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Liver Blood Flow
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The portal vein is a valveless vein and drains blood from the large and small intestines, spleen, stomach, pancreas and gall bladder to the liver. The hepatic portal vein contributes 70% of total liver blood flow and 50%–60% of basal oxygen supply. In the fasting state, the oxygen saturation of portal venous blood is approximately 85%, but this decreases with increased gut activity. The higher O2 saturation in portal venous blood at resting conditions, compared with mixed venous O2 saturation, is due to the high mesenteric arterial shunting through the intestinal capillaries draining into the portal system. The velocity of blood flow in the portal system is 9 cm/s – approximately half that in the hepatic artery. Thus, the hepatic portal system is a low-pressure (5–10 mmHg), low-resistance and low-velocity system. The portal venous pressure depends on the state of constriction/dilatation of mesenteric arterioles and on intrahepatic resistance. The resistance in the portal system is approximately 6%–12% of that in the hepatic artery.
Liver disorders
Published in Rachel U Sidwell, Mike A Thomson, Concise Paediatrics, 2020
Rachel U Sidwell, Mike A Thomson
This occurs when the portal pressure is elevated ≥ 10–12 mmHg (normal = 7 mmHg). Increased portal venous pressure results in collaterals (varices) developing (portosystemic shunting) and a hyperdynamic circulation. These together can cause varices to rupture and result in GI bleeds. Important sites of collaterals (varices): OesophagusAnorectalPeriumbilical (caput medusae. NB: These flow away from the umbilicus)RetroperitonealPerivertebral/perispinal
The Reflex Effects of Hepatic and Mesenteric Afferents on the Circulation
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
As mentioned above, occlusion of the portal vein probably causes an increase in mesenteric venous pressure. It may cause a reduction of portal venous pressure in the liver. However, a decrease in hepatic portal venous pressure may have little effect on renal nerve activity. Liang (1971) reported that reduction of portal venous pressure caused no change in urine flow, suggesting no change in renal nerve activity. For this reason, the effect of a decrease in hepatic portal venous pressure probably can be neglected.
Anticoagulant therapy for splanchnic vein thrombosis: recent updates for patients with liver cirrhosis
Published in Expert Review of Hematology, 2023
Lucia M. Caiano, Nicoletta Riva, Walter Ageno
Thrombosis of the portal venous system increases the portal venous pressure and is a known cause of pre-hepatic portal hypertension [67]. Portal hypertension is considered clinically significant when the hepatic venous pressure gradient (HVPG; i.e. the difference between the pressure in the portal vein and the inferior vena cava) is ≥10 mmHg, since this level was associated with a higher incidence of esophageal varices [68], cirrhosis decompensation, and hepatocellular carcinoma [67]. The risk of variceal rupture, and thus variceal bleeding, depends on the size and location of the varices, and on the level of HVPG (occurring usually when the HVPG is ≥12 mmHg) [69]. In cirrhotic patients, variceal bleeding is one of the elements, which define liver decompensation, the others being development of ascites and hepatic encephalopathy [44], and the transition to decompensated cirrhosis is associated with higher mortality rates.
A Predictive Formula for Portal Venous Pressure Prior to Liver Resection Using Directly Measured Values
Published in Journal of Investigative Surgery, 2020
Masaaki Hidaka, Susumu Eguchi, Takanobu Hara, Akihiko Soyama, Satomi Okada, Takashi Hamada, Shinichiro Ono, Tomohiko Adachi, Kengo Kanetaka, Mitsuhisa Takatsuki
Portal venous pressure has been found to reflect the degree to which the liver parenchyma is damaged.16 Measuring PVP is useful in determining the final indications for surgery also in cirrhotic patients with HCC.2,12–15 In a meta-analysis, morbidity and mortality after hepatectomy were 6.1%, 2.8%, and 41.7%, 34.7%, respectively.17 In addition, Berigotti et al reported that the rate of liver failure after hepatectomy was much higher in patients with portal hypertension (PHT) than in those without PHT.18 In those studies, some defined PHT as platelet count less than 100 × 103 and diameter of the spleen greater than 12 cm, while some used HVPG.19,20 They even reported that long-term recurrence-free survival after hepatectomy was correlated with PVP. Therefore, it is an important development to know the PVP based on preoperatively measured values with ease.21 If the estimated PVP is high, we could make the resection smaller, or, if PVP is within normal range, we would be convinced to perform a larger resection. For those reasons, we established this formula for predicting PVP preoperatively.
Multifocal gastrointestinal varices: a rare manifestation of immunoglobulin G4-related disease
Published in Postgraduate Medicine, 2019
Unlike the well-defined treatments for gastroesophageal varices, the ideal therapeutic intervention for EcV is unknown; however, the concepts are the same. For ectopic or multifocal GI varices, the selection of appropriate approaches should be discussed in a multidisciplinary team [1]. Treatment strategies thus include vasoactive agents (somatostatin or the analogue, octreotide; vasopressin or its analogue, terlipressin) to lower portal pressure, endoscopic therapy (injection sclerotherapy or band ligation) to stop acute bleeding, transjugular intrahepatic portosystemic shunt (TIPS) to decrease intrahepatic portal venous pressure, balloon-occluded retrograde transvenous obliteration (BRTO) to eliminate the gastro-/splenorenal collateral venous flow, partial splenic artery embolization to decrease portal venous flow, or surgery (direct devascularization of varices or splenectomy for long-term control) [1–4].