Is critical closing pressure a determinant of neonatal cerebral blood flow?

1993 ◽  
Vol 33 (3) ◽  
pp. 223-224
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Critical Closing Pressure ◽  
Closing Pressure

Experimental cerebral hemodynamics

1974 ◽  
Vol 41 (5) ◽  
pp. 597-606 ◽  
Author(s):  
Richard C. Dewey ◽  
Heinz P. Pieper ◽  
William E. Hunt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Brain Blood Flow ◽  
Vasomotor Tone ◽  
Vascular Bed ◽  
Critical Closing Pressure ◽  
Closing Pressure

✓ Application of Burton's concept of the critical closing pressure to experimental data on brain-blood flow in the monkey suggests that perfusion pressure, not vascular bed resistance, is the primary variable affecting cerebral blood flow. Perfusion pressure for the cerebral circulation is the mean arterial pressure minus the critical closing pressure (MAP — CCP). Vasomotor tone and intracranial pressure are the major determinants of the critical closing pressure. Changes in either of these variables, therefore, affect perfusion pressure and flow. Data on brain-blood flow at fixed vasomotor tone obtained over wide pressure ranges show little change in vascular bed resistance despite significant changes in flow. The diameter of resistance vessels probably does not change significantly throughout the normal physiological range of cerebral blood flow. The limits of the critical closing pressure in the anesthetized monkey are from 10 to 95 mm Hg. Using these limits, and beginning with the average values for MAP and CCP in 11 awake monkeys breathing room air, the authors present theoretical flow curves in response to changes in intracranial pressure and mean arterial pressure that closely approximate the data reported in man.

Cessation of Diastolic Cerebral Blood Flow Velocity: The Role of Critical Closing Pressure

2013 ◽  
Vol 20 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Georgios V. Varsos ◽  
Hugh K. Richards ◽  
Magdalena Kasprowicz ◽  
Matthias Reinhard ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Critical Closing Pressure ◽  
Closing Pressure

scholarly journals Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects

2017 ◽  
Vol 37 (8) ◽  
pp. 2691-2705 ◽  
Author(s):  
Wesley B Baker ◽  
Ashwin B Parthasarathy ◽  
Kimberly P Gannon ◽  
Venkaiah C Kavuri ◽  
David R Busch ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Continuous Monitoring ◽  
Human Subjects ◽  
Correlation Spectroscopy ◽  
Invasive Technique ◽  
Windkessel Model ◽  
Arterial Blood ◽  
Critical Closing Pressure ◽  
Closing Pressure

The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP −  CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.

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.

Abolition of autoregulation of renal blood flow by acetylcholine

1964 ◽  
Vol 207 (1) ◽  
pp. 123-127 ◽  
Author(s):  
Victor E. Nahmod ◽  
Alfredo Lanari
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Run Off ◽  
Critical Closing Pressure ◽  
Flow Pressure ◽  
Renal Blood Flow Autoregulation ◽  
Autoregulatory Mechanism ◽  
Closing Pressure

In order to study the mechanism of autoregulation of renal blood flow, 36 mongrel dogs were connected in parabiosis according to the Brull method. The following determinations were made: a) flow/pressure curves in innervated and denervated kidneys and b) acetylcholine and arterenol infusion in innervated kidneys. The critical closing pressure and the "run-off" index were also determined in all cases. The results of these experiments show the existence of renal blood flow autoregulation in innervated, denervated, and arterenol-infused kidneys, and the abolition of the autoregulatory mechanism in the acetylcholine-infused kidneys. The run-off index showed a better correlation with renal resistance than with critical closing pressure.

scholarly journals Critical Closing Pressure Determined with a Model of Cerebrovascular Impedance

2012 ◽  
Vol 33 (2) ◽  
pp. 235-243 ◽  
Author(s):  
Georgios V Varsos ◽  
Hugh Richards ◽  
Magdalena Kasprowicz ◽  
Karol P Budohoski ◽  
Ken M Brady ◽  
...  
Keyword(s):  
Blood Flow ◽  
The Novel ◽  
Brain Vessels ◽  
Arterial Blood ◽  
Critical Closing Pressure ◽  
Physiological Values ◽  
Relationship Of ◽  
The Relationship ◽  
Closing Pressure ◽  
Brain Monitoring

Critical closing pressure (CCP) is the arterial blood pressure (ABP) at which brain vessels collapse and cerebral blood flow (CBF) ceases. Using the concept of impedance to CBF, CCP can be expressed with brain-monitoring parameters: cerebral perfusion pressure (CPP), ABP, blood flow velocity (FV), and heart rate. The novel multiparameter method (CCPm) was compared with traditional transcranial Doppler (TCD) calculations of CCP (CCP1). Digital recordings of ABP, intracranial pressure (ICP), and TCD-based FV from previously published studies of 29 New Zealand White rabbits were reanalyzed. Overall, CCP1 and CCPm showed correlation across wide ranges of ABP, ICP, and PaCO2 ( R = 0.93, P < 0.001). Three physiological perturbations were studied: increase in ICP ( n = 29) causing both CCP1 and CCPm to increase ( P < 0.001 for both); reduction of ABP ( n = 10) resulting in decrease of CCP1 ( P = 0.006) and CCPm ( P = 0.002); and controlled increase of PaCO2 ( n = 8) to hypercapnic levels, which decreased CCP1 and CCPm, albeit insignificantly ( P = 0.123 and P = 0.306 respectively), caused by a spontaneous significant increase in ABP ( P = 0.025). Multiparameter mathematical model of critical closing pressure explains the relationship of CCP on brain-monitoring variables, allowing the estimation of CCP during cases such as hypercapnia-induced hyperemia, where traditional calculations, like CCP1, often reach negative non-physiological values.

Distribution of blood flow and the pressure-flow relations of the whole lung

1965 ◽  
Vol 20 (2) ◽  
pp. 175-183 ◽  
Author(s):  
J. B. West ◽  
C. T. Dollery
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pressure Flow ◽  
Mechanical Effects ◽  
Critical Closing Pressure ◽  
Flow Through ◽  
Pulmonary Arterial ◽  
Closing Pressure ◽  
Radioactive Gases

Effects of changes in pulmonary arterial (Pa), venous (Pv), and alveolar (Pa) pressures on the over-all pressure-blood flow relations of an isolated dog lung have been re-examined. In the preparation used, the distribution of blood flow was predictable from previous measurements with radioactive gases. The results showed that the pressure-flow relations of the whole lung were greatly affected by the distribution of blood flow within it. For example, the pulmonary vascular resistance (PVR) of the lung depended on whether all the lung was perfused with blood or not, and thus whether there was an unperfused zone at the top of the lung where Pa was less than Pa ( zone 1). Again the pressure-flow relations of the lung were shown to depend on how much of the lung had a Pv less than Pa ( zone 2), and how much had a Pv which exceeded Pa ( zone 3). The effects on PVR of changing Pv or Pa could be explained on this basis. No evidence of a critical closing pressure in the vessels of the expanded lung was found. It was concluded that although the over-all pressure-flow relations of the whole lung were complicated, the flow through individual vessels could be accounted for by the simple mechanical effects of pressures inside and outside the vessels. hydrostatic effect; pulmonary vascular resistance; Starling resistor; vascular waterfall; critical closing pressure Submitted on May 4, 1964

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