 ± 0.3 ml/min · 100 g) and after termination of hypotension (2.7 ± 0.3 ml/min · 100 g). In two patients nitroprusside produced a 17 and 20% increase, respectively, in cerebral blood flow with no change in cerebral oxygen consumption, together with a marked increase in cardiac output and heart rate.     

Haemodynamic modifications after unilateral subarachnoid anaesthesia evaluated with transthoracic echocardiography

AIM: The aim of the study is the evaluation through transthoracic echocardiography of the haemodynamic modifications due to unilateral subarachnoid anaesthesia with bupivacaine 0.5% given for orthopaedic surgery. METHODS: In this prospective study, at the University Hospital Orthopedics surgical theater, 20 patients underwent orthopaedic surgery on the lower limbs. Unilateral spinal block was performed with hyperbaric bupivacaine 0.5%, 8 mg after a fluid challenge with saline solution 0.9%. Transthoracic echocardiography was performed and cardiac output was calculated from the left ventricular outflow tract (LVOT) with a recently validated technique. Cardiac output, stroke volume, ejection fraction, heart rate, mean arterial pressure were evaluated. These parameters were obtained before anaesthesia (t1), 5 minutes after anaesthesia (t2) and 16 minutes after anaesthesia (t3). RESULTS: Systolic, mean and diastolic arterial pressures after 5 min and 16 min from anaesthesia significantly decreased if compared to basal time (p<0.05 and p<0.001 respectively) while cardiac index (p<0.001) and ejection fraction (p<0.05) decreased only after 16 min from subarachnoid anaesthesia. CONCLUSION: Despite the fluid challenge we can not prevent a significant fall in the blood pressure and a decrease of the left ventricular function calculated with the decrease of cardiac output and of the left ventricular ejection fraction.     

A randomized comparison of labetalol and nitroprusside for induced hypotension

In a randomized study, labetalol-induced hypotension and nitroprusside-induced hypotension were compared in 20 patients (10 in each group) scheduled for major orthopedic procedures. Each patient was subjected to an identical anesthetic protocol and similar drug-induced reductions in mean arterial blood pressure (BP) (50 to 55 mmHg). Nitroprusside infusion was associated with a significant (p < 0.05) increase in heart rate and cardiac output; rebound hypertension was observed in three patients after discontinuation of nitroprusside. Labetalol administration was not associated with any of these findings. Arterial PO₂ decreased in both groups. It was concluded that labetalol offers advantages over nitroprusside.     

Circulatory Changes during High Thoracic Epidural Anaesthesia - Influence of Sympathetic Block and of Systemic Effect of the Local Anaesthetic

Circulatory changes during high thoracic epidural anaesthesia (TEA) were studied in nine healthy volunteers by means of echocardiography and systolic time intervals. The subjects also underwent a physical work test with bicycle ergometry. To evaluate the systemic effect of the local anaesthetic (bupivacaine), the same subjects were investigated 3 weeks later when a corresponding dose of the local anaesthetic was injected intramuscularly instead of epidurally. On the first occasion, after baseline measurements an epidural catheter was inserted at T4 level and 5 ml of 0.5% bupivacaine were injected. This volume led to sensory block within dermatomes T1-T5. On the second occasion all subjects received 8 ml of 0.5% bupivacaine intramuscularly. Heart rate (HR) and systolic blood pressure decreased during TEA, both at rest and during exercise. Following i.m. injection, HR decreased at rest but remained unchanged during exercise. The systolic blood pressure was not affected but the diastolic blood pressure increased during the exercise test. After administration of TEA, stroke volume (SV) decreased 22% and cardiac output (CO) 33%. Following i.m. injection of bupivacaine, SV decreased 8% and CO 20%. The pre-ejection period/left ventricular ejection time ratio increased 23% during TEA and 16% after i.m. injection. The results indicate that the circulatory changes did not seem to be caused entirely by the cardiac sympathetic block, but were due partly to the systemic effect of bupivacaine.     

