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.

Cardio-respiratory and metabolic responses to different levels of compression during submaximal exercise

2011 ◽  
Vol 26 (3) ◽  
pp. 102-106 ◽  
Author(s):  
B Sperlich ◽  
M Haegele ◽  
M Krüger ◽  
T Schiffer ◽  
H-C Holmberg ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Stroke Volume ◽  
Oxygen Saturation ◽  
Arterial Oxygen Saturation ◽  
Peak Oxygen Uptake ◽  
Submaximal Exercise ◽  
Arterial Oxygen ◽  
Different Levels

Objective The effects of knee-high socks that applied different levels of compression (0, 10, 20, 30 and 40 mmHg) on various cardio-respiratory and metabolic parameters during submaximal running were analysed. Methods Fifteen well-trained, male endurance athletes (age: 22.2 ± 1.3 years; peak oxygen uptake: 57.2 ± 4.0 mL/minute/kg) performed a ramp test to determine peak oxygen uptake. Thereafter, all athletes carried out five periods of submaximal running (at approximately 70% of peak oxygen uptake) with and without compression socks that applied the different levels of pressure. Cardiac output and index, stroke volume, arterio-venous difference in oxygen saturation, oxygen uptake, arterial oxygen saturation, heart rate and blood lactate were monitored before and during all of these tests. Results Cardiac output ( P = 0.29) and index ( P = 0.27), stroke volume ( P = 0.50), arterio-venous difference in oxygen saturation ( P = 0.11), oxygen uptake ( P = 1.00), arterial oxygen saturation ( P = 1.00), heart rate ( P = 1.00) and arterial lactate concentration ( P = 1.00) were unaffected by compression (effect sizes = 0.00–0.65). Conclusion This first evaluation of the potential effects of increasing levels of compression on cardio-respiratory and metabolic parameters during submaximal exercise revealed no effects whatsoever.

Appearance of excess lactate in anesthetized dogs during anemic and hypoxic hypoxia

1965 ◽  
Vol 209 (3) ◽  
pp. 604-610 ◽  
Author(s):  
Stephen M. Cain
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Liver Dysfunction ◽  
Hypoxic Hypoxia ◽  
Blood Gas ◽  
Total Oxygen ◽  
Anesthetized Dogs ◽  
Lactate And Pyruvate ◽  
Mixed Venous

Ten anesthetized, splenectomized dogs were made progressively anemic by replacement of blood with warmed dextran to approximate hematocrits of 30, 20, 15, and 10%. A second group of 10 dogs was made progressively hypoxic by having them inspire 11.4, 9.5, 8.0, and 5.9% O2 in N2. Blood gas contents, pH, and gas tensions were measured in arterial and mixed venous bloods. Cardiac output was calculated from the arteriovenous O2 difference and the O2 uptake. Excess lactate was calculated from measured levels of lactate and pyruvate in blood water. Excess lactate appeared at higher mixed venous Po2 in anemic animals than in hypoxic, 40 mm Hg versus 20 mm Hg. When related to total oxygen transport, however, excess lactate appeared at about the same point (12 ml/kg per min) in both groups. Because liver has been shown to reduce its oxygen uptake with any lowering of perfusate oxygen content, it was suggested that the excess lactate measured during both anemic and hypoxic hypoxia in anesthetized dogs is largely the result of liver dysfunction with respect to lactate.

Mechanism and pharmacology of endotoxin shock in sheep

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
Author(s):  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Arterial Oxygen Saturation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Arterial Oxygen ◽  
Marked Rise ◽  
Pulmonary Arterial ◽  
Pressure Fall

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

Hemodynamics in Sepsis

2006 ◽  
Vol 17 (4) ◽  
pp. 435-445
Author(s):  
Tom Ahrens
Keyword(s):  
Intensive Care Unit ◽  
Cardiac Output ◽  
Tissue Oxygenation ◽  
Capillary Flow ◽  
Timely Manner ◽  
Central Venous ◽  
Low Cardiac Output ◽  
High Cardiac Output ◽  
Hemodynamic State ◽  
Mixed Venous

Hemodynamics in sepsis change as sepsis develops. Initial hemodynamics of sepsis often are much different from later stages of sepsis, shifting from low cardiac output states to high cardiac output states. Tissue oxygenation also changes with initial mixed venous oxyhemoglobin (Svo2) or central venous oxyhemoglobin (Scvo2) levels below normal, with later stages reflecting high values. These changes occur as sepsis progresses, producing a marked disturbance in capillary flow and tissue oxygenation. Treatments for these changes in sepsis are different, making the identification of the hemodynamic state essential to optimally treat the patient. Fortunately, hemodynamic monitoring techniques are markedly improved from older techniques such as the pulmonary artery catheter. With noninvasive techniques such as esophageal and external Doppler for measuring hemodynamics, clinicians beyond the intensive care unit can make hemodynamic assessments that were not possible until just recently. This improved assessment should make it much easier to properly identify sepsis and initiate appropriate treatments in a timely manner.

