Static versus dynamic distensibility of the carotid artery in humans.

In clinical studies, the elastic behavior of central arteries is usually assessed by measuring dynamic distensibility. In this study, we aimed to investigate how dynamic and static distensibility of the common carotid artery (D(dyn) and D(stat), respectively) are related in 28 healthy volunteers of 20-71 years. The carotid diameter and its change with the pressure pulse were measured using an ultrasound echo-tracking device. Arterial blood pressure was measured by Finapres and carotid pressure was determined by applanation tonometry. D(dyn) was determined at rest using the pressure pulse, while D(stat) was determined during pressor responses induced by handgrip or cold pressor test. Data are given as mean +/- 1 SD. In younger subjects (<35 years), D(stat) did not differ from D(dyn) (7.0 +/- 3.4 vs. 6.5 +/- 2.1 x 10(-3) x mm Hg(-1), respectively), whereas in older subjects (>35 years), D(stat) was significantly higher than D(dyn) (3.8 +/- 1.4 vs. 2.1 +/- 0.9 x 10(-3) x mm Hg(-1), p < 0.001). For all subjects, D(stat) and D(dyn) decreased with increasing age and mean arterial pressure (MAP). Using stepwise multiple regression analysis, the strongest predictor of D(stat) proved to be MAP, while that of D(dyn) was age. D(stat) was found to be linearly related to the hysteresis loop area of the pressure-diameter relation (r = 0. 94), i.e. to vessel wall viscosity. It is concluded that, with increasing age, static distensibility overestimates the distension capacity of large arteries.

Changes in left ventricular contractility with the phase of respiration.

The end-systolic wall stress (sigma(es))-velocity of circumferential fiber shortening (V(cfsc)) relation was defined during the respiratory cycle, in order to obtain a totally noninvasive measure of left ventricular contractility. Eight young, healthy subjects were studied with echocardiography and calibrated carotid pulse tracings, while performing slow paced breathing. Left ventricular sigma(es) vs. V(efsc) relation was determined by fitting linear regression line to data points obtained at different times during the respiratory cycle. Data are given as mean+/-1SD. Left ventricular sigma(es) and V(efsc) exhibited small but significant changes during the respiratory cycle: sigma(es) was highest in late inspiration (56.9+/-4.8 g/cm2) and lowest in late expiration (49.2+/-3.7 g/cm2); inversely, V(cfsc) was lowest during late inspiration (1.18+/-0.17 circ/s) and highest during late expiration (1.34+/-0.20 circ/s). The relation was significant in each subject (r = -0.64+/-0.13) and remained inverse and significant, when it was determined separately for inspiration and expiration (r = -0.61+/-0.17 and -0.68+/-0.12, respectively). At identical end-systolic wall stress, the velocity of shortening was greater during inspiration then expiration, suggesting that contractility was reduced during the expiratory phase. The reduced expiratory contractility might reflect increased vagal influence on the ventricular myocardium.

Effect of vasoactive drugs on carotid diameter in humans.

We studied whether vasoactive drugs used to determine baroreflex sensitivity influence baroreceptor firing by affecting carotid sinus smooth muscle or simply by stretching the sinus wall through changes in pressure. In six young healthy subjects, the diameter of the carotid artery and its change with arterial pulse were measured with ultrasonography. Blood pressure was measured by Finapres. Phenylephrine and nitroglycerin doses were injected intravenously to raise and lower pressure by approximately 15-25 mmHg. Carotid dimensions increased in all subjects during the phenylephrine-induced rise and decreased during the nitroglycerin-induced fall in pressure. Diastolic diameter changed more than systolic diameter; changes were significantly different from the control value (assessed by single-factor analysis of variance and Scheffé's post hoc test). The systolic pressure-diameter relationship appeared to be nonlinear, with a steeper slope above than below baseline, and contributed significantly to the nonlinearity of the R-R interval-systolic pressure relationship. It is concluded that during drug-induced changes in blood pressure, baroreceptor activity in humans is influenced more by passive stretch than by local smooth muscle contraction.

Relation between baroreflex sensitivity and carotid artery elasticity in healthy humans.

We investigated whether physiological variability in arterial baroreflex sensitivity (BRS) was related to differences in carotid elastic behavior among 19 young healthy subjects (age 18-26 yr). The diameter of the carotid artery (D) and its change during the arterial pulse (delta D) were monitored by a phase-locked echotracking device (UT-4 Hokanson), and pulse pressure (delta P) was measured in the brachial artery by sphygmomanometry. Distensibility coefficient (DC) for the common carotid artery was calculated using the formula DC = (2 x delta D/D)/delta P. Dynamic elastic parameters such as the maximum and mean rate of carotid artery expansion and the dominant harmonic frequency of the diameter curve were also determined. BRS was assessed by regressing R-F.intervals against systolic blood pressure, monitored by finger arterial pressure (FINAPRES), during an elevation of pressure, induced by intravenous bolus injection of phenylephrine. Using correlation and stepwise regression analysis, we found that BRS was significantly related to carotid artery distensibility (r = 0.778, P < 0.001) but was not related to any of the dynamic parameters of carotid pulsation.

