Abstract 16900: Exertional Hemodynamics Among Patients With HFrEF Based on Resting HF Profile

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Cole Buchanan ◽  
Ashley Pratt-Cordova ◽  
Gregory Coe ◽  
Larry A Allen ◽  
Eugene E Wolfel ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiac Index ◽  
Oxygen Uptake ◽  
Ventilatory Threshold ◽  
Peak Oxygen Uptake ◽  
Peak Exercise ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure ◽  
Calorimetry Data

Introduction: HFrEF can be classified by profiles A, B, C or L based on resting pulmonary capillary wedge pressure (PCWP) and cardiac output (Qc). We characterized exertional hemodynamics by HF profile. Methods: HFrEF patients (N=34) completed invasive exercise testing with Swan-Ganz and radial arterial catheterization on upright bicycle. Oxygen uptake was monitored by indirect calorimetry. Data were recorded at supine and upright rest, two exercise stages below ventilatory threshold (steady states 1 and 2), and peak exercise. Participants were stratified into HF profiles based on supine resting hemodynamics including PCWP and cardiac index (CI): Profile A (warm-dry) PCWP≤16mmHg, CI≥2.5L/min/m 2 ; Profile B (warm-wet) PCWP>16mmHg; CI≥2.5L/min/m 2 ; Profile C (cold-wet) PCWP>16mmHg; CI<2.5L/min/m 2 ; Profile L (cold-dry) PCWP≤16mmHg, CI<2.5L/min/m 2 . Results: Demographics are displayed in the table . Peak oxygen uptake (VO 2 ) was severely reduced in all participants ( figure 1 ). Throughout exercise, profile C and L patients had lower stroke volume and Qc, but higher (A-V)O2 difference than profiles A and B ( figure 2 ). Profile B and C patients had higher resting and exertional pulmonary arterial and PCWP filling pressures compared to profiles A and L. Conclusion: Exercise performance among HFrEF patients is not uniform. Exertional hemodynamics vary substantially based on HF profile.

Differential effects of age and type 2 diabetes on dynamic vs. peak response of pulmonary oxygen uptake during exercise

2015 ◽  
Vol 118 (8) ◽  
pp. 1031-1039 ◽  
Author(s):  
Eamonn O'Connor ◽  
Simon Green ◽  
Catherine Kiely ◽  
Donal O'Shea ◽  
Mikel Egaña
Keyword(s):  
Type 2 Diabetes ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Ventilatory Threshold ◽  
Older Men ◽  
Peak Oxygen Uptake ◽  
Peak Exercise ◽  
Middle Aged ◽  
Vascular Conductance

We investigated if the magnitude of the type 2 diabetes (T2D)-induced impairments in peak oxygen uptake (V̇o2) and V̇o2 kinetics was affected by age. Thirty-three men with T2D (15 middle-aged, 18 older), and 21 nondiabetic (ND) men (11 middle-aged, 10 older) matched by age were recruited. Participants completed four 6-min bouts of constant-load cycling at 80% ventilatory threshold for the determination of V̇o2 kinetics. Cardiac output (inert-gas rebreathing) was recorded at rest and 30 and 240 s during two additional bouts. Peak V̇o2 (determined from a separate graded test) was significantly ( P < 0.05) reduced in middle-aged and older men with T2D compared with their respective ND counterparts (middle-aged, 3.2 ± 0.5 vs. 2.5 ± 0.5 l/min; older, 2.7 ± 0.4 vs. 2.4 ± 0.4 l/min), and the magnitude of these impairments was not affected by age. However, the time constant of phase II of the V̇o2 response was only slowed ( P < 0.05) in middle-aged men with T2D compared with healthy counterparts, whereas it was similar among older men with and without T2D (middle-aged, 26.8 ± 9.3 vs. 41.6 ± 12.1 s; older, 40.5 ± 7.8 vs. 41.1 ± 8.5 s). Similarly, the “gains” in systemic vascular conductance (estimated from the slope between cardiac output and mean arterial pressure responses) were lower ( P < 0.05) in middle-aged men with T2D than ND controls, but similar between the older groups. The results suggest that the mechanisms by which T2D induces significant reductions in peak exercise performance are linked to a slower dynamic response of V̇o2 and reduced systemic vascular conductance responses in middle-aged men, whereas this is not the case in older men.

