Haemodynamics and Oxygen Consumption in the Dog During High Epidural Block with Special Reference to the Splanchnic Region

High epidural block (Th I-IV) with bupivacaine was carried out in 16 dogs. Mean arterial blood pressure decreased to 52% of control value owing to nearly equal decreases in systemic vascular resistance and cardiac output. Portal venous blood flow decreased from 25.8 ± 8.6 to 16.7 ±7.2 ml/kg b.w. × min^-1 following epidural block, while hepatic arterial blood flow remained unchanged at 9.1 ± 3.1 ml/kg b.w. × min^-1 owing to a reduction in hepatic arterial resistance of 51 %. Hepatic oxygen uptake was maintained during the epidural block through increased oxygen extraction. However, total oxygen uptake decreased by 18 % and, in spite of this, arteriovenous oxygen content difference increased by 25%, indicating circulatory depression.     

Circulatory effects of short-term hypercapnia during thoracolumbar epidural anaesthesia

In ten elderly patients subjected to extensive thoracolumbar epidural anaesthesia, circulatory changes were studied before and during sympathetic stimulation. Induced hypercapnia was used as a sympathetic stimulus. After establishment of the epidural anaesthesia, which extended from T1 to L2, there were decreases in heart rate, mean arterial blood pressure, cardiac output and systemic vascular resistance. Hypercapnia before the epidural block increased heart rate, arterial blood pressure and cardiac output, while hypercapnia after established epidural block induced only a slight increase in arterial blood pressure. The results indicate that in spite of an extensive epidural block, there are some "escaped" sympathetic nerve fibres that can be mobilized during sympathetic stimulation.     

The Effect of Surgical Stress on Haemodynamics During Neurolept Anaesthesia

The influence of surgical stress on haemodynamics during neurolept anaesthesia (NLA) was studied in ten patients, while they were awake, under anaesthesia prior to surgery and peroperatively. Systemic arterial, pulmonary arterial, right atrial and pulmonary capillary wedge pressures, as well as cardiac output (Q_t), arterial oxygen content and mixed venous oxygen content, were measured. Systemic and pulmonary vascular resistances, arterial-venous oxygen content difference (AVD), oxygen consumption (v_o2 and cardiac index (CI) were calculated.
On institution of anaesthesia, CI fell from 2.8 ±.11 /min. m² to 2.5±0.2 l /min.m² and systolic arterial pressure (SBP) fell from 13.4±0.5 kPa to 10.2±0.3 kPa. During surgery CI rose to 3.3±0.1 1/min.m² and SBP rose to 15.7±0.6 kPa. Prior to anaesthesia, AVD was 40.2±0.2 ml/l Under anaesthesia prior to surgery, AVD did not change, but v_O2 declined from 207±13 ml/min to 171±10 ml/min. During surgery, AVD fell to 30.5±0.3 ml/l, while V_o2 remained unchanged.
It is concluded that NLA has a direct metabolic depressant effect and, in association with surgery, is accompanied by hyperkinetic circulation.     

Cardiovascular Effects of Etomidate Used for Induction and in Combination with Fentanyl-Pancuronium for Maintenance of Anaesthesia in Patients with Valvular Heart Disease

The effects of induction of anaesthesia by etomidate 3 mg·kg-^-1 followed by continuous infusion of etomidate 2 mg·min^-1, fentanyl 0.01 mg·kg^-1 and pancuronium 0.1 mg·kg^-1 were studied in ten patients with valvular heart disease. No haemodynamic changes were seen after injection of etomidate, but after fentanyl was given thew was a significant decline in cardiac index (10%), in mean arterial systemic pressure (20%), in systemic vascular resistance (14%), in left ventricular minute work index (27%) and in right ventricular minute work index (21%) compared to the control values. After supplementing with pancuronium, no further significant changes were seen. There was no significant change in the pulmonary vascular resistance during the whole study. In conclusion, it appears that etomidate is a safe intravenous agent, and is worth further study, in particular in patients with minimal cardiac reserve requiring high inspired oxygen tension.     

