Level of ventilation influences the cardiovascular response to hypoxemia in lambs

2004 ◽  
Vol 82 (12) ◽  
pp. 1113-1117 ◽  
Author(s):  
James E Fewell ◽  
Bonnie J Taylor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Transport ◽  
Cardiovascular Response ◽  
Recovery Period ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Systemic Oxygen ◽  
Cardiovascular Variables

Newborn animals of a number of species display a brisk increase in ventilation followed by a gradual drop toward or below baseline within minutes of exposure to acute hypoxemia. Heart rate and cardiac output (a determinant of systemic oxygen transport along with the arterial oxygen content) appear to follow a similar pattern, but whether or not the cardiovascular response is influenced by the respiratory response is unknown. We therefore carried out experiments in which the level of ventilation was controlled during normoxemia and hypoxemia to test the hypothesis that the level of ventilation influences the cardiovascular response to acute hypoxemia. Six lambs ranging in age from 17 to 22 days were anesthetized, tracheostomized, and instrumented for measurement of cardiovascular variables. A recovery period of at least 3 days was allowed before the study when each lamb was artificially ventilated with a mixture of 70% nitrous oxide and 30% oxygen in nitrogen. A control respiratory frequency (f) of 30 breaths per min was set and a control tidal volume (VT) was chosen to achieve normocapnia. Cardiovascular measurements were made during normoxemia and hypoxemia (FIO2 0.10) 5 min after f or VT was changed to simulate a decrease, no change, or an increase in ventilation. During normoxemia, the level of ventilation had little effect on the measured cardiovascular variables. At control levels of ventilation, hypoxemia caused an increase in cardiac output that was due solely to an increase in stroke volume as heart rate decreased; blood pressure was unchanged. Increasing ventilation during hypo xemia did not augment cardiac output or alter blood pressure as compared with that observed at control levels of ventilation. Decreasing ventilation during hypoxemia, however, decreased cardiac output due to a profound bradycardia; blood pressure increased significantly. Our data provide evidence that the level of ventilation significantly influences the cardiovascular response to hypoxemia in young lambs.Key words: newborn, hypoxemia, cardiovascular, respiration, systemic oxygen transport.

Systemic oxygen transport in induced normovolemic anemia and polycythemia

1962 ◽  
Vol 203 (4) ◽  
pp. 720-724 ◽  
Author(s):  
John F. Murray ◽  
Philip Gold ◽  
B. Lamar Johnson
Keyword(s):  
Cardiac Output ◽  
Oxygen Transport ◽  
Arterial Oxygen Saturation ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Peripheral Vascular ◽  
Arterial Oxygen Content ◽  
Normovolemic Anemia ◽  
Systemic Oxygen ◽  
Negative Linear Relationship

The hemodynamic effects of normovolemic anemia and polycythemia were studied in 14 dogs. Anemia (5 dogs) and polycythemia (5 dogs) were induced by bleeding and simultaneously infusing dextran or packed erythrocytes. Measurements included cardiac output, arterial oxygen saturation, peripheral vascular resistance, and systemic oxygen transport (cardiac output X arterial oxygen content). Cardiac output had a significant negative linear relationship to hematocrit ( r = –0.74, P < 0.01) over the range studied (13–74%). Peripheral resistance fell 46% in anemic animals and increased 152% in four of five polycythemic animals. Arterial saturation was significantly correlated to changes in hematocrit ( r = 0.62, P < 0.01) and cardiac output ( r = –0.55, P < 0.01); these values were due primarily to the linearity encountered in the anemia experiments and a reversal in these relationships tended to occur at high hematocrits. Systemic oxygen transport was maximum at normal hematocrits and decreased in anemia and polycythemia. The data indicate that hemodynamic adjustments in normovolemic anemia and polycythemia are insufficient to maintain normal oxygen delivery.

scholarly journals Refined Multiscale Fuzzy Entropy to Analyse Post-Exercise Cardiovascular Response in Older Adults With Orthostatic Intolerance

Entropy ◽  
2018 ◽  
Vol 20 (11) ◽  
pp. 860 ◽  
Author(s):  
Marcos Hortelano ◽  
Richard Reilly ◽  
Francisco Castells ◽  
Raquel Cervigón
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Orthostatic Intolerance ◽  
Cardiovascular Response ◽  
Recovery Period ◽  
The Elderly ◽  
Fuzzy Entropy ◽  
Post Exercise ◽  
And Gender ◽  
Risk Factors For Falls

