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

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.

scholarly journals Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Spinal Anesthesia ◽  
Cesarean Delivery ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Preeclampsia

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.

scholarly journals COMPARATIVE CHARACTERISTICS OF THE DYNAMICS OF CARDIOVASCULAR AND RESPIRATORY EFFECTS OF PNEUMOPERITONEUM BASED ON CARBON DIOXIDE AND ARGON IN LAPAROSCOPIC CHOLECYSTECTOMY

2021 ◽  
pp. 90-95
Author(s):  
O. L. Tkachuk ◽  
R. L. Parakhoniak ◽  
S. V. Melnyk ◽  
O. O. Tkachuk-Hryhorchuk
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Laparoscopic Cholecystectomy ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Impact ◽  
Abdominal Pressure ◽  
The Mean ◽  
Respiratory Systems

Pneumoperitoneum is one of the most critical components of laparoscopic surgery, which has a negative effect on gas exchange and stress to circulatory buffering system. One of the top priorities of laparoscopic technologies is to minimize the impact on the respiratory and cardiovascular systems, metabolic dynamics and compensatory abilities of homeostasis. The main goal of this research work is to compare the effects of carboxyperitoneum and argonoperitoneum on the intraoperative dynamics of CO2 concentration as well as cardiovascular and respiratory characteristics in patients undergoing laparoscopic cholecystectomy for various forms of cholelithiasis. Materials and methods. Four experimental groups involved patients based on their nosological form of cholelithiasis and the gas used to induce pneumoperitoneum. All patients underwent laparoscopic cholecystectomy by means of standard procedure. Either medical carbon dioxide or medical argon was used to induce pneumoperitoneum. Intraoperative monitoring of blood carbon dioxide levels PaCO2 was performed by taking venous blood every 15 minutes. Capnometry was performed by means of mainstream analysis using “BIOMED” BM1000C modular patient monitor by recording the discrete values of PetCO2 every 15 minutes, as well as by analyzing photocopies of capnography curves every 15 minutes. Intraoperative echocardiography was performed to identify the mean arterial pressure (MAP), heart rate (HR) and cardiac output (CO) in order to assess the effects of different types of pneumoperitoneum on the cardiovascular system. Results. The obtained data confirm the expected difference in the indices of cardiorespiratory functions between patients with acute cholecystitis and cholelithiasis without signs of inflammation. The investigation revealed that under the influence of pneumoperitoneum, heart rate and mean arterial pressure increase, while the cardiac output decreases. The respiratory pressure marker depends more on the intra-abdominal pressure and presumably the patient’s body type than on the presence of inflammatory syndrome. Argon insufflation has a slight negative impact on the cardiovascular system. Particularly, the mean arterial pressure and heart rate increase, while the cardiac output marker is less decreased as compared to the use of carbon dioxide. Abdominal pressure has a significant effect on the cardiovascular and respiratory systems regardless of the used type of gas. The combination of high intra-abdominal pressure with the elevated head end of the operating table, which is a common practise during cholecystectomy, has especially great influence on cardiovascular and respiratory functions. Operation which is carried out at decreased pressure allows reducing the deviations of practically all indices. Conclusions. Thus, the cardiovascular and respiratory systems adapt under the influence of pneumoperitoneum, providing compensation for the negative effects of mechanical and resorptive-metabolic character. Compensatory-adaptive abilities of the cardiovascular and respiratory systems increase with the decrease of intra-abdominal pressure. The use of argon as a working gas for insufflation into the abdominal cavity during laparoscopy reduces the negative impact of pneumoperitoneum on the cardiovascular and respiratory systems, providing a greater reserve of homeostatic and buffer systems of the body.

Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses

1985 ◽  
Vol 59 (1) ◽  
pp. 183-189 ◽  
Author(s):  
T. I. Musch ◽  
G. C. Haidet ◽  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Maximal Exercise ◽  
Submaximal Exercise ◽  
Maximal Heart Rate ◽  
O2 Consumption

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8–12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

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.

