Monitoring of cerebral oximetry in patients with postural orthostatic tachycardia syndrome, Kharraziha et al, 2019

Monitoring of cerebral oximetry in patients with postural orthostatic tachycardia syndrome
Isabella Kharraziha, Hannes Holm, Erasmus Bachus, Olle Melander, Richard Sutton, Artur Fedorowski, and Viktor Hamrefors
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Abstract

Postural orthostatic tachycardia syndrome (POTS) is a disorder of unknown aetiology characterized by orthostatic intolerance and tachycardia with diverse other symptoms, including neurocognitive deficits. Cerebral oximetry non-invasively measures cerebral tissue saturation (SctO2) and has been shown to be informative in syncope evalu- ation. We aimed to assess SctO2 in POTS patients and those with normal response to orthostatic provocation, relative to haemodynamic parameters and symptoms.

Thirty-four patients with POTS (29.1 ± 9.5 years; 26 females) and 34 age-/sex-matched controls with normal head-up tilt tests (HUTs) were included. SctO2 at rest and during HUT were compared between POTS and controls.

The relation between SctO2, systolic blood pressure (SBP), and heart rate (HR) during HUT was linearly assessed. SctO2 values were related to dizziness or syncope during HUT. The minimum SctO2-value during HUT was lower (65.4 ± 5.6 vs. 68.2 ± 4.2%, P = 0.023) and changes in SctO2 from supine to minimum HUT value were more pronounced in POTS patients (5.7 ± 2.9% vs. 4.3 ± 2.1%, P = 0.028). Decrease in SBP from supine to minimum HUT value (P=0.004) and increase in HR from supine to HUT value at 3min (P=0.022) correlated with more pronounced SctO2 decrease in POTS but not controls. SctO2 did not predict syncope or dizziness during HUT.

Postural orthostatic tachycardia syndrome patients have lower cerebral tissue saturation during orthostatic provocation compared with those subjects having normal haemodynamic response to tilt. Orthostatic decrease in cerebral saturation only weakly correlates with HR increase and does not predict vasovagal reflex in POTS. Other hitherto unknown factors may affect cerebral tissue saturation in POTS.

 

For some real-world context for the NIRS device, one use-case is in congenital cardiac surgery. Frequently you need to repair the aortic arch and that compromise the great vessels, including the carotid and vertebral arteries. The NIRS sensor is placed on either side of the head and will warn you if brain hemispheric perfusion is dropping during your reconstruction manoeuvres.

Similar use when implanting a transplanted liver. As the vasculature is reconstructed, you can measure whether/how well the organ is being perfused. It's complemented by on-table Doppler ultrasound studies. (Sometimes when you close the abdomen, there is a configuration change and your nicely formed hepatic arterial anastomosis may get kinked).

 

Yes, this is what seems to be happening in my case. My heart rate doesn't increase as drastically as it used to and is generally lower but the dizziness resulting from being upright is still there and hasn't changed much. I suspect the POTS diagnostic criteria are flawed because one can have much the same illness without the required marked HR increase.

 

I think POTS is a comorbidity to ME relating to a central and likely shared mechanism with a neuroanatomical basis with cellular dysfunction.

 

The doctors involved with ME before CFS (and long before POTS) believed that the problems with temperature control, OI and so on were because of problems in the hypothalamus and that part of the brain. It is a central part of ME to have trouble standing still for any length of time.