Rise In Venous Pressure Research Articles

Spontaneous Thoracic Spinal Epidural Hematoma During Pregnancy

Spontaneous Thoracic Spinal Epidural Hematoma During Pregnancy

Effect of positive end-expiratory pressure on central venous pressure in the closed and open thorax

Objective. The magnitude and mechanism of the rise of central venous pressure (CVP) after positive end-expiratory pressure (PEEP) among patients with cardiac disease is poorly understood. Therefore, the study aimed to compare the magnitude of change in CVP after PEEP in patients with TR (tricuspid regurgitation), high CVP, and high PCWP (pulmonary capillary wedge pressure) and in those with no TR, low CVP, and low PCWP. Additionally, we hypothesized that PEEP in the open thorax would also lead to a rise in CVP. Approach. This prospective, quasi-experimental study was conducted in patients undergoing cardiac surgery. Three consecutive readings of variables were obtained at 1 min intervals after PEEP (5 and 10 cm H2O) application in the closed and open thorax. Patients were stratified a priori into low CVP (<10 cm H2O) and high CVP (≥10 cm H2O), no TR and TR, and low PCWP (<15 mm Hg) and high PCWP (≥15 mm Hg) in the closed and open thorax. Main Results. Sixty-two patients were eligible for final analysis. The mean difference (MD) in ΔCVP (CVP10 cm H2O of PEEP—CVP zero end-expiratory pressure) was 2.33 ± 1.13 (95% CI, 2.04–2.62, P = 0.000) and 1.02 ± 0.77 (95% CI, 0.82–1.22, P = 0.000) in the closed and open thorax, respectively. The increase in CVP was higher among patients who had a lower CVP (2.64 ± 0.9 mm Hg versus 1.45 ± 1.17 mm Hg; p=0.000), in patients without TR (2.64 ± 0.97 mm Hg versus 2.14 ± 1.2 mm Hg, p=0.09) and in patients with a lower PCWP (2.4 ± 0.9 mm Hg versus 2.3 ± 1.4 mm Hg, p=0.67) at 10 cm H2O PEEP in the closed thorax. Significance. The rise in CVP was higher among patients without TR, low CVP, and low PCWP. Zero intrathoracic pressure in the open thorax did not abolish the effect of PEEP on CVP rise altogether.

Valsalva Retinopathy: A Case Report

Valsalva retinopathy is characterised by pre-retinal haemorrhage which presents with unilateral, sudden, painless diminution of vision. Pre-retinal haemorrhage caused by sudden rise in venous pressure was first termed as Valsalva haemorrhage by Duane TD in 1972. It is caused by rupture of superficial retinal capillaries due to increased intra-ocular venous pressure following increase in intra-thoracic or intraabdominal pressure. It resolves in few weeks or month and vision returns to normal depending on the location of the bleed on the retina. Observation, Nd:YAG (neodymium-doped yttrium aluminium garnet) laser and Argon laser hyaloidotomy, vitrectomy are effective treatment options for eyes with Valsalva retinopathy. Here we present a case of a 32 year old female with Valsalva retinopathy with subhyaloid haemorrhageafter an episode of vomiting who was treated with Nd:YAG laser hyaloidotomy with a good visual outcome.The novelty of this case report lies in the fact that although conservative management is practiced more often with similar prognosis, early intervention by Nd:YAG laser hyaloidotomycan benefit the patient with marked improvement and rapid recovery. Key words: Valsalva retinopathy, subhyaloid haemorrhage, Nd:YAG laser hyaloidotomy.

Henle Fiber Layer Hemorrhage in Macular Telangiectasia Type 2: Is Right Eye Dominance Coincidence or Consequence?

