Response of systemic arterial input impedance to volume expansion and hemorrhage

. Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis. Am J Physiol Heart Circ Physiol 286: H267-H275, 2004. First published September 25, 2003 10.1152/ ajpheart.00505.2002-Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) ϭ 5-9 mmHg], high volume (HiV; LVEDP ϭ 16-19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forwardgoing PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 Ϯ 3 ms (HiV) and 103 Ϯ 5 ms (LoV; P Ͻ 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature. lung; arteries; hemodynamics; wave transmission WAVE TRANSMISSION through the heart is poorly understood. Among the clinical syndromes in which wave transmission could be an important, unappreciated factor are the stiff left atrium (LA) syndrome (6, 15) and the Bernheim syndrome (1,5,24). To study the transmission of waves generated in the LA, we created a system where a backward-going wave, originating from the LA, could be detected in the proximal pulmonary artery (PA; backward and forward are defined with respect to PA flow.) To create such a wave in a controlled fashion, we used an LA counterpulsation balloon. Pressure and velocity waveforms in the proximal PA were analyzed to evaluate the effects of LA pressure (P LA ) perturbations.Most commonly, pulsatile arterial phenomena have been characterized using Fourier analysis where the observed waveforms are decomposed into sinusoidal wave trains, and the results are expressed as amplitude and phase as a function of frequency (16,17). This frequency-domain analysis has provided much information. However, wave-intensity analysis where the observed waveforms are decomposed into a succession of infinitesimal wave fronts that are described by their amplitude and time (13,19) allows the interaction of forwardand backward-going waves and their relation to primary hemodynamic parameters (pressure, flow, etc.) to be studied directly. This method utilizes changes in pressure and velocity to evaluate the direction, intensity, and type of waves and has been used recently to study the systemic (18), pulmonary (8,11,22), and coronary circulations...

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“…These values were not different from wave-speed estimations calculated from characteristic impedance (3,4,17).…”

Section: Methodsmentioning

confidence: 45%

Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

Hollander¹,

Dobson²,

Wang³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, a frequency dependence of arterial compliance inherent to arterial blood vessels, as discussed earlier, need not be the only explanation for an observed HR dependence of arterial compliance in intact humans. Because arterial compliance changes with vascular smooth muscle activation, a slight increase in sympathetic outflow may account for the observed effects 1 , 3 , 27 , 41 , 42 . Even though the placing of the oesophageal pacing electrode is painless, our impression during the experiments was that pacing caused considerable anxiety among our study volunteers.…”

Section: Discussionmentioning

confidence: 88%

Effects of Heart Rate on Arterial Compliance in Men

Liang¹,

Gatzka

et al. 1999

Clin Exp Pharma Physio

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1. Arterial compliance is a major determinant of left ventricular afterload. In keeping with earlier experimental data obtained in isolated arterial segments, it has recently been shown in the rat that arterial compliance decreases with an increase in heart rate (HR) induced by atrial pacing. 2. To elucidate the potential relevance of this effect in humans, we investigated nine male volunteers (age 20-30 years; mean 26 years). Systemic arterial compliance (SAC) was measured with the diastolic area method and carotid-to-femoral and femoral-to-dorsalis pedis pulse wave velocities (PWV) were measured to determine regional changes in compliance. Heart rate was first lowered with intravenous metoprolol to 56 +/- 2 b.p.m. and then increased by transoesophageal atrial pacing to 80 and 100 b.p.m. 3. Increasing HR from 56 +/- 2 to 80 b.p.m. by pacing increased mean arterial pressure (MAP) from 78 +/- 2 to 98 +/- 1 mmHg (P < 0.001) and then to 102 +/- 2 mmHg (P = NS). Systemic arterial compliance fell from 0.48 +/- 0.06 to 0.33 +/- 0.04 arbitrary compliance units (ACU; P < 0.01), carotid-to-femoral PWV increased from 6.1 +/- 0.3 to 6.8 +/- 0.4 m/s (P < 0.001) and femoral-to-dorsalis pedis PWV increased from 8.9 +/- 0.4 to 10.1 +/- 0.5 m/s (P < 0.001). Pacing at 100 b.p.m did not change MAP, but did lead to a further decrease in SAC (to 0.24 +/- 0.03 ACU; P < 0.05) and further increases in carotid-to-femoral (7.3 +/- 0.4 m/s; P = NS) and femoral-to-dorsalis pedis PWV (11.3 +/- 0.4 m/s; P < 0.001). 4. We conclude that systemic, central and peripheral compliances decrease in vivo with an increase in HR induced by atrial pacing.

