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.

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.

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.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog

1963 ◽  
Vol 204 (5) ◽  
pp. 895-898 ◽  
Author(s):  
James W. West ◽  
Elwood L. Foltz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Venous Oxygen Saturation

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

Effects of polycythemia and anemia on cardiac output and other circulatory factors

1959 ◽  
Vol 197 (6) ◽  
pp. 1167-1170 ◽  
Author(s):  
Travis Q. Richardson ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Oxygen Transport ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Major Effect ◽  
Right Atrial ◽  
Marked Rise ◽  
Chemical Changes ◽  
Normovolemic Anemia ◽  
The Mean

Normovolemic anemia and polycythemia were studied in 14 dogs. Cardiac outputs increased with anemia and fell with rises in hematocrit. Although many factors—such as chemical changes—may play an important role in these variations in cardiac output, there was an indication that viscosity alone may have a major effect. There was no significant association between changes in cardiac output and the various pressures—mean arterial, mean right atrial, mean pulmonary and mean circulatory. Although the pressures did not change significantly, there was a significant decrease in total peripheral resistance in anemia and a marked rise in polycythemia. It was also found that the maximum number of red cells present for oxygen transport to the tissues was near the mean normal hematocrit of 40.

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.

Saturation of arterial blood with oxygen during maximal exercise

1964 ◽  
Vol 19 (2) ◽  
pp. 284-286 ◽  
Author(s):  
Loring B. Rowell ◽  
Henry L. Taylor ◽  
Yang Wang ◽  
Walter S. Carlson
Keyword(s):  
Oxygen Saturation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Oxygen Intake ◽  
Arterial Oxygen Content ◽  
Good Physical Condition ◽  
Arterial Blood ◽  
Sedentary Group ◽  
Arterial Desaturation ◽  
Sufficient Intensity

The per cent saturation of the arterial blood with oxygen was examined in four men before and during the last 15 sec of a 3-min run of sufficient intensity to elicit a maximal oxygen intake. The measurements were repeated after a 3-month period of intensive conditioning for middle distance running and in a group of four athletes in good physical condition. The per cent saturation in the sedentary group was 95.8 at rest and 93.4 during exhausting exercise; after conditioning the similar figures were 95.4 and 91.4 and, finally, the athletes showed a per cent saturation of 85.2 during the heavy work. The arterial oxygen content during exhausting work was found to be 20.12 ml/100 ml blood in the sedentary group before training, 19.02 after conditioning, and 18.18 in the group of athletes. It is concluded that, in athletes who are well conditioned and pushing themselves close to the limit of their capacity, arterial desaturation can take place. athletic conditioning and arterial oxygen saturation; arterial desaturation in athletes; ventilation and arterial desaturation; oxygen intake and arterial oxygen saturation Submitted on August 5, 1963

scholarly journals Effects of Hematocrit Variations on Cerebral Blood Flow and Oxygen Transport in Ischemic Cerebrovascular Disease

1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Oxygen Transport ◽  
Oxygen Delivery ◽  
Inverse Correlation ◽  
Arterial Oxygen ◽  
Brain Oxygenation ◽  
Arterial Oxygen Content ◽  
Ischemic Cerebrovascular Disease

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.

Oxygen pulse

2021 ◽  
pp. 51-55
Author(s):  
William J.M. Kinnear ◽  
James H. Hull
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Arterial Oxygen Saturation ◽  
Recovery Phase ◽  
Arterial Oxygen ◽  
Low Cardiac Output ◽  
Oxygen Pulse ◽  
A Value ◽  
Peripheral Arterial ◽  
Mixed Venous

This chapter outlines how dividing the volume of oxygen uptake (VO2) by the pulse rate gives an estimate of the stroke volume of the heart. The amount of oxygen taken up with each heartbeat is called the oxygen pulse (O2 pulse). It should increase steadily on exercise to a value above 10 ml/beat and may continue to rise during the recovery phase. A low O2 pulse can be an indicator of low cardiac output. If the maximum VO2 (VO2max) is normal, caution should be used in the interpretation of a low O2 pulse. Sometimes the O2 pulse is abnormal because of a fall in peripheral arterial oxygen saturation (SpO2) or mixed venous oxygen levels.

Sign in / Sign up

Export Citation Format

Share Document