Pulmonary gas exchange effects by nitroglycerin,dopamine and dobutamine during one-lung ventilation in man

The effects of nitroglycerin, dopamine and dobutamine on pulmonary gas exchange were determined in 21 adult patients during two-lung and one-lung ventilation. Nitroglycerin, in I μg·kg^?1·min^?1, decreased cardiac index (CI) andPaO₂ during both two-and one-lung ventilation, and increased in Qs/Qt during one-lung ventilation. There were no significant changes in the measured variables during infusion of dopamine, 5 μg·kg^?1·min^?1. Dobutamine, 5μg·kg^?1·min^?1, increased Cl and PaO₂ did not change during two-lung ventilation. During one-lung ventilation, PaO₂ increased from (mean value ±SD) 168 ± 46 to 201 ± 52 mmHg (P < 0.01) with dobutamine infusion. Qs/Qt decreased from 29.2 ± 7.0 to 26.0 ± 6.2 per cent (P < 0.05) without any change in pulmonary vascular resistance index during one-lung ventilation. We conclude that dobutamine has advantages over dopamine and nitroglycerin during one-lung ventilation.     

Effects of desflurane and propofol on arterial oxygenation during one-lung ventilation in the pig

Background: Desflurane depresses hypoxic pulmonary vasoconstriction (HPV) in vitro. During one-lung ventilation (OLV), HPV may reduce venous admixture and ameliorate the decrease in arterial O₂ tension by diverting blood from the non-ventilated to the ventilated lung. Accordingly, this study compares the effects of desflurane with those of propofol on oxygenation during two-lung (TLV) and OLV in vivo. Methods: Ten pigs (25–30 kg) were premedicated (flunitrazepam 0.4 mg/kg im), anaesthetized (induction: propofol 2 mg/kg iv; maintenance: N₂O/O₂ 50%/50%, desflurane 3%, propofol 50 μg kg^?1 min^?1, and vecuronium 0.2 mg kg^?1 h^?1 iv), orally intubated and mechanically ventilated. Femoral arterial and thermodilution pulmonary artery catheters were placed, and the orotracheal tube was replaced by a left-sided 28-Ch double-lumen tube (DLT) via tracheotomy. After DLT placement, N₂O and propofol were discontinued, FiO₂ was increased to 0.85, and anaesthesia continued randomly with either desflurane (1 MAC) or propofol 200 μg kg^?1 min^?1. Using a cross-over design, in each animal the effects of a), changing from TLV to OLV (left lung) during both desflurane and propofol and b), the effects of changing between the two anaesthetics during OLV were studied. Results: When changing from TLV to OLV, PaO₂ decreased more (P<0.05) during desflurane (mean 75%) than during propofol (mean 60%). Changing between desflurane and propofol during OLV resulted in small but consistent (P<0.05) increases in PaO₂ (mean 15%) during propofol. Conclusion: Consistent with in vitro results on HPV, 1 MAC desflurane impaired in vivo oxygenation during OLV more than did propofol.     

Auswirkungen von Dopexamin Transpulmonales Shuntvolumen bei thorax- chirurgischen Eingriffen mit Ein-Lungen-Beatmung

