What causes vasoplegia (vasodilatory shock)?

From the Guidelines

Vasoplegia is primarily caused by excessive vasodilation and decreased vascular tone, resulting in low blood pressure that responds poorly to vasopressors. It commonly occurs during sepsis, after cardiopulmonary bypass surgery, following anaphylaxis, or during severe systemic inflammatory response syndrome. The underlying mechanism involves dysregulation of the body's vascular control systems, particularly excessive production of nitric oxide and activation of potassium channels in vascular smooth muscle cells 1. Inflammatory mediators like cytokines, complement activation, and oxidative stress contribute significantly to this process. Certain medications such as ACE inhibitors, calcium channel blockers, and phosphodiesterase inhibitors can predispose patients to vasoplegia. Some key points to consider in the management of vasoplegia include:

• The use of vasopressors like norepinephrine (starting at 0.05-0.1 mcg/kg/min) and vasopressin (0.01-0.04 units/min) to maintain adequate perfusion pressure 1.
• The potential benefit of methylene blue (1-2 mg/kg IV over 15-30 minutes) for refractory cases 1.
• The importance of addressing the underlying cause, maintaining adequate fluid status, and providing supportive care in the management of vasoplegia 1. Understanding these pathophysiological mechanisms helps clinicians anticipate, prevent, and effectively treat this potentially life-threatening condition. Key considerations in the treatment of vasoplegia include:
• Early recognition and intervention to prevent end-organ damage.
• The use of vasoactive agents to support blood pressure and perfusion.
• The importance of fluid management and volume assessment to exclude hypovolemia.
• The potential role of other therapies, such as levosimendan and esmolol, in the management of vasoplegia 1.

From the Research

Causes of Vasoplegia

• Vasoplegia is a condition characterized by persistent low systemic vascular resistance despite a normal or high cardiac index, resulting in profound and uncontrolled vasodilation 2
• It may occur due to various conditions, including cardiac failure, sepsis, and post-cardiac surgery 2
• The pathogenesis of vasoplegia involves the activation of contact, coagulation and complement systems and the activation of leukocytes, platelets and endothelial cells resulting in an imbalance in the regulation of the vascular tone leading to postcardiac surgery vasoplegia 3
• Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen sulphide and reactive oxygen species production, are also reviewed 4
• Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the blood vessels, are also discussed 4

Risk Factors for Vasoplegia

• Multiple risk factors have been identified that help predict vasoplegia, including use of angiotensin-converting enzyme inhibitor (ACE-I), calcium channel blockers, amiodarone, heparin, low cardiac reserve (EF < 35%), symptomatic congestive heart failure, and diabetes mellitus 5
• Perioperative risk factors for VPS after cardiac surgery in adults have been identified, and early identification and prompt management of vasoplegia is crucial to prevent development of shock 2

Pathophysiology of Vasoplegia

• The underlying pathophysiology following cardiopulmonary bypass (CPB) consists of resistance to vasopressors (inactivation of Ca2+ voltage gated channels) on the one hand and excessive activation of vasodilators (SIRS, iNOS, and low AVP) on the other 5
• Vasoplegia syndrome is characterized by hypotension refractory to fluid resuscitation or high-dose vasopressors, low systemic vascular resistance, and normal-to-increased cardiac index 6
• The vasoplegic syndrome is encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and trauma 4