Orthostatic intolerance syndrome occurs when the autonomic nervous system is incapacitated and fails to respond to the demands associated with the upright position. Assessing this syndrome among the elderly population is important in order to prevent falls. However, this problem is still challenging. The goal of this work was to determine the relationship between orthostatic intolerance (OI) and the cardiovascular response to exercise from the analysis of heart rate and blood pressure. More specifically, the behavior of these cardiovascular variables was evaluated in terms of refined composite multiscale fuzzy entropy (RCMFE), measured at different scales. The dataset was composed by 65 older subjects, 44.6% (n = 29) were OI symptomatic and 55.4% (n = 36) were not. Insignificant differences were found in age and gender between symptomatic and asymptomatic OI participants. When heart rate was evaluated, higher differences between groups were observed during the recovery period immediately after exercise. With respect to the blood pressure and other hemodynamic parameters, most significant results were obtained in the post-exercise stage. In any case, the symptomatic OI group exhibited higher irregularity in the measured parameters, as higher RCMFE levels in all time scales were obtained. This information could be very helpful for a better understanding of cardiovascular instability, as well as to recognize risk factors for falls and impairment of functional status.

scholarly journals Testing individual baroreflex responses to hypoxia-induced peripheral chemoreflex stimulation

2020 ◽  
Vol 30 (6) ◽  
pp. 531-540
Author(s):  
Hendrik Kronsbein ◽  
Darius A. Gerlach ◽  
Karsten Heusser ◽  
Alex Hoff ◽  
Fabian Hoffmann ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Recovery Period ◽  
Arterial Oxygen ◽  
Heart Rate Regulation ◽  
Peripheral Chemoreflex ◽  
Collective Influence

Abstract Introduction Baroreflexes and peripheral chemoreflexes control efferent autonomic activity making these reflexes treatment targets for arterial hypertension. The literature on their interaction is controversial, with suggestions that their individual and collective influence on blood pressure and heart rate regulation is variable. Therefore, we applied a study design that allows the elucidation of individual baroreflex–chemoreflex interactions. Methods We studied nine healthy young men who breathed either normal air (normoxia) or an air–nitrogen–carbon dioxide mixture with decreased oxygen content (hypoxia) for 90 min, with randomization to condition, followed by a 30-min recovery period and then exposure to the other condition for 90 min. Multiple intravenous phenylephrine bolus doses were applied per condition to determine phenylephrine pressor sensitivity as an estimate of baroreflex blood pressure buffering and cardiovagal baroreflex sensitivity (BRS). Results Hypoxia reduced arterial oxygen saturation from 98.1 ± 0.4 to 81.0 ± 0.4% (p < 0.001), raised heart rate from 62.9 ± 2.1 to 76.0 ± 3.6 bpm (p < 0.001), but did not change systolic blood pressure (p = 0.182). Of the nine subjects, six had significantly lower BRS in hypoxia (p < 0.05), two showed a significantly decreased pressor response, and three showed a significantly increased pressor response to phenylephrine in hypoxia, likely through reduced baroreflex buffering (p < 0.05). On average, hypoxia decreased BRS by 6.4 ± 0.9 ms/mmHg (19.9 ± 2.0 vs. 14.12 ± 1.6 ms/mmHg; p < 0.001) but did not change the phenylephrine pressor response (p = 0.878). Conclusion We applied an approach to assess individual baroreflex–chemoreflex interactions in human subjects. A subgroup exhibited significant impairments in baroreflex blood pressure buffering and BRS with peripheral chemoreflex activation. The methodology may have utility in elucidating individual pathophysiology and in targeting treatments modulating baroreflex or chemoreflex function.

scholarly journals Pain catastrophizing in athletes correlates with pain and cardiovascular changes during a painful cold pressor test

10.4085/16-20 ◽  
2020 ◽  
Author(s):  
Lentini Matylda ◽  
Scalia Joseph ◽  
Berger Lebel Frédérike ◽  
Touma Fadi ◽  
Jhajj Aneet ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiovascular Response ◽  
Pain Catastrophizing ◽  
Cold Pressor Test ◽  
Objective Measure ◽  
Cold Pressor ◽  
Pressor Test ◽  
Cardiovascular Variables

