[Intraoperative indirect monitoring of electrocardiogram].

The electrocardiogram (ECG) is used as a standard monitoring method during anesthesia and operation. But during the operation of severely burnt patients, the electrodes for ECG cannot be placed on the ideal points for the standard limb leads. We tried the indirect monitoring of the ECG. We placed the electrodes on the sheet over the operating table, and connected the patient and the electrodes with water. By this way the ECG similar to the standard limb leads could be recorded. This method is useful for the patients, with such diseases as severe burn, severe atopic dermatitis and epidermolysis bullosa hereditaria.

[Amrinone (50 micrograms.kg-1.min-1) does not impair regional myocardial tissue metabolism during the 40%-decrease of left anterior descending coronary flow].

We investigated the effects of amrinone on metabolism of regional myocardial tissue during the 40%-decrease of left anterior descending coronary (LAD) flow in anesthetized dogs. Fourteen adult mongrel dogs weighing 15.4 +/- 5.1 kg were anesthetized with 0.5% isoflurane in 50% oxygen and ventilated mechanically to maintain normocapnia. After thoracotomy, regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode inserted in the myocardium. Electromagnetic blood flow probes were placed around LAD and circumflex artery. A 23-gauge catheter was inserted into a coronary vein which runs along LAD to obtain coronary venous blood for measuring oxygen content, lactate and pyruvate. A variable constrictor was placed distal to the flow-probe. After decreasing LAD flow for 40%, cardiac index (CI) decreased. Systemic venous resistance was decreased and CI was increased by amrinone (50 micrograms.kg-1.min-1) infusion. Myocardial tissue oxygen tension, venous lactate, lactate extraction, lactate-pyruvate ratio and excess lactate were all unchanged by amrinone. In conclusion, amrinone does not impair myocardial aerobic metabolism and increases CI under the stenosis of coronary artery.

[Effects of arterial carbon dioxide (PaCO2 not equal to 60 mmHg) on regional myocardial tissue oxygen tension and metabolism].

We investigated the effects of increased arterial carbon dioxide (PaCO2 not equal to 60 mmHg) on myocardial tissue oxygen tension and metabolism in anesthetized dogs. Ten adult mongrel dogs weighing 15.3 +/- 4.1 kg were anesthetized with 0.5% isoflurane in 50% oxygen and ventilated mechanically to maintain normocapnia. After thoracotomy, regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode inserted in the myocardium. Electromagnetic blood flow probes were applied on the left anterior descending artery and the circumflex artery. A 23-gauge catheter was inserted into a coronary vein to obtain coronary venous blood for measuring oxygen content, lactate and pyruvate. After control normocapnic ventilation, hypercapnia (PaCO2 62.7 +/- 3.2 mmHg) was induced by adding 10% carbon dioxide to the inspired gas for 20 minutes. As a result, the coronary blood flow and myocardial oxygen tension increased during hypercapnia. The myocardial lactate extraction and coronary venous lactate were unchanged and excess lactate was kept below zero, although coronary venous L/P ratio increased during hypercapnia. These results indicate that hypercapnia (PaCO2 not equal to 60 mmHg) increases coronary blood flow and myocardial oxygen tension, while myocardial aerobic metabolism is not impaired under hypercapnia.

[Evaluation of oxygen insufflation to non-ventilated lung during one-lung anesthesia].

To prevent hypoxemia during one-lung anesthesia, we have devised an oxygen insufflation machine which can insufflate oxygen (0.2-10 l.min-1) and apply CPAP (0-30 cmH2O) selectively to the non-ventilated lung. In all the 8 patients, arterial oxygen tension was maintained above 100 mmHg by using this machine, and was increased significantly from 76.2 +/- 11.2 mmHg (mean +/- SD) during one-lung anesthesia to 118.9 +/- 25.2 mmHg during the use of this machine. In conclusion, the machine prevents hypoxemia effectively during one-lung anesthesia without hindering surgical manipulations.

[Myocardial metabolism, oxygen demand and oxygen supply during prostaglandin E1 induced hypotension].

