Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1304-H1309 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Matthew Coutsos ◽  
Tomoko Ichinose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Linear Relationships ◽  
Before And After ◽  
Spontaneous Baroreflex

Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 ± 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (−2.29 ± 0.5 vs. −5.78 ± 0.7 beats·min−1·mmHg−1; −70.95 ± 11.8 vs. −229.89 ± 29.6 ml·min−1·mmHg−1; and 19.66 ± 4.9 vs. 44.0 ± 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.

Spontaneous baroreflex control of cardiac output during dynamic exercise, muscle metaboreflex activation, and heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1310-H1316 ◽  
Author(s):  
Masashi Ichinose ◽  
Javier A. Sala-Mercado ◽  
Donal S. O'Leary ◽  
Robert L. Hammond ◽  
Matthew Coutsos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex ◽  
Before And After ◽  
Spontaneous Baroreflex

We have previously shown that spontaneous baroreflex-induced changes in heart rate (HR) do not always translate into changes in cardiac output (CO) at rest. We have also shown that heart failure (HF) decreases this linkage between changes in HR and CO. Whether dynamic exercise and muscle metaboreflex activation (via imposed reductions in hindlimb blood flow) further alter this translation in normal and HF conditions is unknown. We examined these questions using conscious, chronically instrumented dogs before and after pacing-induced HF during mild and moderate dynamic exercise with and without muscle metaboreflex activation. We measured left ventricular systolic pressure (LVSP), CO, and HR and analyzed the spontaneous HR-LVSP and CO-LVSP relationships. In normal animals, mild exercise significantly decreased HR-LVSP (−3.08 ± 0.5 vs. −5.14 ± 0.6 beats·min−1·mmHg−1; P < 0.05) and CO-LVSP (−134.74 ± 24.5 vs. −208.6 ± 22.2 ml·min−1·mmHg−1; P < 0.05). Moderate exercise further decreased both and, in addition, significantly reduced HR-CO translation (25.9 ± 2.8% vs. 52.3 ± 4.2%; P < 0.05). Muscle metaboreflex activation at both workloads decreased HR-LVSP, whereas it had no significant effect on CO-LVSP and the HR-CO translation. HF significantly decreased HR-LVSP, CO-LVSP, and the HR-CO translation in all situations. We conclude that spontaneous baroreflex HR responses do not always cause changes in CO during exercise. Moreover, muscle metaboreflex activation during mild and moderate dynamic exercise reduces this coupling. In addition, in HF the HR-CO translation also significantly decreases during both workloads and decreases even further with muscle metaboreflex activation.

scholarly journals Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

2012 ◽  
Vol 303 (7) ◽  
pp. R757-R768 ◽  
Author(s):  
Masashi Ichinose ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
ZhenHua Li ◽  
Tomoko K. Ichinose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Moderate Exercise ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex ◽  
High Level

We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04–0.15 Hz; Hi-F, 0.15–0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (>0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Spontaneous baroreflex control of heart rate during exercise and muscle metaboreflex activation in heart failure

2007 ◽  
Vol 293 (3) ◽  
pp. H1929-H1936 ◽  
Author(s):  
Ferdinando Iellamo ◽  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Marco Pallante ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Response Relationship ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Stimulus Response ◽  
Spontaneous Baroreflex

In heart failure (HF), there is a reduced baroreflex sensitivity at rest, and during dynamic exercise there is enhanced muscle metaboreflex activation (MRA). However, how the arterial baroreflex modulates HR during exercise is unknown. We tested the hypothesis that spontaneous baroreflex sensitivity (SBRS) is attenuated during exercise in HF and that MRA further depresses SBRS. In seven conscious dogs we measured heart rate (HR), cardiac output, and left ventricular systolic pressure at rest and during mild and moderate dynamic exercise, before and during MRA (via imposed reductions of hindlimb blood flow), and before and after induction of HF (by rapid ventricular pacing). SBRS was assessed by the sequences method. In control, SBRS was reduced from rest with a progressive resetting of the baroreflex stimulus-response relationship in proportion to exercise intensity and magnitude of MRA. In HF, SBRS was significantly depressed in all settings; however, the changes with exercise and MRA occurred with a pattern similar to the control state. As in control, the baroreflex stimulus-response relationship showed an intensity- and muscle metaboreflex (MMR)-dependent rightward and upward shift. The results of this study indicate that HF induces an impairment in baroreflex control of HR at rest and during exercise, although the effects of exercise and MRA on SBRS occur with a similar pattern as in control, indicating the persistence of some vagal activity.

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Naoki Fujimoto ◽  
Keishi Moriwaki ◽  
Issei Kameda ◽  
Masaki Ishiyama ◽  
Taku Omori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Circulatory Arrest ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Isometric Handgrip ◽  
Arterial Elastance ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p<0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p<0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

Muscle metaboreflex attenuates spontaneous heart rate baroreflex sensitivity during dynamic exercise