Objective: To study the influence of dopexamine on pulmonary shunt and hypoxic pulmonary vasoconstriction during major thoracic surgery with one-lung ventilation (OLV). Design: Prospective, randomised, placebo-controlled study. Setting: University hospital. Patients: Twenty adult patients undergoing elective pulmonary resection. Anaesthesia: General anaesthesia was performed using propofol, fentanyl, N₂O and vecuronium.Volume-controlled ventilation was performed to maintain normocapnia over the whole investigation period. During OLV, the tidal volume was reduced and the respiratory rate was increased to avoid a peak airway pressure exceeding 40 cm H₂O. Furthermore the FiO₂ was increased to 1,0 and the external PEEP was removed during OLV. Interventions: The patients received either dopexamine at 2 µg/kg/min (group A, n=10) or 0,9% saline as control (group B, n=10) after assessing the baseline values. Measurement and results: The following cardiorespiratory variables were recorded: Heart rate, mean arterial pressure and mean pulmonary arterial pressure. Cardiac output was measured by thermodilution using a continuous cardiac output thermodilution catheter. Arterial and mixed venous blood gas analysis were measured from simultaneously drawn samples. Cardiac index (CI), systemic vascular resistance index, pulmonary vascular resistance index, oxygen delivery index (DO₂I), oxygen consumption index and the venous admixture were calculated using standard formula. Furthermore, pressure-flow-curves were constructed to analyse flow independent changes in the pulmonary vascular resistance. Data were recorded at the following times: After induction of anaesthesia in stable haemodynamics during two-lung ventilation (baseline values, T0), intraoperatively during one-lung ventilation (T1) and postoperatively after re-establishing two-lung ventilation (T2). Patients characteristics, data from the preoperative lung function testing and surgical procedures did not differ significantly between the groups. CI increased in the dopexamine group from 2,5±1,2 l·min^?1·m^?2 (T0) to 3,6±0,9 l·min^?1·m^?2 (T1) and 4,0±1,3 l·min^?1· m^?2 (T2). The course of the intrapulmonary right-to-left shunting did not differ between the groups. In the dopexamine-treated group the DO₂I increased from 430±143 ml·min·m^?2 (T0) to 652±255 ml·min·m^?2 (T1) and 653±207 ml·min·m^?2 (T2). Regarding the pressure-flow-curves there was no difference during OLV between the two groups indicating no major blocking effect of dopexamine on hypoxic pulmonary vasoconstriction. Conclusion: It is concluded that dopexamine can be used to improve haemodynamics and oxygen delivery during thoracic surgery without increasing venous admixture during one-lung ventilation.     

Cerebral oxygénation during prostaglandin E1 induced hypotension

Purpose

To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E₁(PGE₁) during fentanyl-oxygen anaesthesia.

Methods

Ten patients who underwent elective cardiac surgery received infusion of PGE₁. After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO₂) estimated by INVOS 3l00^R, PGE₁ was continuously infused at 0.25-0.65 μg·kg^?1·min^?1 (mean dosage: 410 ± 41.4 mg·kg^?1·min^?1) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO₂. Thirty minutes from the start of drug infusions, administration of PGE₁ was stopped. The same parameters were measured again 10, 30 minutes after the stop of drug infusion.

Results

PGE₁ decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE₁ increased mixed venous saturation, but in contrast did not effect internal jugular pressure, internal jugular oxygen saturation and rSO₂.

Conclusions

These results suggest that PGE₁ is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.     

The effects of increasing concentrations of desflurane on systemic oxygenation during one-lung ventilation in pigs.

During one-lung ventilation (OLV), hypoxic pulmonary vasoconstriction reduces venous admixture and attenuates the decrease in arterial O2 tension by diverting blood from the nonventilated to the ventilated lung. In vitro, increasing concentrations of desflurane depresses hypoxic pulmonary vasoconstriction in a dose-dependent manner. Accordingly, we investigated the effects of increasing concentrations of desflurane on oxygenation during OLV in vivo. Thirteen pigs (25-30 kg) were anesthetized (induction: propofol 2-3 mg/kg IV; maintenance: N2O/O2 50%/50%, desflurane 3%, propofol 50 microg x kg(-1) min(-1), and vecuronium 0.2 mg x kg(-1) x h(-1) IV), orotracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a leftsided, 28F, double-lumen tube was placed via tracheotomy. After double-lumen tube placement, N2O and desflurane were discontinued, propofol was increased to 200 microg x kg(-1) x min(-1), and the fraction of inspired oxygen was adjusted at 0.8. Anesthesia was then continued in random order with desflurane 5%, 10%, or 15% end-tidal concentrations while propofol was discontinued. Whereas mixed venous PO2, mean arterial pressure, cardiac output, and shunt fraction decreased in a dose-dependent manner, PaO2 remained unchanged with increasing concentrations of desflurane during OLV. These findings indicate that, in vivo, increasing concentrations of desflurane do not necessarily worsen oxygenation during OLV. IMPLICATIONS: Oxygenation during one-lung ventilation depends on reflex vasoconstriction in the nonventilated lung. In vitro, desflurane inhibits this reflex dose-dependently. Our results indicate that, in vivo, this does not necessarily translate to dose-dependent decreases in oxygenation during one-lung ventilation.     

