Abstract 16747: The Artificial Pulse of the HeartMate3 LVAD Alters Mean Arterial Pressure Calculation, and the Relationship Between Arterial Pulse Pressure and Pulsatility Index

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lorenzo Braghieri ◽  
Alberto Pinsino ◽  
Giulio Mondellini ◽  
Antonia Gaudig ◽  
Azka Javaid ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pulsatility Index ◽  
Left Ventricular ◽  
Absolute Difference ◽  
Arterial Line ◽  
Arterial Pulse ◽  
Relative Contribution ◽  
Arterial Pulse Pressure

Introduction: The HeartMate (HM3) left ventricular assist device (LVAD) uniquely features an artificial pulse (AP) (designed to reduce blood stasis and simulate physiologic pulsatility) that alters arterial blood pressure (BP) tracings ( Fig. 1A ). Pulsatility Index (PI) corresponds to the magnitude of flow pulse through the LVAD and is used as a surrogate measure of arterial pulse pressure (PP). The effect of the AP on: i) relative contribution of systolic BP (SBP) and diastolic BP (DBP) to mean arterial pressure (MAP) calculation; and ii) association between PP and PI is presently unknown. Thus, we aimed to compare: i) MAP calculations; and ii) relation of PI with PP in HM3 vs HM II (LVAD with no AP) pts with arterial line (A-line) monitoring. Methods: A-line BP and LVAD PI data were prospectively collected in 48 HM3 and 29 HMII pts. MAP was calculated with the formula conventionally used in non LVAD pts (MAP = 2/3 DBP + 1/3 SBP) and compared to A-line MAP. Among HM3 pts, a multiple linear regression model was fit with A-line SBP and DBP as predictor variables, and A-line MAP as the dependent variable to derive the HM3 MAP Formula . The relation between arterial PP and PI in HM3 and HMII pts was assessed using Pearson’s correlation. Results: MAP calculated using the conventional formula accurately estimated A-line MAP in HMII pts, but overestimated A-line MAP in HM3 pts. The HM3 MAP Formula more closely approximated A-line MAP. Mean observed difference (MOD) and mean absolute difference (MAD) between calculated MAPs and A-line MAPs are reported in Fig. 1B . While median PP was similar in HM3 and HMII pts (16 vs 20 mmHg, p=0.11), median PI was significantly higher in HMII pts (3.45 vs 5.6, p<0.001). PI correlated with PP in HMII pts ( r 0.47, p=0.01). However, no significant correlation was found between PI and PP in HM3 pts ( r 0.24, p=0.1; Fig. 1C ). Conclusions: In HM3 pts, the AP significantly alters the relative contribution of SBP and DBP to MAP. Unlike in HM2 pts, PI does not relate to arterial PP in HM3 pts.

scholarly journals Relationship between Stroke Volume and Pulse Pressure during Blood Volume Perturbation: A Mathematical Analysis

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Ramin Bighamian ◽  
Jin-Oh Hahn
Keyword(s):  
Stroke Volume ◽  
Blood Volume ◽  
Fluid Therapy ◽  
Pulse Pressure ◽  
Mathematical Analysis ◽  
Left Ventricular ◽  
Experimental Investigations ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
Relative Change

Arterial pulse pressure has been widely used as surrogate of stroke volume, for example, in the guidance of fluid therapy. However, recent experimental investigations suggest that arterial pulse pressure is not linearly proportional to stroke volume. However, mechanisms underlying the relation between the two have not been clearly understood. The goal of this study was to elucidate how arterial pulse pressure and stroke volume respond to a perturbation in the left ventricular blood volume based on a systematic mathematical analysis. Both our mathematical analysis and experimental data showed that the relative change in arterial pulse pressure due to a left ventricular blood volume perturbation was consistently smaller than the corresponding relative change in stroke volume, due to the nonlinear left ventricular pressure-volume relation during diastole that reduces the sensitivity of arterial pulse pressure to perturbations in the left ventricular blood volume. Therefore, arterial pulse pressure must be used with care when used as surrogate of stroke volume in guiding fluid therapy.

Comparative effects of levosimendan, OR-1896, OR-1855, dobutamine, and milrinone on vascular resistance, indexes of cardiac function, and O2 consumption in dogs

2008 ◽  
Vol 294 (1) ◽  
pp. H238-H248 ◽  
Author(s):  
Patricia N. Banfor ◽  
Lee C. Preusser ◽  
Thomas J. Campbell ◽  
Kennan C. Marsh ◽  
James S. Polakowski ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Myocardial Oxygen Consumption ◽  
Plasma Concentrations ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Dose Dependent