Central and Splanchnic Haemodynamics in the Dog During Controlled Hypotension with Sodium Nitroprusside

The effects of controlled hypotension induced by sodium nitroprusside (SNP) on central and splanchnic haemodynamics were studied in ten artificially ventilated dogs under neurolept anaesthesia. SNP was given intravenously as a continuous infusion in order to maintain a mean arterial blood pressure (MABP) of about 50 mmHg. Observations were made before (control) and at 20 and 60 min after the start of the SNP infusion. The mean SNP dosage was 13.7 micrograms X kg-1 X min-1. Systemic vascular resistance (SVR) decreased by 47%. After 20 min there was a 17% decrease in cardiac output, while the hepatic arterial blood flow was diminished by 39%, and portal venous blood flow by 16%. Cardiac output and portal venous blood flow tended to return towards control values at 60 min, while the hepatic arterial blood flow remained depressed. The total oxygen uptake was unaltered after 20 min, but slightly decreased after 60 min. There were no changes in hepatic or preportal tissue oxygen consumption, nor in hepatic lactate uptake. It is concluded that SNP-induced hypotension was achieved primarily by a profound reduction of SVR, and initially also by a slight decrease in cardiac output. Although splanchnic and hepatic blood flows decreased, there were no signs of hypoxia in the preportal tissues or in the liver.     

Epidural Anesthesia, Hypotension, and Changes in Intravascular Volume

Background: The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available.

Methods: In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch.

Results: Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min.     

Thoracic electrical bioimpedance measurement of cardiac output and cardiovascular responses to the induction of anaesthesia and to laryngoscopy and intubation

Noninvasive methods of determining cardiac output (by thoracic electrical bioimpedance) and arterial pressure (by intermittent oscillometry) were used to record minute-by-minute changes in heart rate, mean arterial pressure, stroke volume, cardiac output and systemic vascular resistance following induction of general anaesthesia and laryngoscopy and intubation in 60 healthy female patients who were either unpremedicated, or premedicated with temazepam or papaveretum-hyoscine. Anaesthesia was induced with a sleep dose (3-5 mg.kg-1) of thiopentone and maintained with 70% nitrous oxide in oxygen with 0.5-1% enflurane. Tracheal intubation was facilitated by administration of vecuronium 0.1 mg.kg-1. Mean arterial pressure and cardiac output decreased maximally 5 min after induction in all premedication groups by mean estimates of 21-25% and 14-22% respectively. Heart rate increased initially one minute after induction, but decreased to less than the baseline value 5 min after induction. Systemic vascular resistance was unchanged. The stimulus of laryngoscopy and tracheal intubation was accompanied by a significant pressor response and tachycardia one minute after intubation (with mean increases in mean arterial pressure and heart rate of 29-34% and 22-33% respectively). The increase in mean arterial pressure was secondary to an increase in systemic vascular resistance (36-57%), and was accompanied by a decrease in stroke volume (-25 to -31%). These changes were significant in all three groups. Cardiac output decreased only in unpremedicated patients. There were wide variations in the different haemodynamic indices.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidural anesthesia worsens uterine blood flow and fetal oxygenation during hemorrhage in gravid ewes.

Recent studies suggest that epidural anesthesia initiated before hemorrhage may improve survival and acid-base status in laboratory animals. However, studies of hemorrhagic shock in nonpregnant animals may not be applicable to less severe hemorrhage in pregnant animals. The purpose of this study was to determine whether epidural anesthesia alters maternal and fetal hemodynamic and acid-base responses to hemorrhage in gravid ewes. Twenty-four experiments were performed in twelve chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0 min: normal saline 500 ml intravenously; 2) T = 15 min: epidural administration of 0.5% bupivacaine (epidural group) or normal saline (control group); 3) T = 30 min: epidural administration of additional 0.5% bupivacaine (epidural group only) if the sensory level of anesthesia was below T10; 4) T = 45 min: maternal hemorrhage 20 ml/kg over 55 min; and 5) T = 110 min: transfusion of collected maternal blood over 55 min. At 45 min (i.e., 30 min after the epidural injection of bupivacaine), epidural bupivacaine resulted in a median sensory level of T9 in the epidural group. At that time, maternal mean arterial pressure was less (P less than 0.05) in the epidural group than in the control group (14 +/- 2% below baseline versus 4 +/- 1% above baseline, respectively). Maternal mean arterial pressure, heart rate, cardiac output, and uterine blood flow, and fetal PO2 and pH all were significantly less during hemorrhage (P less than 0.05) in the epidural group than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glycopyrronium and hypotension following combined spinal-epidural anaesthesia for elective Caesarean section in women with relative bradycardia

