Cerebral critical closing pressure and CO2 responses during the progression toward syncope

2013 ◽  
Vol 114 (6) ◽  
pp. 801-807 ◽  
Author(s):  
K. A. Zuj ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
R. L. Hughson
Keyword(s):  
Lower Body Negative Pressure ◽  
Resistance Index ◽  
Bed Rest ◽  
Tolerance Test ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Cerebral Blood Velocity ◽  
End Tidal ◽  
Closing Pressure

Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BPMCA) and reductions in arterial CO2 as reflected by end-tidal values (PetCO2). It was hypothesized that reductions in PetCO2 increase cerebrovascular tone before a drop in BPMCA that ultimately leads to syncope. Twelve men (21–42 yr of age) completed an orthostatic tolerance test consisting of head-up tilt and progressive lower body negative pressure to presyncope, before and after completing 5 days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BPMCA, and PetCO2 were continuously recorded throughout the test. Cerebrovascular indicators, cerebrovascular resistance, critical closing pressure (CrCP), and resistance area product (RAP), were calculated. Comparing from supine baseline to 6–10 min after the start of tilt, there were reductions in CBFV, PetCO2, BPMCA, and CrCP, an increase in RAP, and no change in cerebrovascular resistance index. Over the final 15 min before syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in PetCO2 ( r = 0.69 ± 0.17 and r = 0.63 ± 0.20, respectively), and BPMCA, which was not reduced until the last minute of the test, was correlated with a reduction in RAP ( r = 0.91 ± 0.09). Post-HDBR, tilt tolerance was markedly reduced, and changes in CBFV were dominated by a greater reduction in BPMCA with no relationships to PetCO2. Therefore, pre-HDBR, changes in PetCO2 with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope, whereas, after 5 days of HDBR, orthostatic responses were dominated by changes in BPMCA.

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Lower Body Negative Pressure ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex ◽  
Underlying Mechanisms ◽  
End Tidal ◽  
Induced Changes ◽  
The Relationship

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA Vmean (middle cerebral artery mean blood velocity) and V̇E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO2 levels (0, 3.5 and 5% CO2). The regression line of the linear relationship between V̇E and PETCO2 (end-tidal CO2) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA Vmean and PETCO2 was not shifted by LBNP-induced changes in PETCO2. However, changes in V̇E from rest to LBNP were more related to changes in MCA Vmean than changes in PETCO2. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO2 from the brain causing hyperpnoea following activation of the central chemoreflex.

WISE-2005: adrenergic responses of women following 56-days, 6° head-down bed rest with or without exercise countermeasures

2007 ◽  
Vol 293 (6) ◽  
pp. R2343-R2352 ◽  
Author(s):  
Heather Edgell ◽  
Kathryn A. Zuj ◽  
Danielle K. Greaves ◽  
J. Kevin Shoemaker ◽  
Marc-Antoine Custaud ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Cardiovascular Responses ◽  
Bed Rest ◽  
Nutritional Supplement ◽  
Exercise Group ◽  
Adrenergic Stimulation

We tested the hypotheses that women completing 56 days, 6° head-down bed-rest (HDBR) would have changes in sensitivity of cardiovascular responses to adrenergic receptor stimulation and that frequent aerobic and resistive exercise would prevent these changes. Twenty-four women, eight controls, eight exercisers (lower body negative pressure treadmill and flywheel resistance exercise), and eight receiving nutritional supplement but no exercise were studied in baseline and during administration of the β-agonist isoproterenol (ISO) and the α- and β-agonist norepinephrine (NOR). In the control and nutrition groups, HDBR increased heart rate (HR) and reduced stroke volume (SV), and there was a significantly greater increase in HR with ISO after HDBR. In contrast, the HR and SV of the exercise group were unchanged from pre-HDBR. After HDBR, leg vascular resistance (LVR) was greater than pre-HDBR in the exercise group but reduced in control and nutrition. LVR was reduced with ISO and increased with NOR. Changes in total peripheral resistance were similar to those of LVR but of smaller magnitude, perhaps because changes in cerebrovascular resistance index were directionally opposite to those of LVR. There were no changes in sensitivity of the vascular resistance responses to adrenergic stimulation. The HR response might reflect a change in sensitivity or a necessary response to the reduction in SV after HDBR in control and nutrition groups. The reduced peripheral vascular resistance after HDBR might help to explain orthostatic intolerance in women. Exercise was an effective countermeasure to the HDBR effects.