To summarize all reported cases of Henle fiber layer (HFL) hemorrhage in the absence of subretinal neovascularization (SRNV) in patients with macular telangiectasia type 2 (MacTel2) and to propose a mechanism for the right-sided predominance of this unique presentation. Perspective. Collection, review, and analysis of all cases in the literature and in the authors' databases of HFL hemorrhage in MacTel2, including analysis of baseline and follow-up multimodal retinal imaging findings of selected cases. Elucidation of the complex interplay of systemic venous pressure with the deep retinal capillary plexus and hypothesis regarding the right-sided predilection of HFL hemorrhage complicating MacTel2. Ten patients presented with a unilateral, characteristic radial macular hemorrhage within the HFL that affected only the right eye in all cases. Absence of SRNV was confirmed by fluorescein angiography and/or optical coherence tomography angiography. The hemorrhage resolved spontaneously in at least 7 of the 10 eyes. The HFL hemorrhage may plausibly be explained by dysfunction of the deep capillary plexus in MacTel2 combined with an acute rise in central venous pressure, for which the right side may be at increased risk. HFL hemorrhage can complicate MacTel2 in the absence of SRNV, and the radial pattern of blood affecting only the right eye is remarkable. The right eye predominance may be multifactorial in etiology. Related factors may include the right-sided predilection of MacTel2 and/or increased right-sided dural sinus drainage related to normal anatomical variation.

Posisi Pasien terhadap Tekanan Vena Sentral

This study aims to identify an increase in central venous pressure in patients given lateral or prone position interventions and to identify the rise in central venous pressure in patients given semi-fowler position intervention in the intensive care unit. This study uses a Quasi-Experimental method with a Case-Control design. The results obtained are the p-value of 0.000, meaning that the research significantly affects the positioning of the central venous pressure (CVP). In conclusion, there was an increase in the average CVP value before and after the passive position intervention was -1,967 cmH2O; on the other hand, there was a decrease in the average CVP value before and after the semi fowler position intervention was 1,867 cmH2O.&#x0D; &#x0D; Keywords: Supine and Semi Fowler Position, Central Venous Pressure

Valsalva retinopathy induced by handstand: a case report

BackgroundValsalva retinopathy is known to occur as a sudden preretinal or sub-internal limiting membrane hemorrhage induced by a rapid rise in venous pressure following increased intrathoracic or intraabdominal pressure. Here we report a case of Valsalva retinopathy that was probably induced by straining that occurred due to following a handstand.Case presentationA 15-year-old boy became aware of decreased visual acuity in his left eye immediately after doing a handstand for approximately 10 s during physical education class, and subsequently visited a local clinic on the same day. Upon examination, a vitreous hemorrhage (VH) in the posterior pole of the fundus was found in his left eye, and he was subsequently referred to our department 7 days later. Upon examination, the VH around the optic nerve head of the left eye appeared to be resolved, and an oval-shaped sub-internal limiting membrane (sub-ILM) hemorrhage was found in the superonasal side of the optic nerve head. No abnormalities were observed in the macular area. Four months later, the sub-ILM hemorrhage was found to have spontaneously resolved. Subsequent fluorescein angiography examinations revealed no abnormal findings at the lesion site.ConclusionsIn this patient, we hypothesize that the Valsalva retinopathy was induced by straining that occurred due to a handstand, and that the resultant sub-ILM hemorrhage progressed to VH.

Early rise in central venous pressure during a spontaneous breathing trial: A promising test to identify patients at high risk of weaning failure?

BackgroundThe spontaneous breathing trial (SBT) assesses the risk of weaning failure by evaluating some physiological responses to the massive venous return increase imposed by discontinuing positive pressure ventilation. This trial can be very demanding for some critically ill patients, inducing excessive physical and cardiovascular stress, including muscle fatigue, heart ischemia and eventually cardiac dysfunction. Extubation failure with emergency reintubation is a serious adverse consequence of a failed weaning process. Some data suggest that as many as 50% of patients that fail weaning do so because of cardiac dysfunction. Unfortunately, monitoring cardiovascular function at the time of the SBT is complex. The aim of our study was to explore if central venous pressure (CVP) changes were related to weaning failure after starting an SBT. We hypothesized that an early rise on CVP could signal a cardiac failure when handling a massive increase on venous return following a discontinuation of positive pressure ventilation. This CVP rise could identify a subset of patients at high risk for extubation failure.MethodsTwo-hundred and four mechanically ventilated patients in whom an SBT was decided were subjected to a monitoring protocol that included blinded assessment of CVP at baseline, and at 2 minutes after starting the trial (CVP-test). Weaning failure was defined as reintubation within 48-hours following extubation. Comparisons between two parametric or non-parametric variables were performed with student T test or Mann Whitney U test, respectively. A logistic multivariate regression was performed to determine the predictive value on extubation failure of usual clinical variables and CVP at 2-min after starting the SBT.ResultsOne-hundred and sixty-five patients were extubated after the SBT, 11 of whom were reintubated within 48h. Absolute CVP values at 2-minutes, and the change from baseline (dCVP) were significantly higher in patients with extubation failure as compared to those successfully weaned. dCVP was an early predictor for reintubation (OR: 1.70 [1.31,2.19], p<0.001).ConclusionsAn early rise in CVP after starting an SBT was associated with an increased risk of extubation failure. This might represent a warning signal not captured by usual SBT monitoring and could have relevant clinical implications.