Haemodynamic changes during induced hypotension — comparison of trimethaphan with prostaglandin E1 assessed using transoesophageal echocardiography

Haemodynamic changes during induced hypotension depend upon the hypotensive agent used. We investigated if, using transoesophageal echocardiography (TEE), we could identify the haemodynamic differences between trimethaphan and prostaglandin E₁. Twenty-nine patients undergoing total hip replacement were selected for study. Hypotension was induced to a mean arterial pressure of 8.0– 9.3 kPa with either trimethaphan (5–20 μg · kg^?1 min^?1) or prostaglandin E₁ (0.5–2.0 μg · kg^?1 min^?1). The left atrial dimension, cardiac output, fractional shortening, pulmonary venous flow and mitral valve flow were evaluated using TEE. During induced hypotension, left atrial dimension decreased in both trimethaphan and prostaglandin E₁ groups (P < 0.05). In the trimethaphan-treated patients systolic velocity in pulmonary venous flow decreased from 41.9 ± 4.8 cm · sec^?1 before induced hypotension to 27.8 ± 4.2 cm · sec^?1 by 30 min after stable hypotension had been established (P < 0.01). The late/early ratio of peak velocity in mitral blood flow decreased in prostaglandin E₁ treated patients. Cardiac output increased from 4.2 ± 0.5 L · min^?1 to 5.3 ± 0.4 L · min^?1 during 30 min hypotension with prostaglandin E₁ administration (P < 0.05), but cardiac output decreased from 5.0 ± 0.5 to 3.5 ± 0.4 L · min^?1 with trimethaphan (P < 0.01). The differences in haemodynamic variables could be attributed to the venule dilatation effect of trimethaphan. We conclude that it was possible to detect the haemodynamic differences between trimethephan and prostaglandin E₁ using TEE.     

Automatic jet ventilation in children anaesthetized by the T-piece circuit

Investigation was carried out in ten children aged between one month and six years, who were anaesthetized by the T-piece circuit. The volume of the reservoir tubing of the T-piece was 250 ml. Ventilation was controlled automatically by oxygen jets which were delivered via an injector attached to the reservoir tubing. The oxygen jets were regulated by an electronically-controlled solenoid valve. The children were ventilated by a tidal volume about 12 ml±kg^?1 at a rate of 12-20 per min depending on their age, while the FGF varied between 3 and 6 l min^?1 depending on their body weight. The resulting FIO₂ ranged between 0.32 and 0.34 which was expected from the oxygen:nitrous oxide mixture (1:2), denoting no mixing of the oxygen jets with the anaesthetic mixture. The PA_co2 was ventilation-dependent, and ranged between 4±6-5±3 kPa (35-41 mmHg). The results suggest that automatic jet ventilation facilitates controlled ventilation in children anaesthetized by the T-piece circuit, while maintaining the original simplicity of the T-piece.;     

Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco_2-20 kPa) at Fio₂ 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco₂ did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min^-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm^-5 (2490±210 vs 3430±200 μN-s-cm^-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio₂ (0.15, 0.10, 0.05) at 30-min intervals, while Fico₂ was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio₂ 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio₂ 0.10, while all buffered animals survived Fio₂ 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio₂ 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia.     

Unilateral high-frequency jet ventilation during one-lung ventilation for thoracotomy

One-lung ventilation is indicated during thoracic operations for bronchopleural fistula, pulmonary abscess, and pulmonary hemorrhage in spite of the possibility of the development of severe hypoxemia. To evaluate methods for improving oxygen transport during one-lung ventilation, we applied high-frequency jet ventilation (HFJV) and continuous positive airway pressure (CPAP) to the nondependent lung following deflation to atmospheric pressure in each procedure, and measured the effects on cardiac output and arterial oxygenation. In each case, the dependent lung was ventilated with conventional intermittent positive pressure ventilation (IPPV).

