scholarly journals Prediction of expiratory desflurane and sevoflurane concentrations in lung-healthy patients utilizing cardiac output and alveolar ventilation matched pharmacokinetic models

Medicine ◽  
2021 ◽  
Vol 100 (6) ◽  
pp. e23570
Author(s):  
Jonas Weber ◽  
Claudia Mißbach ◽  
Johannes Schmidt ◽  
Christin Wenzel ◽  
Stefan Schumann ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Alveolar Ventilation ◽  
Pharmacokinetic Models

Cardiopulmonary effects of continuous pressure breathing in hypothermic dogs

1965 ◽  
Vol 20 (4) ◽  
pp. 669-674 ◽  
Author(s):  
J. Salzano ◽  
F. G. Hall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Negative Pressure Breathing ◽  
Continuous Positive Pressure ◽  
Respiratory Dead Space

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964

Modeling Population Pharmacokinetics of Lidocaine

2001 ◽  
Vol 94 (4) ◽  
pp. 566-573 ◽  
Author(s):  
Jette A. Kuipers ◽  
Fred Boer ◽  
Annemiek de Roode ◽  
Erik Olofsen ◽  
James G. Bovill ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pharmacokinetic Model ◽  
Population Pharmacokinetic ◽  
Ratio Test ◽  
Pharmacokinetic Models ◽  
Population Pharmacokinetic Modeling ◽  
Population Pharmacokinetic Study ◽  
Electrical Bioimpedance ◽  
Demographic Covariates ◽  
The Individual

Background Inclusion of cardiac output and other physiologic parameters, in addition to or instead of, demographic variables might improve the population pharmacokinetic modeling of lidocaine. Methods Thirty-one patients were included in a population pharmacokinetic study of lidocaine. After bolus injection of lidocaine (1 mg/kg), 22 or 10 blood samples per patient were taken from a radial artery. During the experiment, cardiac output was measured using a thoracic electrical bioimpedance method. The following four population pharmacokinetic models were constructed and their performances investigated: a model with no covariates, a model with cardiac output as covariate, a model with demographic covariates, and a model with both cardiac output and demographic characteristics as covariates. Model discrimination was performed with the likelihood ratio test. Results Inclusion of cardiac output resulted in a significant improvement of the pharmacokinetic model, but inclusion of demographic covariates was even better. However, the best model was obtained by inclusion of both demographic covariates and cardiac output in the pharmacokinetic model. Conclusions When population pharmacokinetic models are used for individualization of dosing schedules, physiologic covariates, e.g., cardiac output, can improve their ability to predict the individual kinetics.

Carbon monoxide exchanges between the human fetus and mother: a mathematical model

1977 ◽  
Vol 232 (3) ◽  
pp. H311-H323 ◽  
Author(s):  
E. P. Hill ◽  
J. R. Hill ◽  
G. G. Power ◽  
L. D. Longo
Keyword(s):  
Mathematical Model ◽  
Air Pollution ◽  
Carbon Monoxide ◽  
Cardiac Output ◽  
Human Fetus ◽  
Alveolar Ventilation ◽  
Co Concentration ◽  
Fetal Oxygenation ◽  
Ventilation Rates ◽  
Co Concentrations

A mathematical model was developed to calculate maternal and fetal carboxyhemoglobin concentrations, [HbCO], as functions of time during and after exposure of the mother to various inspired CO concentrations. Effects of variation in alveolar ventilation rates, pulmonary and placental fiffusing capacities, cardiac output, endogenous carbon monoxide production and other factors were studied. Following a change in the inspired CO concentration, fetal HbCO lags behind maternal HbCO by several hours. During CO uptake, fetal HbCO eventually overtakes maternal, and approaches an equilibrium value as much as 10% higher than the mother's. During CO washout the fetal levels again lag behind the mothers. Results indicate that treatment of pregnant women who have elevated HbCO levels with 100% oxygen reduces the time necessary to reduce the maternal HbCO level as expected, but that the rate of fetal CO elimination is not increased as much as that of the mother. Changes in maternal and fetal HbCO were also calculated for a representative exposure to changing inspired CO levels produced by fluctuating levels of air pollution. Finally, the effects of carboxyhemoglobin on fetal oxygenation were studied, including the effects of high altitude and exercise.

