Mechanism of Action
Converted to NO which stimulates cGMP production. Acts as a smooth muscle relaxant and venodilator (why NTG is more of a venodilator than a vasodilator is not known). Note that the process of NO formation is dependent on availability of sulfhydryl (SH) groups and thus tolerance can develop.
Venodilation which decreases filling pressures, venous return, and thus myocardial work. The effects of NTG are dose-dependent.
Dose-Dependent effects of NTG Low dose (< 150 ucg/min): venodilation Higher doses (> 150 ucg/min): arteriolar vasodilation
NTG decreases diastolic blood pressure, however because filling pressures are decreased, theoretically myocardial perfusion can be preserved. The end result of NTG administration is dependent on the totality of its various hemodynamic effects (venodilation, decreased VR, decreased systemic pressure, increased HR).
NTG affects the pulmonary vasculature as well, causing decreases in RAP, PAP, and PCWP.
Potent coronary vasodilator, however total CBF decreases (probably because of autoregulation and the decrease in cardiac work). Dilates collateral vessels and because it decreases LVEDP, may improve subendocardial flow (especially in ischemic areas) despite the fact that total coronary artery blood flow decreases.
First-line agent in virtually all instances of myocardial ischemia. When combined with phenylephrine may offer decrease in preload as well as decrease in heart rate (and possibly increased perfusion pressure and afterload).
Note that the effective dose of NTG may vary substantially, ranging from 5 to 600 ucg/min.
Very short-acting, with resolution within 5 minutes.