Reduced stroke volume during exercise in postural tachycardia syndrome

Masuki, Shizue; Eisenach, JH; Schrage, WG; Johnson, C.E.; Nm, Dietz; Wilkins, BW; Sandroni, Paola; Low, P. A.; Joyner, M. J.

doi:10.1016/j.autneu.2008.10.019

Cited by 9 publications

(15 citation statements)

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“…15 The invasive hemodynamic profile of the 5 POTS patients in this study confirms a significantly reduced peak SV compared to normal patients, consistent with a previous study. 16 We further show that POTS patients had persistently low RAP despite receiving an average of 1 L of normal saline before the test, suggesting that venous capacitance is the issue rather than total intravascular volume. Other studies have also suggested that inadequate peripheral vasoconstriction, 17 cardiac sympathetic dysautonomia, 18 and autoimmune autonomic neuropathy 19 may contribute to symptoms of POTS.…”

Section: Discussionmentioning

confidence: 90%

Unexplained Exertional Dyspnea Caused by Low Ventricular Filling Pressures: Results from Clinical Invasive Cardiopulmonary Exercise Testing

et al. 2016

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To determine whether low ventricular filling pressures are a clinically relevant etiology of unexplained dyspnea on exertion, a database of 619 consecutive, clinically indicated invasive cardiopulmonary exercise tests (iCPETs) was reviewed to identify patients with low maximum aerobic capacity (V O 2 max) due to inadequate peak cardiac output (Qtmax) with normal biventricular ejection fractions and without pulmonary hypertension (impaired: n = 49, V O 2 max = 53% predicted [interquartile range (IQR): 47%-64%], Qtmax = 72% predicted [62%-76%]). These were compared to patients with a normal exercise response (normal: n = 28, V O 2 max = 86% predicted [84%-97%], Qtmax = 108% predicted [97%-115%]). Before exercise, all patients received up to 2 L of intravenous normal saline to target an upright pulmonary capillary wedge pressure (PCWP) of ≥5 mmHg. Despite this treatment, biventricular filling pressures at peak exercise were lower in the impaired group than in the normal group Dyspnea on exertion is a common presenting symptom with a broad differential diagnosis. Often the etiology remains unclear despite a thorough clinical and laboratory investigation. 1,2 Cardiopulmonary exercise testing (CPET) may assist in the diagnostic evaluation by defining the degree of impairment in maximum aerobic capacity (V O 2 max), identifying the limiting organ system (e.g., heart vs. lung), and providing clues as to more specific pathophysiology. When CPET is coupled with invasive hemodynamic monitoring using radial and pulmonary arterial catheters (i.e., invasive CPET [iCPET]), the presence of peripheral and central cardiovascular abnormalities can be better characterized through direct measurements of systemic and pulmonary vascular pressures and systemic and mixed venous oxygen content as well as precise estimation of cardiac output (Qt). 3 For example, these measurements have been used to characterize the exercise-induced increases in ventricular filling pressure and pulmonary arterial pressure in patients with heart failure 4-8 and pulmonary arterial hypertension, 9 respectively. Despite a detailed hemodynamic and metabolic evaluation, nearly 10% of symptomatic patients studied with iCPET in our laboratory had low V O 2 max and low maximum Qt (Qtmax) without a clearly identified cause.During the normal exercise response, sympathetic stimulation and vagal withdrawal increase heart rate (HR), contractility, and mean systemic pressure. Increased respiratory efforts and vigorous limb skeletal muscle contractions also enhance venous return to the heart. Together, these responses increase stroke volume (SV) through the Frank-Starling mechanism. In this study, we tested the hypothesis that failure of these mechanisms to increase cardiac preload during exercise, as evidenced by persistently low ventricular filling pressures, may be the primary limitation of Qtmax in an undiagnosed population of patients with unexplained exercise intolerance. METHODS PatientsFor the single-test cohort, results from 619 consecutive, clinically ...

