Venous Pulse Pressure Research Articles

Spontaneous Intrinsic Hepatic Vascular Oscillations

The liver is well known as a large blood reservoir that can shift both stressed and unstressed volumes passively and actively in response to changes in portal venous and hepatic arterial blood flow, inflow and outflow blood pressures, autonomic nervous stimulation, and various humoral and pathophysiological factors. Not described is the characteristic of the liver to intrinsically modulate its own vascular pressure and volume independent of extrinsic factors.METHODSMale Holtzman rats (n=5) were anesthetized (30 mg/kg sodium pentobarbital, i.p.) and heparinized (500 IU/kg, i.v.), the portal vein and inferior vena cava were isolated and cannulated, the liver was flushed with room temperature normal saline, and the liver quickly removed. Each liver was mounted on a scale in a 37°C chamber (95% O2‐5% CO2) and pump‐perfused (Masterflex) with donor rat blood at a baseline 1 ml/min/g of tissue. The hepatic venous pressure (Phv) was regulated by raising and lowering the blood reservoir. At each Time (see table), portal venous oscillations were counted over 3 to 12 min and the portal venous wavelet pulse pressures (Ppv) were measured over at least 40 wavelets.RESULTSThe portal venous pressures of 3 of the 5 livers oscillated spontaneously. One lasted only 26 min while the others went on for over 200 min. The characteristics of these oscillations varied widely from animal to animal, but there usually was an irregular cycle length and uneven wavelet magnitude that tended to degrade to a diminished size with higher frequency over time (see Figure 1). Rat Time (Min) Maneuver Mean Portal Venous Pulse Pressure (mmHg) Frequency (Wavelets/Min) Frequency (Hz) Cycle Length (Sec) 1 0 Baseline 2.1 ± 0.9 (SD) 8.08 0.135 7.42 95 Baseline 1.5 ± 0.8 16.10 0.268 3.73 107 Change Phv 2.5 ± 1.3 17.00 0.283 3.53 (0 to 10 mmHg) (P<0.001 vs. 95 Min Baseline) 180 Baseline 1.3 ± 0.5 18.67 0.311 3.21 2 0 Baseline 0.8 ± 0.4 14.42 0.240 4.16 60 Baseline 0.4 ± 0.3 20.00 0.333 3.00 130 Baseline 0.4 ± 0.2 23.78 0.396 2.52 3 0 Baseline 0.6 ± 0.3 8.67 0.144 6.92 CONCLUSIONSThis is a very limited data set, providing more questions than answers, but it opens a curiosity to much more investigation to understand the function of these intrinsic hepatic vascular oscillations under normal, reflex, and pathophysiological conditions.

The association between retinal vein pulsation pressure and optic disc haemorrhages in glaucoma.

PurposeTo explore the potential relationship between optic disc haemorrhage, venous pulsation pressure (VPP), ocular perfusion pressures and visual field change in glaucomatous and glaucoma suspect eyes.Materials and methodsThis prospective observational study examined 155 open angle glaucoma or glaucoma suspect eyes from 78 patients over 5 years. Patients were followed with 3 monthly non-mydriatic disc photographs, 6 monthly standard automated perimetry and annual ophthalmodynamometry. The number of disc haemorrhages in each hemidisc was counted across the study period. Visual field rate of change was calculated using linear regression on the sensitivity of each location over time, then averaged for the matching hemifield. VPP and central retinal artery diastolic pressure (CRADP) were calculated from the measured ophthalmodynanometric forces (ODF). The difference between brachial artery diastolic pressure (DiastBP) and CRADP was calculated as an index of possible flow pathology along the carotid and ophthalmic arteries.ResultsMean age of the cohort was 71.9 ± 7.3 Years. 76 out of 155 eyes (49%) followed for a mean period of 64.2 months had at least 1 disc haemorrhage. 62 (81.6%) of these 76 eyes had recurrent haemorrhages, with a mean of 5.94 recurrences over 64.2 months. Using univariate analysis, rate of visual field change (P<0.0001), VPP (P = 0.0069), alternative ocular perfusion pressure (CRADP–VPP, P = 0.0036), carotid resistance index (DiastBP–CRADP, P = 0.0108) and mean brachial blood pressure (P = 0.0203) were significantly associated with the number of disc haemorrhages. Using multivariate analysis, increased baseline visual field sensitivity (P = 0.0243, coefficient = 0.0275) was significantly associated with disc haemorrhage, in conjunction with higher VPP (P = 0.0029, coefficient = 0.0631), higher mean blood pressure (P = 0.0113, coefficient = 0.0190), higher carotid resistance index (P = 0.0172, coefficient = 0.0566), and rate of visual field loss (P<0.0001, coefficient = -2.0695).ConclusionsHigher VPP was associated with disc haemorrhage and implicates the involvement of venous pathology, but the effect size is small. Additionally, a greater carotid resistance index suggests that flow pathology in the ophthalmic or carotid arteries may be associated with disc haemorrhage.

