Cardiopulmonary Effects of Intrathoracic Insufflation in Dogs

2002 ◽  
Vol 38 (6) ◽  
pp. 515-520 ◽  
Author(s):  
Curt M. Daly ◽  
Karen Swalec-Tobias ◽  
Anthony H. Tobias ◽  
Nicole Ehrhart
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Healthy Adult ◽  
Venous Pressure ◽  
Minute Volume ◽  
Mechanical Ventilator ◽  
Central Venous ◽  
Anesthetized Dogs ◽  
Pressure Standard

This study was designed to quantify the effects of incremental positive insufflation of the intrathoracic space on cardiac output (CO), heart rate (HR), arterial pressure (AP), central venous pressure (CVP), and percent saturation of hemoglobin with oxygen (SPO2) in anesthetized dogs. Seven healthy, adult dogs from terminal teaching laboratories were maintained under anesthesia with isoflurane delivered with a mechanical ventilator. The experimental variables were recorded before introduction of an intrathoracic catheter, at intrathoracic pressures (IP) of 0 mm Hg, 3 mm Hg insufflation, and additional increments of 1 mm Hg insufflation thereafter until the SPO2 remained <85% despite increases in minute volume. Finally the variables were measured again at 0 mm Hg IP. The cardiac output and systolic and diastolic AP significantly (P<0.05) decreased at 3 mm Hg IP. Significant decreases in SPO2 were seen at 10 mm Hg IP. Significant increase in CVP was noted at 6 mm Hg IP. Heart rate decreased significantly at 5 to 6 mm Hg IP but was not decreased above 6 mm Hg IP. Given the degree of CO decrease at low intrathoracic pressures, insufflation-aided thoracoscopy should be used with caution and at the lowest possible insufflation pressure. Standard anesthetic monitoring variables such as HR and AP measurements may not accurately reflect the animal’s cardiovascular status.

Hemodynamic response of normal men to graded treadmill exercise

1964 ◽  
Vol 19 (3) ◽  
pp. 457-464 ◽  
Author(s):  
Burton S. Tabakin ◽  
John S. Hanson ◽  
Thornton W. Merriam ◽  
Edgar J. Caldwell
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Treadmill Exercise ◽  
Minute Volume ◽  
Peripheral Vascular ◽  
Carbon Dioxide Elimination ◽  
Oxygen Utilization

The physiologic variables defining the circulatory and respiratory state in normal man have been measured in recumbency, standing at rest and during progressively severe grades of exercise approaching near-maximal levels. Indicator-dilution technique was used for determination of cardiac output with simultaneous radio-electrocardiographic recordings of heart rate. Direct intra-arterial pressure measurements were utilized for calculation of peripheral vascular resistance. Minute volume of ventilation, oxygen utilization, and carbon dioxide elimination were obtained from analysis of expired air collected at the time of each cardiac output determination. A peak mean workload of 1,501 kg-m/min was realized during the treadmill exercise. Increases in cardiac output over the range of exercise employed correlated well with indices of workload such as heart rate, oxygen utilization, and minute volume of ventilation. There was no correlation of stroke volume with these indices. It is concluded from examination of individual stroke-volume responses that a progressive increase in stroke volume is not a necessary or constant phenomenon in adapting to increasing workload. cardiac output in treadmill exercise; dye-dilution cardiac output determinations; arterial pressure during upright exercise; stroke-volume response to graded treadmill exercise; exercise response of cardiac output and stroke volume; peripheral vascular resistance response to position and exercise; treadmill exercise—effects on cardiac output, stroke volume, and oxygen uptake; minute ventilation, cardiac output, and stroke volume during exercise; carbon dioxide elimination during treadmill exercise; heart rate and cardiac output during treadmill exercise; exercise; physiology Submitted on July 12, 1963

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

2004 ◽  
Vol 287 (4) ◽  
pp. H1658-H1662 ◽  
Author(s):  
N. Charkoudian ◽  
E. A. Martin ◽  
F. A. Dinenno ◽  
J. H. Eisenach ◽  
N. M. Dietz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Healthy Humans ◽  
Rapid Changes

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10° head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased ∼2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: −3.1 ± 0.6 and −3.3 ± 1.0 versus −5.0 ± 0.6 units·beat−1·mmHg−1 ( P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Central Venous ◽  
Pressor Test

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

scholarly journals Effects of Different Doses of Magnesium Sulfate on Pneumoperitoneum-related Hemodynamic Changes in Patients Undergoing Gastrointestinal Laparoscopy: a randomized, double-blind, controlled trial

2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Magnesium Sulfate ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Control Group ◽  
Central Venous

Abstract Background: The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods: Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure(CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results: Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4), systemic vascular resistance (T2), and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analog scales at 5 min and 20 min, the level of vasopressin, and the dose of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion: Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.

