Mechanical Effects Of Respiration Research Articles

Role of short-term cardiovascular regulation in heart period variability: a modeling study.

A mathematical model of short-term cardiovascular regulation is used to investigate how heart period variability reflects the action of the autonomic regulatory mechanisms (vagal and sympathetic). The model includes the pulsating heart, the systemic (splanchnic and extrasplanchnic) and pulmonary circulation, the mechanical effect of respiration on venous return, two groups of receptors (arterial baroreceptors and lung stretch receptors), the sympathetic and vagal efferent branches, and a very low-frequency (LF) vasomotor noise. All model parameters were given on the basis of physiological data from the literature. We used data from humans whenever possible, whereas parameters for the regulation loops are derived from dog experiments. The model, with basal parameter values, produces a heart period power spectrum with two distinct peaks [a high frequency (HF) peak at the respiratory rate and a LF peak at approximately 0.1 Hz]. Sensitivity analysis on the mechanism gains suggests that the HF peak is mainly affected by the vagal mechanism, whereas the LF peak is increased by a high sympathetic gain and reduced by a high vagal gain. Moreover, the LF peak depends significantly on the reactivity of resistance vessels and is affected by noise, amplified by the sympathetic control loop at its resonance frequency. The model may represent a new tool to study alterations in the heart period spectrum on the basis of quantitative physiological hypotheses.

Mechanism of blood pressure and R-R variability: insights from ganglion blockade in humans.

Spontaneous blood pressure (BP) and R-R variability are used frequently as 'windows' into cardiovascular control mechanisms. However, the origin of these rhythmic fluctuations is not completely understood. In this study, with ganglion blockade, we evaluated the role of autonomic neural activity versus other 'non-neural' factors in the origin of BP and R-R variability in humans. Beat-to-beat BP, R-R interval and respiratory excursions were recorded in ten healthy subjects (aged 30 +/- 6 years) before and after ganglion blockade with trimethaphan. The spectral power of these variables was calculated in the very low (0.0078-0.05 Hz), low (0.05-0.15 Hz) and high (0.15-0.35 Hz) frequency ranges. The relationship between systolic BP and R-R variability was examined by cross-spectral analysis. After blockade, R-R variability was virtually abolished at all frequencies; however, respiration and high frequency BP variability remained unchanged. Very low and low frequency BP variability was reduced substantially by 84 and 69 %, respectively, but still persisted. Transfer function gain between systolic BP and R-R interval variability decreased by 92 and 88 % at low and high frequencies, respectively, while the phase changed from negative to positive values at the high frequencies. These data suggest that under supine resting conditions with spontaneous breathing: (1) R-R variability at all measured frequencies is predominantly controlled by autonomic neural activity; (2) BP variability at high frequencies (> 0.15 Hz) is mediated largely, if not exclusively, by mechanical effects of respiration on intrathoracic pressure and/or cardiac filling; (3) BP variability at very low and low frequencies (< 0.15 Hz) is probably mediated by both sympathetic nerve activity and intrinsic vasomotor rhythmicity; and (4) the dynamic relationship between BP and R-R variability as quantified by transfer function analysis is determined predominantly by autonomic neural activity rather than other, non-neural factors.

Effects of CPAP therapy on cardiovascular variability in obstructive sleep apnea: a closed-loop analysis

To determine the long-term effects of continuous positive airway pressure (CPAP) therapy on cardiovascular variability, we measured R-R interval (RR), systolic blood pressure (SBP) and respiration (DeltaV) in 13 awake, supine patients with moderate-to-severe obstructive sleep apnea (OSA), before and after ~6 mo of treatment. Using these data, we estimated the dynamics of the following components of a closed-loop circulatory control model: 1) the baroreflex component, 2) the neural coupling of DeltaV to RR or respiratory sinus arrhythmia (RSA), 3) the mechanical effects of respiration (MER) on SBP, and 4) the circulatory dynamics (CID) component, which is responsible for the feedforward effect of RR fluctuations on SBP. Baroreflex and RSA gains increased whereas MER and CID gains decreased in compliant subjects whose average CPAP use was >3 h/night. In contrast, baroreflex, RSA, and MER gains remained unchanged and CID gain increased in noncompliant subjects. Other summary measures were unchanged in both groups, except for mean RR, which increased in compliant patients. Closed-loop analysis provides a simple but sensitive means for quantitatively assessing cardiovascular control in OSA by using data collected from a single, nonintrusive test procedure.

