Inj Noradrenaline and Inj Dopamine mode of action and use

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norepinephrine AND dopamine

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Surviving Sepsis Campaign norepinephrine dopamine vasopressor recommendation

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1. Injection Noradrenaline (Norepinephrine)

Mode of action

Noradrenaline is a sympathomimetic catecholamine that acts mainly on:
  • Alpha-1 receptors: powerful arterial and venous vasoconstriction
    • Raises systemic vascular resistance (SVR)
    • Raises blood pressure and mean arterial pressure (MAP)
  • Alpha-2 receptors: reduces further norepinephrine release from nerve terminals
  • Beta-1 receptors: mild increase in cardiac contractility
It has very little beta-2 activity. The rise in BP may produce reflex bradycardia, so heart rate may not increase despite beta-1 activity.

Main uses

  • First-line vasopressor in septic shock after appropriate fluid resuscitation
  • Acute severe hypotension due to vasodilatory shock, for example:
    • Septic shock
    • Neurogenic shock
    • Anesthesia-related vasodilation
  • Support of BP in critically ill patients while the underlying cause is treated
The Surviving Sepsis Campaign guideline recommends norepinephrine as the first-line vasopressor for adults with septic shock.

Important adverse effects / precautions

  • Excess vasoconstriction can reduce perfusion to skin, kidneys, gut, and limbs
  • Tachyarrhythmias are possible, though usually less frequent than with dopamine
  • Extravasation can cause severe local ischemia and tissue necrosis
  • Give as a titrated continuous IV infusion, preferably through a central venous catheter, with continuous BP and cardiac monitoring

2. Injection Dopamine

Mode of action

Dopamine is an endogenous catecholamine and a precursor of norepinephrine. Its receptor action is dose-dependent:
Infusion rangePredominant receptor effectsMain effect
Low doseDopaminergic D1 receptorsRenal and splanchnic vasodilation
Moderate doseBeta-1 receptorsIncreased heart rate, contractility, and cardiac output
High doseAlpha-1 receptorsVasoconstriction and increased BP
In practice, do not use low-dose dopamine merely to increase urine output or as “renal-dose dopamine.” It has not been shown to protect kidney function in critically ill patients.

Main uses

  • Selected cases of hypotension with low cardiac output, particularly if there is significant bradycardia
  • Cardiogenic shock in limited circumstances, especially when hypotension is present and an alternative is unsuitable
  • Alternative vasopressor only when norepinephrine is unavailable or not appropriate
Dopamine was historically used in septic shock, but it causes more tachyarrhythmias than norepinephrine. Current sepsis guidance favors norepinephrine; dopamine is an alternative where norepinephrine is unavailable, with particular caution in patients at risk of arrhythmia. See the SCCM guideline summary.

Important adverse effects / precautions

  • Tachycardia and arrhythmias, especially atrial fibrillation and ventricular arrhythmias
  • Increased myocardial oxygen demand, which can worsen myocardial ischemia
  • Nausea, headache, peripheral ischemia at high doses
  • Extravasation can cause tissue necrosis
  • Continuous ECG and BP monitoring are required

Quick comparison

FeatureNoradrenalineDopamine
Main receptor actionAlpha-1 > beta-1Dose-dependent D1, beta-1, alpha-1
Dominant clinical effectVasoconstriction, raises MAPRaises cardiac output at moderate dose; vasoconstriction at high dose
Septic shockPreferred first-lineUsually avoided if norepinephrine is available
Arrhythmia riskLowerHigher
Useful whenVasodilatory hypotensionHypotension with low output and marked bradycardia, selected cases
Clinical note: These are high-risk ICU/emergency medicines. They must be administered as titrated infusions under trained supervision with monitoring and treatment of the cause of shock, not simply to normalize the BP.
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