Tommy Symreng

Intrapleural bupivacaine ν saline after thoracotomy—effects on pain and lung function—a double-blind study

The effects of intrapleural (IP) bupivacaine on pain, morphine requirement, and pulmonary function were evaluated in 15 patients for 24 hours after thoracotomy. An IP catheter was placed during surgery. Patients were randomized in a double-blind fashion to receive 1.5 mg/kg of 0.5% bupivacaine IP or saline on two occasions, eight hours apart. A standard anesthetic with thiopental, oxygen, isoflurane, and nondepolarizing muscle relaxant was given. Pain was evaluated with a visual analog pain score every hour, and forced vital capacity (FVC), forced expiratory volume one second (FEV1), peak expiratory flow (PF), and forced expiratory flow 25% to 75% (FEF) were measured 1, 2, 4, 8, and 24 hours postoperatively as well as before and 30 minutes after each IP injection. Arterial blood gases were sampled 1, 2, 8, and 24 hours postoperatively. Plasma bupivacaine concentrations were measured in 10 patients 5, 10, 20, 30, 60, 120, and 180 minutes after IP injection. With each IP bupivacaine injection, the pain score and morphine requirement decreased. There was a significant improvement in all pulmonary function tests in the patients receiving bupivacaine, but no change in the saline controls. The analgesic effect was shortlived (two to five hours), possibly because of loss of bupivacaine in the chest drains. No differences were seen between the two groups after the effect of IP bupivacaine had worn off. Plasma bupivacaine levels had a Cmax of 0.44 to 1.50 micrograms/mL, with a Tmax at 5 to 30 minutes with levels well below 2 to 4 micrograms/mL where increasing toxicity is seen.

Reliability of capnography in identifying esophageal intubation with carbonated beverage or antacid in the stomach

To evaluate the reliability of capnography in identifying esophageal intubation in the presence of a carbonated beverage in the stomach, we first investigated the amount of CO2 released from different carbonated beverages and antacids in a simulated stomach; next we measured the end-expired CO2 level during esophageal ventilation with a carbonated beverage in the stomachs of six swine. CO2 levels of approximately 20% were consistently observed in all carbonated beverages. The CO2 levels obtained with sodium bicarbonate, Maalox, and sodium citrate were 19.3%, 2.0%, and 0%, respectively. CO2 waveforms were observed during esophageal ventilation in five of six animals after intragastric administration of a carbonated beverage. An end-expired CO2 level of 2.5% or more was observed in two swine. The highest end-expired CO2 level measured was 5.3%. We conclude that although capnography is convenient and effective, it lacks all the attributes of an ideal monitor for detecting esophageal intubation.

Inconsistent esophageal doppler cardiac output during acute blood loss

Application of the Doppler principle can provide relatively noninvasive and continuous measurement of cardiac output. However, it is based on certain assumptions that may introduce error. Esophageal Doppler cardiac output was compared with Fick cardiac output during acute blood loss (35-45% estimated blood volume) in eight anesthetized pigs. Mean Fick cardiac output decreased from 4.8 to 1.9 l/min, mean Doppler cardiac output from 4.9 to 2.9 l/min. This was accompanied by a decrease in mean arterial pressure from 119 to 55 mmHg and increase in heart rate from a mean of 115 to 156 beats/min. There was an inconsistent association between the two methods both within and between individual animals. Cubic polynomial regression equations of cardiac output with time indicated small measurement error in Fick (R2: mean 0.93, range 0.99-0.75) as opposed to Doppler (R2: mean 0.67, range 0.93-0.16) cardiac output. In one animal Doppler cardiac output showed an increase with time and in one the Doppler cardiac output measurements were unrelated to time. There was highly variable association comparing Fick versus Doppler cardiac output with correlations ranging from -0.76 to 0.98. A sign test for mean differences indicated that Doppler derived cardiac output was higher than Fick cardiac output, and the chance of this occurring if the true difference was zero was less than 1 in 1,000. A test for homogeneity of correlations was also rejected. Inaccuracies in individual assumptions in the computation of esophageal Doppler cardiac output, especially unaccounted changes in aortic diameter, are responsible for the inconsistent and unpredictable values of Doppler cardiac output obtained in this experimental model of hemorrhage.

Measurement of right atrial oxygen saturation by fiberoptic oximetry accurately reflects mixed venous oxygen saturation in swine.

