Hemodynamic characteristics of postural hyperventilation: POTS with hyperventilation versus panic versus voluntary hyperventilation

Upright hyperventilation occurs in ~25% of our patients with postural tachycardia syndrome (POTS). Poikilocapnic hyperventilation alone causes tachycardia. Here, we examined changes in respiration and hemodynamics comprising cardiac output (CO), systemic vascular resistance (SVR), and blood pressure (BP) measured during head-up tilt (HUT) in three groups: patients with POTS and hyperventilation (POTS-HV), patients with panic disorder who hyperventilate (Panic), and healthy controls performing voluntary upright hyperpnea (Voluntary-HV). Though all were comparably tachycardic during hyperventilation, POTS-HV manifested hyperpnea, decreased CO, increased SVR, and increased BP during HUT; Panic patients showed both hyperpnea and tachypnea, increased CO, and increased SVR as BP increased during HUT; and Voluntary-HV were hyperpneic by design and had increased CO, decreased SVR, and decreased BP during upright hyperventilation. Mechanisms of hyperventilation and hemodynamic changes differed among POTS-HV, Panic, and Voluntary-HV subjects. We hypothesize that the hyperventilation in POTS is caused by a mechanism involving peripheral chemoreflex sensitization by intermittent ischemic hypoxia. NEW & NOTEWORTHY Hyperventilation is common in postural tachycardia syndrome (POTS) and has distinctive cardiovascular characteristics when compared with hyperventilation in panic disorder or with voluntary hyperventilation. Hyperventilation in POTS is hyperpnea only, distinct from panic in which tachypnea also occurs. Cardiac output is decreased in POTS, whereas peripheral resistance and blood pressure (BP) are increased. This is distinct from voluntary hyperventilation where cardiac output is increased and resistance and BP are decreased and from panic where they are all increased.

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Pet CO2 inversely affects MSNA response to orthostatic stress

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.281.3.h1040 ◽

2001 ◽

Vol 281 (3) ◽

pp. H1040-H1046 ◽

Cited By ~ 22

Author(s):

J. Kevin Shoemaker ◽

Debbie D. O'Leary ◽

Richard L. Hughson

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Orthostatic Intolerance ◽

Muscle Sympathetic Nerve Activity ◽

Peripheral Resistance ◽

Burst Frequency ◽

Head Up Tilt ◽

End Tidal ◽

Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

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Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00640.2001 ◽

2002 ◽

Vol 282 (5) ◽

pp. H1804-H1809 ◽

Cited By ~ 50

Author(s):

D. L. Jardine ◽

I. C. Melton ◽

I. G. Crozier ◽

S. English ◽

S. I. Bennett ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Sympathetic Nerve Activity ◽

Vasovagal Syncope ◽

Peripheral Resistance ◽

Blood Pressure Level ◽

Progressive Decline ◽

Vasovagal Reactions ◽

Head Up Tilt ◽

Regression Slopes

The importance of cardiac output (CO) to blood pressure level during vasovagal syncope is unknown. We measured thermodilution CO, mean blood pressure (MBP), and leg muscle mean sympathetic nerve activity (MSNA) each minute during 60° head-up tilt in 26 patients with recurrent syncope. Eight patients tolerated tilt (TT) for 45 min (mean age 60 ± 5 yr) and 15 patients developed syncope during tilt (TS) (mean age 58 ± 4 yr, mean tilt time 15.4 ± 2 min). In TT patients, CO decreased during the first minute of tilt (from 3.2 ± 0.2 to 2.5 ± 0.3 l · min−1 · m−2, P = 0.001) and thereafter remained stable between 2.5 ± 0.3 ( P = 0.001) and 2.4 ± 0.2 l · min−1 · m−2( P = 0.004) at 5 and 45 min, respectively. In TS patients, CO decreased during the first minute (from 3.3 ± 0.2 to 2.7 ± 0.1 l · min−1 · m−2, P = 0.02) and was stable until 7 min before syncope, falling to 2.0 ± 0.2 at syncope ( P = 0.001). Regression slopes for CO versus time during tilt were −0.01 min−1 in TT versus −0.1 l · min−1 · m−2 · min−1in TS ( P = 0.001). However, MBP was more closely correlated to total peripheral resistance ( R = 0.56, P = 0.001) and MSNA ( R = 0.58, P = 0.001) than CO ( R = 0.32, P = 0.001). In vasovagal reactions, a progressive decline in CO may contribute to hypotension some minutes before syncope occurs.

