Pharmacological action: Sodium nitroprusside is a kind of nitrohydrocyanate, which directly acts on the powerful dilator of arteriovenous vascular bed. The drug can directly dilate the resistance and volume vessels, and has a greater effect on afterload than nitroglycerin, so it can reduce the left ventricular filling pressure and increase the cardiac output.
The effect of sodium nitroprusside on acute decompensation in patients with chronic left heart failure is faster and stronger than that of furosemide. Because sodium nitroprusside mainly acts on the resistance blood vessels in coronary circulation, it can cause coronary steal. Sodium nitroprusside can increase the arteriovenous shunt of myocardium and lung, so the increase of total blood flow is not necessarily manifested as the increase of partial blood flow improved by perfusion.
The increase of stroke volume can offset the decrease of peripheral vascular resistance, so the arterial blood pressure will not drop greatly. Heart rate generally does not increase, and may even decrease due to the improvement of hemodynamics. Its mechanism of action is the same as nitrate, which can make vascular endothelial cells release NO and activate guanylate cyclase, increase the level of cGMP in cells and dilate blood vessels.
The specific types of hemodynamic changes and the basis of internal lesions may be helpful to the choice of drugs. For patients with obvious pump dysfunction, increased left ventricular filling pressure, increased peripheral vascular resistance, decreased cardiac output and normal or increased arterial pressure, sodium nitroprusside should be used for short-term intravenous drip.