Nitroprusside Flashcards
What is the mechanism of action of nitroprusside?
Nitroprusside causes arterial and venous dilation by increasing nitric oxide (NO), which leads to increased cyclic GMP and smooth muscle relaxation.
What is the primary physiological effect of nitroprusside?
It reduces both preload and afterload by dilating arteries and veins, leading to a rapid decrease in blood pressure.
Why is nitroprusside preferred over hydralazine in acute heart failure?
It provides immediate afterload reduction without reflex tachycardia, whereas hydralazine can cause significant sympathetic activation.
What are the main clinical indications for nitroprusside?
Hypertensive emergencies, acute heart failure, and afterload reduction in conditions like acute mitral regurgitation or aortic regurgitation.
What medications are commonly first-line in hypertensive emergencies?
Labetalol, nicardipine, clevidipine, and esmolol are preferred in most cases before considering nitroprusside.
Why is nitroprusside often not a first-line agent for hypertensive emergencies?
It has a short half-life, requires continuous infusion, and carries a risk of cyanide toxicity, especially with prolonged use.
What is the most severe adverse effect of nitroprusside toxicity?
Cyanide toxicity, which occurs due to the release of cyanide ions during metabolism.
What are the clinical signs of cyanide toxicity?
Altered mental status, lactic acidosis, confusion, seizures, coma, metabolic acidosis, and cardiovascular collapse.
Is a cherry red skin usually associated with cyanide toxicity?
Yes, cherry-red skin is a classic finding in cyanide toxicity, though it is more commonly associated with carbon monoxide poisoning.
How is cyanide toxicity diagnosed?
Based on clinical suspicion in a patient receiving nitroprusside with sudden metabolic acidosis (elevated lactic acid) and unexplained neurologic symptoms.
What is a good bedside diagnostic measure based on the hemoglobin curves to distinguish cyanide toxicity?
venous oxygen saturation (SvO₂)
What is the treatment for cyanide toxicity?
1) Sodium thiosulfate (converts cyanide to thiocyanate).
2) Hydroxocobalamin (binds cyanide).
3) Sodium nitrite (induces methemoglobinemia to neutralize cyanide).
What is methemoglobinemia and how does it relate to nitroprusside use?
Methemoglobinemia occurs when iron in hemoglobin is oxidized to Fe3+, which cannot bind oxygen, leading to functional anemia.
What are the clinical symptoms of methemoglobinemia?
Cyanosis (‘chocolate cyanosis’), dyspnea, headache, dizziness, and low oxygen saturation despite normal PaO2 on arterial blood gas.
How is methemoglobinemia diagnosed?
Methemoglobin level >1% (normal is <1%), chocolate-colored blood, and pulse oximetry showing low readings that do not improve with oxygen.
What is the treatment for methemoglobinemia?
Methylene blue, which reduces Fe3+ back to Fe2+, restoring normal hemoglobin function.
Why should nitroprusside be avoided in renal failure?
Impaired renal clearance leads to thiocyanate accumulation, increasing the risk of toxicity.
Why does nitroprusside require special handling?
It is light-sensitive and must be protected from light to prevent degradation.
