The role of hypocapnia in the development of syncope during orthostatic stress following plasma volume expansion

Marsh, Clare; Ernsting, J; J, Ernsting,

Abstract

Hypotension is considered to be the cause of syncope during
lower body negative pressure (LBNP). However, hypocapnia
induced by hyperventilation has been observed in subjects
preceding syncope, and may contribute to the onset of syncope
by reducing cerebral blood flow during orthostatic stress
(Morgan et al. 1997). Enhancing the ‘respiratory pump’ may
partially attenuate the reduction in venous return that occurs
during LBNP (Lipsitz et al. 1998; Novak et al. 1998), but the
associated hyperventilation may actually exacerbate orthostatic
intolerance. The aims of this study were to examine the effect of
plasma volume expansion on tolerance to LBNP, and to consider
the role of hypocapnia in the development of syncope.
Following approval by King’s College London Ethics Committee,
five subjects volunteered to participate in the study. Subjects
performed two LBNP stress tests. LBNP was applied at
10 mmHg increments every 3 min until cessation at pre-syncope,
or due to breathing difficulties. Subjects performed one test after
ingesting 12 ml/kg body weight of electrolyte fluid (F trial), and
one test following no fluid (NF trial). Measurements included
change in plasma volume (cyanmethaemoglobin and
microhaematocrit values from venous blood samples
incorporated into equation by Dill & Costill, 1974), end-tidal
PCO2 (nasal catheter), blood pressure (Finapres), heart rate
(ECG). Data presented as means ± S.E.M., and compared using
paired t tests.
Following fluid ingestion, plasma volume increased (P < 0.05) by
3.25 %, and time to cessation of LBNP increased (P < 0.05) by
4.28 min (NF: 18.85 ± 1.28 min; F: 23.13 ± 1.81 min). End-tidal
PCO2 (n = 4) did not change from baseline values during mild
LBNP up to _20 mmHg (NF: 42.13 ± 0.86; F:
42.23 ± 1.66 mmHg). However, as suction pressure increased to
_
30 mmHg and above, end-tidal PCO2 fell. Hypocapnia was
greater during the NF trial, with a significantly lower (P < 0.05)
end-tidal PCO2 at suction of _50 mmHg (NF: 36.24 ± 1.67; F:40.9 ± 1.55 mmHg). Mean end-tidal PCO2 at time of LBNP
cessation were similar between trials (NF: 31.70 ± 3.04; F:
33.27 ± 2.35 mmHg).
In conclusion, the smaller reduction in end-tidal PCO2 during
suction following plasma volume expansion was associated with
increased tolerance to LBNP. Therefore, hypocapnia may be an
important factor that contributes to orthostatic intolerance.
However, plasma volume expansion may play an important role
in reducing the hypocapnic contribution implicated in syncope
during orthostatic stress by perhaps reducing the degree of
hyperventilation that often leads to cerebral vasoconstriction.

• Presentation Conference Type: Poster
• Conference Name: Physiological Society Conference 2004 (J555P)
• Publication Date: Mar 9, 2004
• Deposit Date: Nov 27, 2020
• Publisher URL: https://doi.org/10.1111/j.1469-7793.2004.tb00484.x
• Related Public URLs: http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1469-7793/
• Additional Information: Access Information : This published abstract can be viewed using the link above.; Event Type : Conference