Carbon dioxide, critical closing pressure and cerebral haemodynamics prior to vasovagal syncope in humans

2001 ◽  
Vol 101 (4) ◽  
pp. 351-358 ◽  
Author(s):  
Brian J. CAREY ◽  
Penelope J. EAMES ◽  
Ronney B. PANERAI ◽  
John F. POTTER
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vasovagal Syncope ◽  
Previous History ◽  
Normal Subjects ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Closing Pressure

The cerebrovascular changes that occur prior to vasovagal syncope (VVS) are unclear, with both increases and decreases in cerebrovascular resistance being reported during pre-syncope. This study assessed the cerebrovascular responses, and their potential underlying mechanisms, that occurred before VVS induced by head-up tilt (HUT). Groups of 65 normal subjects with no previous history of syncope and of 16 patients with recurrent VVS were subjected to 70° HUT for up to 30min. Bilateral middle cerebral artery (MCA) cerebral blood flow velocities (CBFVs) were measured using transcranial Doppler ultrasound, along with simultaneous measures of MCA blood pressure, heart rate, and end-tidal and transcutaneous carbon dioxide concentrations. All 16 patients and 14 of the control subjects developed VVS during HUT. During pre-syncope, mean CBFV declined, due predominantly to a decrease in diastolic rather than systolic CBFV (decreases of 44.5±;19.8% and 6.3±;12.9% respectively; P < 0.0001). CO2 levels and indices of cerebrovascular resistance decreased during pre-syncope, while critical closing pressure (CrCP) increased to levels approaching MCA diastolic blood pressure before decreasing precipitously on syncope. Pre-syncopal changes were similar in syncopal patients and syncopal controls. CrCP, therefore, rises during pre-syncope, possibly related to progressive hypocapnia, and may account for the relatively greater fall in diastolic CBFV. Falls in cerebrovascular resistance, therefore, may be offset by rises in CrCP due to hypocapnia, leading to diminished cerebral blood flow during pre-syncope.

scholarly journals Increases in cerebrovascular impedance in older adults

2011 ◽  
Vol 111 (2) ◽  
pp. 376-381 ◽  
Author(s):  
Yong-Sheng Zhu ◽  
Benjamin Y. Tseng ◽  
Shigeki Shibata ◽  
Benjamin D. Levine ◽  
Rong Zhang
Keyword(s):  
Arterial Pressure ◽  
Resistance Index ◽  
The Elderly ◽  
Systemic Circulation ◽  
Applanation Tonometry ◽  
Elderly Subjects ◽  
Cerebrovascular Resistance ◽  
Novel Method ◽  
Young Subjects ◽  
End Tidal

This study explored a novel method for measuring cerebrovascular impedance to quantify the relationship between pulsatile changes in cerebral blood flow (CBF) and arterial pressure. Arterial pressure in the internal or common carotid artery (applanation tonometry), CBF velocity in the middle cerebral artery (transcranial Doppler), and end-tidal CO2 (capnography) were measured in six young (28 ± 4 yr) and nine elderly subjects (70 ± 6 yr). Transfer function method was used to estimate cerebrovascular impedance. Under supine resting conditions, CBF velocity was reduced in the elderly despite the fact that they had higher arterial pressure than young subjects. As expected, cerebrovascular resistance index was increased in the elderly. In both young and elderly subjects, impedance modulus was reduced gradually in the frequency range of 0.78–8 Hz. Phase was negative in the range of 0.78–4.3 Hz and fluctuated at high frequencies. Compared with the young, impedance modulus increased by 38% in the elderly in the range of 0.78–2 Hz and by 39% in the range of 2–4 Hz ( P < 0.05). Moreover, increases in impedance were correlated with reductions in CBF velocity. Collectively, these findings demonstrate the feasibility of assessing cerebrovascular impedance using the noninvasive method developed in this study. The estimated impedance modulus and phase are similar to those observed in the systemic circulation and other vascular beds. Moreover, increases in impedance in the elderly suggest that arterial stiffening, besides changes in cerebrovascular resistance, contributes to reduction in CBF with age.

