Cardio-vascular reserve index (CVRI) during exercise complies with the pattern assumed by the cardiovascular reserve hypothesis.

Objectives: The Cardio-vascular reserve index (CVRI) had been empirically validated in diverse morbidities as a quantitative estimate of the reserve assumed by the cardiovascular reserve hypothesis. This work evaluates whether CVRI during exercise complies with the cardiovascular reserve hypothesis.

Design: Retrospective study based on a database of patients who underwent cardio-pulmonary exercise testing (CPX) for diverse indications.

The approximated cardiovascular reserve index complies with haemorrhage related hemodynamic deterioration pattern: A swine exsanguination model.

Background: To estimate the cardiovascular reserve we formulated the Cardiovascular Reserve Index (CVRI) based on physiological measurements. The aim of this study was to evaluate the pattern of CVRI in haemorrhage-related haemodynamic deterioration in an animal model simulating combat injury.

Methods: Data were collected retrospectively from a research database of swine exsanguination model in which serial physiological measurements were made under anesthesia in 12 swine of haemorrhagic injury and 5 controls.

A novel hypothesis comprehensively explains shock, heart failure and aerobic exhaustion through an assumed central physiological control of the momentary cardiovascular performance reserve.

Background: Heart failure (HF) and shock are incomprehensively understood, inconclusively defined and lack a single conclusive test. The proceedings that preceded and triggered clinical manifestations are occult. The relationships in between different shock and HF types and between each HF type and its matched shock are poorly understood.

A novel heart rate control model provides insights linking LF-HRV behavior to the open-loop gain.

Background: Low-frequency heart rate variability (LF-HRV) at rest has already been successfully modeled as self-sustained oscillations in a nonlinear control loop, but these models fail to simulate LF-HRV decreases either during aerobic exercise or in heart failure patients. Following control engineering practices, we assume the existence of a biological excitation (dither) within the heart rate control loop that softens the nonlinearity and studied LF-HRV behavior in a dither-embedded model.

Methods: We adopted the Ottesen model with some revisions and induced a dither of high-frequency stochastic perturbations.

Hypothesis: Low frequency heart rate variability (LF-HRV) is an input for undisclosed yet biological adaptive control, governing the cardiovascular regulations to assure optimal functioning.

Cardiovascular regulation is considered today as having three levels: autoregulations, neural regulations and hormonal regulations. We hypothesize that the cardiovascular regulation has an additional (fourth) control level which is outer, hierarchical (adaptive) loop where LF-HRV amplitude serves as a reference input which the neural cardiovascular center detects and responses in order to maintain LF-HRV around some prescribed level. Supporting evidences: LF-HRV absence during artificial cardiac pacing may be associated with "pacemaker syndrome" which had not been sufficiently understood regardless of apparently unimpaired cardiovascular performance.

Analysis of direct spectrum measurement of a sinusoidal signal impaired by either fractional Gaussian phase noise or fractional Brownian phase motion.

This article discusses the empirical spectrum (periodogram) of a sinusoidal signal that is phase modulated by either fractional Gaussian noise (fGn) or fractional Brownian motion (fBm). These two cases are of note because they are frequently used to model oscillator phase instabilities known as "1/f noise" and "1/f(3)noise," respectively. This work demonstrates that an fGn phase noise may result in a 1/f-shaped spectrum, as might be expected.

Very low-frequency heart rate variability wave amplitude and sympathetic stimulation--characterization and modeling.

The purpose of this study was to assess the relationship between very low-frequency heart rate variability (LFHR) wave amplitude and the degree of sympathetic stimulation. We developed a computerized system for the controlled increase of heart rate (HR) by isoproterenol (ISP), with which we obtained a series of stabilized HR levels in conscious freely moving rats. We found that LFHR amplitude rises gradually as a function of the average HR for each level until it reaches a point where additional increases in average HR are associated with gradual decrease in LFHR amplitude.

A common origin of the very low frequency heart rate and blood pressure variability--a new insight into an old debate.

The purpose of this study was to assess the exact temporal and amplitude relationship between very low frequency heart rate variability waves and very low frequency blood pressure variability waves. We developed a computerized system based on a modified proportional-integral controller for the controlled increase of heart rate by isoproterenol. Heart rate and blood pressure were measured continuously in conscious tethered rats.