Desflurane-mediated Neurocirculatory Activation in Humans

1996 ◽  
Vol 84 (5) ◽  
pp. 1035-1042 ◽  
Author(s):  
Michael Muzi ◽  
Craig W. Lopatka ◽  
Thomas J. Ebert
Keyword(s):  
Blood Pressure ◽  
Threshold Concentration ◽  
Rate Of Change ◽  
Measured Variable ◽  
Mechanically Ventilated ◽  
Institutional Review ◽  
Isoflurane Group ◽  
Finite Concentration ◽  
Desflurane Concentration ◽  
End Tidal

Background Rapid increases in the inspired concentration of desflurane have been associated with sympathetic activation, tachycardia, hypertension, and in select cases, myocardial ischemia. The current study examined the effects of the rate of change of the desflurane concentration on the sympathetic and hemodynamic responses to desflurane and sought to determine whether a finite concentration (end-tidal) of desflurane consistently initiated these responses. Methods After Institutional Review Board approval, 23 healthy male volunteers were instrumented for electrocardiogram (heart rate (HR)), intraarterial blood pressure, and peroneal nerve microneurography (sympathetic nerve activity (SNA)). Subjects were given propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg), and their lungs were mechanically ventilated for 30 min at a minimum alveolar concentration of 0.5 MAC with either desflurane or isoflurane (random assignment). The end-tidal concentration was increased at either 1% per min (n = 7) or 0.5% per min (n = 7) for desflurane or 0.16% per min (n = 9) for isoflurane (MAC-multiple comparable to 1% per min desflurane group) until 1.5 MAC was reached. HR, blood pressure, and SNA were averaged over 1-min segments from 0.5 to 1.5 MAC levels. Results Awake neurocirculatory variables did not differ among the three groups. At 0.5 MAC, blood pressure had decreased (12-15%) and HR increased (12-20%) similarly in both groups. SNA decreased 77% in the isoflurane group but was not significantly changed in the desflurane groups. In the desflurane groups, the threshold (end-tidal concentration associated with a 10% increase in the measured variable) ranged between 4% and 10% for HR and between 4% and 7.7% for SNA. In the isoflurane group, the threshold occurred between 1.0% and 1.6% for HR and between 0.7% and 1.3% for SNA. The rate of change did not affect the threshold concentration or the peak HR increase in the desflurane groups. In contrast, SNA responses to desflurane were directly proportional to the rate of change. Conclusion There was no consistent threshold for the neurocirculatory activation associated with desflurane, and the HR and SNA thresholds generally were less than 1 MAC. The HR increase associated with desflurane was not rate- or concentration-dependent. In contrast, SNA responses were proportional to the rate of change and the concentration of desflurane.

Rapid 1 % Increases of End-tidal Desflurane Concentration to Greater Than 5% Transiently Increase Heart Rate and Blood Pressure in Humans

1994 ◽  
Vol 81 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Mark A. Moore ◽  
Richard B. Weiskopf ◽  
Edmond I. Eger ◽  
Mimi Noorani ◽  
Lawrence McKay ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Increase Heart Rate ◽  
Desflurane Concentration ◽  
End Tidal

scholarly journals Isoflurane-induced Neuroapoptosis in the Neonatal Rhesus Macaque Brain

2010 ◽  
Vol 112 (4) ◽  
pp. 834-841 ◽  
Author(s):  
Ansgar M. Brambrink ◽  
Alex S. Evers ◽  
Michael S. Avidan ◽  
Nuri B. Farber ◽  
Derek J. Smith ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Rhesus Macaques ◽  
Fold Increase ◽  
Control Group ◽  
Mechanically Ventilated ◽  
Isoflurane Anesthesia ◽  
Primate Brain ◽  
Isoflurane Group ◽  
End Tidal ◽  
Human Primate

Background Brief isoflurane anesthesia induces neuroapoptosis in the developing rodent brain, but susceptibility of non-human primates to the apoptogenic action of isoflurane has not been studied. Therefore, we exposed postnatal day 6 (P6) rhesus macaques to a surgical plane of isoflurane anesthesia for 5 h, and studied the brains 3 h later for histopathologic changes. Method With the same intensity of physiologic monitoring typical for human neonatal anesthesia, five P6 rhesus macaques were exposed for 5 h to isoflurane maintained between 0.7 and 1.5 end-tidal Vol% (endotracheally intubated and mechanically ventilated) and five controls were exposed for 5 h to room air without further intervention. Three hours later, the brains were harvested and serially sectioned across the entire forebrain and midbrain, and stained immunohistochemically with antibodies to activated caspase-3 for detection and quantification of apoptotic neurons. Results Quantitative evaluation of brain sections revealed a median of 32.5 (range, 18.0-48.2) apoptotic cells/mm of brain tissue in the isoflurane group and only 2.5 (range, 1.1-5.2) in the control group (difference significant at P = 0.008). Apoptotic neuronal profiles were largely confined to the cerebral cortex. In the control brains, they were sparse and randomly distributed, whereas in the isoflurane brains they were abundant and preferentially concentrated in specific cortical layers and regions. Conclusion The developing non-human primate brain is sensitive to the apoptogenic action of isoflurane and displays a 13-fold increase in neuroapoptosis after 5 h exposure to a surgical plane of isoflurane anesthesia.