Continuous fiberoptic measurement of mixed venous oxygen saturation (SvO2) via a pulmonary artery catheter is a useful, though invasive, monitoring technique. Continuous right atrial venous oxygen saturation measurement by oximetry offers the potential of a significantly less invasive SvO2 measurement. However, catheter motion, character of the vessel, chamber wall reflection, the filtering technique involved in calculating oxygen saturation, and the streaming of venous blood prior to ventricular mixing may influence the feasibility of continuous right atrial (RA) SvO2 measurement. This study investigated the performance of fiberoptically measured RA SvO2, at a position 2 cm from the tricuspid valve, relative to simultaneously measured pulmonary artery (PA) SvO2. Ten pigs were subjected to circulatory shock or chemically induced lung damage. Over a total monitoring period of approximately 40 hours, 464 paired data points were sampled at 5-minute intervals. The difference between the overall means of RA and PA SvO2 was 0.91% with a standard error of the estimate of 4.7%, a regression equation of RA SvO2=PA SvO2 (0.94 + 2.1) PA So2, and a correlation coefficient of 0.94. Our conclusion, although extrapolated from a pig model, is that fiberoptic SvO2 monitoring may be accomplished less invasively and at a lower cost with a right atrial catheter.

Local Anesthesia and Regional Blockade

If you do not have a sound knowledge of regional anesthesia, this book, which provides new facts and ideas essential for a fresh approach to the best possible use of local anesthetics and regional techniques, will be difficult to read. In the first two chapters, which discuss chemistry, pharmacology, and tissue uptake of local anesthetics and opioids, the need for considerable previous knowledge becomes evident. Carbonation and mixtures of local anesthetics, as well as addition of vasoconstrictors, mgcromolecules, and sustained release formulas for manipulation of the length of blockade are discussed. Lung uptake of endogenous substances and exogenous drugs such as local anesthetics is described very nicely. This buffer probably protects us from acute toxic reactions in connection with inadvertent intervascular injection of local anesthetics. Dr. Lofstr6m provides a superb discussion of the effect

Stable and reproducible porcine model of acute lung injury induced by oleic acid

of local anesthetics on circulation and respiration and clegrly distinguishes effects on smooth muscle, arterial versus venous, splanchnic circulatory, and central nervous system. The discussion about respiration is brief, but includes the increased response to carbon dioxide caused by local anesthetics, and, more important, the decreased response to hypoxemia with combinations of analgetics and local anesthetics. There is a good review of central nervous system and cardiovascular toxicity of local anesthetic agents, a review that is clear in its comparisons of different local anesthetic agents, and there is also a review of recent work on nerve toxicity of local anesthetics. Pathogenesis is divided into mechanical, toxic, and ischemic trauma. This part on peripheral nerves is very well written, but somewhat brief on spinal toxicity. The anatomy of the lumbar epidural subarachnoid spaces is nicely described, with epiduroscopy and spinaloscopy. Anatomic explanations are given for many daily clinical problems. This part is short, clear, very new, and exciting. Sensory and sympathetic block in connection with intraand extradural analgesia is something we all thought that we understood fairly well. Dr. Bengtsson describe? methods for estimation of spread and the factors of importance for spread and duration that cannot be controlled, such as age, weight, and height, as well as the controllable factors of volume, dose, gravity, choice of agent, vasoconstrictor, and injection technique. He also describes the resulting sympathetic blockade, which often is only partial and may even be considerably below the sensory level. Unfortunately, this review is somewhat confusing due to the high number of contradictory results presented. Additionally, the epidural portion is too brief. Motor blockade and bladder function during spinal anesthesia are described. Bromage scale and more recently introduced quantitative isometric muscle strength measurements are compared. Here one finds a very good review of recent studies on motor block compared to sensory block in intradural analgesia. The description of regression compared to modified Bromage scale is interesting and clinically valuable. There are several good clinical comments and recommendations, but the epidural part is brief and not up-to-date, e.g., it is still discussing the use of 0.75% bupivacaine for extensive epidural blocks. An extensive review of the effects of obstetric regional anesthesia on placental blood flow is given. Effects of local anesthetics and epidural anesthesia on coagulation, hemodynamics, fibrinolysis leading to decreased thrombosis, and pulmonary embolism are reviewed. Both these contributions are clear and clinically oriented. The description of the effects of general anesthesia with depression of the immune defense as opposed to regional anesthesia with a lack of immune depression is interesting, but its clinical importance is not yet fully understood. The literature on spinal opiates is growing rapidly, and the pharmacokinetic aspects of this issue are discussed thoroughly. Clinical aspects are described clearly but somewhat superficially. The effect of neuroblockade on trauma and stress response is described in an informative but perhaps somewhat superficial chapter. The authors do make the important distinction between pain relief and block of stress response. The psychological aspects of regional anesthesia are discussed by an experienced anesthesiologist, but there is a conspicuous lack of documentation of the different comments. Music of patients’ own selection might not be the best; white sound or soft music is better according to some reports. The dose recommendation of fentanyl on page 276 must be a typo and should be 0.05-0.1 mg, not “0.5-0.1 mg.” There is a nice presentation of results regarding anes-