The effects of hypotensive anesthesia induced by PGE1 on myocardial metabolism, oxygen demand and oxygen supply were studied. Nine mongrel dogs were anesthetized with pentobarbital and isoflurane. Mean blood pressure (MBP), cardiac output (CO), blood gases (BG), coronary blood flow (CBF), and myocardial tissue oxygen tension (MPO) were measured. Arterial and coronary venous lactate and pyruvate concentrations were also measured. We calculated myocardial oxygen consumption, L/P ratio, excess lactate, oxygen extraction ratio and lactate extraction ratio to estimate the adequacy of myocardial aerobic metabolism. CO and CBF decreased in accordance with MBP depression. Myocardial oxygen consumption decreased significantly with PGE1 administration. Lactate and pyruvate concentrations, L/P ratio, excess lactate and myocardial tissue oxygen tension were unchanged. These results suggest that PGE1 exerts no significant effect on myocardial metabolism during hypotensive anesthesia.

[The effects of adenosine-induced hypotension on myocardial metabolism].

The effects of hypotension induced by adenosine on myocardial metabolism were studied in ten mongrel dogs anesthetized with 0.5% isoflurane. Adenosine was infused intravenously to reduce mean arterial blood pressure by approximately 30% during a period of 20 min. Although heart rate was unchanged, cardiac output increased and coronary blood flow increased 3-fold of the preinfusion value. Oxygen tension of the myocardium, and oxygen extraction as well as lactate extraction of the myocardium decreased. Myocardial oxygen uptake and myocardial lactate uptake were unchanged, but lactate production was observed in three of ten dogs. In addition, coronary venous lactate/pyruvate ratio and excess lactate increased, and excess lactate became positive in five of ten dogs. The results suggest that adenosine-induced hypotension may inhibit the myocardial aerobic metabolism.

[Effect of 10% carbon dioxide on regional myocardial tissue oxygen tension and myocardial metabolism].

We investigated the effects of arterial carbon dioxide tension on myocardial blood flow, tissue oxygen tension and metabolism in the anesthetized dogs. Eighteen adult mongrel dogs weighing 13.4 +/- 3.6 kg were anesthetized with 0.5% isoflurane, intubated and ventilated mechanically with 50% oxygen to maintain normocapnia. Endtidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode inserted to the myocardium. Electromagnetic blood flow probes were applied on the left anterior descending artery and circumflex artery. For cardiac venous blood sampling, a 23G intravenous catheter was inserted into the cardiac veins (great coronary veins) carefully. After normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and hypercapnia was induced by adding 10% carbon dioxide to the inspired gas. The coronary blood flow and myocardial tissue oxygen tension increased during hypercapnia and the myocardial lactate extraction decreased, while excess lactate and cardiac venous L/P ratio increased during hypercapnia. These results indicate that hypercapnia increase coronary flow and myocardial tissue oxygen tension but myocardial aerobic metabolism is impaired during hypercapnia.

[Comparison of standard-dose epinephrine and high-dose epinephrine in cardiopulmonary arrest outside the hospital].

We compared high-dose epinephrine (HDE) with standard-dose epinephrine (SDE) in improving the outcome of resuscitation after out-of-hospital cardiopulmonary arrest. The SDE group received epinephrine 1mg, and the HDE group received epinephrine 5mg respectively every 5 minutes until the return of spontaneous circulation. There were no significant differences between the SDE group and the HDE group in the rate of return of spontaneous circulation, rate of successful resuscitation and neurologic outcome. However, the rate of successful resuscitation tended to be higher in the SDE group. The ineffectiveness of HDE was considered to be due to the existence coronary artery diseases in the majority of patients, or increase in myocardial oxygen demand by the beta 1-adrenergic effects of epinephrine.

Effects of adenosine triphosphate (ATP) on somatosensory evoked potentials in humans anesthetized with isoflurane and nitrous oxide.

In order to examine the usefulness of adenosine triphosphate (ATP) as an adjuvant to anesthesia for surgery requiring intraoperative somatosensory evoked potential (SSEP) monitoring, we have studied the effects of ATP on SSEPs in patients anesthetized with isoflurane and nitrous oxide (N2O). A control recording of SSEP was performed while anesthesia was maintained with 0.5% end-tidal concentration of isoflurane in 60% N2O. The recordings were repeated after an ATP infusion had been added to this basal anesthesia at the rates of 100 micrograms.kg bw-1.min-1 and 200 micrograms.kg bw-1.min-1. SSEP was also studied when end-tidal isoflurane concentration was increased to 1.5% after cessation of ATP infusion. An infusion of ATP combined with 0.5% isoflurane and 60% N2O effectively inhibited an increase in blood pressure during surgery. The amplitude of the cortical component of SSEP was lowered by 1.5% isoflurane, which also increased both cortical and spinal latencies as well as central conduction time (CCT). In contrast ATP infusions at both rates induced no significant changes in latencies, amplitude and CCT. The results indicate that ATP infusion combined with 0.5% isoflurane in 60% N2O can be a useful anesthetic technique for intraoperative SSEP monitoring because adequate anesthetic depth can be maintained by a low concentration of anesthetics without further suppression of SSEPs.