The Effect of Halothane on the Recirculatory Pharmacokinetics of Physiologic Markers 

1997 ◽  
Vol 87 (6) ◽  
pp. 1381-1393 ◽  
Author(s):  
Michael J. Avram ◽  
Tom C. Krejcie ◽  
Claus U. Niemann ◽  
Cheri Klein ◽  
W. Brooks Gentry ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Drug Disposition ◽  
Drug Distribution ◽  
Peripheral Blood Flow ◽  
Dependent Manner ◽  
Pharmacokinetic Models ◽  
Halothane Anesthesia ◽  
Arterial Blood ◽  
Dose Dependent

Background The cardiovascular effects of halothane are well recognized, but little is known of how this affects drug distribution. The effect of halothane anesthesia on physiologic factors that affect drug disposition from the moment of injection was investigated. Methods The dispositions of markers of intravascular space and blood flow (indocyanine green), extracellular space and free water diffusion (inulin), and total body water and tissue perfusion (antipyrine) were determined in four purpose-bred coonhounds. The dogs were studied while awake and while anesthetized with 1%, 1.5%, and 2% halothane in a randomized order determined by a repeated measures Latin square experimental design. Marker dispositions were described by recirculatory pharmacokinetic models based on frequent early and less frequent later arterial blood samples. These models characterize the role of cardiac output and its distribution on drug disposition. Results Halothane caused a significant and dose-dependent decrease in cardiac output. The disposition of antipyrine was most profoundly affected by halothane anesthesia, which increased both nondistributive intercompartmental clearance and volume while decreasing fast and slow tissue clearances and elimination clearance in a halothane dose-dependent manner. Conclusions Halothane-induced changes in blood flow to the compartments of the antipyrine recirculatory model were not proportional to changes in cardiac output. Halothane anesthesia significantly increased (to more than double) the area under the drug concentration versus time curve due to an increase in the apparent peripheral blood flow not involved in drug distribution, despite a dose-dependent cardiac output decrease. Recirculatory pharmacokinetic models include the best aspects of traditional compartmental and physiologic pharmacokinetic models while offering advantages over both.

The Effect of Aminophylline on the Respiration and Pulmonary Circulation

1970 ◽  
Vol 38 (5) ◽  
pp. 549-554 ◽  
Author(s):  
V. Ježek ◽  
A. Ouředník ◽  
J. Štěpánek ◽  
F. Boudík
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Chronic Bronchitis ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Ventilation ◽  
Arterial Oxygen ◽  
Bronchial Obstruction ◽  
Arterial Blood ◽  
Pulmonary Arterial

1. We have examined the effects of aminophylline on the respiration and pulmonary circulation of eleven patients with chronic bronchitis and six patients with peripheral bronchial carcinoma; the latter were free from bronchial obstruction at the time of study. 2. Aminophylline caused an increase in total and alveolar ventilation and a decrease in arterial carbon dioxide tension. Lung diffusing capacity was unaltered in subjects with marked respiratory insufficiency but increased slightly in an additional group of less severely affected patients, and in the control subjects. 3. Mean pulmonary arterial pressure decreased significantly in the patients with chronic bronchitis but not those with lung cancer. A positive correlation was observed between the level of pulmonary arterial pressure during the control period and the decrease after aminophylline. 4. For the group as a whole there was no significant change in cardiac output or arterial oxygen saturation or tension. However, in those subjects in whom the cardiac output was increased, the arterial blood oxygen was reduced despite an increase in alveolar ventilation. The data are interpreted as evidence for a disproportionate part of the increase in cardiac output being directed to poorly ventilated areas of the lung.

Influence of vagal blockade on respiratory and circulatory functions in hypothermic dogs

1962 ◽  
Vol 17 (5) ◽  
pp. 833-836 ◽  
Author(s):  
John Salzano ◽  
F. G. Hall
Keyword(s):  
Cardiac Output ◽  
Body Temperature ◽  
Dead Space ◽  
Alveolar Ventilation ◽  
Normal Body Temperature ◽  
Vagal Blockade ◽  
Physiologic Dead Space ◽  
Anesthetized Dogs ◽  
Output Ratio ◽  
Carbon Dioxide Pressure

Anatomical and physiological dead spaces were enlarged as a result of reduction in body temperature to 28 C in spontaneously respiring anesthetized dogs. Respiratory dead space at 32 C was not significantly different from that at normal body temperature. Vagal blockade resulted in an increase in tidal volume and decrease in respiratory frequency and increased anatomic and physiologic dead space at normal and reduced temperatures. Alveolar ventilation and cardiac output declined equally (percentagewise) with reduction in body temperature to 32 C; at 28 C alveolar ventilation fell more precipitously so that alveolar ventilation-cardiac output ratio (ventilation-perfusion) at 28 C was approximately one-half that at 37 and 32 C. Arterial-alveolar carbon dioxide pressure differences were independent of temperature and vagal blockade. The results indicate no impairment of gas transport or gas exchange at 32 or 28 C in spontaneously respiring anesthetized dogs. Submitted on January 11, 1962

A BASIC software program to estimate cardiac output and alveolar ventilation

1990 ◽  
Vol 20 (4) ◽  
pp. 261-265
Author(s):  
Alain Varray ◽  
Jacques Mercier ◽  
Christian Prefaut
Keyword(s):  
Cardiac Output ◽  
Alveolar Ventilation ◽  
Basic Software ◽  
Software Program
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