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“…Stone and Dujardin 7 and Dujardin et al 28 have demonstrated that aortic smooth muscle tone can be influenced by autonomic reflexes, with resultant changes in pressure-diameter relations and Zc. These reflex changes were studied under the conditions of volume expansion and hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Effect of nitroglycerin on aortic impedance, diameter, and pulse-wave velocity.

Latson

Hunter

Katoh

et al. 1988

Circulation Research

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The effects of an intravenous infusion of 1 |xg/kg/min nitroglycerin were studied on systemic arterial properties in nine acutely instrumented dogs. Aortic impedance and pulse-wave velocity were calculated from measured pressure and flow signals collected during random ventricular pacing. Central aortic diameter was simultaneously determined with ultrasonic dimension crystals. Mean blood pressure was maintained constant to avoid the confounding effects of passive, pressure-induced changes in vascular properties. Nitroglycerin both reduced the amplitude of peripheral vascular reflections and delayed the return of these reflections to the aortic root. This reflection delay was manifested as a consistent leftward shift in both impedance modulus and phase. The magnitude of this reflection delay could not be entirely accounted for on the basis of the measured changes in average pulse-wave velocity along the aorta. ; 2) increased arterial compliance, as determined by both the rate of aortic diastolic pressure decay and pressure-diameter relations in peripheral arteries 6 ; and 3) decreased magnitude of arterial pulse-wave reflections. -3This study used an acute canine preparation to further define the effects of nitroglycerin on systemic arterial properties. We measured the effects of intravenous nitroglycerin on aortic impedance, diameter, and pulse-wave velocity (PWV). The use of spectral analysis techniques, in conjunction with random cardiac pacing, allowed us to determine the impedance spectrum with a frequency resolution as small as 0.1 Hz. Our results indicate that nitroglycerin has significant effects on both the magnitude and timing of peripheral vascular reflections. Materials and Methods In Vivo MethodsNine mongrel dogs (body weight 17-23 kg) were anesthetized with a combination of pentobarbital and fentanyl (initial dose: 12 mg/kg pentobarbital and 50 u.g/kg fentanyl; subsequent infusion: 1.1 mg/kg/hr and 15 u,g/kg/hr, respectively). Instrumentation in all dogs included a nonconstricting ultrasonic flow probe (model T-101, Transonic Systems, Ithaca, New York) in the ascending aorta, a Millar pressure catheter (Houston, Texas) in the ascending aorta, inserted through the right common carotid artery, and a central venous pressure catheter passed through the femoral vein. The Millar catheter was positioned at the same level as the aortic flow probe by palpating the catheter tip within the aorta. Additional instrumentation in seven dogs included a second Millar catheter in the femoral artery, inserted and attached with a nonocclusive purse-string suture, and a pair of ultrasonic crystals on the aortic arch (5-HHz crystals connected to a sonomicrometer; model 401, Schuessler, Cardiff by the Sea, California). These ultrasonic crystals, used to measure aortic diameter, were attached to opposing sides of the aortic adventitia with either fine sutures (tied to a flexible woven backing sheet) and/or a small amount of cyanoacrylate glue.7 Permanent atrioventricular block was produced in all dogs by injection of 40% ...

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Response of systemic arterial input impedance to volume expansion and hemorrhage

Cited by 18 publications

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Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

Effects of Heart Rate on Arterial Compliance in Men

Effect of nitroglycerin on aortic impedance, diameter, and pulse-wave velocity.

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