Intraocular Pressure Reduction Is Associated with Reduced Venous Pulsation Pressure.

PurposeTo explore whether alterations in intraocular pressure (IOP) affect vein pulsation properties using ophthalmodynamometric measures of vein pulsation pressure.Patients and MethodsGlaucoma patients had two retinal vein pulsation pressure (VPP) measurements from upper and lower hemiveins performed by ophthalmodynamometry at least 3 months apart. All subjects had VPP and IOP recorded at two visits, with standard automated perimetry, central corneal thickness (CCT) recorded at the initial visit. Where venous pulsation was spontaneous ophthalmodynamometry could not be performed and VPP was considered equal to IOP. Change in VPP was calculated and binarized with reduction in pressure scored 1 and no change or increase scored as 0. Data analysis used a mixed logistic regression model with change in VPP as response variable and change in IOP, visual field loss (mean deviation), CCT and time interval as explanatory variables.Results31 subjects (20 females) with mean age 60 years (sd 11) were examined with change in VPP being significantly associated with change in IOP (odds ratio 1.6/mmHg, 95% CI 1.2 to 2.1 in the glaucoma patients but not suspect patients (p = 0.0005).ConclusionChange in VPP is strongly associated with change in IOP such that a reduced intraocular pressure is associated with a subsequent reduction in VPP. This indicates that reduced IOP alters some retinal vein properties however the nature and time course of these changes is not known.

Contact lens dynamometry influences the systemic blood circulation: clinical significance

The diastolic and systolic pressure in the ophthalmic artery (OAPdia, OAPsys) as well as the venous pulsation pressure (VPP) can be determined by contact lens dynamometry (CLD). With these parameters, carotid artery stenosis, ocular perfusion, e.g., in glaucoma patients and the cerebrospinal pressure can be examined indirectly. In the underlying study comparative data were collected and it was investigated to what extent CLD itself leads to changes of the systemic blood pressure. In the course of a prospective trial CLD was performed in 162 eyes of 81 healthy volunteers (mean age 41.0 ± 17.3 years). VPP, OAPdia and OAPsys were measured. A mean was calculated from 5 single readings. Directly before and after CLD automated blood pressure measurements according to Riva-Rocci (RR) and the heart rate were obtained in both arms. In the entire group, the mean VPP was 21 ± 9 mmHg on the right side and 19 ± 8 mmHg on the left side. The mean OAPdia was 60 ± 14 mmHg on the right and 67 ± 14 mmHg on the left side. The mean OAPsys was 91 ± 17 and 101 ± 21 mmHg, respectively. The mean variation coefficient from 5 single readings was 13/16 % for VPP (right/left), 7.4/8.2 % for OAPdia and 6.2/6.2 % for OAPsys. The difference between right and left eyes concerning OAPdia and OAPsys was statistically significant (Wilcoxon test; p < 0.001). VPP and OAPsys were not correlated with age, OAPdia showed a weak correlation with age on the right side (Spearman R = 0.23; p = 0.03). Blood pressure (RR) dropped from a mean 137/84 to 135/82 mmHg in the right arm and from 135/84 to 132/83 mmHg in the left arm. The change of the diastolic values of the right side and of the systolic values of the left side reached statistical significance (p < 0.05). The difference of the systolic blood pressure and the heart rate before and after CLD were weakly correlated (Spearman R = - 0.28; p = 0.01). The extent of the systemic blood pressure drop was not correlated with the maximum force affecting the globe. The slightly lower blood pressure after CLD could be related to the oculocardiac reflex. This has to be confirmed in further trials with continuous blood pressure determination. In agreement with literature reports, significant differences between right and left eyes were found regarding OAPdia and OAPsys.

