What is the predominant mechanism for his lightheadedness/syncope?

A 59 year-old man with angina uses sublingual nitroglycerin to relieve his occasional episodes of chest pain. He has never had a myocardial infarction. He tells you that on several occasions his pain has not been completely relieved after taking nitroglycerin, so he has taken double the recommended dose. When he has done this, he has become lightheaded, and most recently, he fainted after standing up. What is the predominant mechanism for his lightheadedness/syncope?

1.Arterial vasoconstriction, increased systemic blood pressure, increased intracranial pressure
2.Arterial vasodilation, increased afterload, decreased cardiac output, decreased cerebral perfusion
3.Decreased myocardial contractility, decreased cardiac output, decreased cerebral perfusion
4.Venous vasoconstriction, decreased preload, decreased cardiac output, decreased cerebral perfusion
5.Venous vasodilation, decreased preload, decreased cardiac output, decreased cerebral perfusion

Correct answer
Venous vasodilation, decreased preload, decreased cardiac output, decreased cerebral perfusion

Nitroglycerin (a nitrate) causes relaxation of venous smooth muscle, leading to decreased venous pressures, and decreased venous return. This leads to decreased end diastolic volume (EDV) and less strain on heart muscle, relieving anginal pain. Using too much nitroglycerin could cause venous pooling and an excessive decrease in cardiac output (since VR = CO). The decrease in CO could cause lightheadedness, and when coupled with positional changes, could cause orthostatic syncope.