The ability of glycopyrronium to reduce the severity of hypotension following subarachnoid block in parturients with a relative bradycardia was evaluated in a double-blind randomised controlled study. Women with a resting heart rate of < or = 80 beat x min(-1) presenting for elective Caesarean section were randomly allocated to receive either glycopyrronium 2 microg x kg(-1) or normal saline intravenously once positioned for combined spinal-epidural anaesthesia. Following spinal injection of 2.6 ml hyperbaric bupivacaine 0.5% and fentanyl 15 microg, women randomly allocated to the saline group were given 6 mg ephedrine so that all parturients received some prophylaxis against hypotension other than the fluid preload. Further ephedrine and fluid boluses were administered if mean arterial pressure fell 20% or more from resting values. Using a sequential analysis technique, analysis after the first 20 subjects indicated the study should be stopped, with no difference in ephedrine requirements or hypotension between the groups. We conclude that pretreatment with glycopyrronium 2 microg x kg(-1) is no more effective than 6 mg ephedrine in preventing hypotension following subarachnoid block in parturients with relatively low resting heart rates.     

Hämodynamische Effekte einer Spinalanästhesie mit 2% Lidocain im Vergleich zu 0,5% isobaryem Bupivacain

BACKGROUND: Our study compared the haemodynamic changes after spinal anesthesia with 2% lignocaine and 0.5% plain bupivacaine. METHODS: A controlled, randomized trial was performed on 30 patients scheduled for arthroscopic knee surgery. 2% lignocaine and 0.5% plain bupivacaine were used for spinal anaesthesia. We measured cardiac output (electrical bioimpedance cardiography), blood pressure and development of sensory blockade before and for 25 minutes after spinal anaesthesia. RESULTS: In patients developing a sensory block below T6 there were no differences between both anaesthetics in haemodynamic parameters. But in patients developing a sensory block at or above T6 there was a greater drop in mean arterial pressure and cardiac output and a faster decrease in heart rate for bupivacaine compared to patients receiving Lignocaine. CONCLUSION: In patients developing a sensory block at or above the T6 dermatome, the decrease in cardiac output and mean arterial pressure in the first 25 min after spinal anaesthesia is smaller when 2% lignocaine rather than 0.5% bupivacaine is used for blockade.     

Epidural anesthesia, hypotension, and changes in intravascular volume

BACKGROUND: The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available. METHODS: In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch. RESULTS: Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min. CONCLUSIONS: Thoracic epidural anesthesia per se does not lead to changes in blood volumes despite a reduction in blood pressure. When fluid is infused, there is a dilution, and the fluid initially seems to be located centrally. Because administration of hydroxyethyl starch and ephedrine has similar hemodynamic effects, the latter may be preferred in patients with cardiopulmonary diseases in which perioperative fluid overload is undesirable.     

Prevention of hypotension during spinal anaesthesia for caesarean section

Twenty-six parturients scheduled to receive spinal anaesthesia for caesarean section were randomized to receive either isotonic saline 750 ml plus 20 ml/kg (group A) or 750 ml plus 500 ml (group B) before subarachnoid administration of bupivacaine 13 mg. Ephedrine 0.15 mg/kg i.v. followed by an infusion 0.4 mg.kg(-1) h(-1) were then administered in group B. In both groups ephedrine 10 mg/min i.v. was given if the mean arterial blood pressure decreased more than 10 mmHg. Despite the fluid preload and large doses of ephedrine noted {median (range), group A 30 mg (10-80), group B 92 mg (25-194)}, hypotension, sometimes accompanied by nausea, still occurred. Mean maternal arterial was significantly lower in group A than in group B 5-10 min after induction of spinal anaesthesia (P < 0.05). There was no difference in the frequency of nausea or vomiting, Apgar score, or pH in umbilical cord blood. One neonate in group A and 2 in group B were acidotic. In conclusion, a reduced volume loading could be compensated with an increased ephedrine administration after induction of spinal anaesthesia, without increasing the incidence of hypotension or other maternal or neonatal complications. However, the fluid volumes and/or ephedrine doses used were not sufficient to prevent hypotension altogether.     