Associations of left atrial volumes and Doppler filling indices with left atrial function in acute myocardial infarction.

SummaryRecent findings suggest that left atrial (LA) function is more strongly related to adverse prognosis than LA volumes. We aimed to evaluate the associations between LA volumes and Doppler filling indices with LA function. Echocardiographic LA volumes (LAVs), mitral valve early (MV‐E) and late (MV‐A) peak flow velocities, and mitral atrioventricular plane tissue‐Doppler early (TD‐e′) and late (TD‐a′) peak velocities were obtained in 320 patients with acute myocardial infarction (AMI) free from atrial fibrillation and more than moderate valvular disease. LA function was estimated as the LA emptying fraction (LAEF), that is 100× (LAVmax‐LAVmin)/LAVmax. LA reservoir volume was calculated as LAVmax‐LAVmin and LA transit volume as LV stroke volume‐reservoir volume. In restricted cubic spline regression analyses with multivariable adjustment, a reduced LAEF was strongly associated with smaller reservoir volume, larger transit volume, LAVmax, LAVpreA and especially LAVmin. MV‐E linearly increased with a lower LAEF, whereas MV‐A decreased but only below LAEF levels of approximately 45%. The resulting E/A ratio showed a sudden increase in LAEF levels below ~45%. Lower TD‐a′ was linearly associated with a lower LAEF. In conclusion, a reduced atrial function was associated with smaller LA reservoir volume, larger LA transit volume, lower TD‐a′, a non‐linear decrease in MV‐A and a non‐linear increase in E/A. Our findings are likely a reflection of the adaptation to sustain LV filling volume and counteracting a rise in pulmonary venous pressure in face of an enhanced LV end‐diastolic pressure.

Liver transplantation for acute liver failure due to hepatitis E in a pregnant patient.

Liver transplantation for acute liver failure due to hepatitis E in a pregnant patient.

Bilateral thalamic developmental venous variations (DVVs) draining into same internal cerebral vein: a case report and review with emphasis on DVVs with outflow restriction

Developmental venous variations (DVVs) are anatomic variations of normal transmedullary veins which are often discovered incidentally. Although they are accepted as benign compensatory venous drainage systems, they may become symptomatic or clinically significant due to flow-related causes. The fragile venous drainage systems increase vulnerability to in-out flow alterations. Increased inflow or decreased outflow causes rise in venous pressure, which may subsequently produce ischemic symptoms. Obstruction or stenosis of the collector vein is the most common cause of decreased outflow of a DVV. However, in the absence of collecting vein stenosis, venous hypertension may still exist due to volume overload. In case of multiple DVVs with single combined drainage pathway, functional outflow restriction may occur due to diminished capability of the vessel to adapt to pressure changes. In this report, we present a case with bilateral thalamic DVVs, which cause parenchymal amorphous calcification and drain into the left internal cerebral vein. A review of the literature on DVVs with outflow restriction including pathophysiological mechanisms is also discussed.

Improved cardiac filling facilitates the postprandial elevation of stroke volume in Python regius.

To accommodate the pronounced metabolic response to digestion, pythons increase heart rate and elevate stroke volume, where the latter has been ascribed to a massive and fast cardiac hypertrophy. However, numerous recent studies show that heart mass rarely increases, even upon ingestion of large meals, and we therefore explored the possibility that a rise in mean circulatory filling pressure (MCFP) serves to elevate venous pressure and cardiac filling during digestion. To this end, we measured blood flows and pressures in anaesthetized Python regius The anaesthetized snakes exhibited the archetypal tachycardia as well as a rise in both venous pressure and MCFP that fully account for the approximate doubling of stroke volume. There was no rise in blood volume and the elevated MCFP must therefore stem from increased vascular tone, possibly by means of increased sympathetic tone on the veins. Furthermore, although both venous pressure and MCFP increased during volume loading, there was no evidence that postprandial hearts were endowed with an additional capacity to elevate stroke volume. In vitro measurements of force development of paced ventricular strips also failed to reveal signs of increased contractility, but the postprandial hearts had higher activities of cytochrome oxidase and pyruvate kinase, which probably serves to sustain the rise in cardiac work during digestion.