Effects of continuous negative extrathoracic pressure ventilation on left ventricular dimensions and hemodynamics in dogs.

It has been reported that continuous negative extrathoracic pressure ventilation (CNETPV) depresses cardiac output less than continuous positive pressure ventilation (CPPV) does, and this difference may be related to the different effects of two ventilatory modes on preload. We performed simultaneous measurements of hemodynamics and left ventricular short axis dimensions by transesophageal echocardiography (TEE) to evaluate left ventricular preload and function during CNETPV and CPPV in normal dogs. Hemodynamic measurements and simultaneous TEE recording were performed at 5 successive periods; 1) the first control period of intermittent positive pressure ventilation (IPPV1), 2) CNETPV with negative end-expiratory pressure (NEEP) of -10 cmH2O (CNET10), 3) CNETPV with NEEP of -15 cmH2O (CNET15), 4) the second control period of IPPV (IPPV2), and 5) CPPV with PEEP of 15 cmH2O (CPPV15). Left ventricular end-systolic and end-diastolic dimension (LVESD and LVEDD), ejection fraction (EF) and fractional shortening (FS) were measured from TEE recordings. Both CNET10 and CNET15 induced no significant changes in hemodynamics and left ventricular dimensions, compared with those during IPPV1. However, CPPV15 reduced cardiac output and stroke volume (SV) and increased heart rate significantly, compared with IPPV2. CPPV15 significantly decreased LVEDD compared with IPPV2. Neither EF nor FS showed any significant change throughout the experiment. These results indicate that CNETPV preserved cardiac output because it maintained the preload and the left ventricular function.

[Effect of hypotensive anesthesia on tissue oxygen tension of the heart, kidney and liver].

The effects of hypotensive anesthesia by prostaglandin E1 (PGE1: 8 dogs) or trimetaphan (TMP: 8 dogs) on tissue oxygenation were studied in 16 mongrel dogs anesthetized with pentobarbital. Mean blood pressure (MBP), heart rate (HR), cardiac output (CO), blood gases (BG), the blood flow and tissue oxygen tension of the heart, the kidney and the liver were measured. The blood flow and oxygen tension were measured by electromagnetic flowmeters and by polarographic oxygen electrodes respectively. PGE1 or TMP was injected intravenously to decrease MBP by 30%. MBP, CO, HR and BG of PGE1 were not significantly different with those of TMP. Coronary blood flow decreased for 12% with PGE1 and for 33% with TMP. Though blood flows of the renal and the hepatic arteries were well maintained with PGE1, they decreased for 36% and 34% respectively with TMP. Oxygen tensions of the myocardium (both outer and inner layers) and the liver were well maintained with PGE1. But with TMP, oxygen tension decreased for 23% in outer layer, for 16% in inner layer and for 31% in the liver. Oxygen tension of the kidney remained unchanged with PGE1 and TMP. The results suggest that PGE1 is more useful for the maintenance of the tissue oxygenation than TMP during hypotensive anesthesia.

[Effect of carbon dioxide (hypocapnia and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary stenosis].

Carbon dioxide (CO2) has been well documented to act as a potent vasodilator of coronary vessels under normal conditions. But there is little data available on the effect of CO2 on the collateral perfusion of patients with coronary insufficiency. We studied the effects of CO2 on the myocardial tissue PO2 in anesthetized dogs with critical coronary stenosis. Twelve mongrel dogs were anesthetized with pentobarbital and ventilated with 100% O2 to maintain normocapnia. Electromagnetic blood flow (BF) probe was applied on the left anterior descending artery (LAD). Regional myocardial PO2 was measured at two different sites using two pairs of monopolar polarographic needle electrodes; one inserted in the epicardial (EPI) layer, and the other in the endocardial (ENDO) layer. These were placed in the regions supplied by LAD and circumflex. Following the baseline recording, critical stenosis of LAD was produced by adjusting a copper-wire clamp occluder until LADBF was reduced by 50%. After a stable normocapnic ventilation, hypocapnia was produced by hyperventilation. To induce hypercapnia, exogenous CO2 was added to the inspired gas stepwise until end-tidal CO2 fraction reached 10%. Hypocapnia resulted in a significant reduction in myocardial PO2 in both EPI and ENDO non-stenotic areas, while hypercapnia increased these PO2 values dose-dependently. After coronary stenosis, hypocapnia resulted in a small but significant reduction of PO2 in endocardial ischemic area. Hypercapnia did not induce any sign of reduced regional myocardial PO2 or evidence of regional or intramural "steal" phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous negative extrathoracic pressure ventilation, lung water volume, and central blood volume. Studies in dogs with pulmonary edema induced by oleic acid.