Impact of lower body negative pressure induced hypovolemia on peripheral venous pressure waveform parameters in healthy volunteers

Lower body negative pressure (LBNP) creates a reversible hypovolemia by sequestrating blood volume in the lower extremities. This study sought to examine the impact of central hypovolemia on peripheral venous pressure (PVP) waveforms in spontaneously breathing subjects. With IRB approval, 11 healthy subjects underwent progressive LBNP (baseline, −30, −75, and −90 mmHg or until the subject became symptomatic). Each was monitored for heart rate (HR), finger arterial blood pressure (BP), a chest respiratory band and PVP waveforms which are generated from a transduced upper extremity intravenous site. The first subject was excluded from PVP analysis because of technical errors in collecting the venous pressure waveform. PVP waveforms were analyzed to determine venous pulse pressure, mean venous pressure, pulse width, maximum and minimum slope (time domain analysis) together with cardiac and respiratory modulations (frequency domain analysis). No changes of significance were found in the arterial BP values at −30 mmHg LBNP, while there were significant reductions in the PVP waveforms time domain parameters (except for 50% width of the respiration induced modulations) together with modulation of the PVP waveform at the cardiac frequency but not at the respiratory frequency. As the LBNP progressed, arterial systolic BP, mean BP and pulse pressure, PVP parameters and PVP cardiac modulation decreased significantly, while diastolic BP and HR increased significantly. Changes in hemodynamic and PVP waveform parameters reached a maximum during the symptomatic phase. During the recovery phase, there was a significant reduction in HR together with a significant increase in HR variability, mean PVP and PVP cardiac modulation. Thus, in response to mild hypovolemia induced by LBNP, changes in cardiac modulation and other PVP waveform parameters identified hypovolemia before detectable hemodynamic changes.

Central retinal venous pulsation pressure in different stages of primary open-angle glaucoma

BackgroundTo evaluate the central retinal venous pulsation pressure (CRVPP) in patients with intraocular pressure (IOP)-controlled early, moderate and advanced open-angle glaucoma and a healthy control group.MethodsCRVPP was measured with a...

Central Venous Pulsations

The translaminar pressure gradient (TLPG) is largely influenced by the difference between intraocular pressure (IOP) and cerebrospinal fluid pressure (CSFP), but modulated by the buffering effect of orbital tissue and pia mater, which limits the reduction in retrolaminar tissue pressure as intracranial CSFP falls below 0 mm Hg. Across the lamina cribrosa, the central retinal vein experiences the greatest pressure gradient (TLPG) of any vein in the body. When CSFP rises, the minimum IOP required to induce venous pulsation pressure (VPP) rises with CSFP (r=0.95, slope=0.90). Lowering IOP in glaucoma patients leads to a reduction in VPP (P=0.0003). The normal human central retinal vein endothelial cells in the lamina region resemble typical arterial endothelia and are quite unlike other venous cells. It is likely that the TLPG is increasing retinal vein shear and in glaucoma this effect is likely to be increased with possible wall effects.

