Browsing by Subject "Blood volume"

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Admittance measurement for early detection of congestive heart failure
(2010-05) Porterfield, John Edward; Pearce, John A., 1946-; Valvano, Jonathan W.; Yilmaz, Ali; Rylander, Henry G.; Feldman, Marc D.
Impedance has been used as a tool for cardiac research since the early 1940’s. Recently there have been many advances in this field in the diagnosis of human heart failure through the measurement of pacemaker and ICD coupled impedance detection to determine the state of pulmonary edema in patients through drops in lung impedance. These new detection methods are far downstream of the initial changes in physiology, which signify heart failure risk, namely, an increased left ventricular (LV) end-diastolic volume (also known as preload). This dissertation presents the first formal validation of the complex admittance technique for more accurate blood volume measurement in vivo in mice. It aims to determine a new configuration of admittance measurement in a large scale animal model (pigs). It also aims to prove that “piggybacking” an admittance measurement system onto previously implanted AICD and bi-ventricular pacemakers is a feasible and practical measurement that will serve as an early warning system for impending heart failure through the measurement of LV preload, which appears before the currently measured drop in lung impedance using previous techniques.
The effect of a single session of intermittent hypoxia on erythropoietin and oxygen-carrying capacity
(2020-05-04) Nagel, Mercedes J.; Lalande, Sophie
Intermittent hypoxia, defined as alternating bouts of breathing hypoxic and normoxic air, has the potential to improve oxygen-carrying capacity through an erythropoietin-mediated increase in hemoglobin mass. The purpose of this study was to determine the effect of a single exposure of intermittent normobaric hypoxia on erythropoietin levels and hemoglobin mass in young healthy individuals. Nineteen healthy individuals (10 women and 9 men, age: 24 ± 4 years, height: 174 ± 11 cm, weight: 72.2 ± 12.2 kg) participated in the study. Participants were randomly assigned to an intermittent hypoxia group (Hyp, n = 10) or a placebo intermittent normoxia group (Norm, n = 9). Intermittent hypoxia consisted of five 4-minute hypoxic cycles at a targeted arterial oxygen saturation of 90% interspersed with 4-minute normoxic cycles. Air was made hypoxic by titrating nitrogen to a breathing circuit connected to a tank of compressed air. Nitrogen was not added to the breathing circuit in the intermittent normoxia condition. Pulmonary gas exchange, arterial oxygen saturation, and hemodynamics, using finger plethysmography, were continuously assessed during the intervention. Erythropoietin levels were measured before and two hours following the completion of the protocol. Hemoglobin mass was assessed using the carbon monoxide rebreathing technique the day before and seven days after exposure to intermittent hypoxia or normoxia. As anticipated, the intermittent hypoxia group had a lower arterial oxygen saturation than the intermittent normoxia group during the intervention (Hyp: 89 ± vs. Norm: 98 ± 1%, p < 0.01), which was equivalent to a lower fraction of inspired oxygen (Hyp: 0.119 ± 0.008, Norm: 0.209 ± 0.001, p < 0.01). Erythropoietin levels did not significantly increase following exposure to intermittent hypoxia (Hyp: 8.2 ± 4.5 to 9.0 ± 4.8, Norm: 8.9 ± 1.7 to 11.1 ± 2.1 mU/ml, p = 0.56). Hemoglobin mass did not change following exposure to intermittent hypoxia (Hyp: 10.6 ± 1.4 to 10.2 ± 1.4, Norm: 9.7 ± 1.6 to 9.4 ± 1.5 g/kg, p = 0.48). Exposure to intermittent hypoxia did not affect mean arterial pressure (Hyp: 91 ± 6 to 90 ± 6, Norm: 93 ± 12 to 93 ± 12 mmHg, p = 0.84) or heart rate (Hyp: 68 ± 8 to 74 ± 9, Norm: 68 ± 8 to 68 ± 8 mmHg, p = 0.27). Respiratory rate, tidal volume, end-tidal CO₂ and total minute ventilation were not affected by intermittent hypoxia. Thus, a 40-minute session of intermittent hypoxia was not sufficient to elicit a rise in erythropoietin levels or hemoglobin mass in young healthy individuals. A longer exposure to intermittent hypoxia at a lower arterial oxygen saturation may be necessary to trigger an erythropoietin-mediated increase in hemoglobin mass in young healthy individuals.
The effect of the menstrual cycle on hemoglobin mass
(2019-05-08) Keller, Melissa Faith; Lalande, Sophie
The impact of the menstrual cycle on oxygen-carrying capacity remains equivocal. Previous studies reported either reductions or no significant changes in hemoglobin concentration during the follicular phase when compared to the luteal phase of the menstrual cycle. Changes in plasma volume associated with fluctuating estrogen and progesterone levels likely contribute to the variations in hemoglobin concentration observed throughout the menstrual cycle. Thus, measures of hemoglobin concentration do not accurately represent the oxygen-carrying capacity of the blood. Hemoglobin mass represents a more direct measure of oxygen-carrying capacity. However, the impact of menstrual blood loss on hemoglobin mass remains unknown. PURPOSE: To determine the effect of the menstrual cycle on hemoglobin mass in pre-menopausal women. METHODS: Twenty-one women (age: 23 ± 6 years, height: 167 ± 7 cm, weight: 66 ± 13 kg) with a regular menstrual cycle using (n = 9) and not using hormonal contraceptives participated in the study. Hemoglobin mass was assessed using the carbon monoxide rebreathing technique on three separate occasions. Visits for women using hormonal contraceptives were scheduled in the early follicular phase (3-5 days post-onset of menses), late follicular phase (14 days post-onset of menses), and mid-to-late luteal phase (10 days after the late follicular visit). Visits for women not using hormonal contraceptives were scheduled in the early follicular phase (3-5 days post-onset of menses), late follicular phase (1-2 days post-surge of luteinizing hormone in urine), and mid-to-late luteal phase (10 days after the late follicular visit). RESULTS: No differences were observed in hemoglobin concentration across phases of the menstrual cycle (early follicular: 12.9 ± 1.3 g/dl, late follicular: 12.7 ± 0.9 g/dl, mid-to-late luteal: 12.8 ± 0.9 g/dl, p = 0.08). Likewise, hemoglobin mass did not significantly differ between menstrual cycle phases (early follicular: 606 ± 73 g, late follicular: 602 ± 73 g, mid-to-late luteal: 606 ± 68 g, p = 0.90). Hemoglobin mass for women using hormonal contraceptive tended to be higher than non-users across the menstrual cycle (early follicular: 629 ± 53 g vs. 590 ± 83 g, late follicular: 635 ± 58 g vs. 577 ± 75 g, mid-to-late luteal: 626 ± 61 vs. 592 ± 71 g, respectively, p = 0.12). CONCLUSION: The menstrual cycle has no significant impact on hemoglobin mass or oxygen-carrying capacity in eumenorrheic women. The use of hormonal contraceptives may improve oxygen-carrying capacity.