The effect of continuous positive-pressure ventilation (CPPV) on extravascular lung water volume has been investigated, but there is only one report which studied the effect of continuous negative extrathoracic pressure ventilation (CNETPV). The effect of CNETPV on central blood volume (CBV) has not been studied. Changes in intrathoracic pressure by CNETPV may alter lung water volume and CBV. In this study the effects of CNETPV on lung water volume and CBV were compared with those of intermittent positive-pressure ventilation (IPPV) and CPPV in dogs with pulmonary edema induced by oleic acid. Nine mongrel dogs were anesthetized and given oleic acid at 0.06 ml/kg intravenously to induce pulmonary edema; CNETPV was applied with a cuirass and a negative thoracic pressure ventilator (Kimura OKT-100) for 1 h. Extravascular lung water volume (as extravascular thermal volume [EVTV]) and CBV were estimated with the double-indicator dilution method using thermal-sodium; PEEP and continuous negative extrathoracic pressure were matched to produce the same increments in FRC. The EVTV increased during CNETPV but did not change during CPPV. The CBV decreased during CPPV but did not change during CNETPV. An increase of transmural pulmonary microvascular pressure was thought to be one of the reasons for the increase in EVTV with CNETPV.

[Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog].

We investigated the effects of arterial carbon dioxide tension on the myocardial tissue oxygen tensions of subepicardium and subendocardium in the anesthetized dogs. The study was done in fourteen open-chest mongrel dogs, weighing 13 +/- 1 kg, anesthetized with sodium pentobarbital (30 mg.kg-1 iv), and mechanically ventilated with 100% oxygen to maintain normocapnia. End tidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode. Two pairs of combined needle sensors were carefully inserted, one in the epicardial and the other in the endocardial layer of the beating heart. Electromagnetic blood flow probe was applied on the left anterior descending artery (LAD). After a stable normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and this mechanical hyperventilation was kept fixed throughout the experiments. To induce hypercapnia, exogenous carbon dioxide was added to the inspired gas step-wise until FECO2 reached 10%. Hypocapnic hyperventilation (PaCO2: 22 mmHg) invariably resulted in a significant reduction of coronary blood flow (LADBF) and left ventricular myocardial tissue PO2 in both epicardial and endocardial layers, while addition of carbon dioxide to the inspired gas (hypercapnic hyperventilation) reversed the change by increased LADBF and arterial PaCO2 in a dose-dependent manner. These results indicate that injudicious and severe hypocapnic hyperventilation may induce impaired myocardial tissue perfusion and oxygenation although normal cardiac output and arterial blood oxygenation are maintained.

[CO diffusing capacity during continuous negative extra-thoracic pressure].

Eight healthy males were studied to compare CO diffusing capacity (DLCO) during spontaneous breathing with that during continuous negative extra-thoracic pressure (CNETP). Mean DLCO was 33.0 +/- 5.1 ml.min-1.mmHg-1 during spontaneous breathing and 33.5 +/- 4.5 ml.min-1.mmHg-1 during CNETP with an end-expiratory negative extra-thoracic pressure (EENETP) of -20 cmH2O, and there was no significant difference between them (P less than 0.05). Pulmonary capillary blood volume, which was measured only in a male, was 76.7 ml during spontaneous breathing and 80.5 ml during CNETP. This change dose not seem to be significant. The results suggest that the effect of pulmonary diffusing capacity changes during EENETP on improvement of oxygenation may not be significant.

[Is ventilatory anaerobic threshold useful for preoperative assessment?].

