Mechanism of pulmonary venous pressure and flow waves

1999 ◽  
Vol 14 (2) ◽  
pp. 67-71 ◽  
Author(s):  
L. R. Hellevik ◽  
P. Segers ◽  
N. Stergiopulos ◽  
F. Irgens ◽  
P. Verdonck ◽  
...  
Keyword(s):  
Venous Pressure ◽  
Pressure And Flow Waves

Invasive therapeutic options in truncal varicosity of the great saphenous vein

VASA ◽  
2006 ◽  
Vol 35 (3) ◽  
pp. 157-166 ◽  
Author(s):  
Hach-Wunderle ◽  
Hach
Keyword(s):  
Minimally Invasive ◽  
Saphenous Vein ◽  
Venous Insufficiency ◽  
Great Saphenous Vein ◽  
Varicose Veins ◽  
Venous Pressure ◽  
Stage Iii ◽  
High Ligation ◽  
Surgical Trauma ◽  
Disease Stages

It is known from current pathophysiology that disease stages I and II of truncal varicosity of the great saphenous vein do not cause changes in venous pressure on dynamic phlebodynamometry. This is possibly also the case for mild cases of the disease in stage III. In pronounced cases of stage III and all cases of stage IV, however, venous hypertension occurs which triggers the symptoms of secondary deep venous insufficiency and all the complications of chronic venous insufficiency. From these facts the therapeutic consequence is inferred that in stages I and II and perhaps also in very mild cases of stage III disease, it is enough "merely" to remove varicose veins without expecting there to be any other serious complications in the patient’s further life caused by the varicosity. Recurrence rates are not included in this analysis. In marked cases of disease stages III and IV of the great saphenous vein, however, secondary deep venous insufficiency is to be expected sooner or later. The classical operation with saphenofemoral high ligation ("crossectomy") and stripping strictly adheres to the recognized pathophysiologic principles. It also takes into account in the greatest detail aspects of minimally invasive surgery and esthetics. In the past few years, developments have been advanced to further minimize surgical trauma and to replace the stripping maneuver using occlusion of the trunk vein which is left in place. Obliteration of the vessel is subsequently performed via transmission of energy through an inserted catheter. This includes the techniques of radiofrequency ablation and endovenous laser treatment. High ligation is not performed as a matter of principle. In a similar way, sclerotherapy using microfoam is minimally invasive in character. All these procedures may be indicated for disease stages I and II, and with reservations also in mild forms of stage III disease. Perhaps high ligation previously constituted overtreatment in some cases. Targeted studies are still needed to prove whether secondary deep venous insufficiency can be avoided in advanced stages of varicose vein disease without high ligation and thus without exclusion of the whole recirculation circuit.

Systemic Effects of ADP-induced Platelet Aggregation and Their Modification by Aspirin and by Pyridinolcarbamate

1973 ◽  
Vol 30 (01) ◽  
pp. 178-190 ◽  
Author(s):  
Itsuro Kobayashi ◽  
Paul Didisheim
Keyword(s):  
Platelet Aggregation ◽  
Venous Pressure ◽  
Systemic Effects ◽  
Central Venous ◽  
Platelet Aggregates ◽  
Induced Changes ◽  
Second Wave ◽  
Carotid Arterial ◽  
Arterial Po2

SummaryADP, AMP, or ATP was injected rapidly intravenously in rats. ADP injection resulted in the f olio wing transient changes: a drop in platelet count, a rise in central venous pressure, a fall in carotid arterial PO2, bradycardia, arrhythmia, flutter-fibrillation, and arterial hypotension. AMP and ATP produced some of these same effects; but except for hypotension, their frequency and severity Avere much less than those following ADP.Prior intravenous administration of acetylsalicylic acid or pyridinolcarbamate, two inhibitors of the second wave of ADP-induced platelet aggregation in vitro, significantly reduced the frequency and severity of all the above ADP-induced changes except hypotension. These observations suggest that many of the changes (except hypotension) observed to follow ADP injection are produced by platelet aggregates which lodge transiently in various microcirculatory beds then rapidly disaggregate and recirculate.