Role of the Baroreflex in Cardiovascular Instability: A Modeling Study

A mathematical model of the short-term arterial pressure control is used to investigate the possible origin of blood pressure waves (Mayer waves) and of heart rate variability signals. The model includes an elastance-variable pulsating heart, the pulmonary and systemic circulation, the mechanical effect of respiration on venous return, and the regulatory actions of two groups of baroreceptors: the high-pressure (i.e., arterial) baroreceptors and the low-pressure (i.e., cardiopulmonary) baroreceptors. The feedback mechanisms work by modulating the peripheral resistances, the venous unstressed volumes, the ventricle end-systolic elastance and the heart period. The last mechanism involves a balance between sympathetic and vagal control actions. The basal value of all parameters in the heart and vascular model has been given to mimic a normal human hemodynamic. Parameters in the feedback regulation mechanisms have been assigned on the basis of open loop experiments in vagotomized dogs (as to the sympathetic arterial baroreflex) and neck chamber or lower body negative pressure experiments in human volunteers (as to vagal response and cardiopulmonary baroreflex). A sensitivity analysis on the gains and time delays of the feedback mechanisms revealed that (i) a significant increase in the gains and time delays (above 9 s) of all the arterial baroreflex sympathetic mechanisms is required to induce instability. In this condition, systemic arterial pressure exhibits spontaneous oscillations with a period of about 20 s, similar to Mayer waves. The control of peripheral resistance seems more important than the venous volume control in the genesis of these oscillations. (ii) An increase in the gain and time delay (above 3 s) of the arterial baroreflex vagal mechanism causes the appearance of unpredictable fluctuations in heart period, with spectral components in the range 0.08–0.12 Hz. These fluctuations originate after a double period bifurcation. (iii) The cardiopulmonary baroreflex plays a less important role in the genesis of the aforementioned instability phenomena.

Effects of exercise load and breathing frequency on heart rate and blood pressure variability during dynamic exercise.

It is known that heart rate (HR) variability decreases with dynamic exercise, but there are only few studies on blood pressure (BP) variability with exercise loads and the effect of breathing pattern has never been investigated. Thus, we studied HR and systolic blood pressure (SBP) signals by spectral analysis (FFT), in 9 healthy subjects, at different breathing frequencies (0.15, 0.2, 0.3, 0.4, 0.5, 0.6 Hz), at rest and during 3 exercise loads (25, 50 and 75% VO2max). BP was measured with a non-invasive device (Finapres) and continuously recorded. The power spectrum of R-R period significantly decreased with exercise loads in the low frequency band (LF: 0.04-0.128 Hz) and in the high frequency band (HF: 0.128-0.65 Hz), but with breathing frequency only in the HF part of the spectrum. The power spectrum of SBP significantly increased with exercise loads in LF and HF bands, and decreased in HF band with increasing breathing frequency. R-R and SBP HF peaks were centered on breathing frequency peaks. Therefore, spectral analysis of HR and SBP confirm the withdrawal of vagal control during exercise, while mechanical effect of respiration on SBP persists. LF/HF ratio of R-R spectral components decreased with increasing load, whereas cardiovascular sympathetic activity is known to rise, suggesting that this ratio is not a good indicator of cardiovascular autonomic modulation during exercise.

Cardiac baroreceptor sensitivity is impaired after acute stroke.

The blood pressure (BP) fall and increased BP variability after acute stroke have been previously described. The underlying pathophysiological mechanisms producing these findings are unclear but may include abnormalities of cardiac baroreceptor reflex arc and/or changes in sympathetic nervous system activity. To date, evidence of impaired cardiac baroreceptor sensitivity (BRS) after stroke is limited to patients with chronic disease as determined by invasive methodology. Therefore, it was proposed to assess cardiac BRS and sympathovagal balance with the use of novel noninvasive techniques after acute stroke. Thirty-seven acute stroke patients underwent simultaneous surface electrocardiographic and noninvasive beat-to-beat BP recording. Cardiac BRS was assessed by power spectral analysis techniques, and sympathovagal balance was determined from the ratio of the low- to high-frequency powers for pulse interval variability. The responses were compared with a control group matched for age, sex, and BP. Median cardiac BRS was significantly lower in stroke patients than in control subjects (high-frequency alpha-index, 4.89 versus 6.50 ms/mm Hg; P = .007; combined alpha-index, 4.65 versus 5.46 ms/mm Hg; P = .02). Median normalized high- but not low-frequency power of systolic BP variability was significantly greater in stroke patients (11.0 versus 6.7 normalized units; P < .001), probably reflecting differences in the mechanical effects of respiration on BP in stroke patients. No significant differences were observed in the power spectrum of pulse interval variability between stroke patients and control subjects. Patients with tight hemisphere strokes, however, had a significant reduction in median high-frequency pulse interval power compared with patients with left hemisphere strokes (8 versus 20 normalized units; P = .03), which may reflect a change in sympathovagal balance in favor of increased sympathetic tone in this group. The impairment of cardiac BRS may be important in explaining the increased BP variability after stroke. There was no significant difference in surrogate measures of sympathovagal activity between acute stroke patients and control subjects, but right hemisphere stroke patients had a significant alteration in the sympathovagal balance of pulse interval variability compared with left hemisphere stroke patients. This sympathetic predominance in right hemisphere strokes may be important in the development of cardiac arrhythmias after stroke. The prognostic implications of these findings need to be further explored.