Levosimendan enhances cardiac contractility via Ca2+ sensitization and induces vasodilation through the activation of ATP-dependent K+ and large-conductance Ca2+-dependent K+ channels. However, the hemodynamic effects of levosimendan, as well as its metabolites, OR-1896 and OR-1855, relative to plasma concentrations achieved, are not well defined. Thus levosimendan, OR-1896, OR-1855, or vehicle was infused at 0.01, 0.03, 0.1, and 0.3 μmol·kg−1·30 min−1, targeting therapeutic to supratherapeutic concentrations of total levosimendan (62.6 ng/ml). Results were compared with those of the β1-agonist dobutamine and the phosphodiesterase 3 inhibitor milrinone. Peak concentrations of levosimendan, OR-1896, and OR-1855 were 455 ± 21, 126 ± 6, and 136 ± 6 ng/ml, respectively. Levosimendan and OR-1896 produced dose-dependent reductions in mean arterial pressure (−31 ± 2 and −42 ± 3 mmHg, respectively) and systemic resistance without affecting pulse pressure, effects paralleled by increases in heart rate; OR-1855 produced no effect at any dose tested. Dobutamine, but not milrinone, increased mean arterial pressure and pulse pressure (17 ± 2 and 23 ± 2 mmHg, respectively). Regarding potency to elicit reductions in time to peak pressure and time to systolic pressure recovery: OR-1896 > levosimendan > milrinone > dobutamine. Levosimendan and OR-1896 elicited dose-dependent increases in change in pressure over time (118 ± 10 and 133 ± 13%, respectively), concomitant with reductions in left ventricular end-diastolic pressure and ejection time. However, neither levosimendan nor OR-1896 produced increases in myocardial oxygen consumption at inotropic and vasodilatory concentrations, whereas dobutamine increased myocardial oxygen consumption (79% above baseline). Effects of the levosimendan and OR-1896 were limited to the systemic circulation; neither compound produced changes in pulmonary pressure, whereas dobutamine produced profound increases (74 ± 13%). Thus levosimendan and OR-1896 are hemodynamically active in the anesthetized dog at concentrations observed clinically and elicit cardiovascular effects consistent with activation of both K+ channels and Ca2+ sensitization, whereas OR-1855 is inactive on endpoints measured in this study.

Effect of arterial pulse pressure and hypoxia on myogenic responses in the gut

1978 ◽  
Vol 235 (2) ◽  
pp. H157-H161 ◽  
Author(s):  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
Vascular Smooth Muscle ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
Circulatory Control ◽  
Myogenic Responses

In intestine, raising venous pressure (PV) elicits a precapillary vasconstriction that has been ascribed to a myogenic mechanism through which passive stretch elicits active contraction of vascular smooth muscle. A previous report from this laboratory indicated that myogenic responses in the gut were largely dependent on control conditions. The purpose of the present study was to determine whether control blood flow rates or the arterial pulse pressure affects the magnitude of myogenic responses. In isolated perfused canine small bowel arterial hypoxia was used to increase blood flow. Myogenic responses to elevated PV were not significantly different in the normoxic and hypoxic periods, indicating that blood flow per se does not greatly alter myogenic responses. When gut loops were perfused with pulsatile arterial pressure, myogenic responses occurred more than twice as frequently as during nonpulsatile pefusion and they had a greater magnitude. The results are consistent with the observation that vascular smooth muscle is stimulated not only by steady stretch but also by the rate of stretch. The results also suggest that the arterial pressure pulse should be considered in the design and interpretation of future studies of local circulatory control.

Isolated diastolic hypertension, pulse pressure, and mean arterial pressure as predictors of mortality during a follow-up of up to 32 years

2002 ◽  
Vol 20 (3) ◽  
pp. 399-404 ◽  
Author(s):  
Timo E. Strandberg ◽  
Veikko V. Salomaa ◽  
Hannu T. Vanhanen ◽  
Kaisu Pitkälä ◽  
Tatu A Miettinen
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Predictors Of Mortality ◽  
Diastolic Hypertension

Hyperinflation-induced cardiorespiratory failure in rats

2009 ◽  
Vol 107 (1) ◽  
pp. 275-282 ◽  
Author(s):  
Jeremy A. Simpson ◽  
Keith R. Brunt ◽  
Christine P. Collier ◽  
Steve Iscoe
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lung Volume ◽  
Troponin T ◽  
Respiratory Acidosis ◽  
Left Ventricular ◽  
Cardiovascular Failure ◽  
Cardiorespiratory Failure ◽  
Arterial Hypoxemia ◽  
Ventricular Afterload

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 ± 43 min; range 82–206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O2 delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.

Evaluation of cardiac output variations with the peripheral pulse pressure to mean arterial pressure ratio

2018 ◽  
Vol 33 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Audrey Tantot ◽  
Anais Caillard ◽  
Arthur Le Gall ◽  
Joaquim Mateo ◽  
Sandrine Millasseau ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Peripheral Pulse
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