scholarly journals The Association Between Arterial Oxygen Level and Outcome in Neurocritically Ill Patients is not Affected by Blood Pressure

2021 ◽  
Author(s):  
Jaana Humaloja ◽  
Markus B. Skrifvars ◽  
Rahul Raj ◽  
Erika Wilkman ◽  
Pirkka T. Pekkarinen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care ◽  
Brain Injury ◽  
Hemodynamic Instability ◽  
Arterial Oxygen ◽  
Admission Diagnosis ◽  
Secondary Brain Injury ◽  
Multivariable Logistic Regression Model ◽  
Mechanically Ventilated ◽  
The Relationship

Abstract Background In neurocritically ill patients, one early mechanism behind secondary brain injury is low systemic blood pressure resulting in inadequate cerebral perfusion and consequent hypoxia. Intuitively, higher partial pressures of arterial oxygen (PaO2) could be protective in case of inadequate cerebral circulation related to hemodynamic instability. Study purpose We examined whether the association between PaO2 and mortality is different in patients with low compared to normal and high mean arterial pressure (MAP) in patients after various types of brain injury. Methods We screened the Finnish Intensive Care Consortium database for mechanically ventilated adult (≥ 18) brain injury patients treated in several tertiary intensive care units (ICUs) between 2003 and 2013. Admission diagnoses included traumatic brain injury, cardiac arrest, subarachnoid and intracranial hemorrhage, and acute ischemic stroke. The primary exposures of interest were PaO2 (recorded in connection with the lowest measured PaO2/fraction of inspired oxygen ratio) and the lowest MAP, recorded during the first 24 h in the ICU. PaO2 was grouped as follows: hypoxemia (< 8.2 kPa, the lowest 10th percentile), normoxemia (8.2–18.3 kPa), and hyperoxemia (> 18.3 kPa, the highest 10th percentile), and MAP was divided into equally sized tertiles (< 60, 60–68, and > 68 mmHg). The primary outcome was 1-year mortality. We tested the association between hyperoxemia, MAP, and mortality with a multivariable logistic regression model, including the PaO2, MAP, and interaction of PaO2*MAP, adjusting for age, admission diagnosis, premorbid physical performance, vasoactive use, intracranial pressure monitoring use, and disease severity. The relationship between predicted 1-year mortality and PaO2 was visualized with locally weighted scatterplot smoothing curves (Loess) for different MAP levels. Results From a total of 8290 patients, 3912 (47%) were dead at 1 year. PaO2 was not an independent predictor of mortality: the odds ratio (OR) for hyperoxemia was 1.16 (95% CI 0.85–1.59) and for hypoxemia 1.24 (95% CI 0.96–1.61) compared to normoxemia. Higher MAP predicted lower mortality: OR for MAP 60–68 mmHg was 0.73 (95% CI 0.64–0.84) and for MAP > 68 mmHg 0.80 (95% CI 0.69–0.92) compared to MAP < 60 mmHg. The interaction term PaO2*MAP was nonsignificant. In Loess visualization, the relationship between PaO2 and predicted mortality appeared similar in all MAP tertiles. Conclusions During the first 24 h of ICU treatment in mechanically ventilated brain injured patients, the association between PaO2 and mortality was not different in patients with low compared to normal MAP.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

scholarly journals General anesthesia in Sapajus nigritus (black capuchin)

2019 ◽  
Vol 47 ◽  
Author(s):  
Pâmela Disarz ◽  
Paula Pancera Adams ◽  
Anderson Luiz De Carvalho ◽  
Stacy Wu ◽  
Camila Lehmckuhl de Lima ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Total Dose ◽  
Physiological State ◽  
Prophylactic Antibiotic ◽  
Orotracheal Intubation ◽  
Anesthetic Induction ◽  
Chemical Restraint ◽  
End Tidal ◽  
Neonatal Tube