Eight patients were studied during posterolateral thoracotomy using double-lumen endobronchial tubes. HFJV or CPAP to the nondependent lung improved arterial oxygenation significantly during both closed and open stages of the surgical procedures (p < 0.008). When the chest was open, HFJV maintained satisfactory cardiac output, whereas CPAP usually decreased cardiac output (p < 0.008). There were no significant differences in mean partial pressure of arterial carbon dioxide between HFJV, CPAP, and deflation to atmospheric pressure.

In conclusion, HFJV to the nondependent lung provides not only satisfactory oxygenation but also good cardiac output, thereby maintaining better oxygen transport than CPAP or deflation to atmospheric pressure, while the dependent lung is ventilated with IPPV during one-lung ventilation for thoracotomy.     

Pulmonary blood flow reduction by prostaglandin F2α and pulmonary artery balloon manipulation during one-lung ventilation in dogs

The purpose of this experimental study was to compare two methods of pulmonary blood flow manipulation during one-lung ventilation (OLV), either reducing pulmonary blood flow to the non-ventilated lung by inflation of a pulmonary artery catheter balloon (PAB) or by infusion of prostaglandin F2 alpha (PGF2 alpha). Seven anaesthetized dogs were intubated with a Kottmeier endobronchial tube and ventilated with 66% O2. Systemic and pulmonary pressures and blood gases, cardiac output and airway pressure were measured, and the venous admixture (QSP/QT) was calculated. During two-lung ventilation (TLV) Pao2 was 43.6 +/- 1.9 kPa (mean +/- s.d.) and (QSP/QT) was 11 +/- 3%. OLV reduced Pao2 to 12.1 +/- 1.6 kPa (P less than or equal to 0.001) and increased QSP/QT to 40 +/- 4% (P less than or equal to 0.001). Mean pulmonary artery pressure and airway pressure increased. PAB inflation caused an increase in Pao2 to 19.9 +/- 2.9 kPa (P less than or equal to 0.02) and a decrease in QSP/QT to 27 +/- 6% (P less than or equal to 0.001). PGF2 alpha infusion (1.2 micrograms kg-1 min-1) into the pulmonary artery of the non-ventilated lung increased Pao2 to 22.4 +/- 3.3 kPa (P less than or equal to 0.001) and decreased QSP/QT to 25 +/- 4 (P less than or equal to 0.001). PGF2 alpha infusion resulted in a small increase in mean systemic and pulmonary artery pressures. During the infusion of 1.2 micrograms kg-1 min-1 of PGF2 alpha no signs of bronchoconstriction were observed. PAB inflation and PGF2 alpha infusion were equally effective in improving oxygenation and reducing venous admixture during OLV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nitrous oxide reduces inspired oxygen fraction but does not compromise circulation and oxygenation during hemodilution in pigs

Background: The use of nitrous oxide (N₂O) during hemodilution has been questioned. Nitrous oxide reduces the inspired oxygen fraction (F₁O₂), depresses myocardial function and may reduce cardiac output (CO) and systemic oxygen delivery (DO_2SY). The aim of this study was to evaluate the importance of the effects of nitrous oxide on systemic and myocardial circulation and oxygenation during extreme, acute, normovolemic hemodilution. Methods: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to 65% N₂O before and after extreme isovole-mic hemodilution (hematocrit 33±1% and 10±1%, respectively). Systemic and myocardial hemodynamics, oxygen delivery and consumption and blood lactate were measured before (at FrO₂ 1.0 and 0.35) and during N₂O exposure. Results: Hemodilution caused an increase in CO from 137±43 to 229±32 ml kg^-1 min^-1 (P< 0.01), a decrease in systemic vascular resistance (from 42±14 to 20±4 mmHg L^-1 min^-1, P < 0.05), a decrease in mean arterial blood pressure (from 119±19 to 100±26 mmHg, P<0.05) and a decrease in DO_2SY from 21.1 ±6.9 to 13.7±2.1 ml kg^-1 min^-1 (P < 0.01). Cardiac venous blood flow increased by 135% (P < 0.01) and cardiac venous saturation from 25±6 to 41±5% (P < 0.05). After hemodilution, changing F_IO₂ from 1.0 to 0.35 reduced arterial blood oxygen content from 59.4±3.7 to 52.3±5.1 ml L^-1 (P < 0.01), mixed venous saturation (SvO₂) from 75±9 to 47±7% (P < 0.05) and DO_2SY from 13.7±2.1 to 11.9+2.3 ml kg^-1 - min^-1 (P < 0.05). Dissolved oxygen at F₁O₂=1.0 and F₁O₂=0.35 constituted 25.4±3.1% and 10.1 ±1.5%, respectively, of systemic oxygen delivery after hemodilution, compared with 10.7±1.2% and 3.9±0.5% before hemodilution (P < 0.01). Left ventricular oxygen delivery and consumption were unchanged. Exposure to N₂O did not affect mean arterial blood pressure or systemic vascular resistance before or after hemodilution. After hemodilution during N₂O-exposure, CO and DO_2SY decreased by 9% (P < 0.01 and P < 0.05, respectively), but no changes in SvO₂, systemic oxygen uptake or arterial lactate were observed. The effect of N₂O on myocardial oxygenation was similar before and after hemodilution; cardiac venous blood flow, left ventricular oxygen delivery and uptake decreased, but no animals showed left ventricular lactate production. Conclusion: Nitrous oxide did not compromise systemic and myocardial circulation and oxygenation during acute normovolemic hemodilution in pigs. Possible adverse effects from the use of nitrous oxide during hemodilution seem to be related to a reduced F_IO₂, reducing the safety margin for systemic oxygen delivery.     

