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The effect of hyperoxia on central blood pressure in healthy subjects

View Article: PubMed Central - PubMed

ABSTRACT

Introduction: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects.

Material and methods: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 ±1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry.

Results: After the first 2 min of hyperoxia, heart rate decreased significantly (65 ±2.6 beats/min vs. 61 ±2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 ±0.4% vs. 99 ±0.2%, p = 0.03; 168 ±8.4% vs. 180 ±8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (–5.1 ±2.9% vs. –1.2 ±2.6%, p = 0.005 and –4.6 ±2.7% vs. –1.2 ±2.6%, p = 0.0015; –1.3 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.003 and –1.1 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.012; 323 ±3.6 ms vs. 330 ±3.5 ms, p = 0.0002 and 326 ±3.5 ms vs. 330 ±3.5 ms, p = 0.021, respectively).

Conclusions: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

No MeSH data available.


Parameters of central blood pressure presented on the original study recordingSEVR – subendocardial viability ratio, ED – ejection duration, AP – augmentation pressure, AI – augmentation index, PP – pulse pressure, AS – area under the curve for systole, AD – area under the curve for diastole.
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Figure 0001: Parameters of central blood pressure presented on the original study recordingSEVR – subendocardial viability ratio, ED – ejection duration, AP – augmentation pressure, AI – augmentation index, PP – pulse pressure, AS – area under the curve for systole, AD – area under the curve for diastole.

Mentions: Brachial blood pressure was measured with a certified automatic oscillometric device: NIS 2000 (ELMED, Augsburg, Germany). Central blood pressure and heart rate were determined using the SphygmoCor system (MM3 model, AtCor Medical, Sydney, Australia). SphygmoCor uses high fidelity applanation tonometry for the non-invasive registration of radial artery pressure waves and computer software for pressure wave analysis. The average pressure wave was calculated from 8-second recordings. The averaged pressure waves were accepted only when the variation of the peak and bottom pressures of individual pressure waves was < 10%. The SphygmoCor device provides a quality index, which represents reproducibility of the waveform. Measurements were performed by two trained physicians (P.A. and A.D.). Intra-observer and inter-observer variability for these investigators based on 150 previously performed studies is 0 ±4% and 0 ±3% respectively. The visually acceptable recordings of a peripheral pulse waveform were allowed when measurements had a quality index (operator index) > 90. The mean operator index was 93.5 ±1.6% in this study. The central pressure wave was automatically calculated from radial pressures by a built-in general transfer function [22, 23]. The aortic systolic, diastolic and mean blood pressures (mm Hg) were calculated from the recorded central waveforms. SphygmoCor makes it possible to determine other parameters from the central pressure wave. These are: time to first shoulder determined by the outgoing pressure wave (T1, ms), time to the peak of the second shoulder determined by the reflected pressure wave (T2, ms), duration of absolute ejection (ED, ms), augmentation pressure (AP) defined as the difference between pressure values at T2 and T1 (mm Hg), and augmentation index (AI) defined as the quotient of augmentation pressure and central pulse pressure (PP) and expressed as a percentage (%) (Figure 1). The augmentation index and augmentation pressure were normalized for a heart rate of 75 beats per minute. The subendocardial viability ratio (SEVR) was also evaluated from recorded central waveforms. The SEVR (also known as the Buckberg index) is an index of myocardial oxygen supply and demand, and is calculated by pulse wave analysis. Originally, SEVR is derived from pressures measured in the aorta and left ventricle [24, 25] and is defined as the ratio of the pressure-time integral in which the numerator is the diastolic pressure-time integral. The diastolic pressure-time integral (expressed in mm Hg × s) indicates subendocardial blood supply, whereas the systolic pressure-time integral (expressed in mm Hg × s) indicates myocardial contraction (oxygen consumption) [26]. In the study, SEVR was calculated using software provided by the producer. This software automatically calculates SEVR from diastolic/systolic aortic area.