Anaesthesia for 1131 patients undergoing proximal femoral fracture repair: a retrospective, observational study of effects on blood pressure, fluid administration and perioperative anaemia

Intra-operative hypotension is a frequent occurrence during anaesthesia for hip fracture surgery in older patients with co-morbidities. We analysed retrospective data from the Brighton Hip Fracture Database to determine the intra-operative fall in systolic blood pressure, and the incidence of absolute (lowest systolic blood pressure < 90 mmHg) and relative (> 20% fall in systolic blood pressure from baseline) hypotension during general or spinal anaesthesia among 1131 non-consecutive patients with hip fracture. General anaesthesia for 489 patients (43.2%) produced a greater mean (SD) fall in systolic blood pressure than spinal anaesthesia for 578 patients (51.1%): 34.2% (13.0%) vs 29.7% (10.8%), respectively (p < 0.0001), mean difference 4.5% (95% CI 3.1-5.9%), and was associated with greater mean (SD) intra-operative fluid administration (1555 (801) ml vs 1375 (621) ml, respectively, p < 0.0001). We observed a correlation between the volume of subarachnoid hyperbaric bupivacaine 0.5% and fall in systolic blood pressure (p = 0.004): compared with patients receiving > 1.5 ml (n = 463), fewer patients receiving ≤ 1.5 ml bupivacaine 0.5% (n = 97) experienced episodes of absolute (31.1% vs 11.3%, p < 0.0001) or relative (83.9% vs 26.8%, p < 0.0001) hypotension. Both mean (SD) intravenous fluid administration (1097 ml (439) vs 1431 ml (638), p < 0.0001) and mean peri-operative fall in haemoglobin concentration (2.1 (1.8) g.dl(-1) vs 2.6 (1.7) g.dl(-1), p = 0.009) were lower in the low-dose spinal group. If these data are confirmed by other researchers, intra-operative hypotension (and consequent haemodilution secondary to reactive fluid administration) in this patient group may be reduced by the simple expedient of administering more cautious general anaesthesia, or reduced volumes of subarachnoid local anaesthetic.     

Effects of hypertonic 75 mg/ml (7.5%) saline on extracellular water volume when used for preloading before spinal anaesthesia

Background: Prevention of hypotension during spinal anaesthesia is commonly achieved using fluid preloading. This may result in a substantial amount of excess free water retained in the body after spinal anaesthesia. We aimed to evaluate the effects of 7.5% hypertonic saline on extracellular water volume and haemodynamics when used for fluid preloading before spinal anaesthesia.
Methods: This randomised double-blind study evaluated the effects of 75 mg/ml (7.5%) hypertonic saline (HS) on extracellular water volume and haematocrit in patients undergoing arthroscopy or other lower limb surgery under spinal anaesthesia. Amounts of 1.6 ml/kg of HS (20 patients) or 13 ml/kg of 9 mg/ml normal saline (20 patients) were administered for preloading before spinal anaesthesia with a 10 mg dose of 0.5% hyperbaric bupivacaine. Etilefrine was administered in order to maintain mean arterial pressure (MAP) at 80% of its baseline value. Whole-body impedance cardiography-derived cardiac index (CI) and extracellular water (ECW) were measured.
Results: There were no significant differences in demographic data or in the number of blocked segments. ECW remained similar in both groups despite the much smaller amount of infused free water in the HS group. There were no significant differences between the groups in CI values during the study. The amount of etilefrine administered was similar in the treatment groups. Dilution of haematocrit was also similar in both groups.
Conclusion: Hypertonic 75 mg/ml (7.5%) saline is an alternative for preloading before spinal anaesthesia in situations where excess free water administration is not desired. It is effective in small doses of 1.6 ml/kg, which increase the extracellular water, plasma volume and cardiac output, and thus maintain haemodynamic stability during spinal anaesthesia.     

