From the Guidelines
Cirrhosis causes hypotension primarily through splanchnic vasodilation and the development of portal hypertension, as evidenced by the most recent study 1.
Pathophysiology of Cirrhosis-Induced Hypotension
The pathogenesis of portal hypertension (PH) in cirrhosis involves an increased intrahepatic resistance to portal flow, which is attributed to structural mechanisms such as fibrous tissue and regenerative nodules, as well as an increased intrahepatic vascular tone (functional component) 1. This leads to the formation of portosystemic collaterals and splanchnic vasodilatation, resulting in increased flow into the gut and into the portal venous system. The increased production of vasodilatory substances like nitric oxide, carbon monoxide, and endocannabinoids contributes to peripheral arterial vasodilation, particularly in the splanchnic circulation 1.
Clinical Implications
The body attempts to compensate for the reduced effective arterial blood volume and decreased systemic vascular resistance through activation of the renin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone release, but these mechanisms eventually become insufficient 1. Additionally, cirrhosis often leads to the development of a hyperdynamic circulation characterized by increased cardiac output and heart rate, which paradoxically cannot maintain normal blood pressure due to the profound vasodilation. Complications of cirrhosis such as ascites and hepatorenal syndrome further contribute to hypotension by causing fluid sequestration and impaired renal function.
Management Considerations
In critically ill patients with cirrhosis, early baseline assessment of volume status, perfusion, and cardiovascular function is crucial, and bedside echocardiography can be useful in evaluating volume status and cardiac function in patients with hypotension or shock 1. A judicious strategy for intravascular volume resuscitation utilizing hemodynamic monitoring tools should be implemented to optimize volume status, and norepinephrine is recommended as the first vasopressor for patients with hypotension with concurrent appropriate fluid resuscitation 1.
From the Research
Pathophysiology of Cirrhosis and Hypotension
- Cirrhosis can lead to hypotension due to various pathophysiological mechanisms, including changes in the renin-angiotensin-aldosterone system 2, 3.
- The renin-angiotensin-aldosterone system is activated in response to decreased effective arterial blood volume, leading to sodium retention and vasoconstriction 4, 5.
- However, in cirrhosis, the activation of this system can be impaired, leading to decreased peripheral resistance and hypotension 2, 3.
Role of Sodium Retention in Cirrhosis
- Sodium retention is a key factor in the development of ascites in cirrhosis, and is mediated by the renin-angiotensin-aldosterone system 4, 5.
- The kidneys retain sodium and water in response to the perceived decrease in effective circulatory volume, leading to ascites formation 5.
- However, this sodium retention can also contribute to hypotension, as the increased fluid volume can lead to decreased peripheral resistance 2, 3.
Impact of Cirrhosis on Cardiovascular Homeostasis
- Cirrhosis can lead to changes in cardiovascular homeostasis, including reduced peripheral resistances, opening of arterovenous shunts, and reduced efficiency of the sympathetic nervous system 2.
- These changes can contribute to hypotension, as the body's ability to maintain blood pressure is impaired 2, 3.
- The development of massive compartmentalization of fluid as ascites can also lead to striking activation of the renin-angiotensin-aldosterone system, which can further contribute to hypotension 2.