scholarly journals Dynamic Arterial Elastance Is Associated With the Vascular Waterfall in Patients Treated With Norepinephrine: An Observational Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Stéphane Bar ◽  
Maxime Nguyen ◽  
Osama Abou-Arab ◽  
Hervé Dupont ◽  
Belaid Bouhemad ◽  
...  
Keyword(s):  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Arterial Elastance ◽  
Clinical Trial Registration ◽  
Ventricular Elastance ◽  
Flow Parameters ◽  
Vascular Flow ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Critical Closing Pressure

Introduction: It has been suggested that dynamic arterial elastance (Eadyn) can predict decreases in arterial pressure in response to changing norepinephrine levels. The objective of this study was to determine whether Eadyn is correlated with determinants of the vascular waterfall [critical closing pressure (CCP) and systemic arterial resistance (SARi)] in patients treated with norepinephrine.Materials and Methods: Patients treated with norepinephrine for vasoplegia following cardiac surgery were studied. Vascular and flow parameters were recorded immediately before the norepinephrine infusion and then again once hemodynamic parameters had been stable for 15 min. The primary outcomes were Eadyn and its associations with CCP and SARi. The secondary outcomes were the associations between Eadyn and vascular/flow parameters.Results: At baseline, all patients were hypotensive with Eadyn of 0.93 [0.47;1.27]. Norepinephrine increased the arterial blood pressure, cardiac index, CCP, total peripheral resistance (TPRi), arterial elastance, and ventricular elastance and decreased Eadyn [0.40 (0.30;0.60)] and SARi. Eadyn was significantly associated with arterial compliance (CA), CCP, and TPRi (p < 0.05).Conclusion: In patients with vasoplegic syndrome, Eadyn was correlated with determinants of the vascular waterfall. Eadyn is an easy-to-read functional index of arterial load that can be used to assess the patient’s macro/microcirculatory status.Clinical Trial Registration:ClinicalTrials.gov #NCT03478709.

A square-pulse flow method for measuring characteristics of the arterial bed

1976 ◽  
Vol 40 (3) ◽  
pp. 425-433 ◽  
Author(s):  
M. G. Bottomley ◽  
G. W. Mainwood
Keyword(s):  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Mean Value ◽  
Pressure Response ◽  
Arterial System ◽  
Response Curves ◽  
Arterial Tree ◽  
Pulse Flow ◽  
Critical Closing Pressure ◽  
Closing Pressure

A device was designed to provide a “square” pulse of blood flow into the arterial system. Pulses were injected into the carotid artery of the rabbit during transient cardiac arrest. Analysis of pressure response curves generated by the flow provides information as to the state of the arterial tree. With certain assumptions it is possible to estimate from these curves lumped values of peripheral resistance, critical closing pressure, and arterial compliance. In a series of 12 rabbits the mean value of peripheral resistance was found to be 0.21 +/- 0.7 mmHg-ml-1-min and critical closing pressure was estimated to be 23.6 +/- 3.8 mmHg. This method gives two possible values for arterial compliance 0.036 +/- 0.010 and 0.055 +/- 0.010 ml-mm-1 based, respectively, on the rise and decay curves of the pressure response. The theory and limitations of the method are discussed. The use of the method is illustrated in following the response to increased PCO2 and hemorrhage.

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

2008 ◽  
Vol 294 (1) ◽  
pp. H293-H301 ◽  
Author(s):  
Xiaoxiao Chen ◽  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Rafat I. Elahi ◽  
...  
Keyword(s):  
Impulse Response ◽  
Mathematical Analysis ◽  
Total Peripheral Resistance ◽  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Noninvasive Measurements ◽  
Extended Technique ◽  
Arterial Blood ◽  
Before And After ◽  
Cardiovascular Simulator