Hemodynamic and Cardiometabolic Effects of Prenalterol in Patients with Gram Negative Septic Shock

The hernodynamic eflects of prenalterol, a new inotropic agent, were investigated in 10 patients with gram negative septic shock. In four of the patients, coronary sinus blood flow (CSF) and myocardial oxygen and lactate extraction were also determined. After baseline hemodynamic measurements, prenalterol was infused intravenously over a 10-min period to a total dose of 150 pg/kg. All patients responded within 15 min after completion of prenalterol infusion by increasing mean arterial pressure from 57±11 to 75 ± 20 mmHg (7.58f 1.46 to 9.97±2.66 kPa), (+32%), ( P<0.01 ) and cardiac index from 2.65±0.40 to 3.80±0.47 l min^-l m^-2 (+44%) ( P < 0.001). There was no change in heart rate or systemic vascular resistance, nor were any arrhythmias recorded. The urinary output increased significantly. After prenalterol, CSF increased from 185kl 4 to 246±14 ml.min-¹, (+33%), (P<0.001) and myocardial oxygen and lactate extraction rose from 19.8±2.1to26.6±2.1 ml O₂.min^-1, (+ 34%) (P<0.00l) andfrom33.2±2.3 to44.7k2.1 μmol.min^-1, (+35%), (P<0.001), respectively. The total body oxygen consumption increased from 287f 13 to 348±23 ml O₂.min^-1, (+21 %), ( P<0.01 ) and the arterial lactate concentration decreased from 5.61±0.55 to 3.94±0. 16 mmol.l^-1, (- 30%), (P<0.01), suggesting improved tissue perfusion. The results demonstrate that prenalterol is a potent, highly selective inotropic agent inducing the same magnitude of increase in blood pressure and cardiac output as reported for dopamine in septic shock.     

Hypotension and respiratory distress caused by rapid infusion of mannitol or hypertonic saline

Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs. The injection of 20 ml of 10% NaCl into the pulmonary artery increased pulmonary arterial pressure and decreased systemic blood pressure by approximately 50% of control values. Injections of solutions of equal hyperosmolar strength, 50 ml of 25% mannitol or 50 ml of 4% NaCl into the pulmonary artery produced no significant elevation of pulmonary arterial pressure, but were associated with comparable decreases in systemic blood pressure. When allowed to vary, cardiac output increased with injections of all three hyperosmolar solutions, yet was still accompanied by falls in systemic blood pressure as large as when cardiac output was held constant. Vagotomy did not prevent these changes in systemic and pulmonary arterial pressure, nor the increase in cardiac output. After five to 10 injections, the decreases in system blood pressure with any of the solutions and the increases in pulmonary arterial pressure with 10% NaCl disappeared and further injections were without effect. It is concluded that adminstration of mannitol probably does not cause pulmonary edema due to fluid overload, nor does it cause heart failure as evidenced by increases in pulmonary arterial pressure. However, rapid injection may cause a fall in blood pressure and may on occasion be accompanied by bronchospasm, especially in sensitive subjects.     

Intrathoracic and pulmonary blood volume during CO2-pneumoperitoneum in humans

Background : Induction of CO₂-pneumoperitoneum may have significant effects on systemic and pulmonary haemodynamics. We hypothesized, that intrathoracic (ITBV) and pulmonary blood volume (PBV) are affected during intra-abdominal CO₂-insufflation, which may be pronounced by positional changes of the patient.
Methods : Sixteen anaesthetized patients were studied before, during and after CO₂-pneumoperitoneum for laparoscopic cholecystectomy. A dye indicator technique was used to assess ITBV and PBV. In addition, gas exchange and haemodynamics were recorded.
Results : In the supine position, induction of CO₂-pneumoperitoneum had no effects on ITBV, PBV and cardiac output. Mean systemic arterial pressure increased from 10.9±1.5 kPa (82±11 mmHg) to 12.7±1.5 kPa (95±11 mmHg, P<0.01). In the reverse Trendelenburg position ITBV decreased from 19.8±5.1 ml . kg^-1 to 16.7±3.7 ml . kg¹ ( P <0.05) during CO₂-insufflation, but increased to control values after 20 min. PBV decreased from 4.2±1.2 ml . kg^-1 to 3.4±1.1 ml . kg^-1 (P<0.05) and remained decreased during CO₂-pneumoperitoneum. Calculated venous admixture was unchanged throughout the study. Deflation of CO₂-pneumoperitoneum increased ITBV (22.4±5.2 ml . kg^-1, P<0.05) and cardiac output above control values.
Conclusions : In anaesthetized-paralyzed patients in the reverse Trendelenburg position intra-abdominal CO₂-insufflation is associated with significant alterations of ITBV and PBV. The release of CO₂-pneumoperitoneum is associated with a re-distribution of blood into the thorax.     

