Abstract P131: Abnormal Blood Pressure Fall During Hyperventilation Maneuver In Postural Tachycardia Syndrome

Abstract

Postural Orthostatic Tachycardia Syndrome (POTS) might have altered endothelial function, causing abnormal vasomotion in the body and in cerebral vessels. Non-cardiac symptoms experienced by these patients suggest that they may be especially sensitive to acute reduction of arterial CO 2 concentration during hyperventilation (HV). We hypothesized HV induces more significant blood pressure (BP) fall with compensatory higher HR increase in POTS. Subjects previously diagnosed with POTS and gender-matched controls were enrolled. ECG, finger BP, and EtCO 2 were continuously recorded during hyperventilation (1breaths/sec) over 30 seconds. Hemodynamic parameters were computed in absolute and change. We studied 14 POTS and 15 controls matched for age (29 ± 2 vs 30 ± 3; p=0.63) and BMI (24.1±0.8 vs 23.0±0.7; p=0.34). At baseline mean HR (79±4 vs 70±3 bpm, p=0.12) was comparable and SBP was higher (113±3 vs 105±2 mmHg, p<0.05) compared to controls. EtCO 2 values were comparable at baseline (35±1 vs 38±1 mmHg, p=0.14) and at the end of the maneuver (20±1 vs 21±1 mmHg, p=0.58). POTS had greater SBP drop (-27±2 vs -19±2 mmHg, p<0.05) and a comparable HR increase (34±3 vs 29±2 bpm, p=0.11), despite POTS reached a higher absolute maximal HR (113±4 vs 99±2 bpm, p<0.05) [Figure]. Recovery time for HR (31±4 vs 34±4 sec, p=0.68) and SBP (27±7 vs 18±4 sec, p=0.42) were similar. POTS have greater SBP drop with less adequate compensatory HR increase during HV. These results suggest that vascular responsiveness to hypocapnia is especially strong in POTS and it can contribute to orthostatic stress and symptoms.