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Dissection of carotid sinus hypersensitivity: the timing of vagal and vasodepressor effects and the effect of body position

Clinical Science ◽

10.1042/cs20100607 ◽

2011 ◽

Vol 121 (9) ◽

pp. 389-396 ◽

Cited By ~ 8

Author(s):

C. T. Paul Krediet ◽

David L. Jardine ◽

Wouter Wieling

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Total Peripheral Resistance ◽

Sympathetic Nerve Activity ◽

Carotid Sinus ◽

Body Position ◽

Muscle Sympathetic Nerve Activity ◽

Peripheral Resistance ◽

Head Up Tilt

We assessed the timing of vagal and sympathetic factors that mediate hypotension during CSM (carotid sinus massage) in patients with carotid sinus hypersensitivity. We hypothesized that a fall in cardiac output would precede vasodepression, and that vasodepression would be exaggerated by head-up tilt. We performed pulse contour analyses on blood pressure recordings during CSM in syncope patients during supine rest and head-up tilt. In a subset we simultaneously recorded muscle sympathetic nerve activity supine. During supine rest, systolic blood pressure decreased from 150±7 to 107±7 mmHg (P<0.001) and heart rate from 64±2 to 39±3 beats/min (P<0.01). Cardiac output decreased with heart rate to nadir (66±6% of baseline), 3.1±0.4 s after onset of bradycardia. In contrast, total peripheral resistance reached nadir (77±3% of baseline) after 11±1 s. During head-up-tilt, systolic blood pressure fell from 149±10 to 90±11 mmHg and heart rate decreased from 73±4 to 60±7 beats/min. Compared with supine rest, cardiac output nadir was lower (60±8 compared with 83±4%, P<0.05), whereas total peripheral resistance nadir was similar (81±6 compared with 80±3%). The time to nadir from the onset of bradycardia did not differ from supine rest. At the onset of bradycardia there was an immediate withdrawal of muscle-sympathetic nerve activity while total peripheral resistance decay occurred much later (6–8 s). The haemodynamic changes following CSM have a distinct temporal pattern that is characterized by an initial fall in cardiac output (driven by heart rate), followed by a later fall in total peripheral resistance, even though sympathetic withdrawal is immediate. This pattern is independent of body position.

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Reduced stroke volume during exercise in postural tachycardia syndrome

Journal of Applied Physiology ◽

10.1152/japplphysiol.00175.2007 ◽

2007 ◽

Vol 103 (4) ◽

pp. 1128-1135 ◽

Cited By ~ 40

Author(s):

Shizue Masuki ◽

John H. Eisenach ◽

William G. Schrage ◽

Christopher P. Johnson ◽

Niki M. Dietz ◽

...

Keyword(s):

Cardiac Output ◽

Arterial Pressure ◽

Stroke Volume ◽

Peripheral Resistance ◽

Cardiovascular Regulation ◽

Open Circuit ◽

Exercise Intolerance ◽

Postural Tachycardia Syndrome ◽

Cycle Exercise ◽

Postural Tachycardia

Postural tachycardia syndrome (POTS) is characterized by excessive tachycardia without hypotension during orthostasis. Most POTS patients also report exercise intolerance. To assess cardiovascular regulation during exercise in POTS, patients ( n = 13) and healthy controls ( n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter), heart rate (HR; measured by ECG), and cardiac output (open-circuit acetylene breathing) were measured. In both positions, mean arterial pressure, cardiac output, and total peripheral resistance at rest and during exercise were similar in patients and controls ( P > 0.05). However, supine stroke volume (SV) tended to be lower in the patients than controls at rest (99 ± 5 vs. 110 ± 9 ml) and during 75-W exercise (97 ± 5 vs. 111 ± 7 ml) ( P = 0.07), and HR was higher in the patients than controls at rest (76 ± 3 vs. 62 ± 4 beats/min) and during 75-W exercise (127 ± 3 vs. 114 ± 5 beats/min) (both P < 0.01). Upright SV was significantly lower in the patients than controls at rest (57 ± 3 vs. 81 ± 6 ml) and during 75-W exercise (70 ± 4 vs. 94 ± 6 ml) (both P < 0.01), and HR was much higher in the patients than controls at rest (103 ± 3 vs. 81 ± 4 beats/min) and during 75-W exercise (164 ± 3 vs. 131 ± 7 beats/min) (both P < 0.001). The change (upright − supine) in SV was inversely correlated with the change in HR for all participants at rest ( R2= 0.32), at 25 W ( R2= 0.49), 50 W ( R2= 0.60), and 75 W ( R2= 0.32) ( P < 0.01). These results suggest that greater elevation in HR in POTS patients during exercise, especially while upright, was secondary to reduced SV and associated with exercise intolerance.