The effect of hyperoxia on central blood pressure in healthy subjects
Parameters of central blood pressure presented on the original study recordingSEVR – subendocardial viability ratio, ED – ejection duration, AP – augmentation pressure, AI – augmentation index, PP – pulse pressure, AS – area under the curve for systole, AD – area under the curve for diastole.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5016570&req=5

Figure 0001: Parameters of central blood pressure presented on the original study recordingSEVR – subendocardial viability ratio, ED – ejection duration, AP – augmentation pressure, AI – augmentation index, PP – pulse pressure, AS – area under the curve for systole, AD – area under the curve for diastole.
Mentions: Brachial blood pressure was measured with a certified automatic oscillometric device: NIS 2000 (ELMED, Augsburg, Germany). Central blood pressure and heart rate were determined using the SphygmoCor system (MM3 model, AtCor Medical, Sydney, Australia). SphygmoCor uses high fidelity applanation tonometry for the non-invasive registration of radial artery pressure waves and computer software for pressure wave analysis. The average pressure wave was calculated from 8-second recordings. The averaged pressure waves were accepted only when the variation of the peak and bottom pressures of individual pressure waves was < 10%. The SphygmoCor device provides a quality index, which represents reproducibility of the waveform. Measurements were performed by two trained physicians (P.A. and A.D.). Intra-observer and inter-observer variability for these investigators based on 150 previously performed studies is 0 ±4% and 0 ±3% respectively. The visually acceptable recordings of a peripheral pulse waveform were allowed when measurements had a quality index (operator index) > 90. The mean operator index was 93.5 ±1.6% in this study. The central pressure wave was automatically calculated from radial pressures by a built-in general transfer function [22, 23]. The aortic systolic, diastolic and mean blood pressures (mm Hg) were calculated from the recorded central waveforms. SphygmoCor makes it possible to determine other parameters from the central pressure wave. These are: time to first shoulder determined by the outgoing pressure wave (T1, ms), time to the peak of the second shoulder determined by the reflected pressure wave (T2, ms), duration of absolute ejection (ED, ms), augmentation pressure (AP) defined as the difference between pressure values at T2 and T1 (mm Hg), and augmentation index (AI) defined as the quotient of augmentation pressure and central pulse pressure (PP) and expressed as a percentage (%) (Figure 1). The augmentation index and augmentation pressure were normalized for a heart rate of 75 beats per minute. The subendocardial viability ratio (SEVR) was also evaluated from recorded central waveforms. The SEVR (also known as the Buckberg index) is an index of myocardial oxygen supply and demand, and is calculated by pulse wave analysis. Originally, SEVR is derived from pressures measured in the aorta and left ventricle [24, 25] and is defined as the ratio of the pressure-time integral in which the numerator is the diastolic pressure-time integral. The diastolic pressure-time integral (expressed in mm Hg × s) indicates subendocardial blood supply, whereas the systolic pressure-time integral (expressed in mm Hg × s) indicates myocardial contraction (oxygen consumption) [26]. In the study, SEVR was calculated using software provided by the producer. This software automatically calculates SEVR from diastolic/systolic aortic area.

View Article: PubMed Central - PubMed

ABSTRACT

Introduction: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects.

Material and methods: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 &plusmn;1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry.

Results: After the first 2 min of hyperoxia, heart rate decreased significantly (65 &plusmn;2.6 beats/min vs. 61 &plusmn;2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 &plusmn;0.4% vs. 99 &plusmn;0.2%, p = 0.03; 168 &plusmn;8.4% vs. 180 &plusmn;8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (&ndash;5.1 &plusmn;2.9% vs. &ndash;1.2 &plusmn;2.6%, p = 0.005 and &ndash;4.6 &plusmn;2.7% vs. &ndash;1.2 &plusmn;2.6%, p = 0.0015; &ndash;1.3 &plusmn;0.7 mm Hg vs. &ndash;0.2 &plusmn;1.2 mm Hg, p = 0.003 and &ndash;1.1 &plusmn;0.7 mm Hg vs. &ndash;0.2 &plusmn;1.2 mm Hg, p = 0.012; 323 &plusmn;3.6 ms vs. 330 &plusmn;3.5 ms, p = 0.0002 and 326 &plusmn;3.5 ms vs. 330 &plusmn;3.5 ms, p = 0.021, respectively).

Conclusions: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

No MeSH data available.