Mechanisms Of Orthostatic Intolerance Research Articles

The Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients with Joint Hypermobility Show Larger Cerebral Blood Flow Reductions during Orthostatic Stress Testing Than Patients without Hypermobility: A Case Control Study

Aims: An abnormal reduction in cerebral blood flow (CBF) during orthostatic stress is common in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a condition with more prevalent joint hypermobility than in the healthy population. As one of proposed underlying mechanisms of orthostatic intolerance in hypermobile patients is vessel laxity, reducing the normal return of blood to the heart during orthostatic stress, we hypothesized that the CBF reduction during tilt-testing would be larger in ME/CFS patients with joint hypermobility than in patients without hypermobility. Methods: In this case-control study, 100 female ME/CFS cases with joint hypermobility, who had undergone tilt-testing with CBF measurements, were compared to 100 female ME/CFS patients without joint hypermobility, matched by age and disease duration. Results: No differences in baseline characteristics were found between groups. The hypermobile patients had significantly more postural orthostatic tachycardia syndrome (POTS) during tilt testing than the non-hypermobile ones. Compared to supine CBF, the degree of CBF reduction during the tilt was significantly larger in hypermobile cases than in the non-hypermobile controls: -32 (6)% vs -23 (7)% (p<0.0001) The larger CBF reduction in hypermobile patients was not only present in POTS patients: -33 (6)% vs -24 (4)%, but also in patients with a normal heart rate and blood pressure response to tilt testing: -31 (6)% vs -22 (9)%: (both p<0.0001). Conclusions: ME/CFS patients with joint hypermobility syndromes have larger CBF reductions during orthostatic stress testing than patients without hypermobility. This larger CBF reduction is independent of the heart rate and blood pressure results of the orthostatic stress test.

Enhanced postoperative recovery: good from afar, but far from good?

Enhanced postoperative recovery programmes (ERAS) were developed about 20years ago based on improved understanding of the pathophysiology of postoperative recovery within an integrated multidisciplinary approach. The results across surgical procedures have been extremely positive with a reduction in hospitalisation and medical complications, without increased re-admission rates. However, several challenges lie ahead including improved implementation of existing scientific evidence, increased focus on post-discharge recovery problems and a need for improved design of future ERAS studies. However, the most important challenges lie within a better understanding and control of undesirable peri-operative pathophysiological responses with subsequent risk of organ dysfunction. These efforts should focus on: the inflammatory and neurohumoral surgical stress responses; fluid management; pain management; blood management; mechanisms of orthostatic intolerance; postoperative cognitive dysfunction; risk factors for thrombo-embolic complications; and mechanisms and prevention of postoperative ileus. Finally, more focus should be made on the different barriers to post-discharge functional recovery and the choice of (pre- and postoperative) rehabilitation. These efforts should be made on a procedure-specific as well as on a patient-specific basis.

Cardiovascular regulation: associations between exercise and head-up tilt.

It was hypothesized that faster cardiorespiratory kinetics during exercise are associated with higher orthostatic tolerance. Cardiorespiratory kinetics of 14 healthy male subjects (30 ± 4 years, 179 ± 8 cm, 79 ± 8 kg) were tested on a cycle ergometer during exercise with changing work rates of 30 and 80 W. Pulmonary oxygen uptake ( ) was measured breath-by-breath and heart rate (HR), mean arterial blood pressure (MAP), and total peripheral resistance (TPR) were measured beat-to-beat. Muscular oxygen uptake ( ) was estimated from HR and . Kinetic parameters were determined by time-series analysis, using cross-correlation functions (CCFmax(x)) between the parameter and the work rate. Cardiovascular regulations of MAP, HR, and TPR during orthostatic stress were measured beat-to-beat on a tilt seat. Changes between the minima and maxima during the 6° head-down tilt and the 90° head-up tilt positions were calculated for each parameter (Δtilt-up). correlated significantly with ΔTPRtilt-up (r = 0.790, p ≤ 0.001). CCFmax(HR) was significantly correlated with ΔHRtilt-up (r = -0.705, p = 0.002) and the amplitude in HR from 30 to 80 W (rSP = -0.574, p = 0.016). The observed correlations between cardiorespiratory regulation in response to exercise and orthostatic stress during rest might allow for a more differential analysis of the underlying mechanisms of orthostatic intolerance in, for example, patient groups.