High–frequency jet ventilation vs continuous positive airway pressure for differential lung ventilation in patients undergoing resection of thoracoabdominal aortic aneurysm

Twenty patients, scheduled for surgical resection of thoracoabdominal aortic aneurysm were divided into two groups according to the type of differential lung ventilation used during graft replacement of the descending thoracic aorta. In the high–frequency jet ventilation (HFJV) group of ten patients, HFJV was applied to the left lung once collapsed and retracted by the surgeon, the patient lying in the right lateral decubitus and being intubated by a Carlens' tube. In the continuous positive airway pressure (CPAP) group of ten patients, CPAP was applied to the left lung at the same mean airway pressure as HFJV (1 kPa). Before anaesthetic induction, an arterial and a Swan–Ganz catheter were inserted for cardiovascular monitoring. The same anaesthetic technique using fentanyl 6 μg·kg^-1, flunitrazepam 0.02 mg kg^-1 and pancuronium 0.1 mg kg^-1 was used for each patient. Haemodynamic and respiratory measurements were made: 15 min after positioning the patients in the right lateral decubitus using two–lung ventilation; 15 min after collapse and retraction of the left lung using one–lung ventilation and 15 min after using differential lung ventilation with CPAP or HFJV. Left lung collapse with conventional one–lung ventilation induced a dramatic decrease in arterial oxygenation: Pao₂/Fio₂ ratio decreased from 43 6 kPa to 20 8 kPa, alveolo–arterial oxygen difference increased from 24 7 kPa to 72 11 kPa and pulmonary shunt increased from 17 2% to 37 3%. Whereas differential lung ventilation with CPAP did not improve any of the respiratory parameters measured, differential lung ventilation with HFJV, significantly increased Pao₂/Fio₂ ratio to 41 14 kPa. Therefore, since HFJV improves gas exchange without altering the conditions of surgical comfort, different lung ventilation with HFJV appears to be superior to differential lung ventilation with CPAP.     

Unilateral high-frequency jet ventilation during one-lung ventilation for thoracotomy

One-lung ventilation is indicated during thoracic operations for bronchopleural fistula, pulmonary abscess, and pulmonary hemorrhage in spite of the possibility of the development of severe hypoxemia. To evaluate methods for improving oxygen transport during one-lung ventilation, we applied high-frequency jet ventilation (HFJV) and continuous positive airway pressure (CPAP) to the nondependent lung following deflation to atmospheric pressure in each procedure, and measured the effects on cardiac output and arterial oxygenation. In each case, the dependent lung was ventilated with conventional intermittent positive pressure ventilation (IPPV). Eight patients were studied during posterolateral thoracotomy using double-lumen endobronchial tubes. HFJV or CPAP to the nondependent lung improved arterial oxygenation significantly during both closed and open stages of the surgical procedures (p less than 0.008). When the chest was open, HFJV maintained satisfactory cardiac output, whereas CPAP usually decreased cardiac output (p less than 0.008). There were no significant differences in mean partial pressure of arterial carbon dioxide between HFJV, CPAP, and deflation to atmospheric pressure. In conclusion, HFJV to the nondependent lung provides not only satisfactory oxygenation but also good cardiac output, thereby maintaining better oxygen transport than CPAP or deflation to atmospheric pressure, while the dependent lung is ventilated with IPPV during one-lung ventilation for thoracotomy.     