Abstract Context: Athletes are often exposed to pain due to injury and competition. There is preliminary evidence that cardiovascular measures could be an objective measure of pain, but the cardiovascular response can be influenced by psychological factors such as catastrophizing. Objectives: The purpose of our study was to use a painful cold pressor test to measure the relationship between catastrophizing, pain, and cardiovascular variables in athletes. Design: Pre-post test. Setting: We completed all measures in a laboratory setting. Participants: Thirty-six male rugby athletes participated in the study. Main outcome measures: We measured catastrophizing with the Pain Catastrophizing Scale and pain with a Numeric Pain Rating Scale. Cardiovascular measures included heart rate, systolic, and diastolic blood pressure, and heart rate variability. Results: During the cold pressor test, participants experienced a significant increase in pain (0 to 4.1±2.2), systolic blood pressure (126.7±16.5mm Hg to 149.7±23.4mm Hg), diastolic blood pressure (76.9±8.3mm Hg to 91.9±11.5mm Hg) and heart rate variability (from 0.0164ms±0.0121 to 0.0400ms±0.0323) (all p&lt;.001). In addition, there was a significant decrease in heart rate after the cold pressor test (p=0.04). There was a significant correlation between athlete's pain catastrophizing to both pain intensity and change in heart rate during the cold pressor test (p=.017 and p=.003 respectively). A significant linear regression indicated pain and catastrophizing explained 29% of the variance of the change in heart rate (p=.003). Conclusion: Athletes who have catastrophizing thoughts are more likely to experience higher levels of pain and a greater cardiovascular response during a painful stimulus. The change in cardiovascular variables may be a good alternative for an objective measure of pain in athletes in the future.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (12) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

Cardiovascular response to submaximal exercise in sustained microgravity

1996 ◽  
Vol 81 (1) ◽  
pp. 26-32 ◽  
Author(s):  
B. E. Shykoff ◽  
L. E. Farhi ◽  
A. J. Olszowka ◽  
D. R. Pendergast ◽  
M. A. Rokitka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Life Sciences ◽  
Submaximal Exercise ◽  
Arterial Blood ◽  
Response To Exercise

Cardiac output (Q), heart rate (HR), blood pressure, and oxygen consumption (VO2) were measured repeatedly both at rest and at two levels of exercise in six subjects during microgravity exposure. Exercise was at 30 and 60% of the workload producing the individual's maximal VO2 in 1 G. Three of the subjects were on a 9-day flight, Spacelab Life Sciences-1, and three were on a 15-day flight, Spacelab Life Sciences-2. We found no temporal differences during the flights. Thus we have combined all microgravity measurements to compare in-flight values with erect or supine control values. At rest, Q in flight was 126% of Q erect (P < 0.01) but was not different from Q supine, and HR in flight was 81% of HR erect (P < 0.01) and 91% of HR supine (P < 0.05). Thus resting stroke volume (SV) in flight was 155% of SV erect (P < 0.01) and 109% SV supine (P < 0.05). Resting mean arterial blood pressure and diastolic pressure were lower in flight than erect (P < 0.05). Exercise values were considered as functions of VO2. The increase in Q with VO2 in flight was less than that at 1 G (slope 3.5 vs. 6.1 x min-1.l-1.min-1). SV in flight fell with increasing VO2, whereas SV erect rose and SV supine remained constant. The blood pressure response to exercise was not different in flight from erect or supine. We conclude that true microgravity causes a cardiovascular response different from that seen during any of its putative simulations.

scholarly journals Association Between Pain Catastrophizing and Pain and Cardiovascular Changes During a Cold-Pressor Test in Athletes

2021 ◽  
Vol 56 (5) ◽  
pp. 473-483
Author(s):  
Matylda Lentini ◽  
Joseph Scalia ◽  
Frédérike Berger Lebel ◽  
Fadi Touma ◽  
Aneet Jhajj ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Diastolic Blood Pressure ◽  
Cardiovascular Response ◽  
Pain Catastrophizing ◽  
Cold Pressor Test ◽  
Objective Measure ◽  
Cold Pressor ◽  
Cardiovascular Variables

Context Athletes are often exposed to pain due to injury and competition. Using preliminary evidence, researchers have shown that cardiovascular measures could be an objective measure of pain, but the cardiovascular response can be influenced by psychological factors, such as catastrophizing. Objective To use a painful cold-pressor test (CPT) to measure the relationship among catastrophizing, pain, and cardiovascular variables in athletes. Design Cohort study. Setting Laboratory. Patients or Other Participants A total of 36 male rugby athletes (age = 24.0 ± 4.6 years, height = 180.0 ± 6.1 cm, mass = 90.5 ± 13.8 kg). Main Outcome Measure(s) We measured catastrophizing using the Pain Catastrophizing Scale and pain using a numeric pain rating scale. Cardiovascular measures were heart rate, systolic and diastolic blood pressure, and heart rate variability. Results During the CPT, participants experienced increases in pain (from 0 to 4.1 ± 2.2), systolic blood pressure (from 126.7 ± 16.5 to 149.7 ± 23.4 mm Hg), diastolic blood pressure (from 76.9 ± 8.3 to 91.9 ± 11.5 mm Hg), and heart rate variability (from 0.0164 ± 0.0121 to 0.0400 ± 0.0323 milliseconds; all P values &lt; .001). In addition, we observed a decrease in heart rate after the CPT (P = .04). We found a correlation between athletes' pain catastrophizing and both pain intensity and change in heart rate during the CPT (P = .02 and P = .003, respectively). Linear regression indicated that pain and catastrophizing explained 29% of the variance in the change in heart rate (P = .003). Conclusions Athletes who had catastrophizing thoughts were more likely to experience higher levels of pain and a greater cardiovascular response during a painful stimulus. The change in cardiovascular variables may be a good objective measure of pain in athletes in the future.

