Resting arteriovenous oxygen difference and exercise cardiac output

1962 ◽  
Vol 17 (6) ◽  
pp. 922-926 ◽  
Author(s):  
H. Duke Thomas ◽  
Carlos Gaos ◽  
T. J. Reeves
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Steady State ◽  
Cardiac Index ◽  
Normal Subjects ◽  
Regression Equation ◽  
Cardiac Patients ◽  
Oxygen Difference

Measurements of the cardiac output utilizing the classical Fick method were carried out in 38 cardiac patients at rest and during exercise. The predicted cardiac output during exercise was calculated by the regression equation derived by Donald et al. ( Clin. Sci. 14: 37, 1955), relating cardiac output to oxygen consumption during the steady state of exercise in normal subjects (cardiac index = 3.708 + 0.00534 x O2 consumption, ml/min m2). The resting arteriovenous oxygen difference was found to correlate much better with the calculated percentage of predicted cardiac index during exercise (γ = 0.547) than did the resting cardiac index (γ = 0.304). The finding of an arteriovenous oxygen difference greater than 5.16 ml/100 cc indicated a strong probability of subnormal cardiac index during exercise relative to the oxygen consumption. Submitted on June 18, 1962

Regulation of the Circulation During Exercise

1956 ◽  
Vol 184 (3) ◽  
pp. 613-623 ◽  
Author(s):  
A. C. Barger ◽  
V. Richards ◽  
J. Metcalfe ◽  
B. Günther
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Steady State ◽  
Rest Period ◽  
Moderate Exercise ◽  
Work Intensity ◽  
Short Bout ◽  
Graded Exercise ◽  
Oxygen Difference

Oxygen consumption and cardiac output (direct Fick) have been measured in normal dogs at rest and during graded exercise on the treadmill up to a work intensity of 5 mph and 10°. Systemic and pulmonary artery pressures have also been recorded. The changes in cardiac output produced ‘at rest’ by excitement were frequently as large as those induced by moderate exercise. A short bout of exercise followed by a rest period was far more efficacious in producing lower and more uniform results during rest and subsequent exercise than a prolonged rest period alone. Under such conditions the ‘steady state’ was reached in 3 minutes or less of exercise. The linear relation between oxygen consumption and cardiac output during exercise in the dog is similar to that observed in man, and in the horse. The possible significance of this similarity is discussed and it is suggested that the data are consistent with the hypothesis that the increase in blood flow during exercise is largely the increase in muscle flow with a constant arteriovenous oxygen difference of approximately 14 vol. %.

Cardiac output response and peripheral oxygen extraction during exercise among symptomatic hypertrophic cardiomyopathy patients with and without left ventricular outflow tract obstruction

Heart ◽  
2014 ◽  
Vol 100 (8) ◽  
pp. 639-646 ◽  
Author(s):  
Christopher H Critoph ◽  
Vimal Patel ◽  
Bryan Mist ◽  
Perry M Elliott
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiac Index ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Non Invasive ◽  
Left Ventricular Outflow ◽  
Oxygen Difference

ObjectiveReduction of left ventricular outflow tract obstruction (LVOTO) often improves symptoms in hypertrophic cardiomyopathy (HCM), but the correlation between exercise performance and measured LVOT gradients is weak. We investigated the relationship between LVOTO and cardiorespiratory responses during exercise.MethodsThe study cohort included 70 patients with HCM (32 with LVOTO, 55 male, age 47±13) attending a dedicated cardiomyopathy clinic and 28 normal volunteers. All underwent cardiopulmonary exercise testing with simultaneous non-invasive haemodynamic assessment using finger plethysmography. Main outcome measures were peak oxygen consumption, cardiac index and arteriovenous oxygen difference.ResultsWhen compared with controls, patients had reduced peak exercise oxygen consumption (22.4±6.1 vs 34.7±7.7 mL/kg/min, p<0.0001) and cardiac index (5.5±1.9 vs 9.4±2.9 L/min/m2, p<0.0001). At all workloads, stroke volume index (SVI) was lower and arteriovenous oxygen difference greater in patients. During all stages of exercise, LVOTO in patients was associated with failure to augment SVI and higher oxygen consumption; cardiac reserve (4.4±2.7 vs 6.3±3.6 L/min, p=0.025) and peak mean arterial pressure (104±16 vs 112±16 mm Hg, p=0.033) were lower. Multivariable predictors of cardiac output response were age (β: −0.11; CI −0.162 to −0.057; p<0.0001), peak LVOT gradient (β: −0.018; CI −0.034 to −0.002; p=0.031) and gender (β: −2.286; CI −0.162 to −0.577; p=0.01). Within the obstructive cohort, different patterns of SV response were elicited in patients with similar clinical features.ConclusionsCardiac reserve is reduced in HCM because of failure of SV augmentation. LVOTO exacerbates this abnormal response, but haemodynamic responses vary significantly. Non-invasive exercise haemodynamic assessment may improve understanding of symptoms and help tailor therapy.