Tissue Plasminogen Activator Release in Chronic Venous Hypertension due to Heart Failure

1992 ◽  
Vol 68 (03) ◽  
pp. 321-324 ◽  
Author(s):  
Irena Keber ◽  
Dušan Keber ◽  
Mojca Stegnar ◽  
Nina Vene
Keyword(s):  
Heart Failure ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Venous Pressure ◽  
Venous Hypertension ◽  
Plasminogen Activator Inhibitor 1 ◽  
Control Subjects ◽  
Tissue Plasminogen ◽  
Pai 1

SummaryIn order to study the effects of chronic venous hypertension due to heart failure on blood fibrinolytic activity, tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor 1 (PAI-1) antigen, t-PA activity and PAI activity were measured before and after venous occlusion of the arm for 20 min in 15 patients with right-sided heart failure, 15 patients with left-sided heart failure, and 30 control healthy subjects. Central venous pressure, measured by observing the jugular veins, was above 15 cm of the blood column in all patients with right-sided heart failure, and normal (below 8 cm) in all patients with left-sided heart failure and control subjects. There was no difference in the basal concentrations of t-PA (11.0, 10.2 and 10.8 ng/ml; all values medians) and PAI-1 antigens and their activities between right and left-sided heart failure and the control subjects. After the occlusion, t-PA antigen increased significantly less in right-sided heart failure (28.6 ng/ml) than in left-sided heart failure and the control subjects (54.5 and 45.9 ng/ml, respectively). It was concluded that the poor increase in fibrinolytic activity that had already been reported in patients with heart failure, was due to low t-PA release during occlusion and not to a high basal PAI level. It was limited to the patients with right-sided heart failure and was probably the consequence of chronic systemic venous hypertension.

Effect of fluid bolus triggers and their combination on fluid responsiveness in optimization phase of severe sepsis and septic shock resuscitation

MedPharmRes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 27-32
Author(s):  
Bien Le ◽  
Dai Huynh ◽  
Mai Tuan ◽  
Minh Phan ◽  
Thao Pham ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Severe Sepsis ◽  
Fluid Responsiveness ◽  
Statistical Significance ◽  
Venous Pressure ◽  
Fluid Bolus ◽  
Low Blood Pressure ◽  
Low Central Venous Pressure ◽  
Sepsis And Septic Shock

Objectives: to evaluate the fluid responsiveness according to fluid bolus triggers and their combination in severe sepsis and septic shock. Design: observational study. Patients and Methods: patients with severe sepsis and septic shock who already received fluid after rescue phase of resuscitation. Fluid bolus (FB) was prescribed upon perceived hypovolemic manifestations: low central venous pressure (CVP), low blood pressure, tachycardia, low urine output (UOP), hyperlactatemia. FB was performed by Ringer lactate 500 ml/30 min and responsiveness was defined by increasing in stroke volume (SV) ≥15%. Results: 84 patients were enrolled, among them 30 responded to FB (35.7%). Demographic and hemodynamic profile before fluid bolus were similar between responders and non-responders, except CVP was lower in responders (7.3 ± 3.4 mmHg vs 9.2 ± 3.6 mmHg) (p 0.018). Fluid response in low CVP, low blood pressure, tachycardia, low UOP, hyperlactatemia were 48.6%, 47.4%, 38.5%, 37.0%, 36.8% making the odd ratio (OR) of these triggers were 2.81 (1.09-7.27), 1.60 (0.54-4.78), 1.89 (0.58-6.18), 1.15 (0.41-3.27) and 1.27 (0.46-3.53) respectively. Although CVP < 8 mmHg had a higher response rate, the association was not consistent at lower cut-offs. The combination of these triggers appeared to raise fluid response but did not reach statistical significance: 26.7% (1 trigger), 31.0% (2 triggers), 35.7% (3 triggers), 55.6% (4 triggers), 100% (5 triggers). Conclusions: fluid responsiveness was low in optimization phase of resuscitation. No fluid bolus trigger was superior to the others in term of providing a higher responsiveness, their combination did not improve fluid responsiveness as well.