Radius Maumenee Syndrome

SummaryOcular injection and increased IOP from elevated episcleral venous pressure are most frequently caused by carotid cavernous fistula. Other causes include large vessel venous obstruction (venous sinus thrombosis and superior vena cava syndrome), Sturge–Weber syndrome, scleritis, thyroid‐related orbitopathy and orbital tumours or orbital varices (Radius &amp; Maumenee 1978; Rhee et al. 2009). Additionally, idiopathic rise in episcleral venous pressure, known as Radius–Maumenee syndrome, can lead to ocular injection with elevated IOP (Radius &amp; Maumenee 1978). The syndrome was originally described by Minas &amp; Podos (1968). The diagnosis is based on the clinical findings of elevated IOP causing glaucomatous optic nerve and visual field damage in association with an open angle and dilated episcleral veins. The diagnosis of Radius–Maumenee syndrome can only be made with confidence after intra‐orbital and intracranial pathology mentioned above has been excluded by MRI.Two case reports will illustrate the typical features of this rare cause of glaucoma.

Effects of head down tilt on episcleral venous pressure in a rabbit model

In humans, changing from upright to supine elicits an approximately 10 mmHg increase in cephalic venous pressure caused by the hydrostatic column effect, but episcleral venous pressure (EVP) and intraocular pressure (IOP) rise by only a few mmHg. The dissociation of the small increases in IOP and EVP compared to the larger increase in cephalic venous pressure suggests a regulatory mechanism controlling EVP. The aim of the present study was to determine if the rabbit model is suitable to study the effects of postural changes on EVP despite its short hydrostatic column. In anesthetized rabbits (n = 43), we measured arterial pressure (AP), IOP, and orbital venous pressure (OVP) by direct cannulation; carotid blood flow (BFcar) by transit time ultrasound, heart rate (HR) by digital cardiotachometer, and EVP with a servonull micropressure system. The goal of the protocol was to obtain measurement of supine EVP for ≈10 min, followed by ≈10 min of EVP measurement with the rabbit in a head down tilt. The data were analyzed by paired t-tests and the results reported as the mean ± standard error of the mean. In a separate group of animals (n = 35), aqueous flow was measured by fluorophotometry. This protocol entailed measurement of aqueous flow in the supine position for ≈60 min, followed by ≈60 min of aqueous flow measurement with the rabbit in a head down tilt. From supine to head down tilt, AP and BFcar were unchanged, IOP increased by 2.3 ± 0.4 mmHg (p < 0.001), EVP increased by 2.4 ± 0.4 mmHg (p < 0.001), OVP increased by 2.5 ± 0.2 mmHg (p < 0.001) and HR decreased by 9 ± 3 bpm (p = 0.002). Head down tilt caused no significant change in aqueous flow. Although the hydrostatic column in the rabbit is shorter than humans, the rabbit model permits sufficiently sensitive measurements of the pressures and systemic parameters likely involved in the EVP responses to posture change. The present results indicate directionally similar EVP and IOP responses to tilt as occur in humans and, as in humans, the responses are smaller than would be expected from the change in the hydrostatic column height. Also, as in humans, the model reveals no change in aqueous flow during head down tilt. We conclude the rabbit model is appropriate for studying the mechanisms responsible for the relative immunity of EVP and IOP to posture change.

