Postural Changes In Heart Rate Research Articles

Exercise alters cerebellar and cortical activity related to working memory in phenotypes of Gulf War Illness.

Gulf War Illness affects 25–32% of veterans from the 1990–91 Persian Gulf War. Post-exertional malaise with cognitive dysfunction, pain and fatigue following physical and/or mental effort is a defining feature of Gulf War Illness. We modelled post-exertional malaise by assessing changes in functional magnetic resonance imaging at 3T during an N-Back working memory task performed prior to a submaximal bicycle stress test and after an identical stress test 24 h later. Serial trends in postural changes in heart rate between supine and standing defined three subgroups of veterans with Gulf War Illness: Postural Orthostatic Tachycardia Syndrome (GWI-POTS, 15%, n = 11), Stress Test Associated Reversible Tachycardia (GWI-START, 31%, n = 23) and Stress Test Originated Phantom Perception (GWI-STOPP, no postural tachycardia, 54%, n = 46). Before exercise, there were no differences in blood oxygenation level-dependent activity during the N-Back task between control (n = 31), GWI-START, GWI-STOPP and GWI-POTS subgroups. Exercise had no effects on blood oxygenation level-dependent activation in controls. GWI-START had post-exertional deactivation of cerebellar dentate nucleus and vermis regions associated with working memory. GWI-STOPP had significant activation of the anterior supplementary motor area that may be a component of the anterior salience network. There was a trend for deactivation of the vermis in GWI-POTS after exercise. These patterns of cognitive dysfunction were apparent in Gulf War Illness only after the exercise stressor. Mechanisms linking the autonomic dysfunction of Stress Test Associated Reversible Tachycardia and Postural Orthostatic Tachycardia Syndrome to cerebellar activation, and Stress Test Originated Phantom Perception to cortical sensorimotor alterations, remain unclear but may open new opportunities for understanding, diagnosing and treating Gulf War Illness.

Hydration Marker Diagnostic Accuracy to Identify Mild Intracellular and Extracellular Dehydration

Identifying mild dehydration (≤2% of body mass) is important to prevent the negative effects of more severe dehydration on human health and performance. It is unknown whether a single hydration marker can identify both mild intracellular dehydration (ID) and extracellular dehydration (ED) with adequate diagnostic accuracy (≥0.7 receiver-operating characteristic-area under the curve [ROC-AUC]). Thus, in 15 young healthy men, the authors determined the diagnostic accuracy of 15 hydration markers after three randomized 48-hr trials; euhydration (water 36ml·kg-1·day-1), ID caused by exercise and 48hr of fluid restriction (water 2ml·kg-1·day-1), and ED caused by a 4-hr diuretic-induced diuresis begun at 44hr (Furosemide 0.65mg/kg). Body mass was maintained on euhydration, and dehydration was mild on ID and ED (1.9% [0.5%] and 2.0% [0.3%] of body mass, respectively). Urine color, urine specific gravity, plasma osmolality, saliva flow rate, saliva osmolality, heart rate variability, and dry mouth identified ID (ROC-AUC; range 0.70-0.99), and postural heart rate change identified ED (ROC-AUC 0.82). Thirst 0-9 scale (ROC-AUC 0.97 and 0.78 for ID and ED) and urine osmolality (ROC-AUC 0.99 and 0.81 for ID and ED) identified both dehydration types. However, only the thirst 0-9 scale had a common dehydration threshold (≥4; sensitivity and specificity of 100%; 87% and 71%, 87% for ID and ED). In conclusion, using a common dehydration threshold ≥4, the thirst 0-9 scale identified mild intracellular and ED with adequate diagnostic accuracy. In young healthy adults', thirst 0-9 scale is a valid and practical dehydration screening tool.

A prospective study of excessive postural heart rate change on head-up tilt.

Healthy subjects with asymptomatic postural tachycardia (≥30bpm) at baseline were evaluated over a 1-year period to determine whether they developed orthostatic symptoms. Subjects were evaluated at baseline and at 1year using the autonomic reflex screen and autonomic symptom profile (ASP). Heart rate increment on HUT did not differ at baseline (40.6±7.5bpm) or at 1year (37.1±11.1bpm; n=26; p>0.05). Orthostatic symptoms measured by the ASP did not reveal significant orthostatic dysfunction throughout follow-up (baseline, 7.88±7.61; 1year, 9.04±6.64; n=26; p>0.05). The ten autonomic domains of the ASP did not reveal a change in autonomic symptoms from baseline (13.56±13.66) to 1-year follow-up (15.12±11.62; n=26; p>0.05). Cardiovagal function was unchanged between baseline and follow-up for both heart rate variability to deep breathing (baseline, 23.9±11.6bpm; 1year, 23.0±9.3bpm; n=26; p>0.05) and Valsalva ratio (baseline, 2.16±0.39; 1year, 2.15±0.33; n=26; p>0.05). These findings further argue that heart rate criteria (≥30bpm) for Postural Tachycardia Syndrome (POTS) are not appropriate in younger individuals and higher postural heart rates do not predispose individuals to the development of POTS.