Effects of pneumatic antishock garment inflation in normovolemic subjects

1989 ◽  
Vol 67 (1) ◽  
pp. 339-345 ◽  
Author(s):  
B. J. Rubal ◽  
M. R. Geer ◽  
W. H. Bickell
Keyword(s):  
Cardiac Output ◽  
Pulmonary Capillary Wedge Pressure ◽  
Vascular Resistance ◽  
Heart Function ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Ventricular Afterload ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

This study examines the effects of inflation of pneumatic antishock garments (PASG) in 10 normovolemic men (mean age 44 +/- 6 yr) undergoing diagnostic catheterization. Seven subjects had normal heart function and no evidence of coronary artery disease (CAD); three patients had CAD. High-fidelity multisensor catheters were employed to simultaneously record right and left heart pressures before PASG inflation and after inflation to 40, 70, and 100 mmHg. A thermal dilution catheter was used to obtain pulmonary capillary wedge pressure and cardiac output. Counterpressure increases greater than or equal to 40 mmHg were associated with significant changes in left and right heart pressures. Right and left ventricular end-diastolic pressures increased 100% (P less than 0.01); mean pulmonary arterial and aortic pressures increased 77 and 25%, respectively (P less than 0.01); systemic vascular resistance increased 22% (P less than 0.05) and pulmonary vascular resistance did not change in normal subjects at maximum PASG inflation. Heart rate, cardiac output, and aortic and pulmonary arterial pulse pressures did not change during inflation in either group. Right and left ventricular end-diastolic pressures and pulmonary capillary wedge pressure were greater (P less than 0.05) in the CAD group compared with the normal subjects during PASG inflation. The data suggest that the primary mechanism whereby PASG inflation induces changes in central hemodynamics in normovolemic subjects is through an acute increase in left ventricular afterload. PASG changes in afterload and pulmonary capillary wedge pressure imply that these devices should be used with caution in patients with compromised cardiac function.

Bradykinin actively modulates pulmonary vascular pressure-cardiac index relationships

1987 ◽  
Vol 63 (1) ◽  
pp. 145-151 ◽  
Author(s):  
D. P. Nyhan ◽  
P. W. Clougherty ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Cardiac Index ◽  
Arterial Pressure ◽  
Pulmonary Capillary Wedge Pressure ◽  
Pulmonary Arterial Pressure ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Beta Adrenergic ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Our objectives were to investigate the pulmonary vascular effects of exogenously administered bradykinin at normal and reduced levels of cardiac index in intact conscious dogs and to assess the extent to which the pulmonary vascular response to bradykinin is the result of either cyclooxygenase pathway activation or reflex activation of sympathetic beta-adrenergic and -cholinergic receptors. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by step-wise constriction of the thoracic inferior vena cava to reduce Q. In intact dogs, bradykinin (2 micrograms X kg-1 X min-1 iv) caused systemic vasodilation, i.e., systemic arterial pressure was slightly decreased (P less than 0.05), Q was markedly increased (P less than 0.01), and mixed venous PO2 and oxygen saturation (SO2) were increased (P less than 0.01). Bradykinin decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) over the entire range of Q studied (140–60 ml X min-1 X kg-1) in intact dogs. During cyclooxygenase pathway inhibition with indomethacin, bradykinin again decreased (P less than 0.05) pulmonary arterial pressure-pulmonary capillary wedge pressure at every level of Q, although the magnitude of the vasodilator response was diminished at lower levels of Q (60 ml X min-1 X kg-1). Following combined administration of sympathetic beta-adrenergic and -cholinergic receptor antagonists, bradykinin still decreased (P less than 0.01) pulmonary arterial pressure-pulmonary capillary wedge pressure over the range of Q from 160 to 60 ml X min-1 X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of menopause and Type 2 diabetes on pulmonary oxygen uptake kinetics and peak exercise performance during cycling

