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λνλ―Όμ λ΄μΈμ± **μΉ΄ν μ½μλ―Ό**μ΄λ©° λ Έλ₯΄μνΌλ€νλ¦°μ μ§μ μ μΈ λμ¬ μ ꡬ체μ λλ€. μμν μ€νμ μΉλ£μμ μ£Όλ‘ μ μ ν μμ‘ μμμ *μ΄ν* νμνμ λΆμμ μ±(νΉν μ νμμ± μΌν¬ λ° κΈμ± μ¬λΆμ )μ κ΄λ¦¬νκΈ° μν΄ μ§μμ μ λ§₯ μ£Όμ (CRI)μΌλ‘ μ¬μ©λ©λλ€. ### μμ μμ½ * **μ©λ μμ‘΄μ ν¨κ³Ό**: λνλ―Όμ μμ©μ²΄ μΉνλ ₯μ μ£Όμ μλμ λ°λΌ κ·Ήμ μΌλ‘ λ³νλ©°, λνλ―Όμ±(νκ΄ νμ₯)μμ λ² ν-1(κ°μ¬ μμ©), μν-1(μΉμ μμ©) ν¨κ³Όλ‘ μ§νλ©λλ€. * **μ μ₯ μ©λ λ Όλ**: κ³Όκ±°μλ νλ¨μ± κΈμ± μ μμμμ μ΄λ¨λ₯Ό μ΄μ§νκΈ° μν΄ 'μ μ©λ' λνλ―Όμ΄ μ¬μ©λμμ΅λλ€. νλμ μ¦κ±°μ λ°λ₯΄λ©΄ μ¬κ΅¬μ²΄ μ¬κ³Όμ¨(GFR)μ μ μνκ² κ°μ νμ§ λͺ»νλ©°, κ°μμμ μ¬μ©μ μ μ¦λμ§ μμκ±°λ λ Όλμ μ¬μ§κ° μκ³ κ³ μμ΄μκ²λ ν΄λ‘μΈ μ μμ΅λλ€. * **μ격ν ν¬μ¬ κ·μΉ**: μ μ© μ λ§₯ λΌμΈκ³Ό μ£Όμ¬κΈ° νν λλ μμ‘ ννλ₯Ό μ¬μ©νμ¬ ν¬μ¬ν΄μΌ ν©λλ€. **νκ΄ μΈ μ μΆ**μ μ¬κ°ν μ‘°μ§ κ΄΄μ¬λ₯Ό μ λ°ν©λλ€.
μμ© κΈ°μ : Dopamine acts directly on **dopaminergic**, **Ξ²1-adrenergic**, and **Ξ±1-adrenergic** receptors, and indirectly by stimulating the release of endogenous norepinephrine from sympathetic nerve terminals. Its effects are highly dose-dependent: * **Low Dose (0.5β2 Β΅g/kg/min)**: Primarily stimulates **D1 and D2 dopaminergic receptors** β vasodilation of renal, mesenteric, coronary, and intracerebral vascular beds. Increases renal blood flow and urine output, but does not appreciably increase GFR. * **Medium Dose (2β10 Β΅g/kg/min)**: Stimulates **Ξ²1-adrenergic receptors** in the myocardium β increases intracellular cAMP β positive inotropic (increased contractility) and mild chronotropic (increased heart rate) effects. Improves cardiac output and organ perfusion. * **High Dose (>10β12 Β΅g/kg/min)**: Overrides dopaminergic effects and strongly stimulates **Ξ±1-adrenergic receptors** in the vasculature β profound vasoconstriction β increases systemic vascular resistance (SVR) and blood pressure. Renal and peripheral blood flows are decreased at these rates.
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- Vasodilatory shock if fluid resuscitation and dobutamine is not successful Β· 2.5-10 micrograms/kg/min Β· IV Β· CRI Β· Titrated to effect Β· If not successful may try adding norepinephrine.