Autonomic nerve function in adult patients with cyclic vomiting syndrome

Cyclic vomiting syndrome (CVS) in adults is a disorder characterized by recurrent and stereotypic episodes of severe nausea and vomiting separated by symptom-free periods. Autonomic dysfunction has been a postulated mechanism for the pathogenesis of this disorder in children but has not been explored in adults. Our goals were to investigate autonomic nerve function in adult patients with CVS. The sympathetic nervous system was evaluated through postural changes in heart rate and blood pressure and sympathetic skin response in the hand and foot. The parasympathetic nervous system was tested through heart rate response to deep breathing [expiration/inspiration (E/I)], Valsalva and postural indices (30 : 15 ratio). All patients had a 4-h standard isotope labeled egg beater meal gastric emptying test (GET). Twenty-two adult (18 female), mean age 35 ± 11 (range 19-61 years), who met Rome III criteria for CVS were included. History of migraine headache was reported in three patients. Five (23%) had pediatric onset. Of 21 patients who completed the test, nine patients had 21 abnormalities detected in their autonomic nerve testing profile and the remaining 12 had normal autonomic function results. Orthostatic tachycardia was observed in two (mean heart rate increase 39 beats min(-1)) and a decline in blood pressure (BP) in three patients (mean BP drop 30/14 mmHg). Parasympathetic abnormalities were elicited in six patients with an abnormal response to deep breathing and E/I index <1.25. Sympathetic nerve dysfunction was reported in seven patients with absent sympathetic skin response in the foot and/or hand. Twelve (57%) of CVS group had rapid GET (<50% retention at 1 h). The frequency of abnormal autonomic nerve function was not significantly higher in rapid GET subgroup. (i) Autonomic nerve dysfunction is common in adult CVS patients, being observed in 43% of our cohort; (ii) Sympathetic abnormalities dominate; and (iii) Rapid gastric emptying, present in 57% of patients, did not correlate with autonomic testing results. These new data provide more insight into the pathophysiology of CVS in adults and help explain the spectrum of clinical manifestations observed in this entity.

Autonomic nerve function in adults with cyclic vomiting syndrome: a prospective study

Cyclic vomiting syndrome (CVS) is a functional gastrointestinal disorder that is characterized by recurrent episodes of intense vomiting. There are several postulated mechanisms involved in its pathogenesis and one potential explanation for this disorder may be linked to autonomic dysfunction. The aim of our study was to evaluate autonomic nerve function in patients with CVS prospectively. We tested the sympathetic nervous system through postural changes in heart rate (HR) and blood pressure and the thermoregulatory sweat test. The parasympathetic nervous system was tested through the HR response to deep breathing (R-R variability on EKG). A total of 20 patients who met Rome III criteria for CVS, 14 (70%) women and 6 (30%) men, and 20 controls were enrolled in the study. A total of 17 (85%) CVS subjects and 2 (10%) controls had abnormalities on thermoregulatory sweat testing (P < 0.001). A total of 7 (35%) patients and one control subject had evidence of postural tachycardia (P = 0.04) with an increase in HR > 30 on standing. Of the subjects, 18 (90%) had either abnormal sudomotor function or postural tachycardia or both. The HR response to deep breathing was normal in 19 (95%) subjects with CVS and 18 (95%) controls. The results of this study suggest that the majority of subjects (90%) with CVS have impairment of the sympathetic nervous system with postural tachycardia and/or sudomotor dysfunction while parasympathetic nerve function appears to be intact. These findings of dysautonomia in CVS have implications in both the diagnosis and treatment of these patients.

