phenylephrine

Pure alpha-1 agonist — vasoconstriction with no inotropy and no chronotropy. Niche roles: peri-operative hypotension, tachyarrhythmias, and LVOT obstruction (HOCM/SAM). Classic error: cardiogenic shock, where afterload without contractility crushes the failing LV.

mechanism

Pure alpha-1 agonist — essentially no beta activity at clinical doses
Arterial and venous constriction → ↑SVR, ↑venous return
Baroreceptor-mediated reflex bradycardia follows the MAP rise (no beta-1 to oppose it)

Net haemodynamics: ↑↑SVR, ↑MAP, ↓HR, ↓CO

dosing

setting	dose
IV bolus	50–200 mcg, repeat q1–2 min
push-dose (dilute)	100 mcg/mL — give 0.5–2 mL
infusion	25–200 mcg/min (≈0.25–3 mcg/kg/min)
spinal/epidural hypotension	50–100 mcg boluses, or low-dose infusion

PK: onset immediate (IV) · duration 5–20 min · metabolised by MAO
Peripherally administrable at dilute concentration — practical advantage in OR and ED

key points

Pressure drug, not a flow drug — if the problem is low CO, phenylephrine makes things worse
HOCM/SAM crash: the intuitive drugs (inotropes, tachycardia) all worsen the obstruction → answer is phenylephrine + fluids + slow the heart (beta-blocker) + stop inotropes
In septic patients with AF/RVR and hypotension, reasonable options are phenylephrine or vasopressin — both raise MAP without chronotropy
If running phenylephrine in a critically ill medical patient for more than a few hours, ask why it isn’t norepinephrine
Right-to-left shunt physiology (e.g. tetralogy spells) — ↑SVR reverses the shunt

avoid in cardiogenic shock

Afterload without inotropy → SV and CO fall further. Not a first-line septic shock agent — inferior to norepinephrine for tissue perfusion and associated with worse outcomes when used as a substitute.

adverse effects

Reflex bradycardia — occasionally profound; problematic if CO is HR-dependent
↓CO — raises MAP while reducing cardiac output and possibly regional (splanchnic, renal) perfusion
Extravasation necrosis (alpha-mediated) — phentolamine as for norepinephrine
Caution in severe PVD, mesenteric ischaemia, high-grade AV block

evidence

Vail, JAMA. 2017 — during the 2011 US norepinephrine shortage, hospitals that switched predominantly to phenylephrine had higher in-hospital mortality in septic shock (absolute risk increase 3.7%) — the strongest available argument against it as a primary septic shock pressor
Little RCT evidence in shock; largely an anaesthesia drug used off-label in critical care