- Treatment of severe hypotension/shock Β· 1-3 micrograms/kg/minute CRI; higher dosages of 3-10 micrograms/kg/min CRI are indicated if greater cardiotonic and BP support are indicated Β· IV Β· CRI Β· Titrated to effect Β· Not a substitute for adequate volume replacement therapy.
- Treatment of severe hypotension/shock after fluid correction and if dobutamine does not give desired effect Β· 1-10 micrograms/kg/min Β· IV Β· CRI Β· Titrated to effect
- Vasodilatory shock if fluid resuscitation and dobutamine is not successful Β· 2.5-10 micrograms/kg/min Β· IV Β· CRI Β· Titrated to effect Β· If not successful may try adding norepinephrine.
- Adjunctive therapy for acute heart failure Β· 1-10 micrograms/kg/min Β· IV Β· CRI Β· Titrated to effect Β· Initially, a dose of 2 micrograms/kg/min is usually used and titrated upward to desired clinical effect. Doses higher than 10 may increase peripheral vascular resistance and heart rate.
- Treatment of severe hypotension/shock Β· 1-3 micrograms/kg/minute CRI; higher dosages of 3-10 micrograms/kg/min CRI are indicated if greater cardiotonic and BP support are indicated Β· IV Β· CRI Β· Titrated to effect Β· Not a substitute for adequate volume replacement therapy.
- Treatment of severe hypotension/shock after fluid correction and if dobutamine does not give desired effect Β· 1-10 micrograms/kg/min Β· IV Β· CRI Β· Titrated to effect
ν¬μ¬ κ²½λ‘
κΈκΈ°
- Pheochromocytoma
- Ventricular fibrillation
- Uncorrected tachyarrhythmias
- Uncorrected hypovolemia (must replace fluids first)
μ΄μλ°μ
- Nausea and vomiting
- Ectopic beats (arrhythmias)
- Tachycardia
- Palpitations
- Hypotension (at low doses) or Hypertension (at high doses)
- Dyspnea
- Vasoconstriction (reduced peripheral circulation)
- Severe tissue necrosis and sloughing (if extravasated)
μ½λ¬Ό μνΈμμ©
- Alpha-adrenergic blockers (e.g., prazosin) Β· May antagonize the vasoconstrictive properties of high-dose dopamine.
- Halogenated hydrocarbon anesthetics (e.g., halothane) Β· May result in increased incidences of ventricular arrhythmias.
- Tricyclic antidepressants Β· May potentiate adverse cardiovascular effects.
- Beta-blockers (e.g., propranolol, metoprolol) Β· May antagonize the cardiac (inotropic/chronotropic) effects of dopamine.
- Diuretics Β· May potentiate urine production effects of low-dose dopamine.
- Monoamine oxidase inhibitors (MAOIs) Β· Can significantly prolong and enhance the effects of dopamine.
- Oxytocic drugs Β· May cause severe hypertension when used concurrently.
- Phenothiazines Β· May antagonize the renal and mesenteric vasodilatation effects of dopamine.
- Vasopressors/Vasoconstrictors Β· Concurrent use may cause severe hypertension.
λͺ¨λν°λ§
- Continuous electrocardiogram (ECG) for cardiac rate and rhythm
- Direct or indirect blood pressure
- Urine output/flow
- IV catheter site (frequent checks for patency and signs of extravasation)
κ³Όμ©λ
Accidental overdosage is primarily manifested by **excessive blood pressure elevation** (severe hypertension) and arrhythmias. * **Treatment**: Because dopamine's half-life is extremely short (~2 minutes), treatment usually consists only of temporarily discontinuing the IV infusion or reducing the rate until parameters normalize. * If the patient's condition fails to stabilize rapidly after discontinuation, the alpha-adrenergic antagonist **phentolamine** may be administered.
VetSheet μ½λ¬Ό λ νΌλ°μ€λ λ©΄ν μμ μ λ¬Έκ°λ₯Ό μν μμ μμ¬κ²°μ 보쑰 λꡬμ΄λ©°, μ λ¬Έμ νλ¨μ΄λ μ μ‘°μ¬μ μ΅μ λΌλ²¨μ λμ νμ§ μμ΅λλ€.