2007 ◽  
Vol 292 (6) ◽  
pp. H2867-H2873 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Tomoko Ichinose ◽  
Marco Pallante ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Intensity ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Moderate Exercise ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Dynamic exercise attenuates spontaneous baroreflex sensitivity (SBRS) in the control of heart rate (HR) during rapid, spontaneous changes in blood pressure (BP). Our objective was to determine whether muscle metaboreflex activation (MRA) further diminishes SBRS. Conscious dogs were chronically instrumented for measurement of HR, cardiac output, mean arterial pressure, and left ventricular systolic pressure (LVSP) at rest and during mild (3.2 km/h) or moderate (6.4 km/h at 10% grade) dynamic exercise before and after MRA (via partial reduction of hindlimb blood flow). SBRS was evaluated as the slopes of the linear relations (LRs) between HR and LVSP during spontaneous sequences of at least three consecutive beats when HR changed inversely vs. pressure (expressed as beats·min−1·mmHg−1). During mild exercise, these LRs shifted upward, with a significant decrease in SBRS (−3.0 ± 0.4 vs. −5.2 ± 0.4, P < 0.05 vs. rest). MRA shifted LRs upward and rightward and decreased SBRS (−2.1 ± 0.1, P < 0.05 vs. mild exercise). Moderate exercise shifted LRs upward and rightward and significantly decreased SBRS (−1.2 ± 0.1, P < 0.05 vs. rest). MRA elicited further upward and rightward shifts of the LRs and reductions in SBRS (−0.9 ± 0.1, P < 0.05 vs. moderate exercise). We conclude that dynamic exercise resets the arterial baroreflex to higher BP and HR as exercise intensity increases. In addition, increases in exercise intensity, as well as MRA, attenuate SBRS.

scholarly journals P714 Contradicting the most basic tenet of black holes: light can, indeed, escape

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
J P Sousa ◽  
J Ribeiro ◽  
L Puga ◽  
C Lourenco ◽  
R Teixeira ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Surgical Correction ◽  
Left Ventricular Ejection ◽  
Functional Mitral Regurgitation ◽  
Heart Team ◽  
Maximal Velocity ◽  
Ventricular Systolic Pressure

Abstract A 69-year-old man with history of non-insulin-treated type 2 diabetes mellitus, arterial hypertension and mixed dyslipidemia presented to the emergency department with chest pain lasting for four days. Immediate twelve-lead electrocardiogram unveiled an inferior ST-segment elevation myocardial infarction (STEMI), prompting emergent coronary angiography, which, in turn, revealed two-vessel disease, specifically proximal ramus intermedius 60-70% stenosis and proximal right coronary artery acute occlusion. Culprit lesion was successfully managed with balloon angioplasty and a single drug-eluting stent implantation. Still, clinical course was noticeable for deterioration, under the form of cardiogenic shock, which required invasive ventilation and intravenous vasopressor support with norepinephrine. Despite biventricular systolic function relative preservation, transthoracic echocardiography disclosed inferior akinesis, right ventricle dilation, mild circumferential pericardial effusion and, particularly, a 2.3cm posteroinferior ventricular septal defect (VSD), in the setting of a 4.4cm2 pseudoaneurism, resulting in left-to-right shunting, quantified through maximal/mean trans-VSD pressure gradients of 84/44mmHg. Further imaging with transesophageal echocardiography and cardiac computed tomography angiography allowing the conception of a 3D-printed model was performed. Surgical correction of the defect followed, achieving partial anatomic success, namely with residual shunting, as of a left ventricular systolic pressure of 80mmHg and a right ventricular systolic pressure of 25mmHg. Patient survived, recovered and got discharged three weeks later. At one-year follow-up, he was hospitalized for acute decompensated heart failure (hemodynamic profile C) twice, with medication non-adherence reported as the main precipitating factor. In addition to a significant remaining left-to-right shunt (maximal velocity 3m/s), adverse cardiac remodeling was recognized, featuring left ventricular ejection fraction of 30-35%, severe functional mitral regurgitation, severe postcapillary pulmonary hypertension and de novo left bundle branch block (QRS duration of 197ms). Having been deemed clinically unsuitable for another surgical correction, patient underwent percutaneous VSD closure with both AmplatzerTM septal and muscular VSD occluders, with a suboptimal result. He is now on New York Heart Association class III heart failure and on the waiting list for both MitraClip and cardiac resynchronization therapy implantation. Reflecting numerous breakthroughs in the management of acute myocardial infarction, incidence of mechanical complications is on the decline. Nevertheless, when they occur, morbidity and mortality remain high. Acquired ventricular septal defects are no exception, demanding the best care from a tertiary hospital heart team. Abstract P714 Figure.

scholarly journals Left ventricular epicardial admittance measurement for detection of acute LV dilation

2011 ◽  
Vol 110 (3) ◽  
pp. 799-806 ◽  
Author(s):  
John E. Porterfield ◽  
Erik R. Larson ◽  
James T. Jenkins ◽  
Daniel Escobedo ◽  
Jonathan W. Valvano ◽  
...  
Keyword(s):  
Heart Failure ◽  
Measurement System ◽  
Systolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Warning Systems ◽  
Ventricular Systolic Pressure ◽  
Volume Measurements ◽  
Admittance Measurement

There are two implanted heart failure warning systems incorporated into biventricular pacemakers/automatic implantable cardiac defibrillators and tested in clinical trials: right heart pressures, and lung conductance measurements. However, both warning systems postdate measures of the earliest indicator of impending heart failure: left ventricular (LV) volume. There are currently no proposed implanted technologies that can perform LV blood volume measurements in humans. We propose to solve this problem by incorporating an admittance measurement system onto currently deployed biventricular and automatic implantable cardiac defibrillator leads. This study will demonstrate that an admittance measurement system can detect LV blood conductance from the epicardial position, despite the current generating and sensing electrodes being in constant motion with the heart, and with dynamic removal of the myocardial component of the returning voltage signal. Specifically, in 11 pigs, it will be demonstrated that 1) a physiological LV blood conductance signal can be derived; 2) LV dilation in response to dose-response intravenous neosynephrine can be detected by blood conductance in a similar fashion to the standard of endocardial crystals when admittance is used, but not when only traditional conductance is used; 3) the physiological impact of acute left anterior descending coronary artery occlusion and resultant LV dilation can be detected by blood conductance, before the anticipated secondary rise in right ventricular systolic pressure; and 4) a pleural effusion simulated by placing saline outside the pericardium does not serve as a source of artifact for blood conductance measurements.

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