Hemodynamic effects of angiotensin, norepinephrine, and bradykinin continuously measured in unanesthetized dogs

1961 ◽  
Vol 201 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Irvine H. Page ◽  
Frederick Olmsted
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Partial Recovery ◽  
Slight Rise ◽  
Abrupt Rise

Cardiac output, arterial pressure, heart rate and the derived functions, peripheral resistance and stroke volume, were registered continuously from intact, unanesthetized, unrestrained dogs. Isoleucyl5- or valyl5-angiotensin octapeptide caused output, heart rate and stroke volume to fall sharply when peripheral resistance rose. When infused for an hour, systolic and diastolic pressure remained elevated with unchanged infusion rate. Heart rate decreased in most animals, stroke volume and cardiac output fell, while peripheral resistance rose. Pentobarbital anesthesia increased somewhat the pressor response and decreased the bradycardia. Norepinephrine elicited, first, an abrupt rise in pressure and peripheral resistance, slight rise in heart rate and stroke volume. Arterial pressure then tended to stabilize, followed by a slow decrease associated with continued depression of cardiac output. Bradykinin caused fall in pressure, partial recovery, then further fall. Heart rate slowed, then rose. Cardiac output rose sharply during the initial fall in arterial pressure and remained elevated during the hypotensive response. Stroke volume was reduced during the initial fall but was reduced less during the rest of the response. Peripheral resistance was decreased sharply.

scholarly journals Cyclohexanone contamination from extracorporeal circuits impairs cardiovascular function

2009 ◽  
Vol 296 (6) ◽  
pp. H1926-H1932 ◽  
Author(s):  
Caitlin S. Thompson-Torgerson ◽  
Hunter C. Champion ◽  
Lakshmi Santhanam ◽  
Z. Leah Harris ◽  
Artin A. Shoukas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Vascular Resistance ◽  
Cardiovascular Function ◽  
Carotid Occlusion ◽  
Cardiac Insufficiency ◽  
Edema Formation ◽  
Extracorporeal Circuits

Extracorporeal circulation provides critical life support in the face of cardiopulmonary or renal failure, but it also introduces a host of unique morbidities characterized by edema formation, cardiac insufficiency, autonomic dysfunction, and altered vasomotor function. We tested the hypothesis that cyclohexanone (CHX), a solvent used in production of extracorporeal circuits and intravenous (IV) bags, leaches into the contained fluids and can replicate these clinical morbidities. Crystalloid fluid samples from circuits and IV bags were analyzed by gas chromatography-mass spectrometry to provide a range of clinical CHX exposure levels, revealing CHX contamination of sampled fluids (9.63–3,694 μg/l). In vivo rat studies were conducted ( n = 49) to investigate the effects of a bolus IV infusion of CHX vs. saline alone on cardiovascular function, baroreflex responsiveness, and edema formation. Cardiovascular function was evaluated by cardiac output, heart rate, stroke volume, vascular resistance, arterial pressure, and ventricular contractility. Baroreflex function was assessed by mean femoral arterial pressure responses to bilateral carotid occlusion. Edema formation was assessed by the ratio of wet to dry organ weights for lungs, liver, kidneys, and skin. CHX infusion led to systemic hypotension; pulmonary hypertension; depressed contractility, heart rate, stroke volume, and cardiac output; and elevated vascular resistance ( P < 0.05). Mean arterial pressure responsiveness to carotid occlusion was dampened after CHX infusion (from +17.25 ± 1.8 to +5.61 ± 3.2 mmHg; P < 0.05). CHX infusion led to significantly higher wet-to-dry weight ratios vs. saline only (3.8 ± 0.06 vs. 3.5 ± 0.05; P < 0.05). CHX can reproduce clinical cardiovascular, neurological, and edema morbidities associated with extracorporeal circulatory treatment.

Response to ventilatory obstruction during steady-state exercise

1960 ◽  
Vol 15 (4) ◽  
pp. 579-582 ◽  
Author(s):  
Burton S. Tabakin ◽  
John S. Hanson
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Oxygen Uptake ◽  
Treadmill Exercise ◽  
Minute Volume ◽  
Normal Male ◽  
Carbon Dioxide Elimination ◽  
Physiological Mechanisms ◽  
Total Period ◽  
Male Subjects

Five normal male subjects, 27–37 years of age, were studied during steady-state treadmill exercise to observe the effects of varying expiratory airway obstruction on minute volume, oxygen consumption and carbon dioxide elimination. A 5-mm-diameter resistance produced significant depressions in minute volume for the duration of the obstructed period. Carbon dioxide elimination showed significant reductions during the first 6 minutes of breathing against resistance. Oxygen uptake, however, was reduced significantly only during the 1st minute of obstructed breathing, but the reduction was great enough so that, despite subsequent rises in oxygen uptake, an ‘oxygen debt’ had already been incurred for the total period of obstruction. Following removal of the resistance, all these values rebounded to levels above those of the original steady state. The physiological mechanisms possibly effecting the response to obstruction are discussed. Submitted on February 24, 1959

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