Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.

Grubb, Blair P.; Gerard, Gary F.; Roush, Kenneth; Temesy‐Armos, Peter; Montford, P; Elliott, Laura; Hahn, Harry; Brewster, Pamela

doi:10.1161/01.cir.84.3.1157

Cited by 229 publications

(143 citation statements)

References 27 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…Altered cerebrovascular control unrelated to changes in PET CO 2 has been reported during LBNP following bed rest (44) and parabolic flight (38). In addition, a paradoxical cerebral vasoconstriction in healthy (5,6,22,38) and orthostatically intolerant (13,14) individuals has been reported during postural stress and LBNP. However, our previous work (38), as well as that of others (8,21), showed that cerebral autoregulation remains intact during HUT in healthy subjects, suggesting that decreases in perfusion pressure were unlikely to be the cause of the decrease in cerebral flow.…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Cerebral blood flow during orthostasis: role of arterial CO₂

Serrador

Hughson²,

Kowalchuk³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Reductions in end-tidal PCO2 (PETCO 2 ) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in PETCO 2 reflected decreases in arterial PCO2 (PaCO 2 ) and their relation to increases in alveolar ventilation (V A) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. PaCO 2 , V A, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in PETCO 2 and PaCO 2 (Ϫ1.7 Ϯ 0.5 and Ϫ1.1 Ϯ 0.4 mmHg, P Ͻ 0.05) during minute 1 of HUT were associated with a significant increase in V A (ϩ0.7 Ϯ 0.3 l/min, P Ͻ 0.05). However, further decreases in Pa CO 2 (Ϫ0.5 Ϯ 0.5 mmHg, P Ͻ 0.05), from minute 1 to the last minute of HUT, occurred even though V A did not change significantly (Ϫ0.2 Ϯ 0.3 l/min, P ϭ not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (Ϫ7 Ϯ 2 and Ϫ8 Ϯ 2%, P Ͻ 0.05) from minute 1 to the last minute of HUT, despite minimal changes in PaCO 2 . These data suggest that decreases in PET CO 2 and PaCO 2 during upright posture are not solely due to increased V A but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in PaCO 2 did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in PaCO 2 play a role in the CBF response to orthostatic stress. transcranial Doppler; cerebral vasoconstriction; head-up tilt IT HAS BEEN WIDELY NOTED that orthostatic stress in humans decreases end-tidal PCO 2 (PET CO 2 ) or arterial PCO 2 (Pa CO 2 ) (1,4,17,27,36,38,41). Because Pa CO 2 is known to be critical in control of cerebral blood flow (CBF) (30), decreased Pa CO 2 during tilt could play a role in orthostatic intolerance through inappropriate cerebral vasoconstriction. It has been hypothesized that hyperventilation in the upright posture reduces Pa CO 2 , compromising CBF and leading to syncope (27).One inherent problem with this previous work is the use of PET CO 2 to represent Pa CO 2 . Previous work has found that although, in the supine position, PET CO 2 is closely matched to Pa CO 2 (i.e., ϳ0.8 mmHg greater), the assumption of the upright posture resulted in the PET CO 2 being ϳ2.9 mmHg lower than Pa CO 2 (4).No studies have directly measured alveolar ventilation (V A) and CBF during head-up tilt (HUT) and characterized their association to Pa CO 2 . On the basis of our previous findings that decreases in PET CO 2 did not relate to changes in minute ventilation (V E) (36), we hypothesized that Pa CO 2 decreases would be attenuated compared with PET CO 2 and would not be the predominant factor in reduced CBF during HUT. METHODS Subjects.Fifteen subjects [10 women and 5 men, averaging 25.3 yr of age (range 21-32 yr), 64.3 Ϯ 20.5 (SD) kg body wt, 174 Ϯ 9 cm] with no history of card...

show abstract

Section: Discussionmentioning

confidence: 98%

“…CFV MCA has been found to decrease with upright tilt (13,17,27,38) and lower body negative pressure (LBNP) (6,22). Concomitant with this decrease in CBF is a drop in PET CO 2 (6,17,22,27,38).…”

Section: Discussionmentioning

confidence: 99%

Cerebral blood flow during orthostasis: role of arterial CO₂

Serrador

Hughson²,

Kowalchuk³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…[16][17][18][19][20] Blood flow velocities (systolic, diastolic, and mean velocities) and the pulsatility and resistive indexes, which derive from the flow velocities, are the most common measurements used. Blood flow velocity increases and the pulsatility and resistive index decrease with arteriolar vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

“…Blood flow velocity increases and the pulsatility and resistive index decrease with arteriolar vasoconstriction. 16,17 The middle cerebral artery, which is frequently insonated under angles of less than 30°and which also supplies blood to approximately 85% of the hemisphere, 16 is the most common intracranial vessel used for transcranial Doppler ultrasonography. There are many studies which show that blood flow velocity and HEPATOLOGY Vol.…”

