Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study

AbstractIt remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm−5*m2 (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility.

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Reversal of hyperdynamic response to continuous endotoxin administration by inhibition of NO synthesis

Journal of Applied Physiology ◽

10.1152/jappl.1992.73.1.324 ◽

1992 ◽

Vol 73 (1) ◽

pp. 324-328 ◽

Cited By ~ 108

Author(s):

J. Meyer ◽

L. D. Traber ◽

S. Nelson ◽

C. W. Lentz ◽

H. Nakazawa ◽

...

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Methyl Ester ◽

Arterial Pressure ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Resistance Index ◽

Volume Index ◽

Systemic Vascular Resistance Index ◽

Cardiovascular Performance

Septic shock is characterized by an increase in cardiac output and a fall in systemic vascular resistance index and mean arterial pressure. Endotoxin alters the smooth muscle function of blood vessels, probably by means of an increased production of the potent vasodilator nitric oxide (NO). The present study was accomplished to determine how the inhibition of NO synthesis influences cardiovascular performance in an ovine model of hyperdynamic endotoxemia. Endotoxemia was induced in five range ewes (41 +/- 2 kg) by continuous infusion of Escherichia coli endotoxin (LPS, 10 ng.kg-1.min-1) over the entire study period. After 24 h of LPS infusion, cardiac output increased from 5.2 +/- 0.3 to 7.9 +/- 0.6 (SE) 1/min (P less than 0.05) and mean arterial pressure and systemic vascular resistance index fell from 92 +/- 5 to 79 +/- 6 mmHg (P = 0.08) and from 1,473 +/- 173 to 824 +/- 108 dyn.s.cm-5.m2 (P less than 0.05), respectively. The pulmonary shunt fraction increased from 0.23 +/- 0.03 to 0.32 +/- 0.03 (P less than 0.05). The intravenous administration of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (25 mg/kg) 24 h after the start of the LPS infusion changed these values to approximately baseline levels over the subsequent 4 h. Although N omega-nitro-L-arginine methyl ester increased pulmonary arterial pressure and pulmonary vascular resistance (P less than 0.05), right and left ventricular stroke volume index showed no significant changes. It is concluded that NO has a major function in cardiovascular performance in endotoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)

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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

Cardiovascular Diabetology ◽

10.1186/s12933-020-01175-5 ◽

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)

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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

10.21203/rs.3.rs-45927/v2 ◽

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.

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The effects of malnutrition on cardiac function in African children

Archives of Disease in Childhood ◽

10.1136/archdischild-2015-309188 ◽

2015 ◽

Vol 101 (2) ◽

pp. 166-171 ◽

Cited By ~ 11

Author(s):

Jonathan A Silverman ◽

Yamikani Chimalizeni ◽

Stephen E Hawes ◽

Elizabeth R Wolf ◽

Maneesh Batra ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Function ◽

Severe Acute Malnutrition ◽

Resistance Index ◽

Stroke Volume Index ◽

Acute Malnutrition ◽

Volume Index ◽

Severe Malnutrition ◽

Systemic Vascular Resistance Index ◽

Malnourished Children

ObjectiveCardiac dysfunction may contribute to high mortality in severely malnourished children. Our objective was to assess the effect of malnutrition on cardiac function in hospitalised African children.DesignProspective cross-sectional study.SettingPublic referral hospital in Blantyre, Malawi.PatientsWe enrolled 272 stable, hospitalised children ages 6–59 months, with and without WHO-defined severe acute malnutrition.Main outcome measuresCardiac index, heart rate, mean arterial pressure, stroke volume index and systemic vascular resistance index were measured by the ultrasound cardiac output monitor (USCOM, New South Wales, Australia). We used linear regression with generalised estimating equations controlling for age, sex and anaemia.ResultsOur primary outcome, cardiac index, was similar between those with and without severe malnutrition: difference=0.22 L/min/m2 (95% CI −0.08 to 0.51). No difference was found in heart rate or stroke volume index. However, mean arterial pressure and systemic vascular resistance index were lower in children with severe malnutrition: difference=−8.6 mm Hg (95% CI −12.7 to −4.6) and difference=−200 dyne s/cm5/m2 (95% CI −320 to −80), respectively.ConclusionsIn this largest study to date, we found no significant difference in cardiac function between hospitalised children with and without severe acute malnutrition. Further study is needed to determine if cardiac function is diminished in unstable malnourished children.

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Cardiovascular responses to exhaustive upright cycle exercise in highly trained older men

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.3.1500 ◽

1994 ◽

Vol 77 (3) ◽

pp. 1500-1506 ◽

Cited By ~ 45

Author(s):

J. L. Fleg ◽

S. P. Schulman ◽

F. C. O'Connor ◽

G. Gerstenblith ◽

L. C. Becker ◽

...