Pneumoperitoneum in healthy humans does not affect central blood volume or cardiac output

BACKGROUND: This study addresses the question of whether the elevation of the mean arterial pressure and central venous pressure in response to pneumoperitoneum for laparoscopic surgery is caused by increases in central blood volume and/or cardiac output. METHODS: Eleven patients in good cardiopulmonary health and scheduled for laparoscopic cholecystectomy, with a mean age of 42 years, were included. After induction of anaesthesia with fentanyl and propofol, radial arterial and central venous lines were introduced. The central blood volume and cardiac output were determined by the indicator-dilution technique, using inline densitometric measurements of indocyanine green (ICG). The measurements were made before and after the establishment of pneumoperitoneum by insufflation of carbon dioxide to an intra-abdominal pressure level of 11-13 mmHg. RESULTS: The mean arterial pressure (62+/-6 mmHg) increased after induction of pneumoperitoneum by 40+/-26% (P<0.05) and the central venous pressure increased from 6+/-4 mmHg to 8+/-6 mmHg (P<0.05). The cardiac output (4.3+/-0.9 L/min) and central blood volume (1.5+/-0.5 L) were not affected by the induction of pneumoperitoneum. CONCLUSIONS: In healthy anaesthetized subjects, the elevation of mean arterial pressure and central venous pressure in response to pneumoperitoneum was not caused by enhancement in cardiac output or central blood volume.     

A comparison of labetalol and nitroprusside for inducing hypotension during major surgery

The hemodynamic and intrapulmonary shunt effects of intravenous labetalol and nitroprusside were compared during induced hypotension for major spinal surgery. A randomized, double-blind protocol was used in which 20 patients, ASA physical status I or II, received either nitroprusside infusion (n = 10) or labetalol bolus injections of 10 mg every 10 min (n = 10) until mean arterial blood pressure was reduced to 55-60 mm Hg. Pulmonary artery pressures were measured and mixed venous samples obtained via a pulmonary artery catheter. Nitroprusside increased heart rate significantly more than labetalol during the period of hypotension. When compared with prehypotension baseline values, nitroprusside increased heart rate significantly with a concomitant significant decrease in systemic vascular resistance. Cardiac output increased significantly 60 min after hypotension was achieved in patients treated with nitroprusside. Systemic vascular resistance decreased significantly below baseline levels in patients treated with labetalol but without changes in cardiac output, heart rate, or mean pulmonary artery pressure. There was a 122% increase in intrapulmonary shunt with nitroprusside administration, compared with an 11% increase with labetalol. Labetalol was effective for inducing hypotension and was not associated with an increase in heart rate, intrapulmonary shunt, or cardiac output as seen with nitroprusside.     

Acute hypotension caused by rapid hypertonic saline infusion in anesthetized dogs

Small volumes (4-6 mL/kg) of 7.5% hypertonic saline solution (HTS) are reported to be effective for resuscitation from circulatory shock. When infused rapidly into either hypovolemic or normovolemic subjects, HTS can cause an immediate and severe hypotension before cardiovascular improvement. In the present study, we examined the hypothesis that the early hypotension produced by HTS was mediated by an acute and transient depression of cardiac contractility. left ventricular pressure and wall motions were measured simultaneously in 10 anesthetized dogs for the assessment of cardiac contractility. Infusion of HTS at 3 mL/kg in 1 min significantly decreased mean arterial blood pressure by 49%, from 95 +/- 4 to 51 +/- 5 mm Hg (P less than 0.05, mean +/- SEM) at 45 s after the onset of infusion. This initial decrease in arterial blood pressure was abrupt and transient (106 +/- 9 s). Concomitantly, cardiac output and coronary blood flow increased significantly from 2.8 +/- 1.0 to 3.9 +/- 1.1 L/min and from 23.7 +/- 5.3 to 49.8 +/- 4.7 mL/min, respectively. Although heart rate remained constant, systolic shortenings of left ventricular diameter and wall thickness increased from 5.6% +/- 0.5% to 7.8% +/- 0.5% and from 13.9% +/- 0.6% to 15.1% +/- 1.2%, respectively, indicating an improvement in cardiac contractility. This was confirmed by subsequent analysis of the left ventricular end-systolic pressure-diameter relationship. Systemic and pulmonary vascular resistance decreased by 60% and 27%, respectively. Despite an initial period of hypotension after rapid infusion of HTS, mean arterial blood pressure, cardiac output, and contractility were all significantly increased at 5 min after HTS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)