Mechanisms of orthostatic intolerance during heat stress.

Heat stress profoundly and unanimously reduces orthostatic tolerance. This review aims to provide an overview of the numerous and multifactorial mechanisms by which this occurs in humans. Potential causal factors include changes in arterial and venous vascular resistance and blood distribution, and the modulation of cardiac output, all of which contribute to the inability to maintain cerebral perfusion during heat and orthostatic stress. A number of countermeasures have been established to improve orthostatic tolerance during heat stress, which alleviate heat stress induced central hypovolemia (e.g., volume expansion) and/or increase peripheral vascular resistance (e.g., skin cooling). Unfortunately, these countermeasures can often be cumbersome to use with populations prone to syncopal episodes. Identifying the mechanisms of inter-individual differences in orthostatic intolerance during heat stress has proven elusive, but could provide greater insights into the development of novel and personalized countermeasures for maintaining or improving orthostatic tolerance during heat stress. This development will be especially impactful in occuational settings and clinical situations that present with orthostatic intolerance and/or central hypovolemia. Such investigations should be considered of vital importance given the impending increased incidence of heat events, and associated cardiovascular challenges that are predicted to occur with the ensuing changes in climate.

Mechanisms Of Orthostatic Intolerance During Passive Heat Stress

Mechanisms Of Orthostatic Intolerance During Passive Heat Stress

New‐Onset Orthostatic Intolerance Following Bariatric Surgery

As bariatric surgery has become an increasingly popular treatment for obesity, we have seen an increasing number of patients present after bariatric surgery with new-onset syncope, near-syncope, and lightheadedness. We retrospectively reviewed patients who had had bariatric surgery referred to our institution for evaluation of orthostatic intolerance. We reviewed history, physical examination, type of bariatric surgery procedure, and tilt table test results in these patients. There were 14 women and one man with mean age 42 +/- 6 years, preoperative body mass index was 49.3 +/- 6.0 kg/m(2), and mean postoperative weight loss was 55.9 kg. Mean onset of symptoms was 5.2 +/- 3.9 months after surgery. Presenting symptoms were lightheadedness in 15 (100%), near-syncope in 11 (73%), and syncope in nine (60%). All but one patient had a positive tilt table test with eight (53%) having a neurocardiogenic response, three (20%) having a dysautonomic response, and (20%) having a postural tachycardia response. The likely mechanism of orthostatic intolerance is autonomic insufficiency in combination with reverse course of obesity-related hypertension. The majority of the patients (12 out of 15) responded to standard therapy for autonomic insufficiency. Some patients may develop significant orthostatic intolerance due to autonomic insufficiency following bariatric surgery, and awareness of the potential association between bariatric surgery and new orthostatic intolerance is important for providing timely care.

Mechanisms of orthostatic intolerance following very prolonged exercise

Nine men completed a 24-h exercise trial, with physiological testing sessions before (T1, approximately 0630), during (T2, approximately 1640; T3, approximately 0045; T4, approximately 0630), and 48-h afterwards (T5, approximately 0650). Participants cycled and ran/trekked continuously between test sessions. A 24-h sedentary control trial was undertaken in crossover order. Within testing sessions, participants lay supine and then stood for 6 min, while heart rate variability (spectral analysis of ECG), middle cerebral artery perfusion velocity (MCAv), mean arterial pressure (MAP; Finometer), and end-tidal Pco(2) (Pet(CO(2))) were measured, and venous blood was sampled for cardiac troponin I. During the exercise trial: 1) two, six, and four participants were orthostatically intolerant at T2, T3, and T4, respectively; 2) changes in heart rate variability were only observed at T2; 3) supine MAP (baseline = 81 +/- 6 mmHg) was lower (P < 0.05) by 14% at T3 and 8% at T4, whereas standing MAP (75 +/- 7 mmHg) was lower by 16% at T2, 37% at T3, and 15% at T4; 4) Pet(CO(2)) was reduced (P < 0.05) at all times while supine (-3-4 Torr) and standing (-4-5 Torr) during exercise trial; 5) standing MCAv was reduced (P < 0.05) by 23% at T3 and 30% at T4 during the exercise trial; 6) changes in MCAv with standing always correlated (P < 0.01) with changes in Pet(CO(2)) (r = 0.78-0.93), but only with changes in MAP at T1, T2, and T3 (P < 0.05; r = 0.62-0.84); and 7) only two individuals showed minor elevations in cardiac troponin I. Recovery was complete within 48 h. During prolonged exercise, postural-induced hypotension and hypocapnia exacerbate cerebral hypoperfusion and facilitate syncope.