Cardiac Output, Oxygen Consumption and Renal Blood Flow in Essential Hypertension

1984 ◽  
Vol 67 (3) ◽  
pp. 313-319 ◽  
Author(s):  
G. M. London ◽  
M. E. Safar ◽  
J. L. Bouthier ◽  
R. M. Gitelman
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Essential Hypertension ◽  
Blood Volume ◽  
Transit Time ◽  
Normal Subjects ◽  
Total Blood Volume ◽  
Total Blood ◽  
Cost Of Energy ◽  
Oxygen Difference

1. Cardiac output, oxygen consumption, total blood volume and mean circulatory transit time were investigated at rest in men with sustained essential hypertension in comparison with normal subjects of the same age and sex. 2. In normal subjects and in patients with hypertension, oxygen consumption was positively correlated to cardiac output. In hypertensives, the slope of the curve was significantly shallower with an increase in arteriovenous oxygen difference. 3. Oxygen consumption in both populations was negatively correlated with mean circulatory transit time but not with total blood volume. 4. In normal subjects, mean circulatory transit time and arteriovenous oxygen difference were positively correlated. The correlation was not significant in hypertensive patients. 5. The study suggests important abnormalities in the transport and cost of energy in erythrocytes of patients with sustained essential hypertension.

scholarly journals Usefulness of Cardiac Index to Predict Early and 30-Day Mortality in Non-Cardiac Patients Being Admitted to Intensive Care Units

2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Vahan Moradians ◽  
Seyed Ali Javad Moosavi ◽  
Mohammad Niyakan Lahiji ◽  
Maryam Izadi
Keyword(s):  
Cardiac Output ◽  
Intensive Care ◽  
Cardiac Index ◽  
Surface Area ◽  
Intensive Care Units ◽  
Body Surface ◽  
Simplified Acute Physiology Score ◽  
The Body ◽  
Acute Physiology Score ◽  
Cardiac Patients

Introduction: Cardiac index is a hemodynamic parameter defined as the ratio of the cardiac output, i.e., the volume of blood ejected from the left ventricle in 1 min, to the body surface area. This study aimed to assess the cardiac index to predict early and 30-day outcomes of non-cardiac patients being admitted to intensive care units using a non-invasive approach. Materials and Methods: This prospective cohort study included 31 non-cardiac patients who were consecutively admitted to the intensive care units of Rasoul-e-Akram Hospital, Tehran, Iran, in 2016. On admission, the simplified acute physiology score II to predict mortality and the cardiac output (by two-dimensional echocardiography) of each patient were determined. The cardiac index was calculated by dividing the cardiac output by the body surface area. In-hospital mortality and complications were assessed, and the association between simplified acute physiology score II and cardiac index was determined. The patients were followed-up 30 days after discharge by telephone to determine late death, occurrence of myocardial infarction, readmission, or re-hospitalization. Results: The mean cardiac index was significantly lower among the patients who died in intensive care units than in those who survived (2.86 ± 0.63 versus 3.70 ± 0.49, p = 0.006). A significant inverse association was found between Simplified Acute Physiology Score II and cardiac index (r = −0.539, p = 0.002). The length of hospital and intensive care units stay was not associated with Simplified Acute Physiology Score -II or cardiac index. The receiver operating characteristic curve analysis revealed that the cardiac index was effective in predicting in intensive care units mortality (area under curve = 0.857, p = 0.007). The best cut-off value for the cardiac index to predict in intensive care units mortality was 3.35, yielding a sensitivity of 83.3% and a specificity of 80.0%. Conclusion: Measuring the cardiac index during intensive care units admission using a noninvasive approach even in non-cardiac patients can predict in intensive care units mortality with high sensitivity and specificity.

Effect of Hypothermia of 2 to 24 Hours on Oxygen Consumption and Cardiac Output in the Dog

1957 ◽  
Vol 188 (3) ◽  
pp. 473-476 ◽  
Author(s):  
Bernard Fisher ◽  
Clem Russ ◽  
E. J. Fedor
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Body Temperature ◽  
The Body ◽  
Anesthetic Agent ◽  
Oxygen Utilization ◽  
Pentobarbital Sodium ◽  
Initial Decrease ◽  
Physiologic Parameters ◽  
Oxygen Difference

The changes occurring in cardiac output and oxygen consumption in short periods of hypothermia are the same when either ether or pentobarbital sodium is used as the anesthetic agent during the induction of hypothermia. Following an initial decrease in oxygen consumption, no further change occurred as long as the body temperature was maintained at a constant level. Cardiac output, arterial-venous oxygen difference, and coefficient of oxygen utilization remain unchanged for longer periods of time than most physiologic parameters studied during prolonged hypothermia at constant temperatures. After about 14 hours they also begin to alter so that by 24 hours the changes are profound. Stagnant anoxemia and marked increased in the coefficient of O2 utilization resulting from the markedly lowered cardiac output, which was 5% of the precooled controls, occurred.