The effects of increasing concentrations of isoflurane and desflurane on pulmonary perfusion and systemic oxygenation during one-lung ventilation in pigs.

During one-lung ventilation (OLV), hypoxic pulmonary vasoconstriction (HPV) reduces venous admixture and attenuates the decrease in arterial oxygen tension by diverting blood from the nonventilated lung to the ventilated lung. In vitro, desflurane and isoflurane depress HPV in a dose-dependent manner. Accordingly, we studied the effects of increasing concentrations of desflurane and isoflurane on pulmonary perfusion, shunt fraction, and PaO(2) during OLV in vivo. Fourteen pigs (30-42 kg) were anesthetized, tracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a left-sided double-lumen tube (DLT) was placed via tracheotomy. After DLT placement, FIO(2) was adjusted at 0.8 and anesthesia was continued in random order with 3 concentrations (0.5, 1.0, and 1.5 minimal alveolar concentrations) of either desflurane or isoflurane. Differential lung perfusion was measured with colored microspheres. All measurements were made after stabilization at each concentration. Whereas mixed venous PO(2), mean arterial pressure, cardiac output, nonventilated lung perfusion, and shunt fraction decreased in a dose-dependent manner, PaO(2) remained unchanged with increasing concentrations of desflurane and isoflurane during OLV. In conclusion, increasing concentration of desflurane and isoflurane did not impair oxygenation during OLV in pigs. IMPLICATIONS: In an animal model of one-lung ventilation, increasing concentrations of desflurane and isoflurane dose-dependently decreased shunt fraction and perfusion of the nonventilated lung and did not impair oxygenation. The decreases in shunt fraction are likely the result of anesthetic-induced marked decreases in cardiac output and mixed venous saturation.     

Continuous Flow Apneic Ventilation

A study was designed to evaluate the adequacy of gas exchange during continuous flow apneic ventilation (CFAV) in dogs. Seventeen dogs (average weight 22.9 kg) were divided into three experimental groups. Group I (n = 7) was anesthetized, paralyzed and ventilated with air using intermittent positive pressure ventilation (IPPV) through a tracheal tube. The tube was removed and each main stem bronchus was cannulated with a 2.5 mm i.d., 4 mm o.d. polyethylene catheter using a fiberoptic bronchoscope. The tracheal tube was replaced to hold the catheters in place. Heated, humidified air was continuously delivered equally to each catheter. Total flows ranged from 8 to 28 1/min (0.4—1.4 1 + kg^-1 min-^-1). Airway pressure (P_aw) in the trachea did not exceed 2 mmHg (0.27 kPa). Adequate gas exchange in terms of arterial oxygen and arterial carbon dioxide tension (Pao₂ and Paco₂) was found after 30 min at flows greater than 16 l · min_-1. Group II (n = 7) was managed similarly to the first group, insufflating endobronchial air using the optimal flow of 1.0 1 · kg ¹ · min^-1 obtained from Group I. CFAV continued for 5 h in all animals. Blood gas samples and measurements of systemic blood pressure, heart rate (HR), pulmonary artery blood pressure, pulmonary artery wedge pressure, cardiac output (Qt), and temperature were taken every 30 min. Group III (n = 3) was anesthetized similarly to the other groups. Pulmonary gas distribution was evaluated in relation to catheter placement using Xe¹³³. Results showed significant differences between Paoj values during CFAV and IPPV; however, all animals were adequately oxygenated. During 5 h of CFAV, adequate CO₂ elimination was achieved in all animals. There was no difference in PaO₂, Paco₂ and shunt fraction (Qs/C}t) with CFAV at 30 min and 5 h. Differences in HR, Qt, and systemic vascular resistance at 30 min and 5 h were related to the hypothermia during the developing course of experimentation. With the catheters above the carina, gas distribution studies demonstrated gas limited to the large airways with no peripheral distribution, resulting in low Pao₂ levels and elevated Paco₂ levels. Endobronchial catheters permitted gas distribution to the peripheral airways, and oxygenation and ventilation were normal.     

