Nitroprusside
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Cardiovascular Pharm (Old)
- Adenosine
- Magnesium
- Nitroprusside
- Nitrates
- Ivabradine
- Digoxin/Digitalis
- Class IA Antiarrhythmics
- Class IB Antiarrhythmics
- Class IC Antiarrhythmics
- Class II Antiarrhythmics
- Class III Antiarrhythmics - Amiodarone
- Class III Antiarrythmics - Sotalol
- Class III Antiarrhythmics - Ibutilide, Dofetilide
- Class IV Antiarrhythmics - Verapamil, Diltiazem
- HMG-CoA Reductase Inhibitors (Statins)
- Ezetimibe
- Fibrates
- PCSK9 Inhibitors (Alirocumab, Evolocumab)
- Fish Oil and Omega-3s
- Milrinone
- Aliskiren
- Hydralazine
- Ranolazine
- Sacubitril
Summary
Nitroprusside is a vasodilating drug that works by causing the direct release of nitric oxide and a subsequent increase in cGMP to lead to smooth muscle relaxation. Nitroprusside is a balanced arterial and venous dilator. Nitroprusside is used first-line in the treatment of hypertensive emergencies, and is associated with dose-dependent cyanide poisoning due to the drug being metabolized to cyanide in the body.
Key Points
- Nitroprusside
- Mechanism
- Potent vasodilator
- Direct release of NO → Increases cGMP
- Does not depend on intracellular metabolism into NO (I like to think that this is why it affects arteries equally)
- relaxes vascular smooth muscle
- Balanced (arteries = veins)
- Contrast vs. nitrates, which primarily target veins
- Nitroprusside targets both preload and afterload
- Direct release of NO → Increases cGMP
- Potent vasodilator
- Indications
- Hypertensive emergency (1st line)
- Favored due to its quick onset and short duration of action
- Acute decompensated heart failure
- Helps to reduce afterload (and preload), reducing the work on the heart
- Sodium Cyanide-Nitroprusside test
- Rapid test to detect cysteine in urine (Cystinuria)
- not pharmacologic; should be thought of as a separate lab test and not a drug
- Hypertensive emergency (1st line)
- Adverse Effects
- Cyanide toxicity
- Metabolized into cyanide and thiocyanate, which limits dosing
- This is how cyanide toxicity may be tested (script) → check out our other video on this
- Treatment by thiosulfate, which adds a sulfur group to CN to help it be cleared by the kidneys as thiocyanate
- Metabolized into cyanide and thiocyanate, which limits dosing
- Hypotension (obvious)
- May cause increased intracranial pressure
- Via vasodilation of cerebral arteries
- Cyanide toxicity
- Mechanism