Figure 1.
Example of left ventricular stroke volume time-series of a representative subject.
The left and right panels display data obtained while the subject was resting supine, and during maximal apnoea, respectively. LVSV: left ventricular stroke volume. The vertical dashed line represents the start of the struggle phase. The raw LVSV tracing was obtained by re-sampling beat-by-beat values to 50 Hz via cubic spline interpolation. The interpolated data was band-pass filtered using an 8th order, zero-phase Butterworth filter with low and high cut-off frequencies of 0.20 and 0.80 Hz (i.e., the broadband of respiratory frequencies). This ‘processed’ data was taken to represent the respiratory variability in LVSV.
Figure 2.
: mean variability observed in the corresponding parameter during the struggle phase; ITP: intrathoracic pressure; HR: heart rate; LVSV: left ventricular stroke volume; CO: cardiac output; MAP: mean arterial blood pressure; TPR: total peripheral resistance; CVRi: cerebrovascular resistance index; CBFV: cerebral blood flow-velocity. The top panel depicts a hypothetical Path model to illustrate the direct and indirect effects of each parameter (X1, X2 and X3) on the terminal endogenous variable (i.e., Y). The symbol ß represents the standardised path coefficient describing the influence of one variable on another. See Methods for further explanation. The hypothesised causal model used to examine the influence of respiratory contractions on the respiratory variability in cerebral blood flow velocity is displayed in the middle-panel. The ‘reduced-fit’ causal model is presented in the bottom-panel. Only those parameters which were identified as significant (P<0.05) mediators of the terminal dependent variable (i.e.,
) are retained in this panel. Solid arrows denote the direction of causality between corresponding parameters. Values located adjacent to arrows represent the standardised coefficient of the corresponding path. Values displayed in bold represent the coefficient of determination (R2) of the relationship between the corresponding parameter and all preceding paths.
Figure 3.
Time-course changes in respiratory, cardiovascular and cerebrovascular variables at rest and during maximal apnoea.
Vertical error bars represent means ± SEM. EP1, EP2 and EP3: first, second and third tertiles of the easy-going phase; SP1, SP2 and SP3: first second and third tertiles of the struggle phase; ITP: intrathoracic pressure; HR: heart rate; LVSV: left ventricular stroke volume; CO: cardiac output; MAP: mean arterial blood pressure; CBFV: cerebral blood flow-velocity; TPR: total peripheral resistance in units of mmHg⋅L−1⋅min; CVRi: cerebrovascular resistance index in units of mmHg⋅cm−1⋅s. The closed and open circles in the top left-hand panel represent expiratory and inspiratory ITP swings, respectively. *Significantly different from previous time-point, P<0.05. †Significantly different from resting value, P<0.05.
Figure 4.
Influence of inspiratory intrathoracic pressure on left ventricular stroke volume during the struggle phase.
LVSV: left ventricular stroke volume; Δ: absolute change in values from beginning until the end of the struggle phase of breath holding; ITPinsp: inspiratory swing in intrathoracic pressure during involuntary respiratory contractions. The solid line represents the line of best-fit determined from simple linear regression. The hashed lines denote the ±95% confidence interval of the regression function.
Figure 5.
Respiratory variability in intrathoracic pressure, cardiovascular and cerebrovascular parameters at rest and during maximal apnoea.
Vertical error bars represent mean coefficients of variation (CV) ± SEM. EP1, EP2 and EP3: first, second and third tertiles of the easy-going phase; SP1, SP2 and SP3: first second and third tertiles of the struggle phase; ITP: intrathoracic pressure; HR: heart rate; LVSV: left ventricular stroke volume; CO: cardiac output; MAP: mean arterial blood pressure; CBFV: cerebral blood flow velocity; TPR: total peripheral resistance; CVRi: cerebrovascular resistance index. aThe standard deviation of ITP is presented here as a measure of respiratory variability instead of CV (see Methods). *Significantly different from previous time-point, P<0.05. †Significantly different from resting value, P<0.05.
Table 1.
The impact of‘respiratory’ variability in intrathoracic pressure and central haemodynamics on cerebral blood flow velocity during the struggle phase.
Figure 6.
The influence of cerebral blood flow velocity on the struggle phase duration.
Δ: absolute change in values from beginning until the end of the struggle phase of breath holding; CBFV: cerebral blood flow velocity; : mean variability observed in the corresponding parameter during the struggle phase. The R2 values presented in these panels are calculated from each independent variable’s zero-order correlation coefficient. The solid lines represents the line of best-fit determined from simple linear regressions. The hashed lines denote the ±95% confidence intervals of the regression functions.