Background: The black capuccin (Sapajus nigritus) is one of the most abundant primate specimens in Brazil. Among population control techniques, vasectomy can be used once it maintains the animal's leading behavior in the group through hormonal presence, production of spermatogenic series, and copula. However, due to their escape behavior, agitation, in addition to the impossibility of knowing the physiological state of these animals beforehand, their capture poses a considerable challenge. Thus, chemical restraint is indispensable and the use of effective and safe anesthetic protocols to animal integrity is of paramount importance. In this scenario, the present study aims to report the anesthesia of a black capuccin submitted to vasectomy.Case: A 1-year-old male, 1.1 kg monkey (Sapajus nigritus) was admitted at a Veterinary Hospital after being found on the ground in a natural reserve in the town of Assis Chateaubriand, in the west of Parana State. After clinical evaluation, the patient was submitted to vasectomy as a birth control method, before his return to the natural area, which presented overpopulation of the species. After preanesthetic examinations, the animal was considered healthy, and thus, premedicated with the combination of dexmedetomidine (10 μg/kg) and ketamine (10 mg/kg), intramuscularly. Anesthetic induction with propofol was performed to effect. Laringeal desensitization was achieved with 2% lidocaine (2 mg/kg), which allowed orotracheal intubation through direct visualization. Anesthesia was maintained with 1% isoflurane in a 0.5 oxygen fraction and spontaneous ventilation using a non-rebreathing circuit. The spermatic cord and the skin were desensitized with lidocaine (2 mg/kg). During the procedure, the animal was monitored for pulse oximetry, electrocardiogram, systolic blood pressure, body temperature, end tidal CO2 (ETCO2), and end tidal isoflurane. The animal also received 10 mL/kg/h ringer lactate throughout anesthesia and 30 mg/kg ampiciline as prophylactic antibiotic. After the completion of the surgery, inhalation anesthesia was interrupted and the animal was allowed to wake up.  Discussion: The combination of 10 µg/kg dexmedetomidine and 10 mg/kg ketamine caused intense muscle relaxation and short-term sedation, which lasted 15 min. Protocol was sufficient for veno puncture and pre-oxygenation, but doses should be increased for longer procedures. Although other authors reported physiologic alterations with higher doses of these drugs, such complications were not observed in the present case. The anesthetic induction was smooth, with no excitement or complications. Propofol was infused at 1 mg/10 s, and a total dose of 10 mg/kg was necessary for induction. This rapid infusion rate could have caused the increase in propofol total dose, as described elsewhere. Propofol and local lidocaine allowed orotracheal intubation with a 2.5 mm uncuffed neonatal tube. During surgery, analgesia was achieved with pre surgical local anesthetic and a single bolus of fentanyl during duct deferens manipulation. During anesthesia, heart rate was maintained between 140 and 170 bpm; systolic blood pressure, between 85 and 110 mmHg; respiratory rate, between 30 and 50 mpm; and ETCO2, between 25 and 30 mmHg. No assistance in ventilation was necessary. The procedure lasted one hour, and extubation occurred seven minutes after the interruption of inhalational anesthetic. Anesthesia and anesthesia recovery occurred without complications, allowing the accomplishment of a short duration surgical procedure. After the post operatory period, the animal was reintroduced to the wild, with authorization of the state environmental agency. In conclusion, low dose dexmedetomidine combined with ketamine is adequate for rapid chemical restraint of black capuccin, and do not cause physiologic alterations during isoflurane anesthesia.

scholarly journals Clinical outcomes of concomitant use of enteral and intravenous sedatives and analgesics in mechanically ventilated patients with COVID-19

2021 ◽  
Author(s):  
Nayoung Kang ◽  
Mohammed A Alrashed ◽  
Eric M Place ◽  
Phuongthao T Nguyen ◽  
Stephen J Perona ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Invasive Mechanical Ventilation ◽  
Institutional Review Board ◽  
Chain Reaction ◽  
Mechanically Ventilated ◽  
Ventilation Time ◽  
Institutional Review ◽  
Significant Difference ◽  
Polymerase Chain ◽  
The Impact

Abstract Disclaimer In an effort to expedite the publication of articles related to the COVID-19 pandemic, AJHP is posting these manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. Purpose To evaluate potential differences in days on mechanical ventilation for patients with coronavirus disease 2019 (COVID-19) based on route of administration of analgesic and sedative medications: intravenous (IV) alone vs IV + enteral (EN). Summary This institutional review board–approved study evaluated ventilation time and fentanyl or midazolam requirements with or without concurrent EN hydromorphone and lorazepam. Patients were included in the study if they were 18 to 89 years old and were admitted to the intensive care unit with a positive severe acute respiratory syndrome coronavirus 2 reverse transcription and polymerase chain reaction or antigen test and respiratory failure requiring invasive mechanical ventilation for more than 72 hours. In total, 100 patients were evaluated, 60 in the IV-only group and 40 in the IV + EN group. There was not a significant difference in ventilation time between the groups (mean [SD], 19.6 [12.8] days for IV + EN vs 15.6 [11.2] days for IV only; P = 0.104). However, fentanyl (2,064 [847] μg vs 2,443 [779] μg; P &lt; 0.001) and midazolam (137 [72] mg vs 158 [70] mg; P = 0.004) requirements on day 3 were significantly higher in the IV-only group, and the increase in fentanyl requirements from day 1 to day 3 was greater in the IV-only group than in the IV + EN group (378 [625] μg vs 34 [971] μg; P = 0.033). Conclusion Addition of EN analgesic and sedative medications to those administered by the IV route did not change the duration of mechanical ventilation in patients with COVID-19, but the combination may reduce IV opioid requirements, decreasing the impact of IV medication shortages.

Sign in / Sign up

Export Citation Format

Share Document