We previously developed a mathematical analysis technique for estimating the static gain values of the arterial total peripheral resistance (TPR) baroreflex ( GA) and the cardiopulmonary TPR baroreflex ( GC) from small, spontaneous beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we extended the mathematical analysis so as to also estimate the entire arterial TPR baroreflex impulse response [ hA( t)] as well as the lumped arterial compliance (AC). The extended technique may therefore provide a linear dynamic characterization of TPR baroreflex systems during normal physiological conditions from potentially noninvasive measurements. We theoretically evaluated the technique with respect to realistic spontaneous hemodynamic variability generated by a cardiovascular simulator with known system properties. Our results showed that the technique reliably estimated hA( t) [error = 30.2 ± 2.6% for the square root of energy ( EA), 19.7 ± 1.6% for absolute peak amplitude ( PA), 37.3 ± 2.5% for GA, and 33.1 ± 4.9% for the overall time constant] and AC (error = 17.6 ± 4.2%) under various simulator parameter values and reliably tracked changes in GC. We also experimentally evaluated the technique with respect to spontaneous hemodynamic variability measured from seven conscious dogs before and after chronic arterial baroreceptor denervation. Our results showed that the technique correctly predicted the abolishment of hA( t) [ EA = 1.0 ± 0.2 to 0.3 ± 0.1, PA = 0.3 ± 0.1 to 0.1 ± 0.0 s−1, and GA = −2.1 ± 0.6 to 0.3 ± 0.2 ( P < 0.05)] and the enhancement of GC [−0.7 ± 0.44 to −1.8 ± 0.2 ( P < 0.05)] following the chronic intervention. Moreover, the technique yielded estimates whose values were consistent with those reported with more invasive and/or experimentally difficult methods.

4950Adiposity gain from 17 to 25 years has a substantial effect on cardiac structure, independent of haemodynamics

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C M Park ◽  
H Taylor ◽  
S Jones ◽  
A Rapala ◽  
S Williams ◽  
...  
Keyword(s):  
Emerging Adulthood ◽  
Repeated Measures ◽  
Smoking Status ◽  
Arterial Compliance ◽  
Large Population ◽  
Peripheral Resistance ◽  
Substantial Effect ◽  
Cardiac Structure ◽  
Arterial Elastance ◽  
Left Ventricle Mass

Abstract Introduction Body mass index (BMI) is independently associated with increased left ventricle mass (LVM) and remodeling in children. However associations from adolescence to emerging adulthood are unknown. Purpose To investigate associations between the change (Δ) in BMI to Δ in cardiac structure from 17 to 25 yrs using a large population-based sample of echocardiography in youth, and to explore the role of possible haemodynamic mediators. Methods 901 participants (61% female) underwent echocardiography, anthropometry and sitting blood pressure (BP) measurements aged 17 yrs and had repeated measures aged 25 yrs. BMI, LVM, concentricity0.67 (LVM/end-diastolic volume0.67), total arterial compliance (TACI), peripheral resistance (TPR) and effective arterial elastance (Ea) were calculated. Regression analysis was used to investigate associations between ΔBMI and ΔLVM indexed to height2.7 (ΔLVMI) and Δconcentricity0.67. Results From 17 to 25 yrs BMI increased by 2.05±2.1 g/m2 in males and 1.80±3.1 kg/m2 in females, LVMI increased by 3.10±6.2g/m2.7 and 2.01±6.0g/m2.7 and concentricity0.67 increased by 0.91±1.2g/ml0.67 and 0.03±1.1g/ml0.67. ΔBMI was associated with ΔLVMI and Δconcentricity0.67 independently of age, socioeconomic status (SES) and smoking status. Haemodynamic measures did not substantially mediate these associations. Table 1 ΔLVMI (g/m2.7) ΔConcentricity0.67 (g/m0.67) Males Females Males Females Model 1: Age, SES and smoking @25 0.78±0.15** 0.53±0.08** 0.12±0.03** 0.083±0.02** + ΔSystolic BP (mmHg) 0.68±0.16** 0.46±0.09** 0.10±0.03* 0.069±0.016** + ΔDiastolic BP (mmHg) 0.83±0.16** 0.47±0.08** 0.12±0.03** 0.074±0.015** + ΔMean Arterial Pressure (mmHg) 0.77±0.17** 0.46±0.08** 0.11±0.03** 0.069±0.015** + ΔPulse Pressure (mmHg) 0.72±0.15** 0.54±0.08** 0.11±0.03** 0.083±0.015** + ΔTACI (ml/m2/mmHg) 0.68±0.16** 0.53±0.08 0.12±0.03** 0.091±0.015** + ΔTPR (mmHg/min/L) 0.76±0.17** 0.65±0.08** 0.10±0.03* 0.072±0.016** + ΔEa (mmHg/ml) 0.73±0.17** 0.54±0.08** 0.11±0.03** 0.083±0.015** Data are β±SE. *p<0.01, **p<0.0001. Discussion BMI gain from adolescence to emerging adulthood has a substantial effect on cardiac structure, independent of haemodynamics. These findings highlight the importance of weight control in early adulthood for good cardiovascular health. Acknowledgement/Funding BHF

Relation of effective arterial elastance to arterial system properties

2002 ◽  
Vol 282 (3) ◽  
pp. H1041-H1046 ◽  
Author(s):  
Patrick Segers ◽  
Nikos Stergiopulos ◽  
Nico Westerhof
Keyword(s):  
Arterial Compliance ◽  
Linear Regression Analysis ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Interaction Model ◽  
Left Ventricular ◽  
Arterial System ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Effective Arterial Elastance