Sevoflurane anaesthesia for one-lung ventilation with PEEP to the dependent lung in sheep: effects on right ventricular function and oxygenation

This study was undertaken to examine the effect of sevoflurane on right ventricular junction, the safety of sevoflurane for onelung ventilation and the effects of PEEP (positive end-expiratory pressure) to the dependent lung in this model using 12 openchest sheep. Haemodynamic variables, including cardiac output, mean arterial blood pressure, right ventricular pressure and pulmonary arterial pressure, and right ventricular segment shortening (sonomicrometry) were measured. First, animals received 2.0, 3.0 or 4.0% sevoflurane for 20 min each, respectively, during two-lung ventilation to measure the dose-dependent haemodynamic effects of sevoflurane. Then one-lung ventilation was performed with a randomized sequence of 0 (ZEEP), 5 and 10 cm H₂O PEEP to the dependent lung under 2.0% sevoflurane anaesthesia after one-hour stabilization. A decrease in systolic segment shortening along with increases in both the end-diastolic and end-systolic lengths of the right ventricle were observed at 3.0 and 4.0% sevoflurane, while global right ventricular function remained substantially unchanged during twolung ventilation. During one-lung ventilation the PaO₂ was greater with 5 cm H₂O PEEP 198 mmHg (± 25 SEM) than with ZEEP 138 mmHg (± 22) or with 10 cm H₂O PEEP 153 mmHg (± 23) (P < 0.05). No differences in haemodynamic variables or segment shortening between ZEEP and PEEPs during one-lung ventilation were observed. We conclude that although sevoflurane causes a dose-dependent depression of right ventricular function, sevoflurane anaesthesia can be safely applied to one-lung ventilation, and that 5 cm H₂O PEEP to the dependent lung can improve arterial oxygenation without causing changes in right ventricular function.     

The effects of amrinone and calcium chloride on pulmonary vasculature and biventricular function in ethchlorvynol-induced lung injury in sheep

The effects of amrinone and CaCl₂ on pulmonary vasculature and biventricular function in sheep with acute lung injury (ALI) were studied. Seven sheep were ventilated with a tidal volume of 10–12 ml.kg^-1 with end-tidal C0₂ of 40 ± 5 mmHg (5.3 ± 0.7 kPa) after acute lung injury was induced with up to 30 mg kg^-1 of ethchlorvynol (ECV). Biventricular function and hemodynamic profiles were estimated with a rapid computerized thermodilution method and modified pulmonary artery catheters after acute lung injury, following a loading dose (1 mg kg^-1) and maintenance dose (5 μg kg^-1 min-1 ) of amrinone and after a bolus dose of CaCl₂ (20 mg kg^-1). ECV successfully induced acute lung damage in sheep, causing significant increases in pulmonary artery pressure (PAP) and pulmonary vascular resistance index (PVRI). Amrinone reversed the unfavorable changes induced by ECV, significantly reducing PAP, PVRI and left ventricular end-diastolic volume (LVEDV). CaCl₂, however, reversed the effect of amrinone and increased PAP, PVRI, and LVEDV but decreased left ventricular ejection fraction.     

Comparative study on the cardio-respiratory change during prostaglandin E1-induced hypotension in the patients in the supine and prone position

