Pulmonary Arterio-venous Pressure Gradient as a Determinant of Increased Venous Admixture

2015 ◽  
pp. 450-454
Author(s):  
D. Kentera ◽  
V. Veljkovic
Keyword(s):  
Pressure Gradient ◽  
Venous Pressure ◽  
Venous Admixture

Hepatic Venous Pressure Gradient Predicts Clinical Decompensation in Patients With Compensated Cirrhosis

2007 ◽  
Vol 133 (2) ◽  
pp. 481-488 ◽  
Author(s):  
Cristina Ripoll ◽  
Roberto Groszmann ◽  
Guadalupe Garcia–Tsao ◽  
Norman Grace ◽  
Andrew Burroughs ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Venous Pressure ◽  
Hepatic Venous Pressure Gradient ◽  
Compensated Cirrhosis

Abstract 1122‐000232: The Importance of Performing Venous Pressure Measurements Following Venous Sinus Stenting for Idiopathic Intracranial Hypertension

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Yazan Radaideh
Keyword(s):  
Pressure Gradient ◽  
Intracranial Hypertension ◽  
Stent Placement ◽  
Idiopathic Intracranial Hypertension ◽  
Venous Pressure ◽  
Sigmoid Sinus ◽  
Venous Sinus ◽  
Pressure Measurements ◽  
Sinus Stenosis ◽  
The Right

Introduction : Although venous sinus stenting is an established treatment for medically refractory idiopathic intracranial hypertension, a subset of patients shows little or no improvement of symptoms after stenting. While this could be related to a number of factors, failure to sufficiently address the pressure gradient is one that can be recognized during the treatment procedure. We describe two patients who had a persistent venous pressure gradient after stent placement. Once identified, a second stent was placed with subsequent resolution of the pressure gradient. Methods : This retrospective chart review identified patients at a single institution who underwent venous sinus stenting and required immediate placement of a second venous sinus stent for a persistent pressure gradient. Results : Two patients with refractory idiopathic intracranial hypertension underwent cerebral angiography with venous manometry. In the first patient, unilateral venous sinus stenosis was present with a maximum pressure of 50 mmHg, which only decreased to 30 mmHg after placement of a right transverse‐sigmoid sinus stent. Subsequent manometry revealed a persistent gradient between the superior sagittal sinus and the right transverse sinus, which resolved after placement of a second stent in this location. In the second patient, bilateral stenosis was observed at the transverse‐sigmoid sinus junction; the maximum venous pressure was 40 mmHg, and a gradient of 30 mmHg was measured at the right transverse‐sigmoid junction, where a venous sinus stent was placed. Venous sinus pressure measurements performed immediately after the stent placement demonstrated a persistent pressure gradient of 20 mmHg in the contralateral transverse‐sigmoid sinus junction, which resolved after contralateral stent placement. Both patients showed sustained improvement in their symptoms at 1 year follow up. Conclusions : In some patients with idiopathic intracranial hypertension and venous sinus stenosis, a single stent may not sufficiently reduce the pressure gradient. A second stent may be required; however, this is only detectable with post‐stent pressure measurements. Performing manometry after stent placement should be routinely performed in order to detect persistent venous pressure gradient.

Antiadrenergic and Antihistaminic Therapy in Hemorrhagic Shock in Dog and Rat

1956 ◽  
Vol 186 (1) ◽  
pp. 79-84 ◽  
Author(s):  
S. Jacob ◽  
Edward W. Friedman ◽  
Sabin Levenson ◽  
Philip Glotzer ◽  
H. A. Frank ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Blood Loss ◽  
Pressure Gradient ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Venous Pressure ◽  
Survival Period ◽  
Effect Of Treatment ◽  
Antihistaminic Drugs

The influence of pretreatment with dibenamine on the development and course of hemorrhagic shock, and the effect of treatment with dibenamine, rapidly acting antiadrenergic drugs, or antihistaminic drugs after hemorrhagic shock had been allowed to become unresponsive to replacement transfusion, were tested in dogs prepared in advance to permit measurement of portal-caval venous pressure gradient. Preliminary dibenamine administration was also tested in rats submitted to hemorrhagic shock. The conclusions were as follows: 1) The protective effect of dibenamine prior to the induction of hemorrhagic shock in the dog consists mainly of a reduction of the bleeding volume. Intrahepatic vasoconstriction is not reduced. A dog which is not under the influence of dibenamine can tolerate a greater degree of blood loss than a dibenaminized dog. After hemorrhagic shock has been allowed to become refractory to replacement transfusion, antiadrenergic and antihistaminic drugs do not reduce intrahepatic vasoconstriction or increase the survival period or the survival rate. 2) Dibenamine given prior to hemorrhage enables the rat to survive a degree of blood loss which is lethal to the untreated rat. This, in part, appears to be due to better blood flow to the respiratory center.

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