Vasopressors and Inotropes
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Direct answer
Noradrenaline is the first-line vasopressor in septic shock, started early and titrated to a mean arterial pressure of at least 65 mmHg, with lactate clearance and urine output confirming perfusion rather than pressure alone. It beat dopamine in the landmark comparison largely on arrhythmia prevention — dopamine's beta-1 dose means atrial fibrillation and ectopy, which is why it left routine first line. Vasopressin 0.03 units/min joins as a fixed, non-titratable second agent that spares catecholamine dose; adrenaline is added when a third pressor is needed. When the problem is pump failure rather than tone — low cardiac output with adequate pressure — the inotrope is dobutamine (beta-1 agonist, 2.5-10 micrograms/kg/min), or milrinone where a less tachycardic, more vasodilating inodilator suits, remembering it accumulates in renal failure.
What you must remember
- Noradrenaline first: start around 0.05 micrograms/kg/min and titrate (commonly to 0.5 or beyond) to mean arterial pressure at least 65 mmHg; central access preferred, short peripheral use now accepted in emergencies with a large-bore line and close surveillance.
- Why dopamine fell: more arrhythmia than noradrenaline at equivalent pressure benefit — including the famous "renal-dose dopamine" that never protected a kidney.
- Vasopressin 0.03 units/min: added at moderate noradrenaline doses, fixed-dose only (not titrated), catecholamine-sparing; stop when weaning.
- Adrenaline: second-line addition in septic shock and first-line in anaphylaxis — but at 0.5 mg intramuscularly for anaphylaxis, not as an infusion.
- Dobutamine 2.5-10 micrograms/kg/min: beta-1 driven inotropy for low-output states; causes tachycardia and can drop pressure through beta-2 effects, so it is paired with noradrenaline when tone is low.
- Milrinone: phosphodiesterase-3 inodilator independent of beta receptors — useful with beta-blocked patients and chronic heart failure, but hypotension-prone and renally cleared, so dose-adjust in kidney injury.
- Hydrocortisone 200 mg/day: for vasopressor-dependent septic shock not responding to catecholamines — refractory-shock adjunct, not routine.
- Monitoring targets: mean arterial pressure 65 mmHg plus perfusion markers — urine output above 0.5 mL/kg/hour, lactate falling, mental status — a pressure number without perfusion is not resuscitation.
A worked shock pathway
A 64-year-old with urosepsis arrives confused, mean arterial pressure 52 mmHg after a litre of crystalloid, lactate 5 mmol/L. Fluids continue judiciously — 30 mL/kg is the opening, not an endless chase — but because the pressure does not respond, noradrenaline starts within the first hour, peripherally if a central line is not yet in, with the target set at 65 mmHg. Cultures and antibiotics land within the hour. At 0.4 micrograms/kg/min of noradrenaline, vasopressin 0.03 units/min is added and hydrocortisone considered if the dose keeps climbing. Her lactate halves over six hours and urine output returns — the two numbers that say the drugs are working, because a normal blood pressure with a rising lactate is a dressed-up death.
Should her scenario shift to cold, mottled limbs with a wedge of pulmonary oedema — septic cardiomyopathy — the problem becomes output, and dobutamine joins the noradrenaline rather than replacing it: inotropy for the pump, pressor for the tone, each titrated to its own endpoint.
How the exam frames it
Receptor pharmacology is the scaffolding: candidates must map alpha-1 (phenylephrine — pure vasoconstriction), beta-1 (dobutamine — inotropy), mixed noradrenaline (alpha-dominant with modest beta-1) and dopamine's dose-dependent receptor parade, then answer the clinical question on top of it. The near-certain stem is "first-line vasopressor in septic shock" — noradrenaline — with dopamine offered specifically to punish older memorisation. The second certainty is the anaphylaxis distractor: adrenaline appears in both lists, but the answer for anaphylaxis is 0.5 mg intramuscularly, not an infusion, and stems love mixing the two. The Indian-context reality is worth one viva line: peripheral noradrenaline, once forbidden, is now accepted practice for early septic shock while central access is obtained — a change that matters most in crowded emergency departments where line placement delays pressors. Milrinone's renal accumulation is the quiet discriminator question in patients with kidney injury on chronic beta-blockers.
Frequently asked questions
Which vasopressor is first line in septic shock?
Noradrenaline, titrated to a mean arterial pressure of at least 65 mmHg — dopamine abandoned because of excess arrhythmia.
At what dose is vasopressin added, and why is it not titrated?
0.03 units/min as a fixed adjunct at moderate noradrenaline doses — higher doses add ischaemia without benefit, so it runs as a catecholamine-sparing constant.
When is dobutamine the right choice?
When cardiac output is low with adequate or high filling pressures and mean arterial pressure — pump failure — often paired with noradrenaline to preserve tone.
Why does milrinone need dose adjustment in renal failure?
It is renally cleared, so accumulation causes prolonged hypotension and arrhythmia in kidney injury.
How is pressor success monitored beyond blood pressure?
Perfusion markers — urine output above 0.5 mL/kg/hour, falling lactate and clearing mentation — confirm that the pressure number is translating into flow.