The anaerobic threshold (VAT), obtained by measurement of ventilatory volume and by expiratory gas analysis, and the anaerobic threshold (LAT), obtained directly from the lactic acid value in the blood, were compared and evaluated during exercise load in 25 patients with mitral valve disease. Exercise loading was performed with an ergometer using a multistep method of increases of 5 W (Group A, 11 cases) or 10 W (Group B, 14 cases) per minute. The oxygen uptake value at the points of 0.5 mmol.l-1 and 1.0 mmol.l-1 increase in the lactic acid values when compared with the starting values were designated as 0.5 LAT and 1.0 LAT. VAT was found in 4 of 11 (36%) patients in Group A and in 12 of 14 (86%) patients in Group B and the ratio obtained was significantly higher in Group B than in A. The 0.5 LAT values for Group A and B were 2.4 +/- 0.5 and 2.2 +/- 0.3, respectively. The 1.0 LAT values were 2.9 +/- 0.7 and 2.7 +/- 0.4, and among the two groups no significant difference was found concerning 0.5 LAT or 1.0 LAT. VAT was seen in 16 or 25 patients and the average VAT value of the 16 was roughly at the midpoint between the average values for 0.5 LAT and 1.0 LAT. Therefore in patients in which VAT was seen with the expiratory gas method, VAT and LAT values were basically equivalent. However, in Group A, VAT was seen in only 4 of 11 patients and it is a fact that it is difficult to find VAT without a suitable exercise load.

Placental transfer and effects of famotidine on neonates.

The effect of famotidine on neonates was studied in 34 obstetric patients who underwent elective cesarean section. In the famotidine group, 20 mg of famotidine was intramuscularly injected at 60 min before induction of anesthesia, and 0.5 mg of atropine was injected at 30 min before induction. In the control group, only atropine was given. Ratio of famotidine concentration in the umbilical venous blood to that in the maternal venous blood was determined as 0.64 +/- 0.13 (mean +/- SD). No significant differences were noted in the Apgar scores, neonatal gastric acidity, and results of liver function tests between the two groups. No side effect, such as the development of gastrointestinal infections, was observed.

[The ventilatory response to CO2 during end-expiratory negative extra-thoracic pressure and PEEP].

The effects of end-expiratory negative extra-thoracic pressure (EENETP) and PEEP on the ventilatory response to CO2 were studied in seven healthy volunteers. The changes in functional residual capacity during EENETP -20 cmH2O and PEEP 5 cmH2O were 13.9 and 12.9 ml.kg-1, respectively. The slopes of CO2 response (minute ventilation/end-tidal CO2) during ZEEP, EENETP and PEEP were 0.913, 0.622, 0.693 l.min-1.mmHg-1, respectively. The slopes during EENETP and PEEP were significantly decreased. These results indicate that EENETP and PEEP could worsen the CO2 response in patients with respiratory failure, especially, with chronic obstructive pulmonary disease in which functional residual capacity is increased.

[Respiratory flow and chest wall motion during negative extrathoracic pressure ventilation in human volunteers].

Respiratory flow and chest wall motion during negative extrathoracic pressure ventilation (NETPV) were compared with those during spontaneous breathing in 8 healthy male volunteers. Chest wall motion was evaluated by separate measurement of the changes in the cross sectional area of rib cage and abdomen, using respiratory inductive plethysmograph. During NETPV, expiratory flow was characterized by a large peak and a rapid decline at the early expiratory phase. NETPV increased the relative contribution of rib cage motion to tidal ventilation, and induced the abdominal paradoxical movements at inspiration in two volunteers. These results indicate that NETPV augments rib cage motion rather than abdominal motion, and this altered mechanics of chest wall may change intrapulmonary distribution of inspired gas.

[Effects of negative extra-thoracic pressure ventilation on extravascular lung water volume and central blood volume in normal dogs].

In negative extra-thoracic pressure ventilation (NETPV), lung water volume and central blood volume (CBV) could increase because of increased venous return and intensified negative interstitial pressure. The effects of NETPV on the extravascular lung water and CBV were examined in ten normal dogs by the double-indicator method using Na and cold water. The lung water volume measured by the method (EVTV) was compared with the lung water volume measured by the gravimetric method (EVLW) in 17 dogs. EVTV did not show any significant change in any ventilation modes compared with IPPV. CBV decreased from 21.9 ml.kg-1 to 19.2 ml.kg-1 in CPPV compared with IPPV (P less than 0.05). EVTV correlated well (r = 0.91, P less than 0.001) with EVLW. In normal dogs, NETPV did not change the lung water volume and CBV. NETPV dogs do not seem to have any disadvantage in respect of lung water volume compared with conventional positive pressure ventilations.