Septic Shock Management

Pathophysiology

A relative deficiency of vasopressin occurs in the early stages of septic shock due to depletion of reserves in the hypothalamic-pituitary axis, contributing to pathological vasodilation and refractory hypotension in patients with septic shock 1
Vasopressin acts mainly through V1a receptors in vascular smooth muscle, producing vasoconstriction independent of catecholamines in patients with septic shock 2
The deficiency of vasopressin becomes more evident during recovery from septic shock, with approximately 60% of patients showing inadequate responses to the osmotic challenge 5 days after recovery in a population of patients with septic shock 1
Angiotensin II, a potent endogenous vasoconstrictor, is also decreased or shows resistance to its effects during septic shock, leading to hypotension in patients with septic shock 1
Administration of synthetic human angiotensin II in patients with vasoplegic shock has been shown to increase systemic vascular resistance without altering cardiac output in a clinical setting 1
Downregulation of alpha-adrenergic receptors occurs, decreasing the vasoconstrictive response to endogenous and exogenous catecholamines in patients with septic shock 1

Norepinephrine is the first-choice vasopressor in septic shock, according to the guidelines from the Society of Critical Care Medicine 3
Vasopressin (up to 0.03 U/min) can be added to norepinephrine to increase mean arterial pressure or decrease the dose of norepinephrine in patients with septic shock, as recommended by the Society of Critical Care Medicine 3
The combination of norepinephrine with dobutamine may be beneficial to counteract excessive vasoconstriction and improve capillary and gastrointestinal blood flow in patients with septic shock, based on evidence from Critical Care Medicine 4