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**λνΈλ‘ν루μλ λνΈλ₯¨(Nitroprusside sodium)**μ μ€νμμ€ νκ²½μμλ§ μ μ μΌλ‘ μ¬μ©λλ λ§€μ° κ°λ ₯νκ³ μ΄λ¨κΈ° μμ©μ νλ **νΌν©ν νκ΄νμ₯μ **μ λλ€. μ£Όμ μμ μμ : * **μ£Όμ μ μμ¦**: κ³ νμ μκΈ°, μ€μ¦ μΉλͺ¨ν μλ₯μ μλ°νλ κΈμ± μ¬λΆμ λ° λΆμμ± μΈνμ± μ¬λΆμ (CHF)μ κ΄λ¦¬. * **νμνμ ν¨κ³Ό**: λλ§₯ λ° μ λ§₯ ννκ·Όμ μ΄μμμΌ μ λΆνμ νλΆνλ₯Ό λΉ λ₯΄κ² κ°μμν΅λλ€. * **μμ ν**: μ¬κ°ν μ νμ ν¨κ³Όμ λ§€μ° μ§§μ λ°κ°κΈ° λλ¬Έμ λ°λμ **μ§μμ μΈ μ§μ λλ§₯ νμ λͺ¨λν°λ§**κ³Ό ν¨κ» μ§μμ μ λ§₯ μ£Όμ (CRI)μΌλ‘ ν¬μ¬ν΄μΌ ν©λλ€. * **λ μ± μν**: μ₯κΈ°κ° μ¬μ©(>48-72μκ°)νκ±°λ κ³ μ©λμ ν¬μ¬νλ©΄, νΉν μ μ₯μ΄λ κ° κΈ°λ₯μ΄ μμλ νμμμ λ μ± λμ¬μ°λ¬Ό(μμνλ¬Ό λ° ν°μ€μμμ°μΌ)μ΄ μΆμ λ μ μμ΅λλ€.
μμ© κΈ°μ : Nitroprusside acts as a **nitric oxide (NO) donor**. * Once in the bloodstream, it interacts with tissue sulfhydryl groups to release NO. * NO activates the enzyme **soluble guanylate cyclase** in vascular smooth muscle cells. * This leads to an increase in intracellular **cyclic guanosine monophosphate (cGMP)**. * Elevated cGMP activates protein kinase G, which reduces intracellular calcium concentrations β **vascular smooth muscle relaxation**. This mechanism causes direct peripheral vasodilation of both arterioles and venules (independent of autonomic innervation), resulting in: * Lowered blood pressure * Significant reduction in total peripheral resistance (afterload) * Reduced left ventricular end-diastolic pressure (preload) * Mild decrease in cardiac output (though in severe heart failure, CO may actually increase due to afterload reduction) * Reflex tachycardia (increase in heart rate)
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- Hypertensive crisis (systolic arterial BP >200 mm Hg) Β· Initiate dose at 0.5 micrograms/kg/minute; increase dosage incrementally every 3-5 minutes until a predetermined target BP is attained. Reduce BP 25% over 4-hour period to allow readaptation of cerebral blood vessels. Β· IV Β· CRI Β· Titrate to effect
- Adjunctive treatment of heart failure (cardiogenic shock; fulminant pulmonary edema) Β· Initiate dose at 0.5 micrograms/kg/minute; increase dosage incrementally every 3-5 minutes. Goal to decrease or maintain mean arterial pressure to support vital organ functions-approx. 70 mmHg. Β· IV Β· CRI Β· Titrate to effect Β· Concurrent use of dobutamine (1-5 micrograms/kg/min) often indicated.
- Adjunctive treatment of heart failure Β· Initiate dose at 0.5 micrograms/kg/minute constant rate infusion and increase by 0.5-1 microgram/minute every 5 minutes to desired systolic pressure (90-100 mmHg). Β· IV Β· CRI Β· Titrate to effect Β· Cats are more sensitive to oxidative damage; keep total dosages to a minimum. Use dedicated line; never flush.
- Catastrophic pulmonary edema Β· As a CRI initiated at 1 microgram/kg/min and carefully titrated to effect by increasing by 1 microgram/kg/min increments every 15 minutes as long as BP remains stable and until perfusion and pulmonary function improves (cats usually requires between 1-2 micrograms/kg/min with the upper limit being 2 micrograms/kg/min). Β· IV Β· CRI Β· Maintain most effective dose for 12-15 hours Β· Systolic BP must remain >90 mm Hg. Wean nitroprusside over 6 hours first, then dobutamine over 6 hours.
- Hypertensive crisis (systolic arterial BP >200 mm Hg) Β· Initiate dose at 1-2 micrograms/kg/minute; increase dosage incrementally every 3-5 minutes until a predetermined target BP is attained. Reduce BP 25% over 4-hour period to allow readaptation of cerebral blood vessels. Β· IV Β· CRI Β· Titrate to effect
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- Compensatory hypertension (e.g., AV shunts, coarctation of the aorta, Cushing's reflex)
- Inadequate cerebral circulation
- Emergency surgery in patients near death
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- Profound hypotension
- Nausea
- Retching
- Restlessness
- Apprehension
- Muscle twitching
- Dizziness
- Infusion site irritation (avoid extravasation)
- Thiocyanate and cyanide toxicity (with prolonged use)
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- General Anesthetics (e.g., halothane, enflurane) Β· May enhance the hypotensive effects of nitroprusside.
- Dobutamine Β· Synergistic effects (increased cardiac output and reduced wedge pressure) may result; often used together beneficially in severe heart failure.
- Other Hypotensive Agents (e.g., beta-blockers, ACE inhibitors) Β· Patients may be more sensitive to the hypotensive effects of nitroprusside.
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- Blood pressure (constant, direct arterial monitoring preferred)
- Acid/base balance (to detect early metabolic acidosis/cyanide toxicity)
- Electrolytes (especially Na+)
- Respiratory effort and thoracic auscultation
- Serum thiocyanate levels (if on prolonged therapy or concurrent renal dysfunction)
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**Acute Overdosage**: Manifests as profound hypotension. * **Treatment**: Reduce or stop the infusion and administer IV fluids. Blood pressure will typically recover within 1-10 minutes. Monitor BP constantly. **Toxicity (Cyanide/Thiocyanate)**: Excessive doses, prolonged therapy (>3 days), depleted hepatic thiosulfate, or severe hepatic/renal insufficiency may lead to cyanogen or thiocyanate toxicity. * **Signs**: Metabolic acidosis (early sign of cyanogen toxicity), tolerance to therapy, delirium (thiocyanate toxicity in dogs). * **Monitoring**: Monitor acid/base status. Serum thiocyanate levels >100 mcg/mL are considered toxic. * **Treatment**: Hydroxocobalamin (Vitamin B12a) may prevent or treat cyanogen toxicity. Contact an animal poison control center for specific antidotal protocols if suspected.
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