Heart rate variability after complete autonomic blockade in man.

In a number of studies, using the autoregressive model for frequency domain analysis of R-R interval fluctuations, the low frequency (LF) component (centered at about 0.1 Hz) is claimed to index sympathetic activity level. The aim of this study was to investigate the mediation mechanism of the LF component by pharmacological blockade. Our results support earlier findings, obtained with the use of fast Fourier transformation, that in supine subjects spectral components of R-R interval variability at around 0.1 Hz are mediated mainly by cholinergic mechanisms. Therefore, the use of the LF component as sympathetic index appears questionable.

Cardiac vagal hyperactivity in adolescent anorexia nervosa.

Adolescent anorexia nervosa, a psychiatric disease with high mortality, is often associated with bradycardia. We studied the vagal control of sinus node function in anorexic subjects, to investigate the mechanism of anorexic bradycardia. Cardiac vagal tone was determined in a group of 11 adolescent anorexic girls and in 11 age- and height-matched controls. Cardiac vagal tone in the anorexic patients was measured as the change in R-R interval in response to complete cholinergic blockade; in addition, non-invasive indices of cardiac vagal tone and baroreflex sensitivity were determined in both anorexic and control subjects. Cardiac vagal tone in anorexic subjects was 465 +/- 52 (SE) ms, about 30% higher than values reported for healthy subjects. Vagal tone values were directly related to percent weight loss (R = 0.69, P = 0.017). Non-invasive indices of both cardiac vagal activity and baroreflex sensitivity were significantly higher in the anorexic group as compared to controls; the percent increase of cardiac vagal tone, however, exceeded the increase of baroreflex sensitivity. Cardiac vagal hyperactivity significantly contributes to the bradycardia of anorexic subjects. The excess vagal activity is only partly explained by enhanced baroreflex sensitivity.

Relation between tonic sympathetic and vagal control of human sinus node function.

BACKGROUND: Clinical conditions, such as heart failure or myocardial infarction are associated with enhanced sympathetic and reduced parasympathetic activity as compared to normal controls. The reciprocal alteration in cardiac autonomic tone likely contributes to the electrical instability of the myocardium. Little information is available on the relation between sympathetic and vagal cardiac control in healthy human subjects. METHODS AND RESULTS: Heart period changes in response to autonomic blockades were measured in 16 young, healthy human subjects. Adrenergic and cholinergic blockades were induced by i.v. propranolol (0.2 mg/kg) and atropine (0.04 mg/kg) in two opposite orders on two occasions; interindividual correlations were performed between the R-R interval responses to propranolol and to atropine obtained under the various blockade conditions, and the magnitude of the responses were compared by a drug x order two factorial ANOVA design. It was found, that previous adrenergic blockade did not reduce the extent of cardioacceleration produced by subsequent cholinergic blockade and that the R-R interval responses to atropine and to subsequently given propranolol did not share significant variance across subjects (r = 0.22, P = 0.234). Also, no interindividual correlation was found between the R-R interval responses to propranolol and to atropine, with the influence of the other, respective, autonomic division already blocked (r = 0.42, P = 0.114). CONCLUSIONS: Under resting conditions, activity levels of cardiac vagal and sympathetic outflows are not related across young, healthy human subjects and peripheral interaction is not manifest between the autonomic divisions.

Relation between baroreflex sensitivity and cardiac vagal tone in humans.

The extent of dependence of cardiac vagal tone on arterial baroreceptor input has been studied in 12 healthy, young adult subjects. Cardiac vagal tone was defined as the chang in R-R interval after complete cholinergic blockade by atropine. Baroreflex sensitivity was determined with the "Oxford-method": R-R interval was regressed against systolic pressure. The interindividual correlation between cardiac vagal tone and baroreflex sensitivity for falling pressures was found to be significant, but not close (R = 0.81, P = 0.002). In each subject, the baroreflex regression line for falling pressures was extrapolated to the post-atropine R-R interval level; 50 mmHg was considered as minimum and 80 mmHg as maximum threshold level for the integrated baroreflex. From the relation between the individual regression lines and the minimum and maximum threshold levels, it was concluded that cardiac vagal tone could be generated by both baroreflex-dependent and -independent mechanisms, the ratio of which varies in different individuals, with the baroreflex-dependent mechanism being the dominant factor.

Noninvasive estimation of pulmonary arterial blood pressure in burned patients with acute respiratory failure.

