Venous hemodynamics. Base equations

The hydrodynamics in tubes with inert walls collapsed by a negative transmural pressure (inside pressure minus outside pressure) set up a fundamental and original approach in venous hemodynamics. Mechanisms of flow regulation and flow limitation can occur especially when the upstream pressure is held constant or when the average flow speed in a cross-section equals the local pressure waves speed. The three baseline equations on mechanics are required to demonstrate these properties: --the tube law, --the equation of motion, --the equation of continuity. It is shown that the behaviour of the tube varies with the nature of the flow (subcritical, critical or supercritical, subsonic, sonic or supersonic, according to the aerodynamics). Though this study does not take all the physiological and biological data into account, it includes indeed the three fundamental aspects on mechanics of the veins. The rheologic equation on the state of the venous wall, normal or pathologic, plays a major and determinant role.     

Venous hemodynamics in axillary venous stasis

By means of venous-occlusion plethysmography in 40 patients (24 men, 16 women) with stasis of the axillary vein the venous return was measured. This was 62.3 +/- 21.5 ml/100 ml/min. on the healthy arm. Long-term venous thromboses had worse return values (43.7%) than short occlusions (71.6% of the healthy side). Responsible for the favourable late results, which express themselves in increasing return values, is in general the development of an efficient collateral circulation and recanalisation, respectively, after thrombolysis or thrombectomy. The plethysmographic measurement of the back flow apart from the phlebography of the arm is recommended for the diagnosis and control of the course of the stasis of the axillary vein.     

Pulsatile hemodynamics in hypertension.

The hemodynamics of hypertension and antihypertensive therapy have generally been approached in terms of the steady-flow load on the heart. Recent evidence, however, suggests that the pulsatile component of hemodynamic load may play a fundamental role in both the development and progression of hypertensive cardiovascular disease and its clinical sequelae. Pulse pressure, a correlate of conduit vessel stiffness, has been shown to be an important independent predictor of clinical events in hypertensive patients and in the general population. Unrecognized effects on pulsatile hemodynamics may account for the differential effects of various agents on left ventricular mass and events. A better understanding of abnormalities in pulsatile load in hypertension will facilitate risk stratification in and treatment of patients with hypertension.     

Venous thromboembolism and cancer.

The literature was reviewed in an attempt to determine whether patients with cancer have an increased risk of venous thromboembolism, i.e. deep vein thrombosis and pulmonary embolism. From case reports it was apparent that various thromboembolic or thrombophlebitic manifestations may be found in a small number of patients, although it is possible that not all cases belong to the same clinical or pathogenetic entity. In clinical series it was found that the risk of postoperative venous thromboembolism was increased in cancer patients, but the possibility that this was due to associated risk factors, rather than to the mere presence of a tumour, could not be excluded. Little is known about patients not undergoing surgery. Retrospective postmortem studies have found more thrombi in patients with malignancy, but a prospective study failed to demonstrate an association between malignancy and pulmonary embolism. It is possible that different types of cancer show various degrees of association with venous thromboembolism. We conclude that further studies should be performed to provide a firm clinical and pathoanatomical basis for investigations into the pathogenesis of venous thromboembolism.     

Intracranial hemodynamics in sleep apnea.

Intracranial pressure changes and poor cerebral perfusion have been reported in sleep apnea syndrome (SAS), but such studies have been limited due to lack of a reliable noninvasive study method. We determined the systolic (VS), diastolic (VD), and mean (VM) cerebral blood flow velocities of the middle cerebral artery in 23 individuals (12 severe SAS patients and 11 control subjects) using transcranial Doppler sonography before sleep, during sleep (NREM and REM) and upon awakening. All three velocities (VS = 87.4 cm/s compared to 104.7 cm/s, VD = 41.6 cm/s compared to 47.7 cm/s, and VM = 57.0 cm/s compared to 67.0 cm/s) were decreased in patients with SAS and VS and VM were significantly lower than in control subjects (p = 0.005 and p = 0.033, respectively). The end-tidal CO2 (PETCO2) in the SAS patients (47.3 mm Hg) compared to the control subjects (41.8 mm Hg) was significantly higher (p = 0.003). When the VM was adjusted to normalized CO2 using the Markwalder's equation, the reduction in velocity in patients with SAS (47.5 cm/s) compared to control subjects (63.0 cm/s) became more significant (p = 0.005). This study shows that cerebral blood flow velocities are lower in patients with SAS compared to control subjects and that transcranial Doppler sonography may be useful in such evaluations.     

