scholarly journals A Novel Control Method for Rotary Blood Pumps as Left Ventricular Assist Device Utilizing Aortic Valve State Detection

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Dmitry Petukhov ◽  
Leonie Korn ◽  
Marian Walter ◽  
Dmitry Telyshev
Keyword(s):  
Heart Rate ◽  
Aortic Valve ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Control Method ◽  
Left Ventricular ◽  
Pump Speed ◽  
Pump Flow ◽  
Blood Pumps ◽  
Rotary Blood Pumps

A novel control method for rotary blood pumps is proposed relying on two different objectives: regulation of pump flow in accordance with desired value and the maintenance of partial support with an open aortic valve by the variation of pump speed. The estimation of pump flow and detection of aortic valve state was performed with mathematical models describing the first- and second generation of Sputnik rotary blood pumps. The control method was validated using a cardiovascular system model. The state of the aortic valve was detected with a mean accuracy of 91% for Sputnik 1 and 96.2% for Sputnik 2 when contractility, heart rate, and systemic vascular resistance was changed. In silico results for both pumps showed that the proposed control method can achieve the desired pump flow level and maintain the open state of the aortic valve by periodically switching between two objectives under contractility, heart rate, and systemic vascular resistance changes. The proposed method showed its potential for safe operation without adverse events and for the improvement of chances for myocardial recovery.

scholarly journals Simulation of Exercise-Induced Syncope in a Heart Model with Severe Aortic Valve Stenosis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Matjaž Sever ◽  
Samo Ribarič ◽  
Marjan Kordaš
Keyword(s):  
Heart Rate ◽  
Aortic Valve ◽  
Vascular Resistance ◽  
Aortic Valve Stenosis ◽  
Case Reports ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Lumped Parameter ◽  
Pulmonary Arterial ◽  
Exercise Induced

Severe aortic valve stenosis (AVS) can cause an exercise-induced reflex syncope (RS). The precise mechanism of this syncope is not known. The changes in hemodynamics are variable, including arrhythmias and myocardial ischemia, and one of the few consistent changes is a sudden fall in systemic and pulmonary arterial pressures (suggesting a reduced vascular resistance) followed by a decline in heart rate. The contribution of the cardioinhibitory and vasodepressor components of the RS to hemodynamics was evaluated by a computer model. This lumped-parameter computer simulation was based on equivalent electronic circuits (EECs) that reflect the hemodynamic conditions of a heart with severe AVS and a concomitantly decreased contractility as a long-term detrimental consequence of compensatory left ventricular hypertrophy. In addition, the EECs model simulated the resetting of the sympathetic nervous tone in the heart and systemic circuit during exercise and exercise-induced syncope, the fluctuating intra-thoracic pressure during respiration, and the passive relaxation of ventricle during diastole. The results of this simulation were consistent with the published case reports of exertional syncope in patients with AVS. The value of the EEC model is its ability to quantify the effect of a selective and gradable change in heart rate, ventricular contractility, or systemic vascular resistance on the hemodynamics during an exertional syncope in patients with severe AVS.

Abstract 323: Acute Reduction of Ambient Air Pressure Lowers Systemic Vascular Resistance and Improves Cardiac Output in Mice in-vivo

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Anmol Shahid ◽  
Vaibhav B Patel ◽  
Gavin Y Oudit ◽  
Michael S McMurtry
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Atmospheric Pressure ◽  
Arterial Compliance ◽  
Ambient Air ◽  
Left Ventricular ◽  
Air Pressure