Managing hyperosmolar hyperglycaemic syndrome

I would like to comment on the Association of British Clinical Diabetologists (ABCD) guidelines for the management of hyperglycaemic emergencies in adults (Practical Diabetes International June 2006, pages 227-231). Although the guidelines are simply and straightforwardly presented, I feel they seriously underplay the severity of hyperosmolar nonketotic coma (which incidentally is a misleading term: it should be abandoned and replaced by hyperosmolar hyperglycaemic syndrome, HHS). I think it is a mistake to describe the management ‘as for DKA [diabetic ketoacidosis] but …’ as there are some significant differences which need to be emphasised. Failure to understand the underlying disorder may lead to inappropriate management. There is no precise or internationally agreed definition of HHS but there is recognition that minor degrees of ketosis and acidosis (arterial pH >7.3, bicarbonate >15mmol/L) are common. Patients with HHS are often elderly and the condition may be the first presentation of type 2 diabetes. It appears to be more common in people of African or Afro-Caribbean origin. In recent years, there have been case reports of HHS occurring in children and young adults — not all with type 2 diabetes. Severe dehydration and pre-renal failure are usual. Unlike DKA, the onset is over many days and, although it is correct to say that vascular complications are common, cerebral oedema is the most serious complication and may present as seizures, progressive confusion, or altered consciousness and lead to permanent neurological damage or death. Correct interpretation of the serum Na is important. Total body Na is low and there may be marked water deficiency. Although the initial Na may be normal or high, it is important to understand that high concentrations of effective solutes such as glucose will cause fluid shifts out of the cell and a dilutional fall in Na. The corrected Na can be calculated by adding 2.4mmol/L for every 5.5mmol/L where the glucose is above normal but, more importantly, it follows that as treatment results in a fall in glucose, there will almost inevitably be a rise in serum Na. Therefore, the rise in Na is expected and predictable — what is important is what is happening to tonicity. Thus, a rising Na alone is not an indication for the administration of hypotonic fluids. Care must be taken to avoid situations which may increase the risk of cerebral oedema. Extracellular hypertonicity causes cellular dehydration which in the brain is resisted by a protective mechanism known as cerebral volume regulation. Water loss is limited by the production of intracellular osmotically active ions and, later, organic osmolytes or idiogenic osmoles. Whilst this rise in cellular osmolality is beneficial in the hyperosmolar state, rapid rehydration with IV fluids may lead to water movement into the cell and swelling occurs before compensatory mechanisms have time to eliminate these solutes. This may be the mechanism which leads to cerebral oedema and is the reason why many argue that hypotonic solutions should be avoided (there is no experimental evidence to justify using less than 0.5N saline) and that slower correction of the hyperosmolality is safer than rapid correction. Assessing the level of dehydration is difficult and often over-estimated. Postural changes in heart rate and BP can be helpful but not always practical. It is rare to need more than twice the usual daily fluid requirements. The aim is to replace approximately 50% of the deficit in the first 12 hours. These patients are often transferred too soon to general medical wards and fluid management left to inexperienced junior medical staff. Severe HHS should be seen soon after admission by diabetes specialists with experience of managing this challenging emergency, and close supervision given until the patient is eating and drinking normally. Adrian Scott*, * Diabetes Centre, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK

Does Heart Rate Predict Mortality in Older, Low‐Level Care Residents?

To determine whether abnormalities in heart rate (HR) were associated with long-term mortality in older, low-level care residents, 179 randomly selected persons aged 65 and older (mean, 83.2+/-7.0 [SD] years; 80% women) were prospectively assessed. At baseline, duplicate measurements of HR and blood pressure were recorded in the supine position and after standing. During the 5-year follow-up period, 97 (54%) participants died. Cox survival analysis revealed no association with total mortality when resting HR was analyzed as a continuous or categoric variable (< or = 60, 61-89, and > 90 bpm). However, HR > or = 90 bpm was associated with increased risk of dying in residents who used a walking aid (relative risk, 3.48; 95% confidence interval, 1.07-11.30; p=0.038). Postural HR change was not associated with mortality risk. The authors concluded that resting HR and postural change in HR are not significant predictors of 5-year mortality in older, low-level care residents, except in persons using a walking aid.

Predictors of the New Onset of Wheezing among Middle-aged and Older Men: The Normative Aging Study

Characteristics potentially associated with the development of wheeze symptoms were examined in a prospective cohort study of 624 middle-aged and older men who initially denied any history of wheezing or asthma. Initial evaluation included spirometry, methacholine challenge testing, allergy skin testing with common aeroallergens, serum total IgE concentration, blood leukocyte count, blood eosinophil count, and postural heart rate change (standing minus supine). The presence or absence of wheezing symptoms at follow-up 3 yr later was assessed by questionnaire. Multiple logistic regression was used to examine initial characteristics as predictors of subsequent wheezing. Current smoking was the strongest independent predictor of the new onset of wheezing (adjusted OR, 14.3; 95% confidence interval (CI), 3.9 to 52.3). The risk of developing new wheezing also increased with age (adjusted OR, 1.6; 95% CI, 0.9 to 2.9 comparing individual subjects 10 yr apart) and postural heart rate change at the initial examination (adjusted OR, 1.8; 95% CI, 1.1 to 3.0 comparing individual subjects differing by 10 beats/min). A significant association between greater methacholine airway responsiveness (PD20FEV1 < or = 16.8 mumol versus PD20FEV1 > 16.8 mumol) and the subsequent development of wheezing was observed among nonsmokers (adjusted OR, 5.2; 95% CI, 2.0 to 13.6) but not among current smokers. Other baseline variables were not independently related to the risk of developing wheezing symptoms. These data suggest that current smoking, age, nonspecific airway responsiveness, and altered autonomic function are independently related to the risk of developing wheezing symptoms in middle-aged and older men.

