Propofol Fails to Attenuate the Cardiovascular Response to Rapid Increases in Desflurane Concentration

1996 ◽  
Vol 84 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Malcolm Daniel ◽  
Edmond I Eger ◽  
Richard B. Weiskopf ◽  
Mariam Noorani
Keyword(s):  
Heart Rate ◽  
Cardiovascular Response ◽  
Peak Plasma ◽  
Random Order ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Desflurane Concentration ◽  
End Tidal ◽  
Catecholamine Concentration ◽  
Epinephrine Concentration

Background A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses. Methods To test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg.kg-1 propofol, anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg.kg-1 propofol was administered either 2 or 5 min before increasing end-tidal desflurane concentration from 4% to 8%. Results Without propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63 +/- 3 beats/min to 108 +/- 5 beats/min, mean +/- SEM; P < 0.01), mean arterial pressure (from 73 +/- 1 mmHg to 118 +/- 6 mmHg; P < 0.01), and epinephrine concentration (from 14 +/- 1 pg.ml-1 to 279 +/- 51 pg.ml-1; P < 0.05). There was no significant change in norepinephrine concentration (from 198 +/- 37 pg.ml-1 to 277 +/- 46 pg.ml-1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158 +/- 35 pg.ml-1, propofol given 2 min before, and 146 + 41 pg.ml-1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses. Conclusions Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans

1989 ◽  
Vol 66 (4) ◽  
pp. 1736-1743 ◽  
Author(s):  
L. B. Rowell ◽  
D. G. Johnson ◽  
P. B. Chase ◽  
K. A. Comess ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous Activity ◽  
Plasma Concentrations ◽  
Random Order ◽  
Sympathetic Nervous Activity ◽  
Severe Hypoxemia ◽  
Arterial Blood ◽  
End Tidal ◽  
Venous Plasma

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20–34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.

Relation of thyroid state to myocardial catecholamine concentration

1963 ◽  
Vol 205 (6) ◽  
pp. 1270-1274 ◽  
Author(s):  
George S. Kurland ◽  
Rupert P. Hammond ◽  
A. Stone Freedberg
Keyword(s):  
Body Weight ◽  
Basal Metabolic Rate ◽  
Fluorescence Spectra ◽  
Alumina Column ◽  
Thyroid State ◽  
Norepinephrine Concentration ◽  
Norepinephrine Content ◽  
Alumina Column Chromatography ◽  
Catecholamine Concentration ◽  
Epinephrine Concentration

The myocardial catecholamine content was measured in euthyroid, thyrotoxic, and hypothyroid rabbits. Male rabbits were made thyrotoxic by injection of l-thyroxine, or were rendered hypothyroid by injection of I131. Body weight, basal metabolic rate, serum protein-bound iodine, and appearance were used as criteria of thyroid state. Myocardial norepinephrine and epinephrine concentrations were measured, after alumina column chromatography, by a modification of the trihydroxyindole method. Fluorescence spectra and paper chromatographic analyses confirmed the identity of the trihydroxyindole-fluorescing material, and revealed no extraneous fluorescing substances. In the heart of the euthyroid rabbit, epinephrine concentration averaged 0.3 ± .2 (sd) µg/g in the atrium, and 0.06 ± .03 µg/g in the ventricle. Norepinephrine concentration averaged 2.9 ± .4 µg/g in the atrium, and 2.2 ± .3 µg/g in the ventricle. In thyrotoxicosis, atrial epinephrine and norepinephrine concentrations were decreased, ventricular epinephrine was unchanged, and ventricular norepinephrine was decreased. In hypothyroidism, atrial epinephrine and norepinephrine were decreased and ventricular epinephrine was unchanged, but in the hypothyroid ventricle, norepinephrine content was markedly increased.

Cardiovascular Responses to Submaximal Concentric and Eccentric Isokinetic Exercise in Older Adults

1999 ◽  
Vol 7 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Elizabeth Thompson ◽  
Theo H. Versteegh ◽  
Tom J. Overend ◽  
Trevor B. Birmingham ◽  
Anthony A. Vandervoort
Keyword(s):  
Older Adults ◽  
Heart Rate ◽  
Perceived Exertion ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Knee Extension ◽  
Resistance Testing ◽  
Exercise Heart Rate ◽  
Arterial Blood ◽  
S Peak

Our purpose was to describe heart rate (HR), mean arterial blood pressure (MAP), and perceived exertion (RPE) responses to submaximal isokinetic concentric (CON) and eccentric (ECC) exercise at the same absolute torque output in older adults. Peak torques for ECC and CON knee extension were determined in healthy older males (n = 13) and females (n = 7). Subjects then performed separate, randomly ordered, 2-min bouts of CON and ECC exercise. Heart rate and MAP increased (p < .001) from resting values throughout both exercise bouts. CON exercise elicited a significantly greater cardiovascular response than ECC exercise after 60 s. Peak HR, MAP, and RPE after CON exercise were greater than after ECC exercise (p < .01). At the same absolute torque output, isokinetic CON knee extension exercise resulted in a significantly greater level of cardiovascular stress than ECC exercise. These results are relevant to resistance testing and exercise in older people.