Regional blood flow and cardiac output during acute hypoxia in the anesthetized dog

1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Head Kidney ◽  
Arterial Oxygen ◽  
Circulatory Effects ◽  
Low Concentrations ◽  
Anesthetized Dogs

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.

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.

Contribution of central and peripheral adaptations to changes in maximal oxygen uptake following 4 weeks of sprint interval training

2018 ◽  
Vol 43 (10) ◽  
pp. 1059-1068 ◽  
Author(s):  
James P. Raleigh ◽  
Matthew D. Giles ◽  
Hashim Islam ◽  
Matthew Nelms ◽  
Robert F. Bentley ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Citrate Synthase ◽  
Interval Training ◽  
Maximal Activity ◽  
Capillary Density ◽  
Oxidative Capacity ◽  
Sprint Interval Training ◽  
Peripheral Arterial

The current study examined the contribution of central and peripheral adaptations to changes in maximal oxygen uptake (V̇O2max) following sprint interval training (SIT). Twenty-three males completed 4 weekly SIT sessions (8 × 20-s cycling bouts at ∼170% of work rate at V̇O2max, 10-s recovery) for 4 weeks. Following completion of training, the relationship between changes in V̇O2max and changes in central (cardiac output) and peripheral (arterial–mixed venous oxygen difference (a-vO2diff), muscle capillary density, oxidative capacity, fibre-type distribution) adaptations was determined in all participants using correlation analysis. Participants were then divided into tertiles on the basis of the magnitude of their individual V̇O2max responses, and differences in central and peripheral adaptations were examined in the top (HI; ∼10 mL·kg−1·min−1 increase in V̇O2max, p < 0.05) and bottom (LO; no change in V̇O2max, p > 0.05) tertiles (n = 8 each). Training had no impact on maximal cardiac output, and no differences were observed between the LO group and the HI group (p > 0.05). The a-vO2diff increased in the HI group only (p < 0.05) and correlated significantly (r = 0.71, p < 0.01) with changes in V̇O2max across all participants. Muscle capillary density (p < 0.02) and β-hydroxyacyl-CoA dehydrogenase maximal activity (p < 0.05) increased in both groups, with no between-group differences (p > 0.05). Citrate synthase maximal activity (p < 0.01) and type IIA fibre composition (p < 0.05) increased in the LO group only. Collectively, although the heterogeneity in the observed V̇O2max response following 4 weeks of SIT appears to be attributable to individual differences in systemic vascular and/or muscular adaptations, the markers examined in the current study were unable to explain the divergent V̇O2max responses in the LO and HI groups.

Oxygen transport in the critically ill

2016 ◽  
Author(s):  
Stephan M. Jakob ◽  
Jukka Takala
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Saturation ◽  
Oxygen Transport ◽  
Oxygen Delivery ◽  
Arterial Oxygen Saturation ◽  
Lactate Concentration ◽  
Mixed Venous Oxygen Saturation ◽  
Arterial Oxygen ◽  
Venous Oxygen Saturation ◽  
Mixed Venous

Adequate oxygen delivery is crucial for organ survival. The main determinants of oxygen delivery are cardiac output, haemoglobin concentration, and arterial oxygen saturation. The adequacy of oxygen delivery also depends on oxygen consumption, which may vary widely. Mixed venous oxygen saturation reflects the amount of oxygen not extracted by the tissues, and therefore provides useful information on the relationship between oxygen delivery and oxygen needs. If not in balance, tissue hypoxia may ensue and arterial lactate concentration increases. This occurs at higher oxygen delivery rates in acute compared with chronic diseases where metabolic adaptions often occur. Arterial and mixed venous oxygen saturation are related to each other. The influence of mixed venous saturation on arterial saturation increases with an increasing intrapulmonary shunt. This chapter discusses interactions between the components of oxygen transport and how they can be evaluated. Various methods for measuring tissue oxygenation and oxygen consumption are also presented, together with their limitations.

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.

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