How does cirrhosis cause hypotension?

From the Guidelines

Cirrhosis causes hypotension primarily through splanchnic vasodilation and the development of portal hypertension, leading to a hyperdynamic circulation with high cardiac output but low blood pressure. This is due to increased production of vasodilatory substances like nitric oxide, carbon monoxide, and endocannabinoids, which cause peripheral arterial vasodilation, particularly in the splanchnic circulation 1. As a result, there is a decrease in effective arterial blood volume and reduced systemic vascular resistance. The body attempts to compensate through activation of the renin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone release, but these mechanisms eventually become insufficient.

Some key factors that contribute to hypotension in cirrhosis include:

• Splanchnic vasodilation, which leads to decreased effective arterial blood volume and reduced systemic vascular resistance
• Development of hepatorenal syndrome, where renal vasoconstriction occurs alongside systemic vasodilation, further compromising blood pressure regulation
• Cirrhotic cardiomyopathy, characterized by impaired cardiac contractility and chronotropic incompetence, which may also contribute to hypotension, especially during stress or infection 1
• Decreased effective arterial blood volume and renal perfusion, resulting from progressive worsening of portal hypertension and the vasodilatory–hyperdynamic circulatory state 1

In managing hypotension in cirrhosis, it is essential to consider the underlying pathophysiological changes and to implement a judicious strategy for intravascular volume resuscitation utilizing hemodynamic monitoring tools, as recommended by recent guidelines 1. The use of vasoconstrictors, such as norepinephrine, and intravenous albumin may be necessary to optimize volume status and blood pressure regulation in critically ill patients with cirrhosis. Additionally, consideration of adrenal insufficiency or an empiric trial of hydrocortisone may be necessary for treatment of refractory shock requiring high-dose vasopressors in patients with cirrhosis 1.

From the Research

Pathophysiology of Cirrhosis and Hypotension

• Cirrhosis leads to portal hypertension, which is characterized by increased intrahepatic vascular resistance and a hyperdynamic circulatory state 2, 3.
• The hyperdynamic circulatory state is marked by a high cardiac output, increased total blood volume, and splanchnic vasodilatation, resulting in increased mesenteric blood flow 2.
• Splanchnic vasodilatation is caused by the activation of various vasoactive systems, including nitric oxide, cyclooxygenase-derivatives, carbon monoxide, and endogenous cannabinoids 3.
• The hyperdynamic circulatory syndrome, which occurs in patients with portal hypertension, is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure 3.

Relationship between Cirrhosis and Hypotension

• The hyperdynamic circulatory state and splanchnic vasodilatation in cirrhosis can lead to a decrease in systemic vascular resistance, resulting in hypotension 3, 4.
• The use of certain medications, such as angiotensin converting enzyme inhibitors and angiotensin II type receptor 1 blockers, can also contribute to hypotension in patients with cirrhosis 2.
• Additionally, the development of ascites, a common complication of cirrhosis, can further worsen hypotension due to the loss of fluid and electrolytes 5.

Hemodynamic Changes in Cirrhosis

• Patients with cirrhosis often exhibit significant hemodynamic changes, including increased cardiac output, decreased systemic vascular resistance, and low arterial blood pressure 3, 6.
• The administration of certain medications, such as octreotide, can also affect systemic hemodynamics in patients with cirrhosis, leading to changes in pulse rate, cardiac output, and blood pressure 6.