Imaging of traumatic adrenal injury

Traumatic adrenal injury is a relatively rare event, reported in 0.15 to 4 % of blunt abdominal trauma cases. The location of the adrenal glands, protected deeply within the retroperitoneum, accounts for the rarity of adrenal trauma. These injuries are unilateral in 75 to 90 % of cases and most commonly afflict the right adrenal gland. While no specific clinical symptoms or signs point directly to adrenal injury, and isolated adrenal injury is rare, the presence of adrenal injury can be an indicator of severe trauma. In fact, mortality rates in series of adrenal injuries range from 7 to 32 %. The most common associated injuries affect the liver, ribs, kidney, or spleen. Three theories of adrenal injury from blunt trauma have been proposed: (1) acute rise in intra-adrenal venous pressure due to compression of the IVC during impact, (2) crushing between the spine and surrounding organs, and (3) deceleration forces shearing the small adrenal arterioles. The most common imaging features include a 2-3-cm oval hematoma, irregular hemorrhage obliterating the adrenal gland, periadrenal hemorrhage or fat stranding, and uniform adrenal swelling with increased attenuation. The differential diagnosis of adrenal abnormalities on trauma CT includes adenoma, carcinoma, myelolipoma, metastases, pheochromocytoma, and tuberculosis. Preexisting adrenal disorders can predispose the adrenal to injury with minor trauma. Most adrenal traumatic injuries are managed conservatively.

Experimental evaluation of portal venous pulsatile flow synchronized with heartbeat intervals: effects of vascular clamping on portal hemodynamics.

We previously showed that blood flow in the portal vein was pulsatile and influenced by both the inferior vena cava and the arterial system in a complex manner (Nihei et al., 38:141-149, 2011). The objective of the present study is to identify determinants of blood flow and to clarify the source of pulsatile flow in the portal vein. Three-breed terminal crossbreed mini-pigs underwent general anesthesia. Pressure and flow in the portal vein, inferior vena cava, hepatic artery, and mesenteric artery were measured simultaneously. Vascular occluders were placed in the inferior vena cava, hepatic artery, and mesenteric artery to examine the effects of clamping on portal venous flow. Clamping of the mesenteric artery altered pressure and flow waves in the portal vein to waveforms similar to those in the inferior vena cava. Waves resembling those of the inferior vena cava superimposed on portal venous flow appeared later than waves of the inferior vena cava. Clamping of the inferior vena cava promptly altered portal venous pressure and flow. Because clamping of the inferior vena cava led to a sharp rise in portal venous pressure, detailed evaluations were not feasible. Clamping of the hepatic artery had no effect on flow-wave pulsation in the portal vein. In the hepatic circulation, flow-wave pulsation in the portal vein is influenced by flow in the inferior vena cava via the sinusoids and by flow in the mesenteric artery via the capillary vessels of the intestine.

Fluid balance monitoring by cuff‐occluded rate of rise of peripheral venous pressure in haemodialysis patients

Cuff-occluded rate of rise of peripheral venous pressure has been proposed to reflect volume changes in experimental studies. The aim of this study was to evaluate changes in cuff-occluded rate of rise of peripheral venous pressure associated with fluid removal by haemodialysis in six adult patients with chronic renal failure on intermittent haemodialysis. Measurements were carried out before and after each haemodialysis session. The volume of fluid removed (indexed to body surface area) linearly correlated with changes in cuff-occluded rate of rise of peripheral venous pressure (r = 0.84; r(2) = 0.70; p = 0.037). Cuff-occluded rate of rise of peripheral venous pressure may be feasible for future clinical monitoring of individual fluid balance.

Pulmonary Venous Hypertension- An On Going Quest for Treatment: Is PDE5 Inhibition the Right Solution?

Pulmonary venous hypertension is pulmonary hypertension resulting from elevated left sided filling pressures. This may result from chronic elevation of left atrial pressures from heart failure; either heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) or from valvular heart disease. This is classified as Group 2 pulmonary hypertension in the Dana point classification [1]. Pulmonary hypertension due to left heart disease is defined as mean pulmonary arterial pressure (mPAP) greater than or equal to 25 mm Hg, pulmonary capillary wedge pressure (PCWP) of greater than or equal to 15 mm Hg and pulmonary vascular resistance (PVR) greater than 3WU. Chronic elevation of left ventricular end diastolic pressures will result in increased left atrial pressures, initially causing passive congestion and rise in pulmonary venous pressures and resulting pulmonary arterial hypertension. This usually reverses readily with diuresis and lowering the left atrial pressures. Transpulmonary gradient (TPG = mPAP – PCWP) is normal at this stage. Continued elevation in PCWP may result in pulmonary vasoconstriction and reactive pulmonary hypertension where the TPG is greater than 12 mm HG and pulmonary vascular resistance (PVR) is greater than 3WU. This reactive pulmonary hypertension responds to diuresis and pulmonary vasodilation with agents such as nipride, nesiritide, inhaled nitric oxide or milrinone. Over time, the passive congestion and vasocontiction causes pulmonary vascular remodeling resulting in abnormalities of elastic fibres, smooth muscle proliferation and endothelial proliferation causing pulmonary arterial remodeling and resulting obliterative arteriopathy which is in part mediated by endothelin and is histologically indistinguishable from pulmonary arterial hypertension [2] Table 1. Epidemiology