Prostaglandin E₁-induced hypotension (25% reduction from the preadministration level in mean arterial pressure) was applied to thirteen patients. Eight patients among them were operated in the supine position (group I) and other five in the prone position (group II). The maintenance dose of PGE₁ was considerably lower in group II than in group I (0.067µg·kg^–1·min^–1 vs. 0.119µg·kg^–1·min^–1). In group I, there was a significant increase in CI, with a significant decrease in SVRI and PVRI during PGE₁-induced hypotension. Such a high dose of PGE₁ (0.119µg·kg^–1·min^–1) was considered to have a direct dilating action on the systemic resistance bed as well as on the pulmonary vasculature. It was considered that the suppression of hypoxic pulmonary vasoconstriction could be a mechanism to increase venous admixture during PGE₁-induced hypotension. In group II, there was no significant increase in CI, and no significant decrease in SVRI and PVRI. PGE₁-induced hypotension can be safely applied to the anesthetized patients, but we should be careful to apply it to the patients in the prone position, because lower dose of PGE₁ can induce severe hypotension, which is not accompanied by the increase in CI as occures in the patients in the supine position.(Hirose M, Yoda K, Sakai K, et al.: Comparative Study on the cardio-respiratory change during prostaglandin E₁-induced hypotention in the patients in the supine and prone position. J Anesth 5: 30–35, 1991)     

Effect of low-dose infusion of prostaglandin E1 on vecuronium-induced neuromuscular blockade

The effect of low-dose (20 ng·kg⁻¹·min⁻¹) infusion of prostaglandin E₁ (PGE₁) on vecuronium-induced neuromuscular blockade was studied. The study population consisted of 24 elderly patients (65–75 years old) and 24 younger adult patients (25–56 years old). They were randomly assigned to the control and PGE₁ groups. The steady-state dose requirement (SSDR) of vecuronium was derived from ondemand infusion of the drug which produced a stable twitch height of 20% of its baseline reading, and recovery time after steady-state infusion was defined as the time for recovery from twitch height from 25% to 75%. The patients in the PGE₁ group received an infusion of PGE₁ 20 ng·kg⁻¹·min⁻¹, while those in the control group received an infusion of normal saline. The SSDR (23.2±9.1 and 34.2±5.9 μg·kg⁻¹. hr⁻¹, respectively;P=0.02) was significantly less and the recovery time (35.0±9.5 and 19.9±4.2 min, respectively;P=0.01) was significantly longer in the elderly than in the younger patients. However, low-dose infusion of PGE₁ significantly increased the SSDR (23.2±9.1 to 37.4±3.7 μg· kg⁻¹·hr⁻¹;P=0.01) and shortened the recovery time (35.0±9.5 to 23.5±4.0 min;P=0.02) in elderly patients. We concluded that low-dose infusion of PGE₁ is effective in preventing the prolonged action of vecuronium in elderly patients.     

Prostaglandin E1 attenuates the hypertensive response to tracheal extubation

Purpose

Tracheal extubation causes hypertension and tachycardia, which may cause imbalance between myocardial oxygen demand and supply in patients at risk of coronary artery disease. We conducted a randomized, controlled study to evaluate the effects of 0.05 or 0.1 μg · kg^?1 · min^?1 prostaglandin E₁, (PGE₁) iv on haemodynamic variables occurring during tracheal extubation and emergence from anaesthesia and compared them in patients receiving either lidocaine or saline.

Methods

Eighty ASA physical status I patients undergoing elective surgery were enrolled in the current study. Anaesthesia was maintained with sevoflurane 1.0%–2.5% (ET concentration) and nitrous oxide 60% in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to receive one of four treatments (n = 20 each): saline (control), 0.05 μg · kg^?1 · min^?1 PGE₁, 0.1 μg · kg^?1 · min^?1 PGE₁, or 1 mg · kg^?1 lidocaine. PGE₁ was infused from completion of surgery until five minutes after tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation.

Results

In the control group, the HR, systolic BP, and diastolic BP increased during tracheal extubation. Administration of 0.1 μg · kg^?1 · min^?1 PGE₁ and 1 mg · kg^?1 lidocaine attenuated the increases in BP although 0.05μg · kg^?1 · min^?1 PGE₁ failed to do so. The inhibitory effect of the 0.1 μg · kg^?1 · min^?1 PGE₁ on BP was similar to that of lidocaine 1 mg · kg^?1 iv. The increase in HR was attenuated by lidocaine but not by PGE₁.

Conclusion

The intravenous infusion of 0.1 μg · kg^?1 · min^?1 PGE₁ given during emergence from anaesthesia and tracheal extubation is a useful method for attenuating the hypertension associated with noxious stimuli during this period.