2015 ◽  
Vol 309 (8) ◽  
pp. R875-R883 ◽  
Author(s):  
Catherine Kiely ◽  
Joel Rocha ◽  
Eamonn O'Connor ◽  
Donal O'Shea ◽  
Simon Green ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oxygen Uptake ◽  
Ventilatory Threshold ◽  
Menopausal Status ◽  
Constant Load ◽  
Peak Oxygen Uptake ◽  
Oxygen Uptake Kinetics ◽  
Peak Exercise ◽  
Age Range

We investigated if the magnitude of the Type 2 diabetes (T2D)-induced impairments in peak oxygen uptake (V̇o2) and V̇o2 kinetics was affected by menopausal status. Twenty-two women with T2D (8 premenopausal, 14 postmenopausal), and 22 nondiabetic (ND) women (11 premenopausal, 11 postmenopausal) matched by age (range = 30–59 yr) were recruited. Participants completed four bouts of constant-load cycling at 80% of their ventilatory threshold for the determination of V̇o2 kinetics. Cardiac output (CO) (inert gas rebreathing) was recorded at rest and at 30 s and 240 s during two additional bouts. Peak V̇o2 was significantly ( P < 0.05) reduced in both groups with T2D compared with ND counterparts (premenopausal, 1.79 ± 0.16 vs. 1.55 ± 0.32 l/min; postmenopausal, 1.60 ± 0.30 vs. 1.45 ± 0.24 l/min). The time constant of phase II of the V̇o2 response was slowed ( P < 0.05) in both groups with T2D compared with healthy counterparts (premenopausal, 29.1 ± 11.2 vs. 43.0 ± 12.2 s; postmenopausal, 33.0 ± 9.1 vs. 41.8 ± 17.7 s). At rest and during submaximal exercise absolute CO responses were lower, but the “gains” in CO larger (both P < 0.05) in both groups with T2D. Our results suggest that the magnitude of T2D-induced impairments in peak V̇o2 and V̇o2 kinetics is not affected by menopausal status in participants younger than 60 yr of age.

Is peak oxygen uptake a determinant of moderate-duration self-paced exercise performance in the heat?

2011 ◽  
Vol 36 (6) ◽  
pp. 863-872 ◽  
Author(s):  
Zachary J. Schlader ◽  
Stephen R. Stannard ◽  
Toby Mündel
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Skin Temperature ◽  
Exercise Performance ◽  
Perceived Exertion ◽  
Peak Oxygen Uptake ◽  
Performance Outcomes ◽  
Peak Exercise ◽  
Thermal Discomfort ◽  
Male Subjects

This study aimed to identify whether reductions in peak oxygen uptake (VO2peak) dictate performance outcomes during 30 min of self-paced exercise in the heat, which is expected to induce minimal hyperthermia. On 4 occasions, 11 male subjects completed peak and self-paced exercise in both hot (HOT, 40.2 ± 0.3 °C) and moderate (MOD; 20.4 ± 0.7 °C) conditions. During peak exercise, submaximal oxygen uptake (VO2) was ∼8% higher in HOT, but VO2peak (MOD, 4.64 ± 0.83 L·min–1; HOT, 4.54 ± 0.77 L·min–1) and peak cardiac output (Qpeak) were similar. Self-paced exercise performance was reduced by ∼21% in HOT. VO2 was similar through 15 min, but lower in HOT thereafter. Relative to MOD, this represented a higher and lower %VO2peak during the initial and latter stages. Cardiac output was similar in both trials (MOD, 31.6 ± 6.6 L·min–1; HOT, 30.1 ± 6.0 L·min–1), representing a similar percentage of Qpeak throughout. Rectal temperature was similar in both conditions until 30 min (MOD, 38.5 ± 0.3 °C; HOT, 38.7 ± 0.3 °C), while skin temperature was higher throughout in HOT (mean: MOD, 32.4 ± 1.1 °C; HOT, 37.3 ± 0.4 °C). Perceived exertion rose similarly in both conditions, while thermal discomfort was higher in HOT. These data indicate that when only skin temperature is elevated, reductions in exercise performance during moderate-duration self-paced exercise are not associated with changes in VO2peak. Rather, increases in VO2 at a given submaximal external workload and (or) thermal discomfort appear to play a larger role.

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

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