Phase-averaged characterization of respiratory sinus arrhythmia pattern.

A method for the accurate time-domain characterization of respiratory sinus arrhythmia (RSA) pattern is presented and applied to two groups of healthy subjects to lay the baseline of RSA patterns and to underlay their features: response to standing, stability in successive recordings, and individuality of the shape of RSA pattern. RSA pattern is evaluated by selective averaging of heart rate (HR) changes from multiple respiratory cycles over the respiratory phase and represents the complete modulating function of HR by respiration. The RSA pattern is evaluated with free respiration and even in cases of severe arrhythmia. Estimation error is 6-8% in magnitude, phase resolution is 0.2 rad, and sensitivity margin for respiratory-related HR variability (HRV) components is 1%. RSA magnitude, phase lag, and expiration-to-inspiration time ratio are derived in addition to the entire pattern. In a group of 10 healthy young adults, a phase lag difference of 11.4 +/- 8.5% (mean +/- SD, P < 0.004) was observed between supine and standing postures, possibly ascribed to breathing mechanics. A second group of 15 healthy young adults at supine rest showed stability of the RSA pattern in successive recordings (several weeks apart) as well as individuality among subjects. This may suggest a nonscalar individual long-term index for cardiorespiratory coupling. The method is complementary to the existing statistical and spectral methods. It allows the complete characterization of the primary RSA components and may provide new insight into the effects of vagal activity and changes in clinical conditions.

Early autonomic malfunction in normotensive individuals with a genetic predisposition to essential hypertension.

One of the primary pathologies associated with hypertension is a complex autonomic dysfunction with evidence of sympathetic hyperactivity and/or vagal withdrawal. We investigated the possibility for early detection of essential hypertension on the basis of the analysis of heart rate (HR) and blood pressure fluctuations, which reflect autonomic control. Young adult normotensive offspring of one hypertensive parent (KHT; n = 12) and normotensive offspring of two normotensive parents (YN; n = 14) participated in this study. ECG, continuous blood pressure, and respiration were recorded during steady-state conditions and under various autonomic challenges. Time-frequency decomposition of these signals was performed with the use of a continuous wavelet transform. The use of the wavelet transform enables the extension of typical HR variability analysis to non-steady-state conditions. This time-dependent spectral analysis of HR allows time-dependent quantification of different spectral components reflecting the sympathetic and parasympathetic activity during rapid transitions, such as an active change in posture (CP). During an active CP from the supine to standing position, KHT demonstrated a significantly greater increase in the low-frequency fluctuations in HR than YN, indicating enhanced sympathetic involvement in the HR response to CP, and a reduced alpha-index, indicating decreased baroreceptor sensitivity. On recovery from handgrip, vagal reactivation was more sluggish in KHT. These results indicate the early existence of malfunctions in both branches of autonomic control in individuals at increased risk of hypertension.

Moderate sodium restriction does not alter lower body negative pressure tolerance.

HYPOTHESIS: Space travel with exposure to microgravity leads to a significant reduction in orthostatic tolerance on return to Earth, for which countermeasures are only partially successful. The purpose of this study was to examine the effect of moderate dietary sodium restriction on tolerance to LBNP. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Subjects were exposed to presyncopal LBNP after consuming their "typical" diet (C) for 5 d and after consuming a sodium restricted (SR) diet for 5 d. Diet sequence was randomized and adherence was verified by 24-h urine collection on the 4th and 5th days of each diet. RESULTS: All subjects reached presyncope during the LBNP, regardless of diet. Urinary sodium excretion was 3390+/-950 mg on the C diet and 1174+/-560 mg on the SR diet. Urinary potassium was not different between the diets. Cumulative stress index scores were 655+/-460 (mm Hg x min) on the C diet and 639+/-388 (mm Hg x min) during SR. Cardiac volumes, BP and total peripheral resistance were not different at any stage of the LBNP between the diets, nor were catecholamines. Plasma renin activity, determined by radioimmunoassay, was significantly higher during SR at rest, and during all stages of LBNP in comparison with the control diet. CONCLUSION: Moderate dietary sodium restriction is not detrimental to orthostatic tolerance.

Cardiovascular effects of the breathhold used in determining pulmonary diffusing capacity.

BACKGROUND: The single-breath technique for determination of the diffusion capacity of the lung for CO (DlCO) requires a 10-s breathhold at total lung capacity. The assumption has been that this breathhold does not alter the components of DlCO, i.e., the diffusion capacity of the membrane (Dm) and the pulmonary capillary blood volume (Qc), and therefore measurement of these variables during breathhold represents these variables as they exist during normal breathing. The purpose of this study was to determine the effect of the 10-s breathhold on cardiac output (Q) and Qc while supine and standing. The hypothesis was that the standing posture would have a greater influence on Q and Qc during the breathhold than would the supine posture. METHODS: Twelve male subjects participated. Q, stroke volume (SV), heart rate (HR), BP (MAP), and total peripheral resistance (TPR) were determined before and during the 10-s breathhold determination of DlCO, Qc, and Dm. RESULTS: Results while supine were compared with those while standing. DlCO was reduced on standing, due mainly to a reduction in Qc. SV and Q decreased significantly during the 10-s breathhold in both postures. Both SV and Q decreased more when standing (-53% and -49.5%, respectively) than when supine (-40.5% and -36.5%, respectively). Thus, the 10-s breathhold caused significant reductions in Q and therefore may alter the measurement of DlCO and Qc. CONCLUSIONS: The greater decline in Q during the measurement of DlCO when standing would suggest that the DlCO and Qc values while breathing might be underestimated in the upright posture.