Keyword(s):

Cardiac Index ◽

Stroke Volume ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Stroke Volume Index ◽

Cardiovascular Responses ◽

Radionuclide Ventriculography ◽

Volume Index ◽

Heart Rates ◽

Peak Vo2

It is unclear whether the markedly enhanced aerobic exercise capacity of older endurance-trained men relative to their sedentary age peers is mediated primarily by central or peripheral cardiovascular mechanisms. To address this question, we performed radionuclide ventriculography with respiratory gas exchange measurements during exhaustive upright cycle ergometry in 16 endurance-trained men aged 63 +/- 7 yr and in 35 untrained men of similar age. As expected, maximal O2 consumption during treadmill exercise was much higher in athletes than in controls. At rest and during fixed submaximal cycle work rates through 100 W, athletes demonstrated lower heart rates and greater stroke volume indexes than controls while maintaining similar cardiac indexes and O2 uptake (VO2). At exhaustion, athletes achieved 53% higher work rates and peak VO2 per kilogram body weight than the sedentary men. The higher peak VO2 in athletes was achieved by a 22.5% larger cardiac index and a 15.6% greater arteriovenous O2 difference. The larger peak cardiac index in the athletes than in sedentary controls was mediated entirely by a greater stroke volume index; peak heart rates were virtually identical. The athletes' greater stroke volume index was achieved through an 11% larger end-diastolic volume index and a 7% higher ejection fraction, both of borderline significance. At exhaustion, athletes demonstrated a lower systemic vascular resistance than controls, despite a higher value at rest. Athletes also showed greater exercise-induced increments in heart rate, stroke volume index, and cardiac index and a greater reduction in systemic vascular resistance from rest to maximal workload.(ABSTRACT TRUNCATED AT 250 WORDS)

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Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

Anesthesiology ◽

10.1097/01.anes.0000311153.84687.c7 ◽

2008 ◽

Vol 108 (5) ◽

pp. 802-811 ◽

Cited By ~ 75

Author(s):

Robert A. Dyer ◽

Jenna L. Piercy ◽

Anthony R. Reed ◽

Carl J. Lombard ◽

Leann K. Schoeman ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Stroke Volume ◽

Spinal Anesthesia ◽

Cesarean Delivery ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Severe Preeclampsia

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.

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Circulatory responses to onset of exercise: role of arterial and cardiac baroreflexes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1985.248.4.h457 ◽

1985 ◽

Vol 248 (4) ◽

pp. H457-H467 ◽

Cited By ~ 12

Author(s):

J. Ludbrook ◽

W. F. Graham

Keyword(s):

Arterial Pressure ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Resistance Index ◽

Systemic Vascular Resistance Index ◽

Receptor Input ◽

Cardiovascular Variables ◽

Tonic Reflex ◽

Cardiac Receptors

Six rabbits were exercised on a moving belt at 13 m/min for 60's. Heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI) were measured. Exercise was done under the following four permutations of input from baroreceptors (B) and cardiac receptors (C): BC, both inputs present; B, only baroreceptor input (intrapericardial procaine); C, only cardiac receptor input (surgical barodenervation); 0, both inputs deleted. The reflex effects on SVRI of the two inputs were calculated as (B - 0) and (C - 0) and their interaction as (BC - 0) - [(B - 0) + (C - 0)]. The effects of baroreceptor input plus interaction on all cardiovascular variables were also calculated, as (BC - C). At rest, (B - 0) and (C - 0) each tonically depressed SVRI without interacting, and (BC - C) tonically depressed SVRI, MAP, and HR. Within 10 s of the start of exercise these tonic effects were abolished, although a small, SVRI-lowering interaction appeared. Suppression of the tonic reflex effects of arterial baroreceptor and cardiac receptor input supported systemic vascular resistance at the onset of exercise and contributed to the rise of arterial pressure.

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Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

Journal of Applied Physiology ◽

10.1152/jappl.1999.86.6.1890 ◽

1999 ◽

Vol 86 (6) ◽

pp. 1890-1896 ◽

Cited By ~ 5

Author(s):

D. Slamowitz ◽

L. Chen ◽

S. M. Scharf

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Stroke Volume ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Cardiovascular Response ◽

Pressor Response ◽

Mechanical Effects

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.

