Vasopressor Selection by Shock Type
Pharmacology II · 9 min read
Pick the right pressor by physiology, not by habit. Norepi for sepsis. Vasopressin for ACE-i vasoplegia. Phenylephrine for AS. The 'why' makes the difference.
Receptor cheat sheet
Before the drug list, lock the receptors. α1: arterial vasoconstriction → ↑ SVR + ↑ BP. α2: central sympatholysis (clonidine, dexmedetomidine). β1: heart — ↑ HR + ↑ contractility. β2: bronchial + arterial dilation, ↓ SVR at low doses. V1 (vasopressin): vascular smooth muscle, cAMP-INDEPENDENT — works in acidosis where adrenergic receptors are downregulated. D1/D2: low-dose dopamine, splanchnic + renal vasodilation (clinically irrelevant after PROCESS-style trials).
Norepinephrine — sepsis first-line
Predominantly α1 with modest β1. Raises SVR without dramatic chronotropy. SOAP-II (NEJM 2010) showed lower mortality + fewer arrhythmias vs dopamine in shock; Surviving Sepsis Campaign 2021 calls norepinephrine the FIRST-LINE vasopressor in septic shock. Dose 0.05-0.5+ mcg/kg/min, titrated to MAP target (≥65 default; some patients with chronic HTN need ≥75). Central line preferred for prolonged infusion (extravasation = phentolamine 5-10 mg in 10 mL saline injected SQ around site).
Norepinephrine drug entry →Vasopressin — the V1 outlier
0.01-0.04 U/min FIXED rate (not weight-based). No chronotropy, no β2 vasodilation. UNIQUE STRENGTH: cAMP-INDEPENDENT vasoconstriction works in acidosis where adrenergic receptors are downregulated. Two big use cases: (1) ACE-i / ARB vasoplegia at induction or post-CPB (the renin-angiotensin axis is suppressed; the body relies on vasopressin for SVR — bolus 1-2 units pre-induction in known refractory HTN ACE-i patients). (2) Pulmonary HTN + RV failure — vasopressin selectively raises SVR WITHOUT raising PVR (unlike phenylephrine which can worsen RV in pulm HTN). VASST trial showed addition of vasopressin to NE in septic shock did not change overall mortality but reduced norepinephrine requirement. Don't titrate above 0.04 U/min — diminishing benefit + ischemia risk.
Phenylephrine — pure α1
Bolus 50-200 mcg or infusion 0.5-5 mcg/kg/min. Pure α1 — vasoconstriction with REFLEX bradycardia. IDEAL for: aortic stenosis (preserves SVR + slows HR), HOCM (raises afterload reduces dynamic LVOT obstruction), spinal-induced hypotension (predictable response). RELATIVE caution in severe pulmonary HTN — pure α may raise PVR more than SVR; vasopressin preferred in true RV failure. Don't pair with significant tachycardia — slowing HR with phenylephrine while heart already strains is a wash.
Epinephrine — the dose-dependent shapeshifter
Low dose (0.01-0.05 mcg/kg/min): predominantly β1 + β2 → ↑ HR + ↑ contractility + bronchodilation + mild vasodilation. High dose (>0.1 mcg/kg/min): α dominates → vasoconstriction + ↑ SVR. INDICATIONS: cardiac arrest 1 mg IV q3-5 min (ACLS), anaphylaxis 10-100 mcg IV titrated (NEVER withhold — see anaphylaxis lecture), refractory shock after norepi + vasopressin, severe bronchospasm refractory to inhaled β2. Watch: ↑ glucose, ↑ lactate (β2-mediated muscle glycogenolysis — interpret lactate cautiously when patient is on epi).
Epinephrine drug entry →Dobutamine + milrinone — when CO is the problem
Cardiogenic shock is a delivery problem, not always a tone problem. Dobutamine 2-20 mcg/kg/min: β1-dominant → ↑ contractility + mild β2 → ↓ SVR. Pair with norepinephrine if SVR drops. Milrinone 0.25-0.75 mcg/kg/min (after 50 mcg/kg load if hemodynamically stable): PDE3 inhibitor → ↑ cAMP → inotrope + pulmonary AND systemic vasodilator. Useful in RV failure (lowers PVR) but lowers SVR too — pair with vasopressor. Renal clearance — adjust dose in renal failure.
Pearl — match physiology, not protocol
Septic shock with refractory HoTN despite norepi 0.5 mcg/kg/min → add vasopressin 0.04 U/min before climbing norepi. Severe AS HoTN → phenylephrine, never propofol-induced vasodilation. Pulmonary HTN with RV failure → vasopressin + iNO + milrinone, NOT phenylephrine. Cardiac arrest → epinephrine 1 mg q3-5; vasopressin no longer routinely recommended (replaced by epi-only in 2010 guidelines + still). Anaphylaxis → epi titrated 10-100 mcg IV every 1-2 min until response — never withhold. ACE-i induction crash → vasopressin bolus 1-2 units + infusion. Cardiogenic shock → norepi + dobutamine OR milrinone (paired with vasopressor) + IABP/Impella + revascularize the cause.
References
- · Surviving Sepsis Campaign 2021
- · SOAP-II Trial NEJM 2010
- · VASST Trial NEJM 2008
- · Stoelting Pharmacology 6e Ch 13