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Postural hypocapnic hyperventilation is associated with enhanced peripheral vasoconstriction in postural tachycardia syndrome with normal supine blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01359.2005 ◽

2006 ◽

Vol 291 (2) ◽

pp. H904-H913 ◽

Cited By ~ 31

Author(s):

Julian M. Stewart ◽

Marvin S. Medow ◽

Neil S. Cherniack ◽

Benjamin H. Natelson

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Flow ◽

Blood Volume ◽

Peripheral Resistance ◽

Impedance Plethysmography ◽

Postural Tachycardia Syndrome ◽

Peripheral Vasoconstriction ◽

Postural Tachycardia ◽

End Tidal

Previous investigations have demonstrated a subset of postural tachycardia syndrome (POTS) patients characterized by normal peripheral resistance and blood volume while supine but thoracic hypovolemia and splanchnic blood pooling while upright secondary to splanchnic hyperemia. Such “normal-flow” POTS patients often demonstrate hypocapnia during orthostatic stress. We studied 20 POTS patients (14–23 yr of age) and compared them with 10 comparably aged healthy volunteers. We measured changes in heart rate, blood pressure, heart rate and blood pressure variability, arm and leg strain-gauge occlusion plethysmography, respiratory impedance plethysmography calibrated against pneumotachography, end-tidal partial pressure of carbon dioxide (PetCO2), and impedance plethysmographic indexes of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during upright tilt to 70°. Ten POTS patients demonstrated significant hyperventilation and hypocapnia (POTSHC) while 10 were normocapnic with minimal increase in postural ventilation, comparable to control. While relative splanchnic hypervolemia and hyperemia occurred in both POTS groups compared with controls, marked enhancement in peripheral vasoconstriction occurred only in POTSHC and was related to thoracic blood flow. Variability indexes suggested enhanced sympathetic activation in POTSHC compared with other subjects. The data suggest enhanced cardiac and peripheral sympathetic excitation in POTSHC.

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Reduced central blood volume and cardiac output and increased vascular resistance during static handgrip exercise in postural tachycardia syndrome

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00439.2007 ◽

2007 ◽

Vol 293 (3) ◽

pp. H1908-H1917 ◽

Cited By ~ 11

Author(s):

Julian M. Stewart ◽

Indu Taneja ◽

Marvin S. Medow

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Blood Volume ◽

Peripheral Resistance ◽

Exercise Intolerance ◽

Low Flow ◽

Postural Tachycardia Syndrome ◽

Central Blood Volume ◽

Normal Flow ◽

Postural Tachycardia

Postural tachycardia syndrome (POTS) is characterized by exercise intolerance and sympathoactivation. To examine whether abnormal cardiac output and central blood volume changes occur during exercise in POTS, we studied 29 patients with POTS (17–29 yr) and 12 healthy subjects (18–27 yr) using impedance and venous occlusion plethysmography to assess regional blood volumes and flows during supine static handgrip to evoke the exercise pressor reflex. POTS was subgrouped into normal and low-flow groups based on calf blood flow. We examined autonomic effects with variability techniques. During handgrip, systolic blood pressure increased from 112 ± 4 to 139 ± 9 mmHg in control, from 119 ± 6 to 143 ± 9 in normal-flow POTS, but only from 117 ± 4 to 128 ± 6 in low-flow POTS. Heart rate increased from 63 ± 6 to 82 ± 4 beats/min in control, 76 ± 3 to 92 ± 6 beats/min in normal-flow POTS, and 88 ± 4 to 100 ± 6 beats/min in low-flow POTS. Heart rate variability and coherence markedly decreased in low-flow POTS, indicating uncoupling of baroreflex heart rate regulation. The increase in central blood volume with handgrip was absent in low-flow POTS and blunted in normal-flow POTS associated with abnormal splanchnic emptying. Cardiac output increased in control, was unchanged in low-flow POTS, and was attenuated in normal-flow POTS. Total peripheral resistance was increased compared with control in all POTS. The exercise pressor reflex was attenuated in low-flow POTS. While increased cardiac output and central blood volume characterizes controls, increased peripheral resistance with blunted or eliminated in central blood volume increments characterizes POTS and may contribute to exercise intolerance.

