Preliminary investigations into the effects of breathing retraining techniques on end-tidal carbon dioxide measures in patients with asthma and healthy volunteers during a single treatment session

Physiotherapy ◽  
2007 ◽  
Vol 93 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Anne Bruton ◽  
Mary Armstrong ◽  
Claire Chadwick ◽  
Denise Gibson ◽  
Kate Gahr
Keyword(s):  
Carbon Dioxide ◽  
Healthy Volunteers ◽  
Treatment Session ◽  
Single Treatment ◽  
End Tidal Carbon Dioxide ◽  
Breathing Retraining ◽  
End Tidal ◽  
Single Treatment Session

Phase I Safety Assessment of Intrathecal Neostigmine Methylsulfate in Humans 

1995 ◽  
Vol 82 (2) ◽  
pp. 331-343 ◽  
Author(s):  
David D. Hood ◽  
James C. Eisenach ◽  
Robin Tuttle
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Healthy Volunteers ◽  
Nausea And Vomiting ◽  
Severe Nausea ◽  
End Tidal Carbon Dioxide ◽  
End Tidal ◽  
Ice Water

Background In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. Methods After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. Results Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. Conclusions The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.

Trends in Anesthesia-related Death and Brain Damage

2006 ◽  
Vol 105 (6) ◽  
pp. 1081-1086 ◽  
Author(s):  
Frederick W. Cheney ◽  
Karen L. Posner ◽  
Lorri A. Lee ◽  
Robert A. Caplan ◽  
Karen B. Domino
Keyword(s):  
Carbon Dioxide ◽  
Pulse Oximetry ◽  
Brain Damage ◽  
Adverse Outcomes ◽  
Malpractice Claims ◽  
End Tidal Carbon Dioxide ◽  
Carbon Dioxide Monitoring ◽  
Permanent Brain Damage ◽  
End Tidal ◽  
Closed Claims

Background The authors used the American Society of Anesthesiologists Closed Claims Project database to determine changes in the proportion of claims for death or permanent brain damage over a 26-yr period and to identify factors associated with the observed changes. Methods The Closed Claims Project is a structured evaluation of adverse outcomes from 6,894 closed anesthesia malpractice claims. Trends in the proportion of claims for death or permanent brain damage between 1975 and 2000 were analyzed. Results Claims for death or brain damage decreased between 1975 and 2000 (odds ratio, 0.95 per year; 95% confidence interval, 0.94-0.96; P < 0.01). The overall downward trend did not seem to be affected by the use of pulse oximetry and end-tidal carbon dioxide monitoring, which began in 1986. The use of these monitors increased from 6% in 1985 to 70% in 1989, and thereafter varied from 63% to 83% through the year 2000. During 1986-2000, respiratory damaging events decreased while cardiovascular damaging events increased, so that by 1992, respiratory and cardiovascular damaging events occurred in approximately the same proportion (28%), a trend that continued through 2000. Conclusion The significant decrease in the proportion of claims for death or permanent brain damage from 1975 through 2000 seems to be unrelated to a marked increase in the proportion of claims where pulse oximetry and end-tidal carbon dioxide monitoring were used. After the introduction and use of these monitors, there was a significant reduction in the proportion of respiratory and an increase in the proportion of cardiovascular damaging events responsible for death or permanent brain damage.

Exercise end-tidal carbon dioxide pressure: a new prognostic marker after acute myocardial infarction?

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
J Ferreira ◽  
P Rio ◽  
A Castelo ◽  
I Cardoso ◽  
S Silva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Carbon Dioxide ◽  
Acute Myocardial Infarction ◽  
Prognostic Marker ◽  
Systolic Function ◽  
Prognostic Role ◽  
End Tidal Carbon Dioxide ◽  
Carbon Dioxide Pressure ◽  
End Tidal ◽  
Maximal Effort

Abstract Funding Acknowledgements Type of funding sources: None. Background Although several cardiopulmonary exercise testing (CPET) parameters have already proved to predict prognosis, there is increasing interest in finding variables that do not require maximal effort. End-tidal carbon dioxide pressure (PETCO2), an indirect indicator of cardiac output, is one of such variables. Studies in heart failure populations already suggest its role as a prognostic factor. However, data concerning other populations are still scarce. Purpose To assess the association between exercise PETCO2, cardiac biomarkers and systolic function following acute myocardial infarction (AMI) and to evaluate its potential prognostic role in this population. Methods A retrospective single-centre analysis was conducted including patients who underwent symptom-limited CPET early after AMI. We assessed PETCO2 at baseline (PETCO2-B), at anaerobic threshold (PETCO2-AT) and at peak exercise and calculated the difference between PETCO2-AT and PETCO2-B (PETCO2-difference). We analysed their association with B-natriuretic peptide (BNP), maximal troponin after AMI as well as with left ventricular ejection fraction (LVEF) 1 year after. Results We included 40 patients with a mean age of 56 years (87.5% male), assessed with CPET a median of 3 months after AMI (80% of which were ST-elevation myocardial infarctions). Average respiratory exchange ratio was 1,1 with 48% of patients not reaching maximal effort. Mean PETCO2-AT was 37mmHg, with a mean increase from baseline of 6mmHg (PETCO2-difference). There was a significant positive correlation between all the PETCO2 variables measured and BNP values at time of AMI and on follow-up (best correlation for PETCO2-AT with BNP at AMI hospitalization, r = 0.608, p < 0.001). Maximal troponin was not correlated with PETCO2. Both PETCO2-AT and PETCO2-difference were significantly and positively correlated with LVEF 1-year post-AMI (r = 0.421, p = 0.040 and r = 0.511, p = 0.011, respectively). Conclusion PETCO2-AT and PETCO2-difference are both correlated with BNP, an established prognostic marker, and with medium-term systolic function after AMI, suggesting their potential prognostic role in this population. Further studies with larger samples are required to confirm the results of this pilot study and assess PETCO2 as a definite predictor of prognosis after AMI.

Sign in / Sign up

Export Citation Format

Share Document