Cardiac output response to standing and treadmill walking

1961 ◽  
Vol 16 (2) ◽  
pp. 283-288 ◽  
Author(s):  
John T. Reeves ◽  
Robert F. Grover ◽  
S. Gilbert Blount ◽  
Giles F. Filley
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Venous Blood ◽  
Normal Subjects ◽  
Treadmill Walking ◽  
Whole Body ◽  
Output Response ◽  
Total Body ◽  
Response To Exercise ◽  
Oxygen Difference

Cardiac output measurements during cardiac catheterization were obtained in normal subjects for several grades of treadmill exercise. Femoral venous blood was sampled and the A-V oxygen difference for the exercising leg obtained. Measurements of central and femoral A-V oxygen difference and total oxygen uptake were also obtained in normal subjects during supine rest and during standing. When subjects merely stood, the A-V oxygen difference for the leg increased (whether the leg bore weight or not) much more than did that for the whole body. During treadmill walking femoral A-V oxygen difference was usually no greater than that during standing. Cardiac output was smaller and total body A-V oxygen difference was greater for treadmill walking than for supine bicycle exercise in which comparable levels of oxygen uptake were achieved. It is clear that change in posture alters the cardiac output response to exercise. An important aspect of the altered response was a marked difference in the circulation within the leg for these two postures both at rest and during exercise. Submitted on August 8, 1960

The Effect of Massage on Oxygen Consumption at Rest

1995 ◽  
Vol 23 (01) ◽  
pp. 37-41 ◽  
Author(s):  
Tommy Boone ◽  
Rae Cooper
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Healthy Adult ◽  
Statistical Significance ◽  
Lower Extremities ◽  
Treatment Session ◽  
Adult Males ◽  
Significant Difference ◽  
Metabolic Measurement ◽  
Oxygen Difference

This study determined the effect of massage on oxygen consumption at rest. Ten healthy, adult males (mean age = 28 years) volunteered to serve as subjects. During the Control Session, each subject was placed in the supine position on a massage table to remain motionless for 30 minutes. During the Treatment Session, each subject received a 30-minute sports massage of the lower extremities. Oxygen consumption was determined via the Beckman Metabolic Measurement Cart, which was upgraded to estimate cardiac output using the CO 2 rebreathing (equilibrium) method. Paired t-tests were used for all tests of statistical significance. There was no significant difference in the subjects' oxygen consumption with the massage. Also, there were no significant differences in heart rate, stroke volume, cardiac output, and arteriovenous oxygen difference during the massage. These findings indicate (1) that massaging the lower extremities results in neither an increase nor a decrease in the subjects' expenditure of energy at rest and (2) that the energy cost of metabolism at rest is determined by the same central and/or peripheral adjustments.

Effect of beta-adrenergic blockade during exercise on ventilation and gas exchange

1976 ◽  
Vol 41 (6) ◽  
pp. 886-892 ◽  
Author(s):  
H. V. Brown ◽  
K. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Steady State ◽  
Minute Ventilation ◽  
Co2 Flux ◽  
Normal Subjects ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Co2 Output ◽  
Ventilatory Effects

The ventilatory effects of beta-adrenergic blockade during steady-state exercise were studied in eight normal subjects using intravenous propranolol hydrochloride (0.2 mg/kg). Heart rate decreased in all subjects by an average of 17%. Coincident with the phase of decreasing heart rate was a significant decrease in both minute ventilation (VE) and CO2 output (VCO2), averaging 9.6 and 9.2%, respectively. Both functions returned to prepropranolollevels after heart rate had reached its reduced steady-state value. The change in VE was significantly correlated with the change in VCO2 (r = 0.85, Pless than 0.005), and was associated with negligible changes in endtidal CO2 tensions and ventilatory equivalents for CO2. We interpret these studies as showing that the transient isocapnic hypopnea concomitant with an acute reduction in cardiac output was secondary to a transient decrease in CO2 flux (cardiac output x mixed venous CO2 content). This decrease in VE appearsto be induced by the acute decrease in cardiac output (“cardiodynamic hypopnea”), in fashion similar to the previously described cardiodynamic hyperpnea.

Evidence favoring a cardiac mechanism in irreversible hemorrhagic shock

1961 ◽  
Vol 201 (5) ◽  
pp. 893-896 ◽  
Author(s):  
Jack W. Crowell ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Pulmonary Artery ◽  
Hemorrhagic Shock ◽  
Left Atrial ◽  
Peripheral Resistance ◽  
Arterial System ◽  
Operating Parameters ◽  
The Right ◽  
Oxygen Difference

Shock was induced in 55 dogs by removing blood until the arterial pressure had fallen to 30 mm Hg. The pressure was kept at this level for as long as 10 hr by constantly adding additional blood to the reservoir. The hematocrit was kept constant to prevent large variations in the viscosity. Mean pressures of the right and left atrium, the pulmonary artery, and the systemic arterial system were recorded as well as oxygen consumption and A-V oxygen difference. Total peripheral resistance and cardiac output were calculated. That period of time during which the animal passed from a reversible stage of shock to an irreversible stage of shock was studied. It was found that no significant change occurred in oxygen consumption, cardiac output, or peripheral resistance during this transition phase. However, changes did occur in the operating parameters of the heart. The left atrial pressure began rising with the transition from reversible to irreversible shock and continued rising until death of the animal. It is suggested that irreversible hemorrhagic shock is due to acute cardiac failure.

Sign in / Sign up

Export Citation Format

Share Document