Accuracy of the FEF CO2 detector in the assessment of endotracheal tube placement

Background and Methods.Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (Sao2) and arterial oxygen saturation (Sao2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. Results.During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, Sao2, and Svo2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in Sao2, Svo2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables.Conclusion: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion. (Crit Care Med 1991; 19:405)

Continuous, in vivo pulmonary venous admixture from fiberoptically measured hemoglobin saturations.

The sensitivity and reliability of the FEF end-tidal CO2 detector were investigated for its suitability in the assessment of correct placement of an endotracheal tube. Sensitivity was determined by having eight blinded volunteers observe the color change in the FEF detector with the administration of different volumes and varying CO2 concentrations of gas mixture. The color change in the FEF detector was also assessed during esophageal ventilations before and after administration of carbonated beverage into the stomach of swine and during cardiopulmonary resuscitation in swine. An interpersonal variation was present among the blinded observers during the color-matching process. Different colors were observed with the same volume and CO2 concentration of gas mixture. During esophageal ventilations before or after the administration of carbonated beverage, the FEF detector was neither accurate nor rapid in identifying esophageal placement of the endotracheal tube. The “C” color was displayed during the initial six ventilations in one swine, and esophageal intubation would have been missed. The FEF detector could (by displaying a “C” color) identify one of six correctly intubated swine during cardiopulmonary resuscitation. In conclusion, the FEF CO2 detector does not have the characteristics to reliably assess the correct placement of an endotracheal tube.

Reduced venous admixture in hemorrhagic hypovolemia: maintenance of arterial oxygenation by selective pulmonary vascular collapse

In six anesthetized swine, pulmonary venous admixture (Qsp/Qt) was calculated by four methods: a) Qsp/Qt 1, fiberoptically measured arterial and mixed venous Hgb saturation (SaO2 and SvO2), PaO2 and PvO2 derived from saturations; b) Qsp/Qt 2, fiberoptically measured SaO2 and SvO2, PaO2 and PvO2 measured by blood gas analysis; c) Qsp/Qt 3, PaO2 and PvO2 measured by blood gas analysis, SaO2 and SvO2 derived from tensions; d) Qsp/Qt 4, SaO2 and SvO2 measured by bench oximetry, PaO2 and PvO2 derived from saturations. Input from the fiberoptic catheters was fed into a computer programmed to calculate Qsp/Qt 1 every 20 sec. Fifty-eight of these values were compared with simultaneously calculated Qsp/Qt 2, 3, and 4. There was no difference between fiberoptic and derived SaO2 or fiberoptic and cooximetric SvO2. Correlations and slopes for Qsp/Qt 1 with Qsp/Qt 2, 3, and 4 were significant (p less than .05). Comparing mean differences, Qsp/Qt 1 was significantly different only from Qsp/Qt 3 (p less than .01). We conclude that dual oximetry reliably tracks Qsp/Qt.

Ventilatory and metabolic changes during high efficiency hemodialysis.

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p < .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p < .05) and an increase in mean VD/VT from 0.39 to 0.54 (p < .05). Arterial Hgb saturation (Sao2) increased from 88 ± 7% to 90 ± 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p < .001). VD/VT had an inverse correlation with cardiac output (r = −.90), MAP (r = −.82), Qsp/Qt (r = −.83), MPAP (r = −.77), and Svo2 (r = −.92, p < .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios. (Crit Care Med 1990; 18:208)