Anesthesia and analgesia
-
Anesthesia and analgesia · May 1999
Which countries publish in important anesthesia and critical care journals?
Using a MEDLINE-based analysis, we studied the national origin of articles published in important anesthesia, pain, critical care, and emergency medicine journals. All journals in English listed in the Science Citation Index (SCI) of Journal Citation Reports under the subheadings Anesthesiology (n = 17) and Emergency Medicine & Critical Care (n = 13) were analyzed with the help of MEDLINE. Issues from 1996 and 1997 were included and summarized. Letters, abstracts, editorials, meeting reports, and news were not included. MEDLINE printouts were studied, and we classified the country of origin of the first author. The following subsets were defined: Anesthesia, Regional Anesthesia and Pain, Clinical Monitoring and Computing, Intensive Care Medicine and Resuscitation, and Emergency Medicine and Trauma. A total of 10,643 publications in 30 journals were published during 1996 and 1997. Of the 30 journals, 17 originate in the United States (US) and 8 from United Kingdom (UK). In 14 of the 17 US journals, >50% of the publications came from the US. The US was the most active nation, with a total of 4,283 articles (40.2% of all contributions), followed by the UK with 1,418 articles (13.3%). When looking at the number of publications with regard to inhabitants or impact factor per million inhabitants, small highly industrialized nations (Finland 35.41 and Sweden 33.9 articles/million inhabitants) were significantly more active than large highly industrialized countries (US 16.2, Germany 6.1, Japan 4.5 articles/million inhabitants). It is presumed that indicators of productivity in medical research are the number of articles published and the cumulative impact factor. During 1996 and 1997, the US was the most active nation with regard to publications in important journals in the areas of anesthesia, pain, critical care, and emergency medicine. Small highly industrialized nations, however, had a higher activity rate than larger countries. ⋯ In a MEDLINE-based analysis, we examined the number of publications in important anesthesia, pain, critical care, and emergency medicine journals (n = 30) for the years 1996 and 1997 and analyzed these with regard to national origin. The United States was by far the most active nation in this medical area (4283 articles [40.2%]), followed by the United Kingdom (13.3%). With regard to publications per million inhabitants, small highly industrialized nations contributed overproportionally to publications in this area.
-
Anesthesia and analgesia · May 1999
Small-dose inhaled nitric oxide attenuates hemodynamic changes after pulmonary air embolism in dogs.
Inhaled nitric oxide (NO) has been used to treat pulmonary hypertension. Experimental studies have suggested therapeutic effects of NO after pulmonary microembolism. We evaluated the protective effects of NO in dogs during a pulmonary air embolism (PAE). NO (3 ppm) was administered to six anesthetized mongrel dogs (NO group) but not to the seven dogs in the control group. After 20 min, each dog received a venous air injection of 2.5 mL/kg. Hemodynamic evaluation was performed, and blood samples were drawn for blood gas analysis before and after NO inhalation and 5-60 min after the PAE. Both arterial blood pressure and cardiac output were decreased in the control group for >15 min after PAE, whereas NO-treated animals showed only transient hypotension. NO attenuated the pulmonary hypertension after PAE, as demonstrated by small (P < 0.05) increases in pulmonary artery pressure and pulmonary vascular resistance index in NO-treated animals (90% and 135%, respectively) compared with the controls (196% and 282%, respectively). These hemodynamic effects of NO were associated with higher mixed venous O2 tensions and saturations in the NO group compared with the controls. We conclude that small-dose NO (3 ppm) attenuated the hemodynamic changes induced by PAE in dogs. This protective effect of NO on hemodynamics is not accompanied by improvement in pulmonary oxygenation in this setting. ⋯ In this study, we evaluated the protective effects of inhaled nitric oxide in a pulmonary air embolism setting. Nitric oxide attenuated the hemodynamic changes induced by pulmonary air embolism without improving pulmonary oxygenation.
-
Anesthesia and analgesia · May 1999
Blood pressure is maintained despite profound myocardial depression during acute bupivacaine overdose in pigs.
Bupivacaine-induced cardiovascular collapse is a feared complication because of the difficulty in restoring stable circulation (1). Early recognition is important so that the injection of bupivacaine can be discontinued. We used an animal model of near-cardiac arrest from bupivacaine infusion to identify the sequence of hemodynamic events that precedes bupivacaine-induced cardiovascular collapse. Twelve pigs (23-25 kg) were sedated with ketamine and anesthetized with halothane. Arterial blood pressure and cardiac output were measured. Bupivacaine (3.75 mg/mL) was administered at a rate of 5.73 mL/min (approximately 1 mg x kg(-1) x min(-1)) through a central venous catheter until severe ventricular arrhythmia occurred. Blood pressure and heart rate were unchanged, but cardiac output decreased by 40% with increasing doses of bupivacaine. Calculated peripheral resistance increased by 54%. The QRS complex of the surface electrocardiogram widened, and the R-wave amplitude decreased 80%, together with the decrease in cardiac output. T-wave amplitude increased initially but returned toward baseline at the largest bupivacaine doses. The plasma concentration of bupivacaine after the infusion was 16+/-6.8 microg/mL. ⋯ The increase in vascular resistance that accompanies acute bupivacaine overdose maintains blood pressure but masks severe myocardial depression.