Background: Humans have lower risk for myocardial infarction and stroke at higher altitudes. The mechanism is unknown. We previously demonstrated that acute reductions in ambient air pressure result in enhanced arterial vasodilation ex vivo using a myograph model of murine resistance arteries. Enhanced vasodilation might increase effective arterial compliance in vivo , thus we further hypothesized a reduction in systemic vascular resistance in vivo as a result of lowered ambient air pressure. Methods: In-vivo Pressure Volume Loops: A novel hypobaric chamber was designed and constructed with the capacity to hold a single anaesthetized mouse and simulate a variety of lowered air pressures within the chamber. The design of the chamber allowed for monitoring of murine heart rate, respiratory rate, & blood oxygen saturation at all times. Using inhaled isoflurane to anesthetize the animal, a closed-chest left-ventricular catheterization procedure was performed within the chamber on free-breathing adult male C57-WT mice (n=8) during consecutive acute exposures to the three air pressure steps: 754 mmHg (control or room atmospheric pressure), 714 mmHg (p1) and 674 mmHg (p2). Results: In-vivo : Total systemic vascular resistance was reduced by acute exposure to lower air pressure (10.09±0.15 mmHg*min/μL at control vs. 8.11±1.45 and 8.18±1.24 mmHg*min/μL at p1 and p2, respectively; p<0.05). Cardiac output was significantly improved by lowering atmospheric pressure below room pressure (7.36±0.15 mL/min at control versus 9.71±1.45 mL/min and 9.59±1.77 mL/min at p1 and p2, respectively; p<0.05). Significant increases in stroke volume with a reduction in air pressure were also observed (p<0.05 for p1 and p2 vs. control). We did not note significant changes in heart rate, mean arterial pressure, or contractility of the mice with lowered atmospheric pressure. Conclusion: Acute reductions in ambient air pressure lower systemic vascular resistance, and increase cardiac output and stroke volumes in vivo .

Effects of enhanced ventricular filling on cardiac pump performance in exercising dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1886-1890 ◽  
Author(s):  
L. D. Horwitz ◽  
J. Lindenfeld
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Increase Stroke Volume ◽  
Normal Increase ◽  
Ventricular Filling

The extent to which the normal increase in stroke volume during exercise can be augmented by increasing preload by dextran infusion was studied in seven dogs. Each dog ran 3 min on a level treadmill at mild (3–4 mph), moderate (6–8 mph), and severe (9–13 mph) loads during the control study and immediately after 10% dextran 14 ml/kg iv. During severe exercise dextran-augmented stroke volume (+5.4 ml or 19% vs. exercise without dextran, P less than 0.01) and left ventricular end-diastolic diameter and pressure did not change heart rate, aortic pressure, or maximum derivative of left ventricular pressure but decreased systemic vascular resistance by 16%. Similar increases in stroke volume and preload after dextran occurred during mild and moderate exercise when arterial pressure and heart rate were unchanged or increased and systemic vascular resistance was decreased. Thus altering preload above those levels normally encountered during exercise is a potential mechanism to increase stroke volume and cardiac output.

Exercise Capacity in Patients Supported With Rotary Blood Pumps Is Improved by a Spontaneous Increase of Pump Flow at Constant Pump Speed and by a Rise in Native Cardiac Output

2011 ◽  
Vol 35 (7) ◽  
pp. 682-690 ◽  
Author(s):  
Luc Jacquet ◽  
Olivier Vancaenegem ◽  
Agnès Pasquet ◽  
Pascal Matte ◽  
Alain Poncelet ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Exercise Capacity ◽  
Pump Speed ◽  
Pump Flow ◽  
Blood Pumps ◽  
Rotary Blood Pumps

scholarly journals 443 Arterial hypertension in aortic valve stenosis: a critical update

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Christian Basile ◽  
Ilaria Fucile ◽  
Maria Virginia Manzi ◽  
Federica Ilardi ◽  
Anna Franzone ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Aortic Valve ◽  
Aortic Stenosis ◽  
Arterial Hypertension ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Mechanical Obstruction ◽  
Mineralocorticoid Receptor Antagonist ◽  
All Cause Mortality

Abstract Aims Aortic stenosis (AS) is a very common valve disease and is associated with high mortality once it becomes symptomatic. Arterial hypertension (HT) has a high prevalence among patients with AS leading to worst left ventricle remodelling and faster degeneration of the valve. HT also seems to interfere with the assessment of the severity of AS leading to an underestimation of the real degree of stenosis. Treatment of HT in AS has historically been associated with reluctance due to both the lack of clear guidelines and the fear of adverse effects, but the most recent evidence shows as several drugs that can be used. Methods The pathophysiology of the combination of AS and HT is the association of a first fixed mechanical obstruction of the aortic root and a second obstruction due to systemic vascular resistance. Consequently, a decrease in systemic vascular resistance through, for example, the administration of vasodilators could theoretically cause a drop in systemic pressure due to the fixed mechanical obstruction given by the stenosis which prevents an increase in cardiac output. This theory was the basis for avoiding vasodilators in patients with AS. Results There is a unanimous opinion on maintaining blood pressure values of 130–139 mmHg of systolic and 70–90 mmHg of diastolic, but there is not the same agreement on which drugs to adopt to achieve the aforementioned values. Renin-Angiotensin-Aldosterone system inhibitors are certainly the first-line treatment thanks to their cardioprotective, plaque stabilizing, and antiarrhythmic effect since they are also associated with increased survival rates and greater left ventricular mass reduction in patients after surgical or transcatheter aortic valve replacement for severe AS. If blood pressure is not yet controlled, the addition of a beta-blocker should be considered: metoprolol has the greatest literature, showing not only an improvement in haemodynamic and metabolic performance but also a reduction in mortality in patients who already presented with coronary artery disease. Mineralocorticoid receptor antagonist can be used, among them eplerenone has been studied and can be useful to relieve symptoms of patients with a flare-up of heart failure by reducing the preload, provided that a close fluid and echocardiographic monitoring is implemented. Conclusions The use of phosphodiesterase 5 inhibitors can improve the haemodynamic status of patients with aortic stenosis and reduce the level of left ventricular hypertrophy, as well as improve pulmonary circulation and exercise tolerability of patients with AS, however it should be considered that in other studies sildenafil was associated with a worse clinical outcome. Calcium channel blocker are one the most used medications in patients with HT, but their use was associated with a 7-fold relative risk of all-cause mortality independent of known confounders and was also associated with an adverse effect on treadmill exercise and higher risk of all-cause mortality in patients with AS.

