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Hypotension from vasoplegia—a critical condition that can persist when RAAS becomes dysregulated and fails to restore hemodynamic stability1,2

Vasoplegia is marked by refractory hypotension, most often surfacing in the hours following CPB3

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Profound vasodilation

Endothelial injury reduces the expression and activity of ACE, leading to impaired ANG II formation and excess production of vasodilatory angiotensin metabolites1,4-6

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Impaired perfusion

Despite high cardiac output, hypotension leads to inadequate tissue perfusion, reduced oxygen extraction, and tissue hypoxia4,6,7

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Multi-organ damage

Sustained hypotension drives
damage across vital end organs,
including the kidneys, heart, and lungs, that can ultimately lead to organ failure6,7

Early aggressive treatment of vasoplegia-related hypotension is vital8

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Hypotension from vasoplegia—a critical condition that can persist when RAAS becomes dysregulated and fails to restore hemodynamic stability1,2

Vasoplegia is marked by refractory hypotension, most often surfacing in the hours following CPB3

Left Light_Circle-1

Profound vasodilation

Endothelial injury reduces the expression and activity of ACE, leading to impaired ANG II formation and excess production of vasodilatory angiotensin metabolites1,4-6

Middle Grey 02-3

Impaired perfusion

Despite high cardiac output, hypotension leads to inadequate tissue perfusion, reduced oxygen extraction, and tissue hypoxia4,6,7

Right Dark Organs-1

Multi-organ damage

Sustained hypotension drives damage across vital end organs, including the kidneys, heart, and lungs, that can ultimately lead to organ failure6,7

RAAS pathway dysfunction drives hypotension, a hallmark of vasoplegia pathophysiology1

Early aggressive treatment of vasoplegia-related hypotension is vital8

RAAS pathway dysfunction drives hypotension, a hallmark of vasoplegia pathophysiology1

Under normal conditions, the RAAS
pathway increases blood pressure in
response to hypotension

 
The kidneys release renin into the bloodstream in response to low blood pressure9


Renin cleaves angiotensinogen, produced in the liver, to ANG I9


ACE, expressed by pulmonary endothelial cells, converts ANG I into ANG II9



ANG II maintains hemodynamic stability by
• Inducing vasoconstriction9
• Triggering norepinephrine and vasopressin release9,10


How RAAS pathway dysfunction
perpetuates hypotension

 
The kidneys release renin into the bloodstream in response to low blood pressure9

Renin cleaves angiotensinogen, produced in the liver, to ANG I9

In vasoplegia, endothelial injury in the lungs or bypass of the lungs during CPB reduces the expression and activity of ACE, thereby limiting conversion of ANG I into ANG II and leading to excess production of vasodilatory angiotensin metabolites11,12
ANG II depletion contributes to hypotension by
• Preventing vasoconstriction9
• Stimulating renin release and leading to excess production of vasodilatory angiotensin metabolites9,12

Under normal conditions,
the RAAS pathway increases blood
pressure in response to hypotension

 



 

 

 

 

 

The kidneys release renin into the bloodstream in response to low blood pressure9
Renin cleaves angiotensinogen, produced in the liver, to ANG I9

ACE, expressed by pulmonary endothelial cells, converts ANG I into ANG II9


ANG ll maintains
hemodynamic stability by
• Inducing vasoconstriction9
• Triggering norepinephrine and
vasopressin release9,10 

How RAAS pathway dysfunction
perpetuates hypotension

 

 

 

 

 

 

 

 

The kidneys release renin into the bloodstream in response to low
blood pressure9
Renin cleaves angiotensinogen, produced in the liver, to ANG I9

In vasoplegia, endothelial injury in the
lungs or bypass of the lungs during CPB reduces the expression and activity of ACE, thereby limiting conversion of ANG I into ANG II and leading to excess production of vasodilatory angiotensin metabolites11,12

RAAS dysfunction limits ANG II production—impairing blood pressure restoration in vasoplegia1

ANG II depletion contributes
to hypotension by
• Preventing vasoconstriction9
• Stimulating renin release and leading to excess production of vasodilatory angiotensin metabolites9,12

RAAS dysfunction limits ANG II production—impairing blood pressure restoration in vasoplegia1

ACE=angiotensin-converting enzyme; ANG=angiotensin; CPB=cardiopulmonary bypass; RAAS=renin-angiotensin-aldosterone system.

References: 1. Klijian A, et al. J Cardiothorac Vasc Anesth. 2021;35(1):51-58. 2. Ltaief Z, et al. J Clin Med. 2022;11(21):6407. 3. Busse LW, et al. Crit Care. 2020;24(1):36. 4. Boisramé-Helms J, et al. Curr Vasc Pharmacol. 2013;11(2):150-160. 5. Miranda M, et al. Am J Physiol Heart Circ Physiol. 2016;311(1):H24-H35. 6. Parrillo JE, et al. Ann Intern Med. 1990;113(3):227-242. 7. Annane D, et al. Lancet. 2005;365(9453):63-78. 8. Tsiouris A, et al. Gen Thorac Cardiovasc Surg. 2017;65(10):557-565. 9. Fountain JH, et al. StatPearls; 2023. Accessed January 14, 2025. https://www.ncbi.nlm.nih.gov/books/NBK470410/ 10. Tibi S, et al. J Clin Med. 2023;12(14):4566. 11. Papazisi O, et al. Cardiovasc Drugs Ther. 2022;36(4):739-748. 12. Bellomo R, et al. Am J Respir Crit Care Med. 2020;202(9):1253-1261.

ACE=angiotensin-converting enzyme; ANG=angiotensin; CPB=cardiopulmonary bypass; RAAS=renin-angiotensin-aldosterone system.

References: 1. Klijian A, et al. J Cardiothorac Vasc Anesth. 2021;35(1):51-58. 2. Ltaief Z, et al. J. Clin. Med. 2022;11(21):6407. 3. Busse LW, et al. Crit Care. 2020;24(1):36. 4. Boisramé-Helms J, et al. Curr Vasc Pharmacol. 2013;11(2):150-160. 5. Miranda M, et al. Am J Physiol Heart Circ Physiol. 2016;311(1):H24-H35. 6. Parrillo JE, et al. Ann Intern Med. 1990;113(3):227-242. 7. Annane D, et al. Lancet. 2005;365(9453):63-78. 8. Tsiouris A, et al. Gen Thorac Cardiovasc Surg. 2017;65(10):557-565. 9. Fountain JH, et al. StatPearls; 2023. Accessed January 14, 2025. https://www.ncbi.nlm.nih.gov/books/NBK470410/ 10. Tibi S, et al. J ClinMed. 2023;12(14):4566. 11. Papazisi O, et al. Cardiovasc Drugs Ther. 2022;36(4):739-748. 12. Bellomo R, et al. Am J Respir Crit Care Med. 2020;202(9):1253-1261.

© 2025 Innoviva Specialty Therapeutics™. All rights reserved.
NP-GIA-US-0001 | 12/25
© 2025 Innoviva Specialty Therapeutics™. All rights reserved.
NP-GIA-US-0001 | 12/25