Retinal Vein Pulsation Is in Phase with Intracranial Pressure and Not Intraocular Pressure

As efforts to noninvasively measure intracranial pressure (ICP) increase, we thought it important to investigate the timing of retinal venous pulsation in relation to the intraocular and intracranial pressure pulses. Neurosurgical patients undergoing continuous direct ICP monitoring had video recordings of ICP, IOP, and retinal venous pulsation waveforms taken with constant timing relative to the cardiac cycle using pulse oximetry. Video frames of the maxima and minima of these parameters, including retinal vein diameter, were identified. The times from pulse oximetry "beep" to these parameters were measured and converted into a percentage of the respective cardiac cycle. A total of 338 measurements from nine subjects with a mean age of 39 years, mean ICP of 4.4 mm Hg and IOP 15.1 mm Hg were taken. Vein diameter minima occurred an insignificant 0.6% of cardiac cycle before ICP minima (P = 0.6620) and a significant 3.2% after IOP minima (P = 0.0097) and significantly later than IOP (51%) and ICP maxima (74%, all P < 0.0001). Maximum vein diameter occurred an insignificant 2.0% before IOP maxima (P = 0.2267) and was significantly different from IOP and ICP minima (P < 0.00001). Mean venous pulsation pressure between the two eyes was significantly associated with ICP (r = 0.89, P = 0.0075). During pulsation, central retinal vein collapse occurs in time with IOP and ICP diastole. Venous collapse is not induced by intraocular systole. These results suggest that ICP pulse pressure dominates the timing of venous pulsation.

Inaccuracy of pulse oximetry in patients with severe tricuspid regurgitation

The accuracy of pulse oximetry was studied in a group of patients with severe tricuspid regurgitation. Measurements of arterial oxygen saturation from a finger and an ear probe were compared with those from a radial arterial blood sample analysed in vitro. Lower values were obtained using the pulse oximeter; the difference ranged from +2% to -11%. The discrepancies between pulse oximeter and laboratory oximeter readings were greater in this group of patients than in a control group who did not have tricuspid regurgitation. There was, however, no correlation between the magnitude of this discrepancy and either the peak central venous pressure or the venous pulse pressure.

Pulse Oximetry and Circulatory Kinetics Associated with Pulse Volume Amplitude Measured by Photoelectric Plethysmography

Through a catheter placed in a superficial vein on the finger, we observed a pulsatile venous pressure. To delineate the relationship between the pulsatile venous pressure and the pulse volume amplitude (PVA) recorded by photoelectric plethysmography (PEPG), both tracings were simultaneously recorded. When the PVA changed acutely or gradually, the venous pulse pressure and mean venous pressure simultaneously followed the same trend. We also found that mean PVO2 (135 mm Hg) was greater when the PVA and venous pulse pressure increased above the level (50 mm Hg) observed when they decreased. These findings suggested that the finger pulse detected by PEPG, as well as by pulse oximetry, is caused by pulsations in veins rather than by pulsations in arterial beds. In experiments to evaluate the validity of this hypothesis, we found that the average value of hemoglobin saturation (%SaO2) measured by the pulse oximeter of the dependent fingertip and finger base when dependent was 1.5% and 7.8% lower than when the fingertip and finger base were elevated. Also, the PVA detected by the pulse oximeter followed the same trend as %SaO2. This finding was explained by venous congestion in the dependent finger. On the basis of the high venous pressure, the behavioral trends between the PVA and venous pressure, the high PVO2, and the low %SaO2 and PVA in the dependent finger, we conclude that the PVA of the PEPG is determined mainly by venous pulse volume generated by shunting of arterial pulse via open arteriovenous (AV) anastomoses in the cutaneous circulation.

Arterial and venous pressures in the human umbilical cord

Measurements of the pressure in the umbilical arteries and vein were made during eleven cesarean sections performed under general anesthesia. The maternal blood pressure was recorded at the same time. Nine of the babies were normal with no signs of depression. In 8 cases the average umbilical arterial pressure was 88 mm. Hg with an average pulse pressure of 12 mm. Hg. In 3 of the cases arterial spasm precluded measurement of the arterial pulse pressure. In the umbilical vein the average pressure was 41 mm. Hg and no venous pulse pressure was observed. The high venous pressure is discussed in the light it throws on the pressure gradients of the placenta. A further observation was made at the fourteenth week of pregnancy. The lower transplacental pressure gradient which was present suggests that the modes of transplacental interchange between fetus and mother become modified as pregnancy proceeds and the fetus assumes its full role as the organizer of development.