Venous pressure and exercise tolerance.

Compared to the number of contractions obtained when a blood pressure cuff on the upper arm was at zero pressure, inflation of the cuff to pressures ranging between 5 and 40 mm Hg resulted in an augmentation of the number of hand contractions that could be performed prior to the development of ipsilateral severe fatigue or intolerable pain. Cuff pressures of 60 mm Hg reduced the number of contractions below the control level. These results are consistent with the concept that exercise during venous congestion facilitates the washout of the toxic catabolite presumed to be produced during muscular contraction.     

Hemorheology, hemodynamics and microcirculation. 1

The microcirculation constitutes an ubiquitous vascular network presenting a mesh pattern, and comprising different types of vessels, arterioles, small veins, capillaries, arteriovenous shunts or similar structures, and lymphatics. Many dimensions have to be recognized, or simply mentioned, if one is to understand the hemodynamic and hemorheological particulars of this territory, which differ, in many aspects, from those specific to the macrocirculation (number and length of the vessels, diameter and cross section, intercapillary distance, geometric characteristics, intravascular pressure, pressure gradient, pressure-volume relationship, flow rate, mean velocity of plasma and RBC, velocity profile, local hematocrit, in situ viscosity, kinematic viscosity, wall shearing conditions, local oxygen transport, aggregation and deformability of RBC, leukocyte properties, etc.). The flow rate in capillary tubes and capillary vessels of the living organism varies with many factors, such as proximal hemodynamics, hemorheological characteristics of blood (fibrinogen, macro- and micro-hematocrit), some known effects (Farheus, Farheus Lindqvist), local diameter, the plasma layer which plays the role of the limiting layer, the endothelial film, the wall effect, and so forth. Models of the circulation have been propounded, none of which takes into account the whole of these phenomena due to their great complexity. Hemodynamic and hemorheological interactions provide for a better understanding of certain concepts, such as vascular resistance, hindrance, capacitance, local flow rates, real capillary opening and closing, development of two-directional functional shunts, autoregulation, pressure-volume relationship, critical closing pressure, circulatory current slowing effect, sequelae of intravascular aggregation of formed blood elements.     

Chronic Venous Insufficiency and Venous Ulceration

OBJECTIVE: To review and summarize the literature on the normal venous circulation of the leg, and the epidemiology, pathophysiology, and treatment of chronic venous insufficiency (CVI).
DATA SOURCES: English-language articles identified through a MEDLINE search (1966 –1996) using the terms venous insufficiency or varicose ulcer and epidemiology, pathophysiology, diagnosis, and clinical trial (pt), and selected cross-references.
STUDY SELECTION: Articles on epidemiology, pathophysiology, and treatment of CVI. Randomized, controlled studies were specifically sought for treatment efficacy.
DATA EXTRACTION: Data were manually extracted from selected studies and reviews; emphasis was placed on information relevant to the general internist.
DATA SYNTHESIS: Chronic venous insufficiency is a common primary care problem associated with significant morbidity and health care costs. The clinical spectrum of disease ranges from minor cosmetic concerns to severe fibrosing panniculitis and ulceration. Duplex Doppler ultrasonography may be the single best test to rule out deep venous thrombosis and other entities that can mimic CVI. Leg elevation and compression stockings are effective treatments for CVI; recalcitrant cases may require intermittent pneumatic compression. Topical antiseptics, antibiotics, enzymes, or growth factors offer no clear advantages in ulcer healing. Ulcer dressings remain a matter of convenience, cost, and physician judgment. The role of surgery in CVI appears to be limited.
CONCLUSIONS: Chronic venous insufficiency is a recalcitrant, recurrent medical problem. This condition can be managed by primary care physicians with relatively inexpensive treatment modalities in association with lifestyle modification.
KEY WORDS: venous circulation, of the leg; venous insufficiency, chronic; varicose ulcer.     

Angiotensin dependence of endothelium-mediated renal hemodynamics.