scholarly journals Effect of Exercise-Induced Reductions in Blood Volume on Cardiac Output and Oxygen Transport Capacity

2021 ◽  
Vol 12 ◽  
Author(s):  
Janis Schierbauer ◽  
Torben Hoffmeister ◽  
Gunnar Treff ◽  
Nadine B. Wachsmuth ◽  
Walter F. J. Schmidt
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Oxygen Saturation ◽  
Blood Volume ◽  
Oxygen Transport ◽  
Arterial Oxygen ◽  
Peripheral Oxygen Saturation ◽  
Heart Volume ◽  
Arterial Oxygen Content ◽  
Oxygen Transport Capacity

We wanted to demonstrate the relationship between blood volume, cardiac size, cardiac output and maximum oxygen uptake (V.O2max) and to quantify blood volume shifts during exercise and their impact on oxygen transport. Twenty-four healthy, non-smoking, heterogeneously trained male participants (27 ± 4.6 years) performed incremental cycle ergometer tests to determine V.O2max and changes in blood volume and cardiac output. Cardiac output was determined by an inert gas rebreathing procedure. Heart dimensions were determined by 3D echocardiography. Blood volume and hemoglobin mass were determined by using the optimized CO-rebreathing method. The V.O2max ranged between 47.5 and 74.1 mL⋅kg–1⋅min–1. Heart volume ranged between 7.7 and 17.9 mL⋅kg–1 and maximum cardiac output ranged between 252 and 434 mL⋅kg–1⋅min–1. The mean blood volume decreased by 8% (567 ± 187 mL, p = 0.001) until maximum exercise, leading to an increase in [Hb] by 1.3 ± 0.4 g⋅dL–1 while peripheral oxygen saturation decreased by 6.1 ± 2.4%. There were close correlations between resting blood volume and heart volume (r = 0.73, p = 0.002), maximum blood volume and maximum cardiac output (r = 0.68, p = 0.001), and maximum cardiac output and V.O2max (r = 0.76, p &lt; 0.001). An increase in maximum blood volume by 1,000 mL was associated with an increase in maximum stroke volume by 25 mL and in maximum cardiac output by 3.5 L⋅min–1. In conclusion, blood volume markedly decreased until maximal exhaustion, potentially affecting the stroke volume response during exercise. Simultaneously, hemoconcentrations maintained the arterial oxygen content and compensated for the potential loss in maximum cardiac output. Therefore, a large blood volume at rest is an important factor for achieving a high cardiac output during exercise and blood volume shifts compensate for the decrease in peripheral oxygen saturation, thereby maintaining a high arteriovenous oxygen difference.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (1) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

Oxygen transport of colloidal fluorocarbon suspensions in asanguineous rabbits

1975 ◽  
Vol 229 (4) ◽  
pp. 1045-1049 ◽  
Author(s):  
F Gollan ◽  
M Aono ◽  
A Flores
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Oxygen Content ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Oxygen Utilization ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
Hypervolemic Hemodilution

In anesthetized, oxygen-breathing rabbits, the entire blood volume was exchanged with a 20% colloidal fluorocarbon fluid suspension of high gas solubility. In contrast to the control animals with acute isovolemic and hypervolemic hemodilution, the fluorocarbon suspension prevented the decrease in arterial oxygen content below a hematocrit of 13%. However, the more pronounced effect of the fluorocarbon suspension on oxygen delivery occurred at higher hematocrits and was due to its efficiency as a plasma expander, since it increased the cardiac output even above the level of the hypervolemic hemodilution group. The fluorocarbon suspension also raised arterial blood pressure and total peripheral resistance due to its increased viscosity. Thus, in mild hemodilution, the fluorocarbon suspension kept oxygen utilization in the normal range by increasing cardiac output, and in extreme hemodilution it improved oxygen utilization by also raising the arterial oxygen content and arterial blood pressure. The survival time of the isovolemic control animals was 31.6 min, it was extended to 57.8 min in the hypervolemic control animals, and the rabbits with the fluorocarbon suspension lived for 124.8 min.

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