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Fractional spinal anesthesia and systemic hemodynamics in frail elderly hip fracture patients

10.21203/rs.3.rs-1053831/v1 ◽

2021 ◽

Author(s):

Fredrik Olsen ◽

Mathias Hård af Segerstad ◽

Keti Dalla ◽

Sven-Erik Ricksten ◽

Bengt Nellgård

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Hip Fracture ◽

Spinal Anesthesia ◽

Resistance Index ◽

Stroke Volume Index ◽

Volume Index ◽

Systemic Vascular Resistance Index ◽

Hemodynamic Effects ◽

Systemic Hemodynamic

Abstract Background: Aging and frailty make the elderly patients susceptible to hypotension following spinal anesthesia. The systemic hemodynamic effects of spinal anesthesia are not well known. In this study, we examine the systemic hemodynamic effects of fractional spinal anesthesia following intermittent microdosing of a local anesthetic and an opioid.Methods: We included 15 patients aged over 65 with considerable comorbidities, planned for emergency hip fracture repair. Patients received a spinal catheter and cardiac output monitoring using the LiDCOplus system. Invasive mean arterial pressure (MAP), cardiac index, systemic vascular resistance index, heart rate and stroke volume index were registered. Two doses of bupivacaine 2.25 mg and fentanyl 15µg were administered with 25 minutes in between. Hypotension was defined as a fall in MAP by >30% or a MAP <65 mmHgResults: The incidence of hypotension was 30%. Hypotensive patients (n=5) were treated with low doses of norepinephrine (0.003-0.12 µg/kg/min). MAP showed a maximum reduction of 17% at 10 minutes after the first dose. Cardiac index, systemic vascular resistance index and stroke volume index decreased by 10%, 6%, and 7%, respectively, while heart rate was unchanged over time. After the first dose, none of the systemic haemodynamic variables were affected.Conclusion: Fractional spinal anesthesia causes a low incidence of hypotension, induced mainly by a systemic venodilation, causing a decrease in venous return and fall in cardiac output. Our results show that fractional spinal anesthesia is a safe technique from a hemodynamic point of view and is probably underutilized in high-risk, elderly hip fracture patients

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A proof of principle study of atomoxetine for the prevention of vasovagal syncope: the Prevention of Syncope Trial VI

EP Europace ◽

10.1093/europace/euz250 ◽

2019 ◽

Vol 21 (11) ◽

pp. 1733-1741 ◽

Cited By ~ 4

Author(s):

Robert S Sheldon ◽

Lucy Lei ◽

Juan C Guzman ◽

Teresa Kus ◽

Felix A Ayala-Paredes ◽

...

Keyword(s):

Cardiac Index ◽

Stroke Volume ◽

Vasovagal Syncope ◽

Resistance Index ◽

Stroke Volume Index ◽

Study Drug ◽

Norepinephrine Transporter ◽

Volume Index ◽

Head Up Tilt ◽

Invasive Techniques

Abstract Aims There are few effective therapies for vasovagal syncope (VVS). Pharmacological norepinephrine transporter (NET) inhibition increases sympathetic tone and decreases tilt-induced syncope in healthy subjects. Atomoxetine is a potent and highly selective NET inhibitor. We tested the hypothesis that atomoxetine prevents tilt-induced syncope. Methods and results Vasovagal syncope patients were given two doses of study drug [randomized to atomoxetine 40 mg (n = 27) or matched placebo (n = 29)] 12 h apart, followed by a 60-min drug-free head-up tilt table test. Beat-to-beat heart rate (HR), blood pressure (BP), and cardiac haemodynamics were recorded using non-invasive techniques and stroke volume modelling. Patients were 35 ± 14 years (73% female) with medians of 12 lifetime and 3 prior year faints. Fewer subjects fainted with atomoxetine than with placebo [10/29 vs. 19/27; P = 0.003; risk ratio 0.49 (confidence interval 0.28–0.86)], but equal numbers of patients developed presyncope or syncope (23/29 vs. 21/27). Of patients who developed only presyncope, 87% (13/15) had received atomoxetine. Patients with syncope had lower nadir mean arterial pressure than subjects with only presyncope (39 ± 18 vs. 69 ± 18 mmHg, P < 0.0001), and this was due to lower trough HRs in subjects with syncope (67 ± 30 vs. 103 ± 32 b.p.m., P = 0.006) and insignificantly lower cardiac index (2.20 ± 1.36 vs. 2.84 ± 1.05 L/min/m2, P = 0.075). There were no significant differences in stroke volume index (32 ± 6 vs. 35 ± 5 mL/m2, P = 0.29) or systemic vascular resistance index (2156 ± 602 vs. 1790 ± 793 dynes*s/cm5*m2, P = 0.72). Conclusion Norepinephrine transporter inhibition significantly decreased the risk of tilt-induced syncope in VVS subjects, mainly by blunting reflex bradycardia, thereby preventing final falls in cardiac index and BP.

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