Section: Discussionmentioning

confidence: 99%

Increased cerebrovascular resistance in cirrhotic patients with ascites

et al. 1998

View full text Add to dashboard Cite

Studies assessing regional hemodynamics in patients with cirrhosis and ascites have shown vasodilation in the splanchnic circulation and vasoconstriction in the renal circulation and in the brachial and femoral artery vascular territories. The aim of this study was to assess the cerebral vascular resistance in cirrhotic patients with ascites. The resistive index in the middle cerebral artery (an index of the cerebral vascular resistance) and in a renal interlobar artery were measured by Doppler ultrasonography in 7 healthy subjects: 13 patients with compensated cirrhosis and 24 patients with ascites (13 with renal failure). The arterial blood pressure and the activity of the renin-angiotensin and sympathetic nervous systems, as estimated by plasma renin activity and plasma norepinephrine concentration, respectively, were also measured. The resistive index in the middle cerebral artery was significantly increased in patients with ascites (0.68 ؎ 0.05, mean ؎ SD) as compared with patients without ascites (0.60 ؎ 0.01, P F .05) and with healthy patients (0.52 ؎ 0.01, P F .01). Renal resistive index was also increased in patients with ascites (0.77 ؎ 0.01) compared with the other two groups (0.68 ؎ 0.02 and 0.62 ؎ 0.00, respectively; P F .001). The resistive index in the middle cerebral artery showed a direct correlation with renal resistive index (r ‫؍‬ .73, P F .01), plasma renin activity (r ‫؍‬ .61, P F .01), and norepinephrine (r ‫؍‬ .53, P F .01). The resistive index in the middle cerebral artery showed an inverse correlation with mean arterial pressure (r ‫,54.؊؍‬ P F .01). These results indicate that in patients with cirrhosis and ascites there is a cerebral vasoconstriction which is probably related with the arterial hypotension and the overactivity of vasoconstrictor systems. (HEPATOL-OGY 1998;28:39-44.)Portal hypertension in cirrhosis is associated with a hyperdynamic circulation, which is characterized by hypervolemia, high cardiac output, arterial hypotension, and low peripheral vascular resistance. 1 These circulatory abnormalities are thought to be secondary to a splanchnic arteriolar vasodilation related to the increase in portal pressure. Portal hypertension in experimental animals is associated with a generalized splanchnic arteriolar vasodilation. 2,3 There is indirect evidence that this also occurs in human cirrhosis, as hepatic blood flow is usually normal or increased in these patients, even though 60% to 80% of portal flow is shunted through the collateral circulation. 4 In addition, the mean transit time in the splanchnic vascular bed is substantially reduced in alcoholic cirrhotic patients, which indicates a hyperkinetic splanchnic circulation in these patients. 5 Finally, studies using echo-Doppler have documented increased splenic and mesenteric blood flow in patients with cirrhosis. 6,7 Investigations assessing regional circulations in human cirrhosis are also consistent with that concept. Renal blood flow is reduced and renal vascular resistance is increased in most patients with cirrhosi...

show abstract

“…In human studies, it has been shown that vasodilatation occurs in muscle vascular beds during vasodepressor syncope, but vasoconstriction may develop in skin 24 and brain. 25 In the study of baroreceptors, it has been demonstrated that reflex control of HR and vascular resistance may be quantitatively dissociated. 26 Thus, the differences of HR and vascular resistance between patients with vasovagal and vasodepressor syncope represent the difference in vagal activation and discrepancy in sympathetic inhibition in the peripheral vascular system.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic significance of heart rate in neurally mediated syncope

Chan

Wang

et al. 2004

Clinical Cardiology

View full text Add to dashboard Cite

SummaryBackground: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear.Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope.Methods: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20).Results: The baseline hemodynamic data (mean ± standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 ± 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 ± 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic

show abstract

Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.

Cited by 229 publications

References 27 publications

Cerebral blood flow during orthostasis: role of arterial CO₂

Cerebral blood flow during orthostasis: role of arterial CO₂

Increased cerebrovascular resistance in cirrhotic patients with ascites

Hemodynamic significance of heart rate in neurally mediated syncope

Contact Info

Product

Resources

About

Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.

Cited by 229 publications

References 27 publications

Cerebral blood flow during orthostasis: role of arterial CO2

Cerebral blood flow during orthostasis: role of arterial CO2

Increased cerebrovascular resistance in cirrhotic patients with ascites

Hemodynamic significance of heart rate in neurally mediated syncope

Contact Info

Product

Resources

About

Cerebral blood flow during orthostasis: role of arterial CO₂

Cerebral blood flow during orthostasis: role of arterial CO₂