Correlations among critical closing pressure, pulsatility index and cerebrovascular resistance

2004 ◽  
Vol 30 (10) ◽  
pp. 1329-1335 ◽  
Author(s):  
Hung-Yi Hsu ◽  
Chang-Ming Chern ◽  
Jon-Son Kuo ◽  
Terry Bo-Jau Kuo ◽  
Ying-Tsung Chen ◽  
...  
Keyword(s):  
Pulsatility Index ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Closing Pressure

Critical closing pressure explains cerebral hemodynamics during the Valsalva maneuver

1999 ◽  
Vol 86 (2) ◽  
pp. 675-680 ◽  
Author(s):  
Suzanne L. Dawson ◽  
Ronney B. Panerai ◽  
John F. Potter
Keyword(s):  
Blood Pressure ◽  
Valsalva Maneuver ◽  
Intrathoracic Pressure ◽  
Pulse Interval ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Critical Closing Pressure ◽  
Pressure Changes ◽  
Closing Pressure ◽  
Phase Iv

The Valsalva maneuver (VM), a voluntary increase in intrathoracic pressure of ∼40 mmHg, has been used to examine cerebral autoregulation (CA). During phase IV of the VM there are pronounced changes in mean arterial blood pressure (MABP), pulse interval, and cerebral blood flow (CBF), but the changes in CBF are of a much greater magnitude than those seen in MABP, a finding to date attributed to either a delay in activation of the CA mechanism or the inability of this mechanism to cope with the size and speed of the blood pressure changes involved. These changes in CBF also precede those in MABP, a pattern of events not explained by the physiological process of CA. Measurements of CBF velocity (transcranial Doppler) and MABP (Finapres) were performed in 53 healthy volunteers (aged 31–80 yr). By calculating beat-to-beat values of critical closing pressure (CCP) during the VM, we have found that this parameter suddenly drops at the start of phase IV, providing a coherent explanation for the large increase in CBF. If CCP is included in the estimation of cerebrovascular resistance, a temporal pattern more consistent with an autoregulatory response to the MABP overshoot is also found. CCP is intricately involved in the control of CBF during the VM and should be considered in the assessment of CA.

scholarly journals Does hypercapnia-induced impairment of cerebral autoregulation affect neurovascular coupling? A functional TCD study

2013 ◽  
Vol 115 (4) ◽  
pp. 491-497 ◽  
Author(s):  
Paola Maggio ◽  
Angela S. M. Salinet ◽  
Ronney B. Panerai ◽  
Thompson G. Robinson
Keyword(s):  
Cerebral Autoregulation ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Neurovascular Coupling ◽  
Relative Contribution ◽  
Middle Cerebral Arteries ◽  
Critical Closing Pressure ◽  
Area Product ◽  
End Tidal ◽  
Closing Pressure

Neurovascular coupling (NVC) and dynamic cerebral autoregulation (dCA) are both impaired in the acute phase of ischemic stroke, but their reciprocal interactions are difficult to predict. To clarify these aspects, the present study explored NVC in a healthy volunteer population during a surrogate state of impaired dCA induced by hypercapnia. This study aimed to test whether hypercapnia leads to a depression of NVC through an impairment of dCA. Continuous recordings of middle cerebral arteries cerebral blood flow velocity (CBFv), blood pressure (BP), heart rate, and end-tidal CO2 were performed in 19 right-handed subjects (aged >45 yr) before, during, and after 60 s of a passive paradigm during normocapnia and hypercapnia. The CBFv response was broken down into subcomponents describing the relative contributions of BP (VBP), critical closing pressure (VCrCP), and resistance area product (VRAP). VRAP reflects myogenic activity in response to BP changes, whereas VCrCP is more indicative of metabolic control. The results revealed that hypercapnia significantly affected NVC, with significant reductions in the relative contribution of VCrCP to the paradigm-induced increase in CBFv. The present study suggests that hypercapnia impairs both dCA and NVC, probably acting through an impairment of the metabolic component of CBF control.

Assessing cerebrovascular autoregulation from critical closing pressure and resistance area product during upright posture in aging and hypertension

2014 ◽  
Vol 307 (2) ◽  
pp. H124-H133 ◽  
Author(s):  
Andrew D. Robertson ◽  
Heather Edgell ◽  
Richard L. Hughson
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Pulse Wave ◽  
Uncontrolled Hypertension ◽  
Upright Posture ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Pressure Independent ◽  
Area Product ◽  
Closing Pressure