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Prior head-down tilt does not impair the cerebrovascular response to head-up tilt

Journal of Applied Physiology ◽

10.1152/japplphysiol.00871.2014 ◽

2015 ◽

Vol 118 (11) ◽

pp. 1356-1363 ◽

Cited By ~ 4

Author(s):

Changbin Yang ◽

Yuan Gao ◽

Danielle K. Greaves ◽

Rodrigo Villar ◽

Thomas Beltrame ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Peripheral Resistance ◽

Resistance Index ◽

Cardiovascular Responses ◽

Mean Flow ◽

Cerebrovascular Autoregulation ◽

Arterial Blood ◽

Head Up Tilt ◽

S Period

The hypothesis that cerebrovascular autoregulation was not impaired during head-up tilt (HUT) that followed brief exposures to varying degrees of prior head-down tilt (HDT) was tested in 10 healthy young men and women. Cerebral mean flow velocity (MFV) and cardiovascular responses were measured in transitions to a 60-s period of 75° HUT that followed supine rest (control) or 15 s HDT at −10°, −25°, and −55°. During HDT, heart rate (HR) was reduced for −25° and −55°, and cardiac output was lower at −55° HDT. MFV increased during −10° HDT, but not in the other conditions even though blood pressure at the middle cerebral artery (BPMCA) increased. On the transition to HUT, HR increased only for −55° condition, but stroke volume and cardiac output transiently increased for −25° and −55°. Total peripheral resistance index decreased in proportion to the magnitude of HDT and recovered over the first 20 s of HUT. MFV was significantly less in all HDT conditions compared with the control in the first 5-s period of HUT, but it recovered quickly. An autoregulation correction index derived from MFV recovery relative to BPMCA decline revealed a delay in the first 5 s for prior HDT compared with control but then a rapid increase to briefly exceed control after −55° HDT. This study showed that cerebrovascular autoregulation is modified by but not impaired by brief HDT prior to HUT and that cerebral MFV recovered quickly and more rapidly than arterial blood pressure to protect against cerebral hypoperfusion and potential syncope.

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Autonomic dysfunction in post-COVID patients with and witfhout neurological symptoms: a prospective multidomain observational study

Journal of Neurology ◽

10.1007/s00415-021-10735-y ◽

2021 ◽

Author(s):

Alex Buoite Stella ◽

Giovanni Furlanis ◽

Nicolò Arjuna Frezza ◽

Romina Valentinotti ◽

Milos Ajcevic ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Orthostatic Intolerance ◽

Neurological Symptoms ◽

Postural Tachycardia Syndrome ◽

Symptom Scale ◽

Autonomic Symptom ◽

Postural Tachycardia ◽

Ambulatory Services

AbstractThe autonomic nervous system (ANS) can be affected by COVID-19, and dysautonomia may be a possible complication in post-COVID individuals. Orthostatic hypotension (OH) and postural tachycardia syndrome (POTS) have been suggested to be common after SARS-CoV-2 infection, but other components of ANS function may be also impaired. The Composite Autonomic Symptom Scale 31 (COMPASS-31) questionnaire is a simple and validated tool to assess dysautonomic symptoms. The aim of the present study was to administer the COMPASS-31 questionnaire to a sample of post-COVID patients with and without neurological complaints. Participants were recruited among the post-COVID ambulatory services for follow-up evaluation between 4 weeks and 9 months from COVID-19 symptoms onset. Participants were asked to complete the COMPASS-31 questionnaire referring to the period after COVID-19 disease. Heart rate and blood pressure were manually taken during an active stand test for OH and POTS diagnosis. One-hundred and eighty participants were included in the analysis (70.6% females, 51 ± 13 years), and OH was found in 13.8% of the subjects. Median COMPASS-31 score was 17.6 (6.9–31.4), with the most affected domains being orthostatic intolerance, sudomotor, gastrointestinal and pupillomotor dysfunction. A higher COMPASS-31 score was found in those with neurological symptoms (p < 0.01), due to more severe orthostatic intolerance symptoms (p < 0.01), although gastrointestinal (p < 0.01), urinary (p < 0.01), and pupillomotor (p < 0.01) domains were more represented in the non-neurological symptoms group. This study confirms the importance of monitoring ANS symptoms as a possible complication of COVID-19 disease that may persist in the post-acute period.

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Control of Blood Pressure and the Distribution of Blood Flow

International Journal of Technology Assessment in Health Care ◽

10.1017/s0266462300012551 ◽

1991 ◽

Vol 7 (S1) ◽

pp. 79-84 ◽

Cited By ~ 1

Author(s):

Hans T. Versmold

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cardiac Output ◽

Peripheral Resistance ◽

Systemic Blood Pressure ◽

Adrenergic Innervation ◽

Systemic Blood ◽

Low Cardiac Output ◽

Neurohumoral Control ◽

The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

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