Effective arterial elastance ( E a), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E max, the slope of the LV end-systolic pressure-volume relation, E a/ E max has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance ( R; 0.6–1.8 mmHg · ml−1 · s) and total arterial compliance (C; 0.5–2.0 ml/mmHg) covering the human pathophysiological range. E a, E a/ E max, LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E a, R/ T (where T is cycle length), and 1/C: E a= −0.13 + 1.02 R/ T + 0.31/C, indicating that R/ T contributes about three times more to E a than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E a and E a/ E max but can result in differences of 10% in stroke work and 50% in maximal power.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

scholarly journals Vascular-ventricular coupling during exercise is not affected by exaggerated blood pressures in endurance-trained athletes

2019 ◽  
Vol 127 (3) ◽  
pp. 753-759 ◽  
Author(s):  
Katharine D. Currie ◽  
Zion Sasson ◽  
Jack M. Goodman
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Peripheral Vascular ◽  
Arterial Elastance ◽  
Coupling Index ◽  
Cardiovascular Performance ◽  
Stage 1

This study sought to examine whether cardiovascular performance during exercise, assessed using the vascular-ventricular coupling index (VVC), was affected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. Subjects were middle-aged endurance-trained men and women. Blood pressure measurements and left ventricular echocardiography were performed in a semiupright position at rest and during steady-state cycling at workloads that elicited 100–110 beats/min ( stage 1) and 130–140 beats/min ( stage 2). These data were used to calculate effective arterial elastance index ( EaI), left ventricular end-systolic elastance index ( ELVI), and their ratio (VVC). Additional measurements of left ventricular volumes and function (i.e., stroke volume, cardiac output, and longitudinal strain) and indirect assessments of peripheral vascular function (i.e., total arterial compliance and peripheral vascular resistance) were examined. Fourteen subjects with EBP (EBP+, 50% men) and 14 sex-matched subjects without EBP (EBP−) participated, with results presented as EBP+ versus EBP−. EaI and ELVI increased from rest to exercise while VVC decreased, but only ELVI was different between groups at stage 1 [7.6 (1.8) vs. 6.4 (1.0) mmHg·ml−1·m−2, P = 0.045] and stage 2 [10.3 (1.6) vs. 8.0 (1.7) mmHg·ml−1·m−2, P < 0.001]. Additional comparisons revealed no group difference in the contribution of the Frank-Starling mechanism or left ventricular and peripheral vascular function during exercise. The cardiovascular adjustment to exercise in athletes with EBP is achieved through a matched increase in both EaI and ELVI, and the absence of between-group differences in left ventricular or peripheral vascular function suggests that other factors may contribute to the EBP response. NEW & NOTEWORTHY Cardiovascular performance during submaximal exercise, assessed using vascular-ventricular coupling, is unaffected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. The underlying mechanisms of EBP in athletes remain unknown as changes in left ventricular and peripheral vascular function during exercise were similar in athletes with and without EBP.

Effect of unilateral resistance training on arterial compliance in elderly men

2007 ◽  
Vol 32 (4) ◽  
pp. 670-676 ◽  
Author(s):  
Fleur Poelkens ◽  
Mark Rakobowchuk ◽  
Kirsten A. Burgomaster ◽  
Maria T.E. Hopman ◽  
Stuart M. Phillips ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistance Training ◽  
Arterial Compliance ◽  
Stiffness Index ◽  
Elderly Men ◽  
Arterial Diameter ◽  
Healthy Elderly ◽  
Arterial Blood ◽  
The Impact ◽  
Peak Blood

An increase in age coincides with a decrease in arterial compliance, which is related to a higher risk for cardiovascular accidents. Evidence regarding the effects of resistance training on arterial compliance is conflicting. Currently, little information is available about the effect of resistance training on arterial compliance in elderly men. We assessed the impact of 10 weeks of unilateral arm and leg resistance training on carotid, brachial, and femoral arterial compliance in 12 healthy elderly men (mean age ± SD, 71 ± 7 y). Arterial compliance was evaluated before, after 4 weeks, and after 10 weeks of unilateral resistance training by simultaneously measuring arterial diameter and blood pressure in each artery. There were no significant differences in arterial compliance or stiffness index in any of the arteries examined after 10 weeks of training. However, after 10 weeks of resistance training, resting heart rate decreased from 76 ± 4 beats/min to 61 ± 3 beats/min (p < 0.05), plasma glucose decreased from 6.0 ± 0.9 to 5.1 ± 0.9 mmol/L (mean ± SE) (p < 0.05), and carotid artery peak blood flow increased from 1831 mL/min to 2245 mL/min (p < 0.05). There were no significant changes in resting arterial blood pressure. Unilateral resistance training for 10 weeks does not alter peripheral and central arterial compliance elderly men.