Static cerebral autoregulation (sCA) is believed to be resistant to aging and hypertensive pathology. However, methods to characterize autoregulation commonly rely on beat-by-beat mean hemodynamic measures and do not consider within-beat pulse wave characteristics that are impacted by arterial stiffening. We examined the role of critical closing pressure (CrCP) and resistance area product (RAP), two measures derived from the pulse wave, across supine lying, sitting, and standing postures in young adults, normotensive older adults, and older adults with controlled and uncontrolled hypertension ( N = 80). Traditional measures of sCA, using both intracranial and extracranial methods, indicated similar efficiency across all groups, but within-beat measures suggested different mechanisms of regulation. At rest, RAP was increased in hypertension compared with young adults ( P < 0.001), but CrCP was similar. In contrast, the drop in CrCP was the primary regulator of change in cerebrovascular resistance upon adopting an upright posture. Both CrCP and RAP demonstrated group-by-posture interaction effects ( P < 0.05), with older hypertensive adults exhibiting a rise in RAP that was absent in other groups. The posture-related swings in CrCP and RAP were related to changes in both the pulsatile and mean components of arterial pressure, independent of age, cardiac output, and carbon dioxide. Group-by-posture differences in pulse pressure were mediated in part by an attenuated heart rate response in older hypertensive adults ( P = 0.002). Examination of pulsatile measures in young, elderly, and hypertensive adults identified unique differences in how cerebral blood flow is regulated in upright posture.

scholarly journals Influence of sex, menstrual cycle, and oral contraceptives on cerebrovascular resistance and cardiorespiratory function during Valsalva or standing

2017 ◽  
Vol 123 (2) ◽  
pp. 375-386 ◽  
Author(s):  
Syed Abidi ◽  
Misha Nili ◽  
Stephania Serna ◽  
Simon Kim ◽  
Christopher Hazlett ◽  
...  
Keyword(s):  
Blood Flow ◽  
Menstrual Cycle ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Valsalva Maneuver ◽  
Resistance Index ◽  
Cycle Phase ◽  
Cerebrovascular Resistance ◽  
Cardiac Output Index ◽  
End Tidal

Women experience orthostatic intolerance more than men, and they experience faintness more in the early follicular [i.e., low-hormone (LH)] than luteal [i.e., high-hormone (HH)] phase of the menstrual cycle. Men ( n = 13, 25.8 ± 1.8 yr old) and women in the LH ( days 2–5; placebo) and HH ( days 18–24; high dose) phases of the menstrual cycle with (OC; n = 14, 22.0 ± 0.8 yr old) or without (NOC; n = 12, 21.8 ± 0.5 yr old) oral contraceptive (OC) use underwent the Valsalva maneuver and a supine-sit-stand protocol. Blood pressure, normalized stroke volume [stroke volume index (SVi)], cardiac output index, heart rate, end-tidal CO2, and middle cerebral artery (MCA) blood flow velocity were measured. When subjected to the Valsalva maneuver, all women had a greater increase in diastolic and mean MCA blood flow velocity than men ( P ≤ 0.065), with no significant effect of menstrual cycle phase or OC use. When subjected to the supine-sit-stand protocol, men had lower MCA blood flow velocity ( P < 0.038) than all women, and SVi was higher in men than in the NOC group in all postures ( P < 0.011) and in the OC group in the LH phase of the menstrual cycle during standing ( P = 0.010). Only men experienced higher resistance index ( P < 0.001) and pulsatility index ( P < 0.001) with standing. The OC group had lower end-tidal CO2 ( P = 0.002) than the NOC group ( P = 0.030) and men ( P ≤ 0.067). SVi ( P = 0.004) and cardiac output index ( P = 0.008) were higher in the OC than NOC group. A tendency toward a lower mean MCA blood flow velocity ( P = 0.058) and higher SVi ( P = 0.059) and pulsatility index ( P = 0.058) was noted in the HH than LH phase. Mean arterial pressure was higher in the OC than NOC group in the LH phase ( P = 0.049) and lower in the HH than LH phase ( P = 0.014). Our results indicate that cycling estrogens/progestins can influence ventilatory, cardiovascular, and/or cerebrovascular physiology. NEW & NOTEWORTHY We have found sex differences in the cerebrovascular response to the Valsalva maneuver and standing. Men have greater cerebral vasoconstriction (or women have greater cerebral vasodilation) during late phase II of the Valsalva maneuver, and the cerebrovascular resistance index increases in men, but not in women, during standing. Furthermore, our findings indicate that both the menstrual cycle phase and oral contraceptive use can influence cardiovascular function both at rest and during active standing.

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