Fentanyl Augments the Blockade of the Sympathetic Response to Incision (MAC-BAR) Produced by Desflurane and Isoflurane 

1998 ◽  
Vol 88 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Malcolm Daniel ◽  
Richard B. Weiskopf ◽  
Mariam Noorani ◽  
Edmond I. Eger
Keyword(s):  
Nitrous Oxide ◽  
Cardiovascular Response ◽  
Dependent Manner ◽  
Surgical Incision ◽  
Arterial Blood ◽  
Adrenergic Response ◽  
The Mean ◽  
End Tidal ◽  
Inhaled Anesthetic ◽  
Dose Dependent

Background Heart rate (HR) or mean arterial blood pressure (MAP) may increase in response to incision despite the absence of a motor response. The authors hypothesized that the MAC-BAR (minimum alveolar concentration of an anesthetic that blocks adrenergic response to incision) for isoflurane would exceed that for desflurane, and that fentanyl would decrease the MAC-BAR for each anesthetic in a dose-dependent manner. Methods Seventy-one patients were randomly allocated to one of six groups: desflurane or isoflurane without fentanyl or with 1.5 or 3 microg/kg fentanyl given intravenously 5 min before surgical incision. Anesthesia was induced with 2 mg/kg propofol given intravenously, and tracheal intubation facilitated with 0.1 mg/kg given intravenously. The first patient in each group received 1 MAC (end-tidal) of the inhaled anesthetic in 60% nitrous oxide (0.55 MAC), balance oxygen, maintained for at least 10 min before incision. The response was considered positive if the HR or MAP increased 15% or more. If the response was positive, the end-tidal concentration given to the next patient was 0.3 MAC greater; if the response was negative, the end-tidal concentration was 0.3 MAC less. The MAC-BAR level was calculated as the mean of four independent cross-over responses in each group. Results Desflurane and isoflurane anesthesia with 60% nitrous oxide did not change HR (P &gt; 0.05) and decreased MAP (P &lt; 0.05) before incision. Plasma epinephrine and norepinephrine concentrations after anesthesia and before incision were normal in all groups. The MAC-BAR level, without fentanyl, did not differ (P &gt; 0.05) between desflurane (1.30 +/- 0.34 MAC [mean +/- SD]) and isoflurane (1.30 +/- 0.18 MAC). Fentanyl given at 1.5 microg/kg intravenously equivalently (P &gt; 0.05) reduced the MAC-BAR for desflurane (to 0.40 +/- 0.18 MAC; P &lt; 0.05) and isoflurane (to 0.55 +/- 0.00 MAC; P &lt; 0.05), but a further increase in fentanyl to 3 microg/kg caused no greater decrease in the MAC-BAR for desflurane (0.48 +/- 0.16 MAC) and isoflurane (0.40 +/- 0.30 MAC). Conclusions Clinically attainable doses of desflurane and isoflurane, in 60% nitrous oxide (0.55 MAC), block the cardiovascular response to surgical incision at 1.3 MAC. Fentanyl given at 1.5 microg/kg decreases the MAC-BAR for each agent with no further decrease produced by 3 microg/kg fentanyl.

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

Ventilatory responses to cardiac output changes in patients with pacemakers

1981 ◽  
Vol 51 (5) ◽  
pp. 1103-1107 ◽  
Author(s):  
P. W. Jones ◽  
W. French ◽  
M. L. Weissman ◽  
K. Wasserman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Blood Gas ◽  
Cardiac Pacemakers ◽  
Ventilatory Responses ◽  
Mean Delay ◽  
Arterial Blood ◽  
End Tidal

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

2004 ◽  
Vol 97 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Philip N. Ainslie ◽  
Marc J. Poulin
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Blood Flow Velocity ◽  
Acute Hypoxia ◽  
Random Order ◽  
Transcranial Doppler Ultrasound ◽  
Individual Variability ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
End Tidal

This study examined the effect of high, normal, and uncontrolled end-tidal Pco2 (PetCO2) on the ventilatory, peak cerebral blood flow velocity ( V̄p), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal Po2 was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (PetCO2 +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure V̄p in the middle cerebral artery. The slopes of the linear regressions of ventilation, V̄p, and MAP with arterial O2 saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia ( P < 0.05). Strong, significant correlations were observed between ventilation, V̄p, and MAP with each PetCO2 condition. These data suggest that 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2) in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PetCO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in V̄p and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high V̄p and MAP responses to hypoxia.

