Anesthesia advanced circulatory life support

The constellation of advanced cardiac life support (ACLS) events, such as gas embolism, local anesthetic overdose, and spinal bradycardia, in the perioperative setting differs from events in the pre-hospital arena. As a result, modification of traditional ACLS protocols allows for more specific etiology-based resuscitation. Perioperative arrests are both uncommon and heterogeneous and have not been described or studied to the same extent as cardiac arrest in the community. These crises are usually witnessed, frequently anticipated, and involve a rescuer physician with knowledge of the patient's comorbidities and coexisting anesthetic or surgically related pathophysiology. When the health care provider identifies the probable cause of arrest, the practitioner has the ability to initiate medical management rapidly. Recommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community. Adapting ACLS algorithms and considering the differential diagnoses of these perioperative events may prevent cardiac arrest

Induction and decay of short-term heat acclimation

“The original publication is available at www.springerlink.com”. Copyright SpringerThe purpose of this work was to investigate adaptation and decay from short-term (5-day) heat acclimation (STHA). Ten moderately trained males (mean ± SD age 28 ± 7 years; body mass 74.6 ± 4.4 kg; 4.26 ± 0.37 l min−1) underwent heat acclimation (Acc) for 90-min on 5-days consecutively (T a = 39.5°C, 60% RH), under controlled hyperthermia (rectal temperature 38.5°C). Participants completed a heat stress test (HST) 1 week before acclimation (Acc), then on the 2nd and 8th day (1 week) following Acc (T a = 35°C, 60% RH). Seven participants completed HSTs 2 and 3 weeks after Acc. HST consisted of 90-min cycling at 40% peak power output before an incremental performance test. Rectal temperature at rest (37.1 ± 0.4°C) was not lowered by Acc (95% CI −0.3 to 0.2°C), after 90-min exercise (38.6 ± 0.5°C) it reduced 0.3°C (−0.5 to −0.1°C) and remained at this level 1 week later (−0.5 to −0.1°C), but not two (0.1°C −0.4 to 0.5°C; n = 7) or 3 weeks. Similarly, heart rate after 90-min exercise (146 ± 21 b min−1) was reduced (−13: −6 to −20 b min−1) and remained at this level after 1 week (−13: −6 to −20 b min−1) but not two (−9: 6 to −23 b min−1; n = 7) or 3 weeks. Performance (746 s) increased 106 s: 59 to 152 s after Acc and remained higher after one (76 s: 31 to 122) but not two (15 s: −88 to 142 s; n = 7) or 3 weeks. Therefore, STHA (5-day) induced adaptations permitting increased heat loss and this persisted 1 week but not 2 weeks following Acc.Peer reviewe

An ironman triathlon does not lead to a change in body mass in female triathletes

In 16 female nonprofessional Ironman triathletes, body mass, percent body fat, and skeletal muscle mass were determined before and after an Ironman race in order to detect changes. Selected hematological and urinary variables as well as percent total body water were measured in order to quantify a change in hydration status. Body mass, skeletal muscle mass, percent body fat, and percent body water did not change (p > 0.05). Plasma volume increased significantly by 8.1(13.7) % (p < 0.05). The significant increase in plasma volume, plasma urea concentration, and urinary specific gravity after the race was associated with a significant fall in hematocrit and plasma sodium concentration (p < 0.05). In contrast to studies of male Ironman triathletes, we could not detect a decrease in body mass in female Ironman triathletes. The statistically insignificant loss of 0.6 kg in body mass was smaller than reported in studies of male athletes

Myocardial tissue damage in rabbits injected with group A streptococci, types M1 and M22. Role of bacterial immunoglobuhn G-binding surface proteins

Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, Our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG Bps) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IEG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular changes resembling the picture seen in APSGN. In the present study, cardiac tissue material from rabbits injected with GAS was investigated. After 8 or more weeks of intravenous (i.v.) injections, minimal changes were seen in those animals receiving an IgG non-binding GAS strain, type T27, whereas those animals receiving either of two IgG-binding GAS strains, types M1 or M22, developed strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence of streptococcal IgG-binding activity. Our results demonstrate that myocardial tissue changes may be induced in the rabbit by i.v. injection of whole heat-killed GAS of at least two M serotypes. Conceivably, induction of immune complexes by bacterial IqG BPs may lead to myocardial deposition of IgG, in turn triggering a series of events, involving the complement system and proinflammatory cytokines, with resulting tissue damage. Though many virulence factors may be involved in the development of ARF and APSGN, and a given GAS strain will never cause both, our results may suggest a new pathogenetic mechanism common to these two major non-suppurative complications