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Section: Discussionmentioning

confidence: 90%

Unexplained Exertional Dyspnea Caused by Low Ventricular Filling Pressures: Results from Clinical Invasive Cardiopulmonary Exercise Testing

et al. 2016

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“…Low stroke volume and physical deconditioning are also possible explanations for the fluctuations in SAP and PP (16). For example, it has been suggested that a steeper Frank-Starling relationship could be operating after bed rest deconditioning in people with smaller and less distensible hearts (13), meaning that small changes in left ventricular end-diastolic volume could provoke greater changes in stroke volume that are translated into greater variability in SAP and PP.…”

Section: Variability In Hemodynamic Responses To Tiltmentioning

confidence: 99%

Cardiovascular dynamics in healthy subjects with differing heart rate responses to tilt

Ramírez-Marrero¹,

Charkoudian²,

Hart³

et al. 2008

Journal of Applied Physiology

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MJ. Cardiovascular dynamics in healthy subjects with differing heart rate responses to tilt. J Appl Physiol 105: 1448 -1453, 2008. First published August 28, 2008 doi:10.1152/japplphysiol.90796.2008.-Orthostatic stress such as head-up tilt (HUT) elicits a wide range of heart rate (HR) and arterial pressure (AP) responses among healthy individuals. In this study, we evaluated cardiovascular dynamics in healthy subjects with different HR responses to HUT, but without autonomic dysfunction. We measured AP (brachial artery) and HR (ECG) during 5 min of 60°H UT in 76 healthy normotensive individuals. We then chose individuals on the basis of the extremes of HR responses to HUT (high ϭ ⌬HR Ն 20 beats/min, and low ϭ ⌬HR Յ 10 beats/min; n ϭ 15 per group). Peak HR during HUT was 87 Ϯ 10 beats/min in the high and 69 Ϯ 14 beats/min in the low group (P Ͻ 0.05). High HR responders had lower systolic pressure at baseline (121 Ϯ 9 vs. 129 Ϯ 11 mmHg, P Ͻ 0.05) and during HUT (120 Ϯ 10 vs. 131 Ϯ 13 mmHg, P Ͻ 0.05), and higher plasma norepinephrine (NE) response to HUT (⌬NE: 156.9 Ϯ 17.8 vs. 89.0 Ϯ 17.2 pg/ml; P Ͻ 0.05). ⌬NE during HUT was also significantly correlated with ⌬HR when all 76 subjects were included in a regression analysis (r ϭ 0.39; P Ͻ 0.001). Pulse pressure was lower during HUT in high HR responders compared with low HR responders (45 Ϯ 1 vs. 55 Ϯ 2 mmHg, P Ͻ 0.05). High HR responders also had larger fluctuations in systolic and pulse pressure during HUT (coefficient of variation ϭ 10.7 Ϯ 0.7 vs. 5.7 Ϯ 0.3%; 7.9 Ϯ 0.5 vs. 4.1 Ϯ 0.4%, respectively, P Ͻ 0.05). Sex distribution was different between groups (high: 5 women, 10 men; low: 10 women, 5 men). Higher HR with lower AP during HUT is consistent with normal baroreflex mechanisms of integration. Although interindividual variability appears to be a fundamental part of cardiovascular regulation, the mechanisms of these differences and the sex discrepancy requires further investigation. baroreflex; arterial pressure; orthostasis; sympathetic nervous system; norepinephrine NORMAL cardiovascular dynamics during orthostasis include the displacement of blood from the central circulation into the lower extremities, reduction of venous return, and decreased stroke volume and cardiac output (10). Arterial pressure (AP) is usually not significantly altered during orthostasis in normal individuals due to rapid baroreflex-mediated increases in heart rate (HR) and sympathetic vasoconstrictor nerve activity (5, 22), resulting in increased total peripheral resistance via norepinephrine (NE) secretion (8, 10). These well-synchronized cardiovascular events prevent major abrupt changes in AP and the development of symptoms during orthostatic stress. In autonomic disorders such as the postural tachycardia syndrome (POTS), patients experience exaggerated increases in HR responses (Ն30 beats/min) to head-up tilt (HUT). These patients also present with symptoms of heart palpitations, dizziness, and headaches in the upright posture even when AP appears well maintained although less st...

