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202 13. Bleeding and thrombosis in cirrhosis

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CHAPTER

Peripheral vasculature in portal hypertension

Seong Hee Kang

1,2,3,4

and Soon Koo Baik

1,2,3

Department of Internal Medicine, Wonju Severance Christian Hospital, Yonsei University Wonju College of Medicine,

Wonju, Korea

Regeneration Medicine Research Center, Yonsei University Wonju College of Medicine, Wonju, Korea

Cell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine, Wonju, Korea

Department of Internal Medicine, Inje University College of Medicine, Seoul, Korea

Introduction

In 1628, William Harvey first established that blood circulation is a continuous circuit controlled by the heart,

which dispelled the belief that the liver controlled a separate venous circulation and played a major role in blood

circulation (see also Chapter 1). Following technological advances and the availability of modalities for accurate

measurement of cardiovascular phenomena, Kowalski and Abelmann confirmed that cirrhosis is associated with

cardiovascular disturbances; they specifically proved that alcoholic cirrhosis led to increased cardiac output and

a reduction in the systemic vascular resistance (SVR) and blood pressure. These researchers ascribed this hyper-

dynamic circulation to a circulating vasodilator produced by live r. This seminal research performed 50 years ago

launched the modern era of “cardio-hepatology” the study of cardiovascular disturbances associated with liver

disease. From its early days as an obscure scientific curiosity, this area of stu dy has evolved into a clinically

important specialty, and currently, it is widely recognized that cardiovascular disorders contribute to the patho-

genesis of several complications of liver disease, including variceal bleeding, ascites, hepatorenal syndrome, and

hepatopulmonary syndrome. We discuss various aspects of the peripheral vasculature in portal hypertension

and cirrhosis, focusing mainly on the hyperdynamic circulation, but also including the concept of the alterations

in peripheral arterial and venous circulations and several regulatory mechanisms controlling the organ systems.

Hyperdynamic circulation

Hyperdynamic circulation is characterized by increas ed cardiac output and heart rate and decreased SVR with

low arterial blood pressure

[14]. These hemodynamic alterations occur as a complication of portal hypertension

[5]. Although the exact mechanisms that lead to hemodynamic instability remain unclear, abnormalities in

regional vascular beds, including the hepatic, mesenteric/splanchnic, renal, pulmonary, skeletal muscle, and

cerebral circulation are implicated as contributors to this phenomenon.

Clinical features of hyperdy namic circulation

Hyperdynamic circulation is readily evident when well established, patients typically present with easily iden-

tifiable clinical manifestations of tachycardia, hypotension, and bounding pulses. Hyperdynamic circulation by

itself is not distressing to patients; however, this phenomenon is clinically important because it tends to aggra-

vate or precipitate complications of portal hypertension. The degree of hyperdynamic circulation is associated

with advanc ing liver failure; patients with end-stage liver failure usually develop significant peripheral

203

Cardio-Hepatology.

DOI:

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