scholarly journals Multiple-input nonlinear modelling of cerebral haemodynamics using spontaneous arterial blood pressure, end-tidal CO 2  and heart rate measurements

2016 ◽  
Vol 374 (2067) ◽  
pp. 20150180 ◽  
Author(s):  
V. Z. Marmarelis ◽  
G. D. Mitsis ◽  
D. C. Shin ◽  
R. Zhang
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Prediction Error ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Cerebral Haemodynamics ◽  
Functional Connection ◽  
Arterial Blood ◽  
End Tidal

In order to examine the effect of changes in heart rate (HR) upon cerebral perfusion and autoregulation, we include the HR signal recorded from 18 control subjects as a third input in a two-input model of cerebral haemodynamics that has been used previously to quantify the dynamic effects of changes in arterial blood pressure and end-tidal CO 2 upon cerebral blood flow velocity (CBFV) measured at the middle cerebral arteries via transcranial Doppler ultrasound. It is shown that the inclusion of HR as a third input reduces the output prediction error in a statistically significant manner, which implies that there is a functional connection between HR changes and CBFV. The inclusion of nonlinearities in the model causes further statistically significant reduction of the output prediction error. To achieve this task, we employ the concept of principal dynamic modes (PDMs) that yields dynamic nonlinear models of multi-input systems using relatively short data records. The obtained PDMs suggest model-driven quantitative hypotheses for the role of sympathetic and parasympathetic activity (corresponding to distinct PDMs) in the underlying physiological mechanisms by virtue of their relative contributions to the model output. These relative PDM contributions are subject-specific and, therefore, may be used to assess personalized characteristics for diagnostic purposes.

scholarly journals Hemodynamic effects of acute stressors in the conscious rabbit

1998 ◽  
Vol 274 (3) ◽  
pp. R814-R821 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Sensory Stimulation ◽  
Cardiovascular Responses ◽  
Baroreflex Control ◽  
Conscious Rabbit ◽  
Air Jet ◽  
Arterial Blood

Chronically instrumented, conscious rabbits were used to test the hypothesis that sensory stimulation with an air jet or oscillation produces differential hemodynamic changes that may be appropriate for an active or a passive behavioral response, respectively. Both stressors increased arterial pressure, central venous pressure, and hindquarters blood flow and produced visceral vasoconstriction. Neither stimulus altered hindquarters conductance. Although air jet increased heart rate and cardiac output, oscillation did not. The two stressors affected arterial baroreflex control of heart rate differently. Oscillation reset arterial pressure to a higher level with no change in heart rate maximum or minimum, whereas air jet reset both heart rate and arterial pressure to higher levels. Neither stressor affected baroreflex sensitivity. We conclude that the conscious rabbit shows at least two distinct cardiovascular responses when exposed to acute stressors. Air jet produces a cardiovascular response including tachycardia, which resembles the defense reaction and appears appropriate for active defense or flight. The response to oscillation, on the other hand, appears better suited for a passive response such as “freezing” behavior. During exposure to either stressor, the baroreflex is altered to allow simultaneous increases in heart rate and arterial blood pressure, but the sensitivity is maintained, allowing normal moment to moment control of heart rate.

Adrenomedullary origin of the hindquarter vasodilation during the transposition response of the rat

1988 ◽  
Vol 66 (1) ◽  
pp. 18-21
Author(s):  
S. Sakata ◽  
J. Iriuchijima
Keyword(s):  
Blood Flow ◽  
Adrenal Medulla ◽  
Home Cage ◽  
Cardiovascular Response ◽  
Systemic Arterial Pressure ◽  
Plasma Catecholamine ◽  
Plasma Adrenaline ◽  
Arterial Blood ◽  
Radioenzymatic Assay ◽  
Catecholamine Concentration

Transposing a rat from the home cage to a new cage produces a cardiovascular response (transposition response) characterized by an increase in hindquarter blood flow with unchanged systemic arterial pressure. Arterial blood samples were collected from rats before and during this response for radioenzymatic assay of catecholamines. During the transposition response, the concentration of adrenaline and noradrenaline in plasma increased about six- and two-fold, respectively. Ablation of the adrenal medulla prevented these changes in plasma catecholamine concentration. Constant i.v. infusion of adrenaline, at rates producing a hindquarter flow approximately matching that observed during the transposition response, evoked an increase in plasma adrenaline concentration also approximately matching the increase observed during the transposition response. It is concluded that the increase in plasma adrenaline secreted from the adrenal medulla is the main cause of the increase in hindquarter blood flow in the transposition response.

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