Dopamine is a **dose-dependent catecholamine**: D₁/D₂ at low dose, **β₁ inotropy** at moderate dose, and **α₁ vasoconstriction** at high dose.
It raises **CO** and **HR**, but carries **higher arrhythmia risk** than dobutamine/norepinephrine.
Dose **2–20 mcg/kg/min**, central line preferred; **avoid** for “renal protection,” and **treat extravasation with phentolamine.
# 1) Receptor-level action → clinical effects
**Receptors (dose-dependent):**
* **D₁/D₂ (≈1–3 mcg/kg/min)** → renal/mesenteric vasodilation, natriuresis (the classic “renal dose” effect).
**Clinical reality:** renal-protective strategy **not recommended**—no outcome benefit.
* **β₁ (≈3–10 mcg/kg/min)** → ↑ inotropy/chronotropy → ↑ CO, modest ↑ MAP.
* **α₁ (≥10–20 mcg/kg/min)** → vasoconstriction → ↑ SVR/MAP; tachyarrhythmia risk rises.
**Clinical effects from the above:**
* **Heart:** ↑ contractility (β₁), ↑ HR; may precipitate **AF/VT**.
* **Vessels:** low dose vasodilation (splanchnic/renal), moderate → little net change, high dose **vasoconstriction**.
* **Kidney:** ↑ diuresis at low dose in some, **but no proven renal protection**.
* **Metabolic:** can raise blood glucose, lactate (β-agonism).
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# 2) Vial strength, preparation & basic PK (+ disadvantages)
**Supply / prep**
* Common vials/amps: **200 mg/5 mL** (40 mg/mL).
* Typical infusions: **200 mg/50 mL (4 mg/mL)** or **400 mg/50 mL (8 mg/mL)** in 0.9% saline or 5% dextrose. Use **central line** if possible; guard against extravasation.
**PK you feel at the bedside**
* **Onset:** 2–5 min; **peak** ~10 min.
* **Offset:** 5–10 min after stopping.
* **Metabolism:** MAO & COMT (hepatic, renal, plasma) → inactive metabolites.
* **t½:** ~2 min.
**Disadvantages (from PD/PK)**
* **Tachyarrhythmias**, ↑ myocardial O₂ demand, **variable BP response** (esp. hypovolaemia).
* High-dose **vasoconstriction** may impair splanchnic perfusion.
* **Less predictable** than norepinephrine; higher arrhythmia rates in shock.
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# 3) Practical dosing
## A. Anaesthesia / OR (post-CPB or LV dysfunction)
* **Start:** **2–5 mcg/kg/min**, titrate q5–10 min by 2–5 mcg/kg/min.
* **Typical range:** **2–20 mcg/kg/min** (rarely higher).
* If hypotension with low SVR → may need **norepinephrine** adjunct rather than pushing dopamine high.
## B. ICU (shock, LCOS-Low Cardiac Output Syndrome)
* **Low cardiac output with relative bradycardia:** dopamine reasonable if you want **inotropy + HR** in one drug.
* **Septic shock:** **not first-line** (use **norepinephrine**); dopamine only if **bradycardic, low arrhythmia risk**, and limited access to other agents.
* **Cardiogenic shock:** can be used, but **arrhythmia risk > dobutamine**; many centres prefer **dobutamine ± norepinephrine**.
**Handy rate example (70 kg, 5 mcg/kg/min):**
* Using **8 mg/mL** (8000 mcg/mL): mL/h = (70×5×60) / 8000 ≈ **2.6 mL/h**.
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# 4) Special populations — dosing cautions
### Pregnancy
* Use only if benefits outweigh risks (maternal shock). Can reduce uterine blood flow at high doses (α₁ vasoconstriction).
### Lactation
* Poor oral bioavailability; clinically minimal infant exposure with short maternal use.
### Hepatic impairment
* Metabolised by MAO/COMT widely (not solely hepatic). No strict adjustment; **titrate to effect**.
### Renal impairment
* Metabolites renally excreted; haemodynamics guide dosing. **Do not use** for “renal protection.”
### Obesity
* Start low; titrate to haemodynamic targets. (Most dose to **actual body weight**, but watch for excessive tachycardia.)
### Paediatrics
* **Start 2–5 mcg/kg/min**, titrate to 20 mcg/kg/min max under specialist monitoring (more arrhythmia-prone).
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# 5) Drug interactions (clinically key)
* **MAO inhibitors** (or within 14 days): **massively potentiated** effect → severe hypertension/arrhythmias; **avoid or start at tiny doses with extreme caution**.
* **TCAs / SNRIs:** enhance pressor responses.
* **β-blockers:** blunt inotropy/chronotropy; unopposed α may ↑ SVR (context-dependent).
* **Inhalational anaesthetics (esp. halothane)**: **sensitise myocardium** to catecholamine-induced arrhythmias—use the lowest effective dose.
* **Other pressors/inotropes:** additive effects; coordinate with norepinephrine/dobutamine rather than stacking high dopamine alone.
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# 6) Significant complications & management
| Complication | Mechanism / Features | What to do |
| -------------------------------------------------- | -------------------------------------- | --------------------------------------------------------------------------------------------------------------------------------------------------------- |
| **Tachyarrhythmias (AF/VT), myocardial ischaemia** | β₁ stimulation ↑ HR/O₂ demand | Reduce/stop; correct electrolytes; consider **esmolol** (careful), switch to **dobutamine** or **norepinephrine** strategy. |
| **Hypertension with low output** | Excess α₁ tone | Titrate down; balance with inodilator (e.g., dobutamine/milrinone) if needed. |
| **Extravasation → local ischaemia/necrosis** | Intense α₁ vasoconstriction in tissues | **Stop infusion, leave cannula**, **infiltrate phentolamine 5–10 mg in 10–15 mL saline** around site ASAP; elevate/heat pack; surgical consult if severe. |
| **Gut/limb hypoperfusion** (high dose) | Vasoconstriction | Lower dose; switch agent; ensure MAP/flow balance. |
| **Endocrine effects (rare clinically)** | Dopaminergic pituitary inhibition | Usually not limiting; note possible ↓ prolactin transiently. |
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