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“…A multivariable stepwise logistic regression model was used to assess the predictors of deconditioning. Comparisons between 2 groups of categorical variables were analyzed with 2 or Fisher exact tests and for continuous variables with a 2-sample t test or Wilcoxon rank-sum test, as appropriate. All statistical analysis was performed using JMP 9 (SAS Institute, Cary, NC).…”

Section: Statistical Considerations Data Are Reported As Median Andmentioning

confidence: 99%

“…Cardiovascular changes attributable to deconditioning are similar to those seen after prolonged bedrest and space flight. We have emphasized a reduction in stroke volume, 2 whereas others have emphasized cardiac atrophy. 3 To a variable degree, orthostatic tachycardia has been shown to be reversible with a structured exercise program.…”

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confidence: 99%

Deconditioning in patients with orthostatic intolerance

et al. 2012

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Objective: To study the frequency and degree of deconditioning, clinical features, and relationship between deconditioning and autonomic parameters in patients with orthostatic intolerance. Methods:We retrospectively studied all patients seen for orthostatic intolerance at Mayo Clinic between January 2006 and June 2011, who underwent both standardized autonomic and exercise testing.Results: A total of 184 patients (84 with postural orthostatic tachycardia syndrome [POTS] and 100 without orthostatic tachycardia) fulfilled the inclusion criteria. Of these, 89% were women, and median age was 27.5 years (interquartile range [IQR] 22-37 years). Symptom duration was 4 years (IQR 2-7.8). Of the patients, 90% had deconditioning (reduced maximum oxygen uptake [VO 2max %] Ͻ85%) during exercise. This finding was unrelated to age, gender, or duration of illness. The prevalence of deconditioning was similar between those with POTS (95%) and those with orthostatic intolerance (91%). VO 2max % had a weak correlation with a few autonomic and laboratory parameters but adequate predictors of VO 2max % could not be identified. Conclusion:Reduced VO 2max % consistent with deconditioning is present in almost all patients with orthostatic intolerance and may play a central role in pathophysiology. This finding provides a strong rationale for retraining in the treatment of orthostatic intolerance. None of the autonomic indices are reliable predictors of deconditioning. Neurology ® 2012;79:1435-1439 GLOSSARY BP ϭ blood pressure; DBP ϭ diastolic blood pressure; HR ϭ heart rate; HUT ϭ head-up tilt; II E ϭ early phase II; II L ϭ late phase II; MET ϭ metabolic equivalent; OI ϭ orthostatic intolerance; POTS ϭ postural orthostatic tachycardia syndrome; PP ϭ pulse pressure; RER ϭ respiratory exchange ratio; SBP ϭ systolic blood pressure; TST ϭ thermoregulatory sweat test; VM ϭ Valsalva maneuver; VO 2max ϭ maximum oxygen uptake; VR ϭ Valsalva ratio.The postural tachycardia syndrome (POTS) is a disorder of orthostatic intolerance mostly affecting young and middle-aged women. The pathophysiology of POTS and the role of deconditioning in this syndrome are poorly understood. 1 Recent evidence suggests that POTS is strongly associated with cardiovascular deconditioning. Cardiovascular changes attributable to deconditioning are similar to those seen after prolonged bedrest and space flight. We have emphasized a reduction in stroke volume, 2 whereas others have emphasized cardiac atrophy.3 To a variable degree, orthostatic tachycardia has been shown to be reversible with a structured exercise program.3-6 Some researchers advocate that POTS is a disorder of deconditioning alone and can be cured by reconditioning. However, a recent study reported that even though orthostatic tachycardia improves with regular exercise, patients' symptoms remain, 5 suggesting that deconditioning may be a secondary mechanism in patients with POTS. A comprehensive study formally assessing exercise capacity (the gold standard to assess for deconditioning) in a la...

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Reduced stroke volume during exercise in postural tachycardia syndrome

Cited by 9 publications

References 0 publications

Unexplained Exertional Dyspnea Caused by Low Ventricular Filling Pressures: Results from Clinical Invasive Cardiopulmonary Exercise Testing

Unexplained Exertional Dyspnea Caused by Low Ventricular Filling Pressures: Results from Clinical Invasive Cardiopulmonary Exercise Testing

Cardiovascular dynamics in healthy subjects with differing heart rate responses to tilt

Deconditioning in patients with orthostatic intolerance

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