scholarly journals Dynamic control of maximal ventricular elastance via the baroreflex and force-frequency relation in awake dogs before and after pacing-induced heart failure

2010 ◽  
Vol 299 (1) ◽  
pp. H62-H69 ◽  
Author(s):  
Xiaoxiao Chen ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Masashi Ichinose ◽  
Soroor Soltani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transfer Function ◽  
Transfer Functions ◽  
Dynamic Properties ◽  
System Response ◽  
Force Frequency ◽  
Arterial Baroreflex ◽  
Ventricular Elastance ◽  
Arterial Blood ◽  
Frequency Relation

We investigated to what extent maximal ventricular elastance ( Emax) is dynamically controlled by the arterial baroreflex and force-frequency relation in conscious dogs and to what extent these mechanisms are attenuated after the induction of heart failure (HF). We mathematically analyzed spontaneous beat-to-beat hemodynamic variability. First, we estimated Emax for each beat during a baseline period using the ventricular unstressed volume determined with the traditional multiple beat method during vena cava occlusion. We then jointly identified the transfer functions (system gain value and time delay per frequency) relating beat-to-beat fluctuations in arterial blood pressure (ABP) to Emax (ABP→ Emax) and beat-to-beat fluctuations in heart rate (HR) to Emax (HR→ Emax) to characterize the dynamic properties of the arterial baroreflex and force-frequency relation, respectively. During the control condition, the ABP→ Emax transfer function revealed that ABP perturbations caused opposite direction Emax changes with a gain value of −0.023 ± 0.012 ml−1, whereas the HR→ Emax transfer function indicated that HR alterations caused same direction Emax changes with a gain value of 0.013 ± 0.005 mmHg·ml−1·(beats/min)−1. Both transfer functions behaved as low-pass filters. However, the ABP→ Emax transfer function was more sluggish than the HR→ Emax transfer function with overall time constants (indicator of full system response time to a sudden input change) of 11.2 ± 2.8 and 1.7 ± 0.5 s ( P < 0.05), respectively. During the HF condition, the ABP→ Emax and HR→ Emax transfer functions were markedly depressed with gain values reduced to −0.0002 ± 0.007 ml−1 and −0.001 ± 0.004 mmHg·ml−1·(beats/min)−1 ( P < 0.1). Emax is rapidly and significantly controlled at rest, but this modulation is virtually abolished in HF.

Differential contribution of central command to the cardiovascular responses during static exercise of ankle dorsal and plantar flexion in humans

2011 ◽  
Vol 110 (3) ◽  
pp. 670-680 ◽  
Author(s):  
Nan Liang ◽  
Tomoko Nakamoto ◽  
Seina Mochizuki ◽  
Kanji Matsukawa
Keyword(s):  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Plantar Flexion ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Central Command ◽  
Static Exercise ◽  
Maximum Increase ◽  
Arterial Blood ◽  
Differential Contribution

To examine whether central command contributes differently to the cardiovascular responses during voluntary static exercise engaged by different muscle groups, we encouraged healthy subjects to perform voluntary and electrically evoked involuntary static exercise of ankle dorsal and plantar flexion. Each exercise was conducted with 25% of the maximum voluntary force of the right ankle dorsal and plantar flexion, respectively, for 2 min. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and stroke volume, cardiac output (CO), and total peripheral resistance were calculated. With voluntary exercise, HR, MAP, and CO significantly increased during dorsal flexion (the maximum increase, HR: 12 ± 2.3 beats/min; MAP: 14 ± 2.0 mmHg; CO: 1 ± 0.2 l/min), whereas only MAP increased during plantar flexion (the maximum increase, 6 ± 2.0 mmHg). Stroke volume and total peripheral resistance were unchanged throughout the two kinds of voluntary static exercise. With involuntary exercise, there were no significant changes in all cardiovascular variables, irrespective of dorsal or plantar flexion. Furthermore, before the force onset of voluntary static exercise, HR and MAP started to increase without muscle contraction, whereas they had no significant changes with involuntary exercise at the moment. The present findings indicate that differential contribution of central command is responsible for the different cardiovascular responses to static exercise, depending on the strength of central control of the contracting muscle.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

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