Endothelium-derived relaxing factor has been shown to regulate renal blood flow, and inhibition of its synthesis increases blood pressure and renal vascular resistance and decreases renal blood flow. Using the substrate antagonist NW-nitro-L-arginine methyl ester (L-NAME), we tested whether renal vasoconstriction induced by endothelium-derived relaxing factor synthesis inhibition could be mediated in part by angiotensin II. In 14 control rats, 10 mg/kg body wt L-NAME increased blood pressure from 106 +/- 6 to 126 +/- 6 mm Hg (p < 0.001), increased renal vascular resistance by 74% (from 19.3 +/- 2.6 to 33.6 +/- 2.9 resistance units), and decreased renal blood flow by 34% (from 5.9 +/- 0.5 to 3.9 +/- 0.3 ml.min-1.g kidney wt-1, p < 0.005). When six rats were treated with 10 mg/kg body wt of the angiotensin receptor antagonist DuP 753, L-NAME increased blood pressure from 84 +/- 4 to 106 +/- 4 mm Hg (p < 0.001); however, renal vascular resistance increased by only 27% (from 13 +/- 2 to 17 +/- 3 resistance units, p < 0.01; p < 0.05 different from control value) and renal blood flow was unchanged. Likewise, after pretreatment of six rats with 32 micrograms/100 g body wt of the angiotensin converting enzyme inhibitor enalaprilat, L-NAME increased blood pressure from 88 +/- 5 to 124 +/- 6 mm Hg (p < 0.001) and renal vascular resistance by 54% (from 12 +/- 1 to 18 +/- 3 resistance units, p < 0.01; p < 0.05 different from control value) but renal blood flow was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Portal hemodynamics in chronic liver disease.

Portal hypertension is a result of interplay of numerous static and dynamic forces. Portal hemodynamic characterization involves pressure and flow studies which in turn estimate portal pressure. Hepatic venous pressure gradient is the gold standard for determining portal pressure. Portal hemodynamic measurement has helped to understand the pathogenesis and prognosis of chronic liver disease and to define clinically important hepatic venous pressure gradients. Management strategies for ascites and prevention of variceal hemorrhage have been influenced by hemodynamic studies in animals and humans. The hemodynamics in non-cirrhotic portal fibrosis is ambiguous. The role of portal hemodynamic studies outside clinical trials needs further study.     

Venous emergencies. Personal experience and viewpoint

Based on a casuistic report of 226 cases, the authors propose a classification of venous emergencies, including acute deep thrombo-phlebites (with their anatomo-clinical and topographical varieties), the complications of varicose disease, venous traumatism and anorectal venous thrombosis. The authors touch on problems associated with clinical and paraclinical diagnosis, prophylaxis and active surgical therapy, respectively thrombectomy, ligation of the long saphenofemoral junction, the treatment of varico-phlebitis and urgent traumatic lesions, the thrombectomy and radical cure of haemorrhoids. The coupling of any of these affections presents a potential of great seriousness, sometimes a major vital risk which necessitates immediate therapeutic intervention. The classification of the idea of "venous emergency" in comparison with that of "arterial emergency", is outlined, and the authors mention that a surgical treatment in these affections is to be preferred.     

Venous wall ultrastructure in generalized venomegaly.

The ultrastructure of the v. colica sinistra in a case of generalized vasomegaly in man was examined. Elastic material was found in three forms: as a lightly osmiophil amorphous material bordering on myocytes, as a highly osmiophil elastic membrane, and as highly osmiophil slim elastic fibres of different orientation in the tunica media and adventitia. The slightly osmiophil elastic material is assumed to be newly formed by pinocytotic activity of the myocytes. The highly osmiophil elastic material indicates its impairment. No typical atherosclerotic changes were found in the examined vein. Based on a comparison with previous findings in the case of vasomegaly of the a. mesenterica inferior, the authors conclude that the venomegaly phenomenon is connected with degenerative changes in the elastic material of the vessel wall.     

Venous prostaglandin-like activity in diarrhoeal states.

Prostaglandin E2-like activity was determined in peripheral venous blood of control subjects and in patients with acute gastroenteritis and active ulcerative colitis, using a bioassay method. No significant diurnal variations of prostaglandin levels were detected in the control group, while significantly raised venous plasma prostaglandin-like activity was detected in acute gastroenteritis and in active ulcerative colitis.