The heart is not necessarily empty at syncope.

BACKGROUND: Although extensively investigated, the mechanism(s) of post-spaceflight orthostatic intolerance has not been elucidated. Several researchers have proposed that the "trigger" for syncope is an empty ventricle, initiated when a hypercontractile state, possibly due to a sudden surge in epinephrine, causes the walls of the left ventricle to touch leading to a profound sympatho-inhibition and intense vagal stimulation. HYPOTHESIS: A markedly reduced left ventricular end systolic volume (LVESV) achieved during progressive, presyncopal-limited lower body negative pressure (LBNP) is the trigger for syncope. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Changes in left ventricular end-diastolic volume and LVESV were measured, using two-dimensional echocardiography, at each stage of LBNP from rest up to presyncope (PS). Plasma venous catecholamine concentrations were measured at the end of each stage by high performance liquid chromatography (HPLC) with electrochemical detection. RESULTS: All subjects reached PS. Three men became bradycardic at presyncope while five remained tachycardic. LVESV decreased by 28% at PS with no evidence of ventricular cavity obliteration. Norepinephrine increased by 44% from rest to PS, but no epinephrine surge was detected (35% increase from rest to PS). CONCLUSION: These data indicate that it is possible to initiate syncope with only a 28% decrease in LVESV, and that sympatho-inhibition and bradycardia are not required elements for syncope to occur.

Validation of impedance cardiography during lower body negative pressure.

BACKGROUND: Both echocardiographic and impedance cardiographic techniques have been used individually for the determination of stroke volume (SV) during lower body negative pressure (LBNP). Impedance cardiography has not been validated during LBNP. HYPOTHESIS: The purpose of this study was to determine both the absolute values for SV and the change in SV for each stage of LBNP using both impedance and echocardiographic techniques during staged LBNP to presyncope. The hypothesis was that there would be no difference between the two techniques for either the absolute values of SV or for the change in SV with each stage of LBNP. METHODS: There were 16 men who volunteered to undergo LBNP. LBNP was lowered in 10 mmHg stages for 5 min per stage until presyncope was reached. Left ventricular SV was determined by two-dimensional echocardiography and impedance cardiography. Both the absolute values for SV and the change in SV from baseline at each stage of LBNP were compared for the two methods. RESULTS: There were no significant differences between the two techniques for the measurement of either the absolute SV or the change in SV with LBNP. The two methods correlated highly with r = 0.89 for the absolute SV values and r = 0.93 for the change in SV. Graphical analysis with the Bland-Altman analysis showed little bias in the impedance measurement for SV (-0.031 ml) and the change in SV (-2.7 ml). CONCLUSIONS: Impedance cardiography was a reliable measure of SV, as well as the change in SV, during LBNP stress to presyncope.

Bioelectric impedance as an index of thoracic fluid.

BACKGROUND: Thoracic electrical impedance (TEI) has been suggested as a means to monitor thoracic fluid changes. It was hypothesized that TEI would correlate significantly with an intrathoracic blood volume (pulmonary capillary blood volume) during postural shifts. METHODS: TEI was compared with pulmonary capillary blood volume (Vc) in six men and six women during postural stress. The diffusion capacity for carbon monoxide (DLCO) was used to determine Vc. Subjects were supine for 15 min and then stood quietly for 5 min. Measurements were made at the end of each period. Heart rate (HR), stroke volume (SV), and BP were determined for each posture. RESULTS: Women had higher TEI values at rest, confirming previous data. Cardiopulmonary variables change similarly for each gender on standing. TEI correlated significantly with Vc (p<0.01), and Vc was significantly correlated with SV (p<0.01). Total lung capacity and residual volumes were unchanged with posture. CONCLUSION: It is concluded that TEI can serve as a useful clinical and research monitor of thoracic fluid volume changes, even small volume changes, and correlates with a measured thoracic fluid compartment.

Pulmonary capillary blood volume during lower body negative pressure: effect of gender.

BACKGROUND: The purpose of this study was to examine the changes in pulmonary capillary blood volume (VC) in men and women during lower body negative pressure (LBNP). Additionally, the components of lung diffusion capacity were measured and evaluated for the effect of gender and LBNP. METHODS: There were 6 men and 6 women who underwent a staged LBNP protocol to -40 mm Hg. The diffusion of the lung for carbon monoxide (DLCO) was determined at two levels of inspired oxygen (21% and 60%). DLCO was separated into the diffusion capacity of the membrane (DLM) and the diffusion capacity of blood. RESULTS: During supine rest, DLCO values for men were larger than for women and were 39.8 +/- 3.8 and 32.2 +/- 2.2 ml.min-1.mm-1 Hg, respectfully. DLCO decreased equally with each stage of LBNP for men and women. VC during supine rest was greater for men (131 +/- 8 ml) than for women (92.7 +/- 7 ml). VC also declined with each stage of LBNP, and the decline was similar for men and women. DLM did not change with LBNP. CONCLUSION: The decrease in DLCO with LBNP is due to the reductions in thoracic blood volume in both men and women. These thoracic blood volume changes do not explain the previously reported reduced tolerances to LBNP for women because the reductions in thoracic blood volume were similar for men and women.