Virtual conductance, real hypotension: what happens when we stand up too fast?

cardiovascular physiologists have long been curious about the mechanisms of fainting, and the goal of understanding why people faint under a variety of conditions has taken researchers to the ends of the Earth, and beyond. Some of these investigations have focused on adaptation to extreme

Simulation study of the effects of hypovolaemia on cardiovascular response to orthostatic stress.

To investigate the role played by hypovolaemia in the mechanism of orthostatic intolerance, a mathematical model was developed. The model consisted of seven sub-models that describe: the redistribution of blood induced by lower body negative pressure (LBNP); filling of the left ventricle; contracting of the left ventricle; interaction between the left ventricle and peripheral circulation; and baroreflex regulation. The model was evaluated using experimental data. Using the model, computer simulations were performed to investigate the effects of hypovolaemia on the cardiovascular response to LBNP. The simulation results indicated that, first, when the blood loss is less than 5%, blood pressure can be maintained in the normal range by the baroreflex regulatory mechanism, even with high LBNP application; secondly, when the blood loss is between 15 and 20%, heart rate and blood pressure can be kept in the normal range if LBNP is not applied, but blood pressure falls sharply with LBNP application; and, thirdly, when the blood loss is 25%, the cardiovascular system is in an unstable state (heart rate: 116 beat min (-1), systolic blood pressure: 97 mmHg; diastolic blood pressure: 77 mmHg), even without any LBNP, and becomes more unstable with LBNP. The simulation results support the hypothesis that hypovolaemia is a cause of orthostatic intolerance.

Neurally mediated hypotension and chronic fatigue syndrome

A substantial body of clinical evidence now supports an association between various forms of hypotension and both idiopathic chronic fatigue and the chronic fatigue syndrome (CFS). Patients with CFS have a high prevalence of neurally mediated hypotension, and open treatment of this autonomic dysfunction has been associated with improvements in CFS symptoms. Randomized trials are now in progress to evaluate the efficacy of treatments directed at neurally mediated hypotension in those with CFS patients, and the results of these trials should help guide more basic inquiries into the mechanisms of orthostatic intolerance in affected individuals.

Cardiovascular and Catecholamine Responses to Head‐Up Tilt in the Diagnosis of Recurrent Unexplained Syncope in Elderly Patients

To increase understanding of the mechanisms causing syncope in patients over the age of 60, hemodynamic and hormonal responses to 60 minutes of 60 degree head-up tilt were examined in 10 patients with recurrent syncope of unknown origin and five controls with no history of syncope. Nine of 10 patients and all five controls experienced orthostatic intolerance on the tilt table. Syncope or pre-syncope occurred later in controls than in those syncope patients who had exact reproduction of their clinical symptoms (median time 52 versus 22 minutes, P = 0.05). Three different mechanisms of orthostatic intolerance were identified in the 14 subjects: (1) vasovagal syncope, n = 9 (sudden hypotension +/- bradycardia); (2) dysautonomic syncope, n = 3 (immediate and gradual parallel declines in both systolic and diastolic pressures with blunted increase in heart rate); (3) psychogenic or vestibular reaction, n = 2 (orthostatic intolerance without hemodynamic changes). Vasovagal syncope patients showed a significant increase in plasma norepinephrine from baseline to maximum level during tilt (100 +/- 39% increase, P = 0.03) and a subsequent decrease at the time of syncope (30 +/- 5% decrease, P = 0.01), while plasma epinephrine increased markedly from baseline to the time of syncope (827 +/- 154% increase, P = 0.0003). Dysautonomic syncope patients had lower supine levels of norepinephrine compared to vasovagal syncope patients (182 +/- 30 versus 614 +/- 146 pg/mL, P = 0.008) and no significant change in norepinephrine over time; epinephrine levels increased significantly less than in vasovagal patients (net change 38 +/- 8 versus 189 +/- 56 pg/mL, P = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)