Effects of scopolamine on immediate postural changes in heart rate and R—R variance in humans

AbstractTo examine the anticholinergic effects of scopolamine, postural tests were performed in nine healthy male volunteers after they received intravenous infusions of 0.2mg of scopolamine, 0.4 mg of glycopyrrolate, or placebo on separate days under double‐blind randomized conditions. Compared to the placebo and glycopyrrolate conditions, scopolamine produced a significantly exaggerated HR response to standing from supine posture. Scopolamine also produced a significant increase in R‐R variance during supine deep breathing and standing conditions as compared to glycopyrrolate and placebo conditions. At the same time, scopolamine also produced a significant dry mouth. These findings suggest that the effects of scopolamine in low doses on the above cardiac variables are vagomimetic.

Decreased R‐R variance in panic disorder patients

To investigate autonomic function in panic disorder patients (n = 30), we compared postural changes in heart rate and the R-R interval variance in patients and normal controls (n = 20). There was no significant difference in the immediate changes in heart rate upon standing between the groups. R-R variance was significantly decreased during resting supine condition in patients as indicated by the corrected standard deviation of the R-R intervals. The standing R-R variance was significantly lower than that of normal controls as indicated by the corrected standard deviations, the corrected mean consecutive difference and the corrected standard deviation of the mean consecutive difference of the R-R intervals, suggesting an increase in vagal withdrawal in patients, especially upon standing. If this finding is specific to panic disorder patients, it may be a useful peripheral marker for this condition.

Postural changes in heart rate during imipramine treatment : V.K. Yeragani, M.D., R. Pohl, M.D., R. Balon, M.D., C. Ramesh (by invitation), D. Glitz, M.D. (by invitation) Lafayette Clinic, Detroit, Michigan 48207

Postural changes in heart rate during imipramine treatment : V.K. Yeragani, M.D., R. Pohl, M.D., R. Balon, M.D., C. Ramesh (by invitation), D. Glitz, M.D. (by invitation) Lafayette Clinic, Detroit, Michigan 48207

Voluntary control of systolic blood pressure during postural change.

ABSTRACTThe effects of biofeedback and voluntary control procedures on systolic blood pressure and heart rate during postural change were investigated in 30 normotensive men. Systolic pressure was measured with a continuous blood pressure tracking cuff, and blood pressure feedback was provided on a beat‐to‐beat basis. Postural changes in pressure, and corresponding heart rate changes, were examined in three experimental groups (N = 10 each). In two groups, subjects were given feedback training to increase or to decrease systolic blood pressure. In the third group, subjects were simply asked to increase their pressure but were not given feedback about their performance. Voluntary control of systolic pressure was attempted while subjects were seated and during postural change—sitting to standing. Subjects were also instructed to maintain voluntary blood pressure control in subsequent no‐feedback test trials. During postural change, voluntary control procedures caused significant alterations in tonic levels of systolic pressure, but phasic blood pressure reactivity was unaffected. With respect to postural changes in heart rate, both tonic and phasic treatment effects were observed. Implications of the findings for basic and clinical research are discussed.

Postural hypotension and tachycardia during hydralazine--isosorbide dinitrate therapy for chronic heart failure.

Supine and upright hemodynamic measurements were performed in 10 patients with chronic congestive heart failure, before and during vasodilator therapy with hydralazine and isosorbide dinitrate. This combination of drugs produced significant improvement in supine hemodynamic measurements, with the pulmonary capillary wedge pressure decreasing from 26 +/- 5 to 18 +/- 5 mm Hg (mean +/- SD, p less than 0.01) and stroke volume index increasing from 25 +/- 6 to 39 +/- 6 ml/m2 (p less than 0.01), without any significant change in heart rate (HR) or mean arterial pressure (MAP). However, with the patients upright, HR rose significantly (87 +/- 17 to 99 +/- 17 beats/min, p less than 0.05) and MAP fell (84 +/- 10 to 66 +/- 11 mm Hg, p less than 0.001) compared with measurements before treatment. These patients also exhibited potentially deleterious postural changes in HR, MAP, cardiac output, stroke volume index and stroke work index during therapy with the combination of hydralazine and isosorbide dinitrate. Although diuretic therapy (which had been withheld for 12 hours in eight subjects but only for 6 hours in two others) may have played a role in producing these changes, postural hypotension or tachycardia was not noted before vasodilator therapy or during therapy with nitrates or hydralazine. Repeat catheterization after 3 months in six patients revealed a lessening of the postural effects. These findings indicate the need to perform upright as well as supine hemodynamic measurements during the initiation of vasodilator therapy and suggest the need for particular caution in patients with ischemic heart disease.