Hemodynamic effects of epinephrine: concentration-effect study in humans

1985 ◽  
Vol 58 (4) ◽  
pp. 1199-1206 ◽  
Author(s):  
J. R. Stratton ◽  
M. A. Pfeifer ◽  
J. L. Ritchie ◽  
J. B. Halter
Keyword(s):  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Hemodynamic Effects ◽  
Plasma Epinephrine ◽  
Ventricular Performance

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study 

2020 ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background: In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function.Methods: In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results: Baseline characteristics were not different in the empagliflozin (n=22) and placebo (n=20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 hrs; day 1: 48.4 ± 34.7 g/24 hrs; p<0.001) as well as urinary volume (1740 ± 601 mL/24 hrs to 2112 ± 837 mL/24 hrs; p=0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/e’) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p=0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/sec; day 1: 0.73 ± 0.2 m/sec; p=0.003). Conclusions: Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function.

The Heart-Pump Interaction: Effects of a Microaxial Blood Pump

2002 ◽  
Vol 25 (11) ◽  
pp. 1082-1088 ◽  
Author(s):  
J. Stoliński ◽  
C. Rosenbaum ◽  
W. Flameng ◽  
B. Meyns
Keyword(s):  
Cardiac Cycle ◽  
Differential Pressure ◽  
Blood Pump ◽  
Pump Performance ◽  
Failing Heart ◽  
Pump Flow ◽  
Heart Pump ◽  
Blood Pumps ◽  
Clinical Conditions ◽  
Rotary Blood Pumps

Background: When we use rotary blood pumps as an assist device, an interaction takes place between the pump performance and the native heart function (native heart influences pump performance and vice versa). The interaction between native heart and rotary blood pump can be useful to predict recovery of the failing heart. Methods: The rotary blood pumps used were microaxial catheter-mounted pumps with an external diameter of 6.4mm (Impella, Aachen, Germany). The pump-heart interaction was studied in five juvenile sheep with a mean body weight of 68.5 ± 8.7 kg. The pumps were introduced via the left carotid artery and placed in transvalvular aortic position. Recorded parameters were pump speed (rpm), generated flow (L/min) and differential pressure (mm Hg) obtained at high frequency rate of data recordings (25 sets of data per second). This allowed continuous analysis of the pump performance during cardiac cycle. Under clinical conditions the interaction was studied in a 60-year-old male, in whom the device was applied due to postcardiotomy heart failure after myocardial infarction. Results: Heart-pump interaction was analyzed based on pump flow differential pressure. This relationship, analyzed continuously during cardiac cycle, presents as a loop. The dynamic contribution of the heart to the flow generated by the pump leads to continuous fluctuation in the pressure head and the creation of hysteresis. The improved function of the failing heart under clinical conditions after seven days of mechanical support was expressed by: increased hysteresis of the loop caused by increased gradient of flow generated during cardiac cycle, a more pronounced ventricular ejection phase that indicates more dynamic heart contribution to the generated flow, and finally increased gradient of the differential pressure during cardiac cycle, caused predominantly by increased aortic pressure and decreased left ventricle pressure during diastolic phase. Conclusions: The heart-pump interaction based on the pump flow-differential pressure relationship can be useful in predicting the possibility to wean the patient from the device.

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