Cardiopulmonary Interactions in the Cardiac Patient in the Intensive Care Unit

Critically ill cardiac patients often undergo mechanical ventilation. The interplay between pulmonary and cardiac mechanics is complicated and in many cases may result in impaired transfer of O2 from the atmosphere to the tissues. This article addresses the principles of pulmonary and peripheral gas exchange, as well as the mechanical effects of respiration on the circulation.

Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model.

A beat-to-beat model of the cardiovascular system is developed to study the spontaneous short-term variability in arterial blood pressure (BP) and heart rate (HR) data from humans at rest. The model consists of a set of difference equations representing the following mechanisms: 1) control of HR and peripheral resistance by the baroreflex, 2) Windkessel properties of the systemic arterial tree, 3) contractile properties of the myocardium (Starling's law and restitution), and 4) mechanical effects of respiration on BP. The model is tested by comparing power spectra and cross spectra of simulated data from the model with spectra of actual data from resting subjects. To make spectra from simulated data and from actual data tally, it must be assumed that respiratory sinus arrhythmia at rest is caused by the conversion of respiratory BP variability into HR variability by the fast, vagally mediated baroreflex. The so-called 10-s rhythm in HR and BP appears as a resonance phenomenon due to the delay in the sympathetic control loop of the baroreflex. The simulated response of the model to an imposed increase of BP is shown to correspond with the BP and HR response in patients after administration of a BP-increasing drug, such as phenylephrine. It is concluded that the model correctly describes a number of important features of the cardiovascular system. Mathematical properties of the difference-equation model are discussed.

Arterial pressure pulsation during nonpulsatile biventricular bypass experiments: possible idioperipheral pulsation.

During nonpulsatile biventricular bypass (NPBVB) experiments, regular fluctuations of arterial pressure were observed in all five long-term animals whose ventricles were fibrillated. Analysis of the characteristics of this fluctuation was performed retrospectively. The pulse pressure of this fluctuation increased gradually after the first 2 weeks. They were 6.7, 7.6, 10.2, and 12.4 mm Hg on the fortieth, sixtieth, eightieth, and ninetieth postoperative day, respectively, in the animal surviving for 99 days. Cycle rate was generally high for the first 40 days, and then decreased to approximately 40 cycles/min in calves alive for greater than 90 days. The beat rate of these arterial pressure fluctuations was lower than atrial but similar to respiratory cycle rates. However, no flow fluctuations were observed in conjunction with the arterial pressure oscillations. Therefore, neither atrial contractions nor the mechanical effects of respiration were causing the pressure pulsations. Though further investigations are necessary, it is highly suggestive that this phenomenon was derived from the vasomotor center and can be called "idioperipheral pulsation." It is conceivable that the NPBVB animals adapted to the nonpulsatile condition by adding active pulsatile components of their own to maintain adequate peripheral circulation.

Nasal Vasomotor Oscillations in the Cat Associated with the Respiratory Rhythm

Asymmetrical nasal vasomotor oscillations mediated via the cervical sympathetic nerve have been observed in the spontaneously breathing cat. The vasomotor activity persists after abolition of spontaneous respiration with a neuromotor relaxant agent indicating that the vasomotor activity originates in the respiratory areas of the brain and is not due to any of the mechanical effects of respiration. The nasal vasomotor activity is abolished on hyperventilation indicating that it may be driven from a central respiratory oscillator. The vasomotor activity exhibits a reciprocal activity with oscillations in sympathetic activity alternating from one nasal passage to the other and this may be due to a direct relationship with a nasal cycle in the cat.