Table 3.

Vasopressors for management of septic shock

Drug	Receptor activity	Potential biomarkers to guide treatment	Hemodynamic and organ-specific effects	Specific patient groups who may benefit
Norepinephrine	α1, α2, β1, and β3 receptor agonist		* Marked increase in MAP *Minimal increase in CO and HR	* First-line vasopressor for most patients
Dopamine	DA1 and DA2 agonist		* Moderate increase in MAP and CO * Tachycardia and arrhythmias * Impaired hypothalamic and hypophysis function	* If norepinephrine not available
Epinephrine	β-1, β-2, and α-1 receptor activity (dose-dependent)		* Marked increased in MAP and HR * Moderate increase in CO * Tachycardia and arrhythmias * Decrease in splanchnic perfusion at high doses * Major metabolic effects (acceleration of glycolysis, thermogenic effect, hypokalemia…)	* If anaphylactic component is suspected * Bradycardia septic shock * Refractory septic shock with myocardial dysfunction but the combination norepinephrine + dobutamine may be preferable (modulating doses of dobutamine according to CO)
Phenylephrine	Pure α1 agonist		* Marked increase in MAP * Decrease in CO * Decrease in splanchnic perfusion	* If norepinephrine not available
Metaraminol	α1 agonist		* Similar to low dose norepinephrine	* Short-term strategy in vasodilatory shock until more effective vasopressors available
Vasopressin	VPR1 and VPR2 agonist	LNPEP SNP angiopoetin vasopressin/copeptin	* Marked increase in MAP * Minimal increase in HR and lower incidence of arrhythmias * Minimal increase or even decrease in CO * Improvement in GFR * Impairment in splanchnic perfusion, especially at high doses * Increased risk of digital necrosis * Potential pro-aggregant effect * May improve endothelial permeability	* Patients with arrhythmias * Patients with significant AKI * Avoid in patients with peripheral ischemia *In future, identification of ideal patients using biomarkers
Terlipressin	VPR1 >  > VPR2 agonist	LNPEP SNP vasopressin/copeptin	* Marked increase in MAP * Minimal increase in HR and lower incidence of arrhythmias *Minimal increase or even decrease in CO * Improvement in GFR *Impairment in splanchnic perfusion, especially at high doses *Increased risk of digital necrosis *Potential pro-aggregant effect * May improve endothelial permeability	*Patients with arrhythmias *Patients with significant AKI *Patients with cirrhosis-associated hepatorenal syndrome and systemic inflammatory syndrome * Avoid in patients with peripheral ischemia *In future, identification of ideal patients using biomarkers
Selepressin	VPR1 agonist	LNPEP SNP angiopoetin vasopressin/copeptin	* Marked increased in MAP * Minimal impact on HR and CO * Improve endothelial permeability * Impairment in splanchnic perfusion * Increased risk of myocardial ischemia	*Not available
Angiotensin II	Angiotensin I and angiotensin II receptor	ang I/ang II ratio renin AGTRAP	* Marked increase in MAP * Minimal increase in CO * Tachycardia * Improved GFR—Faster liberation from RRT * Increased risk of pulmonary embolism * Increased risk of fungal infections	* Patients with refractory septic shock * Patients receiving RRT *In future, identification of ideal patients using biomarkers

AF = atrial fibrillation; AGTRAP = angiotensin II receptor associated protein; AKI = acute kidney injury; VPR = vasopressin receptor; DA = dopamine; LNPEP leucyl and cystinyl aminopeptidase; RCT = randomized controlled trial; RAAS = renin–angiotensin–aldosterone system; RRT = renal replacement therapy; SNP = single nucleotide polymorphism; CO = cardiac output; HR = heart rate; GFR = glomerular filtration rate; MAP = mean arterial pressure