Right ventricular end–systolic pressure–volume relation during propofol infusion

The effects of propofol on right ventricular function were studied in 11 ICU patients who needed sedation for acute respiratory failure or neurological diseases. Right ventricular function was studied using a thermodilution method at patients' bedside. Right ventricular ejection fraction (RVEF), cardiac output (CO), right ventricular end–diastolic volume (RVEDV), right ventricular end–systolic volume (RVESV), right ventricular end–systolic pressure (RVESP) and pulmonary capillary wedge pressure (PCWP) were obtained from a modified Swan–Ganz catheter. Calculation of right ventricular end–systolic pressure–volume relation (ESPVR) allowed to assess changes in right ventricular inotropic state. A baseline ESPVR was obtained before propofol infusion: RVESP = 0.21 RVESV + 2.4, r = 0.83, P < 0.0001. Then, patients were given an induction dose of 1 to 2.5 mg kg^-1 propofol over 1 min followed by a continuous infusion of 3 mg kg^-1 h^-1. During propofol infusion heart rate, mean arterial pressure, PCWP, CO, systemic vascular resistance and RVEF significantly decreased. No change in RVEDV and RVESV was observed. ESPVR was significantly altered with a dramatic decrease in the slope of the relation: RVESP = 0.12 RVESV + 6.9 ( P < 0.001 from baseline). Dobutamine was used in five patients with clinically significantly cardiac dysfunction and restored the slope of the ESPVR to the baseline value: RVESP = 0.22 RVESV + 6.3 (NS from baseline). In the study patients, propofol altered the inotropic state of the right ventricle.     

Splanchnic circulation following coeliac plexus block

Both the capacitance vessels and the resistance vessels of the splanchnic area are innervated by the sympathetic nerve fibers. We investigated the effect of abdominal visceral sympathectomy on splanchnic circulation, and the effect of altered splanchnic circulation on systemic circulation in ten mongrel dogs. Abdominal visceral sympathectomy was induced by coeliac plexus block with 1 ml/kg (body weight) of 1 % lidocaine infiltrated around the coeliac artery. Comparison was made with infiltration of physiologic saline of the same volume. The saline infiltration caused no significant changes in the hemodynamic parameters of systemic and splanchnic circulation. Mean arterial pressure decreased significantly from 18.2 ±2.0 to 14.4±1.9 kPa following the coeliac plexus block, with a concomitant decrease in the cardiac index from 2.63 ± 0.46 to 2.30 ± 0.54 1 × min^-1 × m^-2, while systemic vascular resistance was unchanged. Portal vein blood flow, hepatic artery blood flow and, therefore, splanchnic blood flow decreased by 8 to 17%. Portal vascular and hepatic artery resistances were not affected by abdominal sympathectomy. It was concluded that the capacitance vessels in splanchnic circulation are dilated during abdominal sympathetic denervation, causing a blood shift from systemic to splanchnic circulation. On the other hand, the resistance vessels in splanchnic circulation are affected little by abdominal visceral sympathectomy.     

Pulmonary shunt and cardiovascular responses to CPAP during nitroprusside-induced hypotension.

The effects of continuous positive airway pressure (CPAP) on cardiovascular dynamics and pulmonary shunt (QS/QT) were investigated in 12 dogs before and during sodium nitroprusside infusion that decreased mean arterial blood pressure 40-50 per cent. Before nitroprusside infusion, 5 cm H2O CPAP significantly, P less than .05, decreased arterial blood pressure, but did not significantly alter heart rate, cardiac output, systemic vascular resistance, or QS/QT. Ten cm H2O CPAP before nitroprusside infusion produced a further decrease in arterial blood pressure and significantly increased heart rate and decreased cardiac output and QS/QT. Nitroprusside caused significant decreases in arterial blood pressure and systemic vascular resistance and increases in heart rate, but did not change cardiac output or QS/QT. Five cm H2O CPAP during nitroprusside did not further alter any of the above-mentioned variables. However, 10 cm H2O CPAP decreased arterial blood pressure, cardiac output, and QS/QT. These data indicate that nitroprusside infusion rates that decrease mean arterial blood pressure by 40-50 per cent do not change cardiac output or QS/QT. During nitroprusside infusion low levels of CPAP do not markedly alter cardiovascular dynamics, but high levels of CPAP (10 cm H2O), while decreasing QS/QT, produce marked decreases in arterial blood pressure and cardiac output.