Pulmonary arterial hypertension develops in acute respiratory failure and mostly an enhanced PADd-PCWP gradient has an important effect on the outcome of that complication. Considering that this critical state of septic burned patients may last for weeks, the long-term direct monitoring of pulmonary arterial blood pressure with indwelling Swan-Ganz catheter is impossible because of the high risk of endocarditis. Therefore, the aim of this study was to elaborate a noninvasive method to estimate the pulmonary arterial hypertension. Determination of cardiac index and pulmonary arterial blood pressure was carried out with Swan-Ganz catheter, P32 Statham transducer, cardiac output computers (Gould IM 1000, Marquette 7010). Extended systolic time interval measurements (with Medicor 661 polygraph completed by PC program package) were performed simultaneously in 7 burned patients (av. age 38.7 ys, means of TBS 38%) with acute respiratory failure at 38 occasions. The values of cardiac indices with the two methods were practically the same CI t = 3.4 +/- 1.21 1/min/m2 CI s = 3.1 +/- 1.10 1/min/m2; regression equation: CI s = 0.874 CIt + 0.135, r = 0.98, n = 38. Close correlations have been found between PAPm and PO2/FiO2 (r = 0.75), as well as between PAP values and some noninvasively measured hemodynamic data. Using these interrelations: 1) regression equations for PAPs., PAPm, PAPd, PCWP, PVRI were elaborated (r values: 0.855, 0.869, 0.681, 0.644, 0.817 respectively); 2) discriminant analysis with noninvasive parameters correctly classified the cases at critical PAPd-PCWP gradient (greater than 4 mm/Hg) in 84%. These results suggest that a continuous noninvasive hemodynamic and blood gas monitoring completed with a periodic bedside computer analysis of the PC-processed data for calculation of the pulmonary arterial pressure may be enough for the therapy during the long-term critical periods.

Outcome prediction in adult respiratory distress syndrome using discriminant analysis of cardiorespiratory data.

In order to examine the prognostic value of different cardiopulmonary variables in adult respiratory distress syndrome the data of 30 patients with this illness were studied retrospectively. The patients were divided into 3 groups: Group A: survivors (9 cases, 40 examinations), Group B: early stage nonsurvivors (8 cases, 37 examinations), Group C: late stage nonsurvivors (19 cases, 89 examinations). In 6 nonsurvivor patients a few measurements were done in the early and late stage, too. There were highly significant differences between Groups A and C (mean pulmonary arterial pressure, pulmonary arterial diastolic pressure minus pulmonary capillary wedge pressure, left ventricular stroke work index, systemic and pulmonary vascular resistance, inspired oxygen fraction, arterial oxygen tension per inspired oxygen fraction, mixed venous oxygen saturation, pulmonary shunt fraction, and oxygen delivery, but the differences in relation to other groups were less prominent. Using a step-wise discriminant analysis, it was found that the oxygenation parameters alone determined the outcome correctly in 68-75%. Extending the analysis to haemodynamic variables the result improved (72-80%). Similar prediction was obtained when parameters potentionally measurable by noninvasive methods were analysed (69-80%). These results suggest that it is possible to predict the outcome of ARDS correctly without any invasive monitoring technique.

Anacrotic "notch" on the upstroke of external carotid curve may indicate a critically high systolic pulmonary arterial pressure value.

Acute respiratory failure is followed by decreased left ventricular performance probably due to the right ventricle dilatation induced by pulmonary hypertension and intraventricular septal shift to the left. An anacrotic notch on the upstroke slope of the carotid curve was detected in 22 of 36 hemodynamic studies with simultaneous ECG, PCG and external pulse carotid curve recording in 7 burned patients with acute respiratory failure. Comparing the values (x +/- SEM) obtained in group with notch and in group without notch, PAPs, PAPm, PVRI were higher (56 +/- 2.30 mmHg; 32 +/- 0.99 mm Hg; 543 +/- 56.8 dyn x s/cm5/m2 versus 32 +/- 1.08 mm Hg; 20 +/- 0.9 mm Hg; 173 +/- 14.7 dyn x s/cm5/m2) and CI and LVSWI were lower (2.6 +/- 0.17 l/min/m2; 25.8 +/- 2.41 g x m/m2; versus 3.8 +/- 0.26 l/min/m2; 38.3 +/- 2.82 g x m/m2) in group with notch. As it is shown by 11 paired measurements where the notch disappeared immediately after starting vasodilator therapy PAPs, PAPm, PVRI decreased (from 54 +/- 3.1, 35 +/- 0.8 mm Hg, 498 +/- 64.1 dyn x s/cm5/m2 to 35 +/- 0.8, 21 +/- 1.1 mmHg, 189 +/- 18.4 dyn x s/cm5/m2 respectively) and heart performance improved. Since the left ventricle contractility (characterized by EF, PCWP, ICT) was normal in both groups, our findings suggest that critically high PAPs values (over 40 mmHg) cause a septal bulging at the beginning of the systole which in turn narrows the left ventricle outflow tract. Regarding to the clinical importance of the deteriorated biventricular function at the critically high PAPs evidenced by notch phenomenon on carotid curve but measurable only by indwelling pulmonary arterial catheterization always being a source of infection, the noninvasive parameters as independent variables were entered into canonical discriminant analysis. The ratio of the correctly classified cases was 89%.