Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Abstract

BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation‐associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO 2.Methods and ResultsFifty‐eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO 2 <30 Torr during head‐up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat‐to‐beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO 2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head‐up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO 2 in hyperventilation by addition of exogenous CO 2 into a rebreathing apparatus. With added CO 2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control.ConclusionsWe conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

Cerebral blood flow remains reduced after tilt testing in myalgic encephalomyelitis/chronic fatigue syndrome patients

“…Third, a large number of studies using transcranial Doppler have shown that cerebral blood flow velocity is influenced by P ET CO 2 ( Del Pozzi et al, 2014 , Immink et al, 2014 , Laffey and Kavanagh, 2002 , Novak et al, 1998 , Sato et al, 2012 , Stewart et al, 2018a , Stewart et al, 2018b ). Using extracranial Doppler, this finding was also confirmed in our previous study ( van Campen et al, 2020c ).…”

Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness : Consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN)

“…CO 2 recordings are useful to detail the pathophysiological cascade as hypocapnia may precede reflex syncope (Norcliffe-Kaufmann et al, 2008). Adding CO 2 recordings to TTT may also be of clinical interest as it may help to identify POTS subtypes that are consequent upon postural hyperventilation (Stewart et al, 2018) or episodes of hyperventilation in those who report dizziness without concomitant hypotension (Naschitz et al, 2000).…”

2018 Chinese Pediatric Cardiology Society (CPCS) guideline for diagnosis and treatment of syncope in children and adolescents

“…Other causes of TLOC, including epilepsy, metabolic disorders (such as hypoglycemia, hypoxemia, hyperventilation syndrome [10]), poisoning, transient ischemic attack of the vertebral basilar artery system, ''pseudo-syncope" caused by psychological factors [6,11] and TLOC from head trauma are easily misdiagnosed as syncope in the clinic. These diseases do not produce transient cerebral ischemia, so they should be strictly differentiated from syncope (Ⅱa; A).…”