Rapidly progressive glomerulonephritis as presenting feature of systemic lupus erythematosus in a Bangladeshi male patient: a rare case report

2020 ◽  
Vol 10 (2) ◽  
pp. 137-138
Author(s):  
Samiha Haque ◽  
Ishrat Jahan ◽  
Tufayel Ahmed Chowdhury ◽  
Muhammad Abdur Rahim ◽  
Mehruba Alam Ananna ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Venous Pressure ◽  
Rapidly Progressive Glomerulonephritis ◽  
Initial Response ◽  
Systemic Lupus ◽  
Renal Manifestation ◽  
Rare Case Report ◽  
Diagnostic Work ◽  
Work Up

Rapidly progressive glomerulonephritis is one of the most dramatic and tragic presentations of lupus nephritis (LN) or renal manifestation of systemic lupus erythematosus (SLE). A 35-year-old Bangladeshi gentleman presented with worsening oedema, scanty, high colored, frothy urine and deteriorating renal function. He had puffy face, anaemia, oedema, normal jugular venous pressure (JVP), high blood pressure (150/90 mm Hg), ascites and bilateral pleural effusions. Diagnostic work-up confirmed SLE with class IV LN. His initial response to specific therapy showed improvement Birdem Med J 2020; 10(2): 137-138

Endogenous Heparinoids Detected by anti-Xa Activity are Present in Blood during Acute Variceal Bleeding in Cirrhosis. A Prospective Study

2014 ◽  
Vol 23 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Christos Triantos ◽  
Emmanuel Louvros ◽  
Maria Kalafateli ◽  
Anne Riddell ◽  
Ulrich Thalheimer ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Variceal Bleeding ◽  
Blood Cells ◽  
Venous Pressure ◽  
White Blood Cells ◽  
International Normalized Ratio ◽  
Ulcer Bleeding ◽  
Factor X ◽  
Packed Red Blood Cells ◽  
Bacterial Peritonitis

Background & Aims: Endogenous heparinoids have been detected by thromboelastography and quantified by clotting based anti-Xa activity assays in patients with cirrhosis, but their presence in variceal bleeding has not been established yet.Methods: Clotting based anti-Xa activity was measured in A) 30 cirrhotics with variceal bleeding, B) 15 noncirrhotics with peptic ulcer bleeding, C) 10 cirrhotics without infection or bleeding, and D) 10 cirrhotics with hepatocellular carcinoma (HCC).Results: Anti-Xa activity was not detected in ulcer bleeders or in cirrhotics without infection or bleedingbut was present in seven (23%) variceal bleeders (median levels: 0.03 u/mL (0.01-0.07)) and was quantifiable for 3 days in six of seven patients. Four of seven variceal bleeders with anti-Xa activity present had HCC (p=0.023). Age, creatinine, platelet count and total infections the second day from admission were significantly correlated with the presence of measureable anti-Xa levels (p=0.014, 0.032, 0.004 and 0.019, respectively). In the HCC group, anti-Xa activity was present in three patients (30%) [median levels: 0.05 u/mL (0.01-0.06)].Conclusions: In this study, variceal bleeders and 30% of the patients with HCC had endogenous heparinoids that were detected by a clotting based anti-Xa activity assay, whereas there was no anti Xa activity present in patients with cirrhosis without infection, or bleeding or HCC, nor in those with ulcer bleeding. Thus, the anti-Xa activity is likely to be a response to bacterial infection and/or presence of HCC in cirrhosis.List of abbreviations: AFP, alpha-fetoprotein; aPTT, activated partial thromboplastin time; CP, Child-Pugh; FXa, activated factor X; GAGS, glycosaminoglycans; Hb, hemoglobin; HCC, hepatocellular carcinoma; HVPG, hepatic venous pressure gradient; INR, International normalized ratio; LMWHs, low molecular weight heparins; MELD, Model for End-stage Liver Disease; PPP, platelet-poor plasma; PRBC, packed red blood cells; PT, prothrombin time; SBP, sponataneous bacterial peritonitis; TEG, thromboelastography; WBC, white blood cells.

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