The Oscillating Component of the Internal Jugular Vein Flow: The Overlooked Element of Cerebral Circulation

The jugular venous pulse (JVP) provides valuable information about cardiac haemodynamics and filling pressures and is an indirect estimate of the central venous pressure (CVP). Recently it has been proven that JVP can be obtained by measuring the cross-sectional area (CSA) of the IJV on each sonogram of an ultrasound B-mode sonogram sequence. It has also been proven that during its pulsation the IJV is distended and hence that the pressure gradient drives the IJV haemodynamics. If this is true, then it will imply the following: (i) the blood velocity in the IJV is a periodic function of the time with period equal to the cardiac period and (ii) the instantaneous blood velocity is given by a time function that can be derived from a flow-dynamics theory that uses the instantaneous pressure gradient as a parameter. The aim of the present study is to confirm the hypothesis that JVP regulates the IJV blood flow and that pressure waves are transmitted from the heart toward the brain through the IJV wall.

The “systolic volume balance” method for the noninvasive estimation of cardiac output based on pressure wave analysis

Cardiac output (CO) monitoring is essential for the optimal management of critically ill patients. Several mathematical methods have been proposed for CO estimation based on pressure waveform analysis. Most of them depend on invasive recording of blood pressure and require repeated calibrations, and they suffer from decreased accuracy under specific conditions. A new systolic volume balance (SVB) method, including a simpler empirical form (eSVB), was derived from basic physical principles that govern blood flow and, in particular, a volume balance approach for the conservation of mass ejected into and flowed out of the arterial system during systole. The formulas were validated by a one-dimensional model of the systemic arterial tree. Comparisons of CO estimates between the proposed and previous methods were performed in terms of agreement and accuracy using “real” CO values of the model as a reference. Five hundred and seven different hemodynamic cases were simulated by altering cardiac period, arterial compliance, and resistance. CO could be accurately estimated by the SVB method as follows: CO = C × PPao/( T − Psm × Ts/Pm) and by the eSVB method as follows: CO = k × C × PPao/ T, where C is arterial compliance, PPao is aortic pulse pressure, T is cardiac period, Psm is mean systolic pressure, Ts is systolic duration, Pm is mean pressure, and k is an empirical coefficient. SVB applied on aortic pressure waves did not require calibration or empirical correction for CO estimation. An empirical coefficient was necessary for brachial pressure wave analysis. The difference of SVB-derived CO from model CO (for brachial waves) was 0.042 ± 0.341 l/min, and the limits of agreement were −0.7 to 0.6 l/min, indicating high accuracy. The intraclass correlation coefficient and root mean square error between estimated and “real” CO were 0.861 and 0.041 l/min, respectively, indicating very good accuracy. eSVB also provided accurate estimation of CO. An in vivo validation study of the proposed methods remains to be conducted.

Nonlinearity and fractality in the variability of cardiac period in the lizard, Gallotia galloti: effects of autonomic blockade

Both nonlinear and fractal properties of beat-to-beat R-R interval variability signal (RRV) of freely moving lizards ( Gallotia galloti) were studied in baseline and under autonomic nervous system blockade. Nonlinear techniques allowed us to study the complexity, chaotic behavior, nonlinearity, stationarity, and regularity over time of RRV. Scaling behavior of RRV was studied by means of fractal techniques. The autonomic nervous system blockers used were atropine, propranolol, prazosin, and yohimbine. The nature of RRV was linear in baseline and under β-, α1- and α2-adrenoceptor blockades. Atropine changed the linear nature of RRV to nonlinear and increased its stationarity, regularity and fractality. Propranolol increased the complexity and chaotic behavior, and decreased the stationarity, regularity, and fractality of RRV. Both prazosin and yohimbine did not change any of the nonlinear and fractal properties of RRV. It is suggested that 1) the use of both nonlinear and fractal analysis is an appropriate approach for studying cardiac period variability in reptiles; 2) the cholinergic activity, which seems to make the α1-, α2- and β-adrenergic activity interaction unnecessary, determines the linear behavior in basal RRV; 3) fractality, as well as both RRV regularity and stationarity over time, may result from the balance between cholinergic and β-adrenergic activities opposing actions; 4) β-adrenergic activity may buffer both the complexity and chaotic behavior of RRV, and 5) neither the α1- nor the α2-adrenergic activity seem to be involved in the mediation of either nonlinear or fractal components of RRV.

Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

Blood lipids may detrimentally affect autonomic and circulatory control. We tested the hypotheses that acute elevations in free fatty acids and triglycerides (acute hyperlipidemia) impair baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA: sympathetic BRS), increase MSNA at rest, and augment physiological responses to exercise. Eighteen young adults were examined in this randomized, double-blinded, and placebo-controlled study. BRS was determined using the modified Oxford technique before (pre) and 60 min (post) after initiating infusion of Intralipid (0.8 ml·m−2·min−1) and heparin (1,000 U/h) (experimental; n = 12) to induce acute hyperlipidemia, or saline (0.8 ml·m−2·min−1) and heparin (1,000 U/h) (control; n = 6). Responses to isometric handgrip to fatigue (IHG) were also determined. Blood pressure increased more ( P < 0.05) in experimental than control subjects during the infusion. MSNA at rest (14 ± 2 vs. 11 ± 1 bursts/min), cardiovagal (19.8 ± 1.8 vs. 19.1 ± 2.4 ms/mmHg pre and post, respectively) and sympathetic BRS (−5.5 ± 0.6 vs. −5.2 ± 0.4 au·beat−1·mmHg−1), and the neural and cardiovascular responses to IHG were unchanged by acute hyperlipidemia (pre vs. post) in experimental subjects. Similarly, MSNA at rest (10 ± 2 vs. 12 ± 2 bursts/min), cardiovagal (22.1 ± 4.0 vs. 21.0 ± 4.6 ms/mmHg) and sympathetic BRS (−5.8 ± 0.5 vs. −5.5 ± 0.5 au·beat−1·mmHg−1), and the neural and cardiovascular responses to IHG were unchanged by the infusion in control subjects. These data do not provide experimental support for the concept that acute hyperlipidemia impairs reflex cardiovagal or sympathetic regulation in humans.

Cyclooxygenase inhibition and baroreflex sensitivity in humans

Animal studies suggest that prostanoids (i.e., such as prostacyclin) may sensitize or impair baroreceptor and/or baroreflex responsiveness depending on the site of administration and/or inhibition. We tested the hypothesis that acute inhibition of cyclooxygenase (COX), the rate-limiting enzyme in prostanoid synthesis, impairs baroreflex regulation of cardiac period (R-R interval) and muscle sympathetic nerve activity (MSNA) in humans and augments pressor reactivity. Baroreflex sensitivity (BRS) was determined at baseline (preinfusion) and 60 min after (postinfusion) intravenous infusion of a COX antagonist (ketorolac; 45 mg) (24 ± 1 yr; n = 12) or saline (25 ± 1 yr; n = 12). BRS was assessed by using the modified Oxford technique (bolus intravenous infusion of nitroprusside followed by phenylephrine). BRS was quantified as the slope of the linear portion of the 1) R-R interval-systolic blood pressure relation (cardiovagal BRS) and 2) MSNA-diastolic blood pressure relation (sympathetic BRS) during pharmacological changes in arterial blood pressure. Ketorolac did not alter cardiovagal (19.4 ± 2.1 vs. 18.4 ± 2.4 ms/mmHg preinfusion and postinfusion, respectively) or sympathetic BRS (−2.9 ± 0.7 vs. −2.6 ± 0.4 arbitrary units·beat−1·mmHg−1) but significantly decreased a plasma biomarker of prostanoid generation (plasma thromboxane B2) by 53 ± 11%. Cardiovagal BRS (21.3 ± 3.8 vs. 21.2 ± 3.0 ms/mmHg), sympathetic BRS (−3.4 ± 0.3 vs. −3.2 ± 0.2 arbitrary units·beat−1·mmHg−1), and thromboxane B2 (change in −1 ± 12%) were unchanged in the control (saline infusion) group. Pressor responses to steady-state incremental (0.5, 1.0, and 1.5 μg·kg−1·min−1) infusion (5 min/dose) of phenylephrine were not altered by ketorolac ( n = 8). Collectively, these data indicate that acute pharmacological antagonism of the COX enzyme does not impair BRS (cardiovagal or sympathetic) or augment pressor reactivity in healthy young adults.