Postoperative intracranial haemorrhage and remote cerebellar haemorrhage

Dear Editor, We have read with great interest the exhaustive paper of Seifman et al. about “Postoperative intracranial haemorrhage: a review” published inNeurosurgical Review January 2011 [10]. However, we think that the chapter “remote intracranial haemorrhage” particularly the emerging field of “remote cerebellar hemorrhage” deserves further elaboration and attempts to highlight and clarify the pathogenetic mechanisms. Cerebellar haemorrhage after supratentorial craniotomy has been reported in 0.6–4.9% of all supratentorial craniotomies particularly after unruptured aneurysms surgery, epilepsy surgery and spinal surgery with opening of the dura [1–7, 9, 10, 12]. Although its venous origin has been recognised, the pathogenesis of cerebellar haemorrhage is unclear. Haemorrhage is often characterised by a typical, streaky bleeding pattern due to blood spreading in the upper cerebellar vermis and foliae (“Zebra sign”) [1]. The proposed pathogenetic mechanisms include: (a) increase of venous and venular transmural pressure due to the reduction of intracranial pressure caused by removal of a space-occupying mass and enhanced by CSF drainage; (b) increase of venous pressure as a consequence of head position; (c) tearing of superior vermian veins due to mechanical shifting of the cerebellum which results from intraoperative and or postoperative CSF withdrawal; and (d) transtentorial pressure gradient between the supratentorial and infratentorial venous system due to withdrawal of CSF [1, 8, 11, 12]. In our opinion, cerebellar haemorrhage may be caused by an increase in transmural venous pressure (intravascular venous pressure minus extravascular pressure; that is, in normal status, equal to intracranial pressure) related either to venous pressure rise favoured by head position or to intracranial pressure decrease determined by CSF withdrawal or through the concomitance of both factors. We suggest that the main decisive critical factor for this peculiar complication is a “normal” intracranial pressure [5]. This feeling originates from the fact that surgery for unruptured aneurysms, drug-resistant temporal lobe epilepsy and spine pathology shares a condition of normal intracranial pressure. A state of normal intracranial pressure makes transmural pressure forces balance at level of venous–venular system more sensitive to changes related either to an increase of venous pressure and/or to CSF withdrawal. The rare occurrence of cerebellar haemorrhage when surgery is performed in conditions of high intracranial pressure, such as in ruptured aneurysms, also supports our point of view. Therefore, in order to avoid remote cerebellar haemorrhage, above all when surgery is performed in state of likely normal intracranial pressure, special attention should be paid, during the pre-, intraand postoperative management, to the factors related to the increase of transmural venous pressure such as head position, CSF withdrawal and drugs that reduce intracranial pressure [5].

Valsalva haemorrhagic retinopathy after push-ups

An 18-year-old man presented with sudden painless blurring of vision in the right eye, after a few rounds of push-up exercises. He was a college student. Our patient had no history of vascular disease or blood dyscrasias. His right vision was 20/200, and his left vision was 20/20. Retinal examination of the right eye showed a crescent shaped subhyaloid haemorrhage overlying the macula (figure A). Whole blood count, prothrombin time, and activated partial thromboplastin time, were within normal limits. A Nd:YAG laser hyaloidectomy was done, and 3 months later our patients' right vision had improved to 20/40 (figure B). Valsalva retinopathy occurs because of a sudden rise in intraocular venous pressure, causing retinal capillaries to spontaneously rupture. Push-up exercises are valsalva manoeuvres that increase intrathoracic pressure against a closed glottis, causing diminished venous return to the heart, reduced stroke volume, and an increase in venous system pressure. The outcome of valsalva haemorrhagic retinopathy is generally good, with newer treatments such as laser hyaloidectomy improving recovery time.

Estimation of peripheral venous pressure and cuff-occluded rate of rise of peripheral venous pressure in healthy adults

Estimation of peripheral venous pressure and cuff-occluded rate of rise of peripheral venous pressure in healthy adults