scholarly journals Effects of Different Doses of Magnesium Sulfate on Pneumoperitoneum-related Hemodynamic Changes in Patients Undergoing Gastrointestinal Laparoscopy

2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Magnesium Sulfate ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Control Group ◽  
Central Venous

Abstract Background: The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods: Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure(CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results: Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4), systemic vascular resistance (T2), and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analog scales at 5 min and 20 min, the level of vasopressin, and the dose of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion: Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastolic pressure determines autonomic responses to pressure perturbation in humans

1989 ◽  
Vol 66 (2) ◽  
pp. 800-807 ◽  
Author(s):  
J. S. Sanders ◽  
D. W. Ferguson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Diastolic Pressure ◽  
Human Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity ◽  
Normal Human

Arterial baroreceptors reflexly regulate sympathetic and heart rate responses to alteration of blood pressure. The primary mechanical determinant of arterial baroreceptor activity in humans remains unclear. We examined the influence of systolic, diastolic, pulse, and mean arterial pressures on efferent muscle sympathetic nerve activity (MSNA, microneurography) and heart rate responses during perturbation of arterial pressure in 10 normal human subjects [age 25 +/- 2 (SE) yr]. We directly measured arterial pressure, heart rate, and MSNA during intravenous vasodilator infusion (nitroprusside, 6 +/- 1 micrograms.kg-1.min-1, n = 6; or hydralazine, 16 +/- 2 mg, n = 4) while central venous pressure was held constant by simultaneous volume expansion. Changes in arterial pressures were compared with changes in heart rate and MSNA over 3-min periods of vasodilator infusion during which we observed increases in systolic and pulse pressures with simultaneous decreases in mean and diastolic pressures. During vasodilator infusion, there were increases in systolic (124.2 +/- 2.1 to 131.7 +/- 2.9 Torr, P less than 0.001) and pulse pressures (57.0 +/- 2.2 to 72.7 +/- 2.7 Torr, P less than 0.001) although mean arterial pressure fell (88.0 +/- 2.6 to 80.4 +/- 2.7 Torr, P less than 0.001) because of decreases in diastolic pressure (67.2 +/- 3.0 to 59.0 +/- 2.7 Torr, P less than 0.001). The changes in arterial pressures were accompanied by simultaneous increases in heart rate (66.4 +/- 3.0 to 92.6 +/- 4.8 beats/min, P less than 0.001) and MSNA (327 +/- 59 to 936 +/- 171 U, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit

1996 ◽  
Vol 81 (1) ◽  
pp. 266-273 ◽  
Author(s):  
G. Raimondi ◽  
J. M. Legramante ◽  
F. Iellamo ◽  
S. Cassarino ◽  
G. Peruzzi
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Response Patterns ◽  
Central Venous ◽  
Frequency Stimulation ◽  
End Tidal ◽  
Stimulation Of

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Hemodynamic effects of blood loss during a passive response to a stressor in the conscious rabbit

2004 ◽  
Vol 286 (2) ◽  
pp. R373-R380 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Loss ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Freezing Behavior ◽  
Cardiovascular Changes ◽  
Conscious Rabbit ◽  
Air Jet ◽  
Arterial Blood

In the conscious rabbit, exposure to an air jet stressor increases arterial pressure, heart rate, and cardiac output. During hemorrhage, air jet exposure extends the blood loss necessary to produce hypotension. It is possible that this enhanced defense of arterial pressure is a general characteristic of stressors. However, some stressors such as oscillation (OSC), although they increase arterial pressure, do not change heart rate or cardiac output. The cardiovascular changes during OSC resemble those seen during freezing behavior. In the present study, our hypothesis was that, unlike air jet, OSC would not affect defense of arterial blood pressure during blood loss. Male New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood until mean arterial pressure decreased to 40 mmHg. We repeated the experiment in each rabbit on separate days in the presence and absence (SHAM) of OSC. Compared with SHAM, OSC increased arterial pressure 14 ± 1 mmHg, central venous pressure 3.3 ± 0.4 mmHg, and hindquarter blood flow 34 ± 4% while decreasing mesenteric conductance 32 ± 3% and not changing heart rate or cardiac output. During normotensive hemorrhage, OSC enhanced hindquarter and renal vasoconstriction. Contrary to our hypothesis, OSC (23.5 ± 0.6 ml/kg) increased the blood loss necessary to produce hypotension compared with SHAM (16.8 ± 0.6 ml/kg). In nine rabbits, OSC prevented hypotension even after a blood loss of 27 ml/kg. Thus a stressful stimulus that resulted in cardiovascular changes similar to those seen during freezing behavior enhanced defense of arterial pressure during hemorrhage.

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

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