doctorbetty Posted July 3, 2012 Report Share Posted July 3, 2012 Nitrospray will cause vasodilation of coronary arteries and therefore improve myocardial oxygen supply to the heart, reducing myocardial oxygen demand. This makes sense to me. Why does my drug guide state that myocardial oxygen CONSUMPTION will decrease? This seems counterintuitive... I would think that if there is more oxygen available, consumption should increase. Can anyone explain? Is it b/c the heart is not working as hard and therefore requires less oxygen? I thought the reason angina is relieved is b/c oxygen is more readily available to CONSUME. Thanks in advance! Link to comment Share on other sites More sharing options...
pheochromocytoma Posted July 3, 2012 Report Share Posted July 3, 2012 venodilation is also a result -> decrease preload = decreased wall stress = decrease 02 cons. Also, vasodilation -> decreased afterload = decreased wall stress = decreased 02 cons. Link to comment Share on other sites More sharing options...
doctorbetty Posted July 3, 2012 Author Report Share Posted July 3, 2012 Thanks for the explanation. Thinking in terms of myocardial wall stress makes more sense. I will review this topic some more... I wish we learned this stuff in nursing... the course is way too general for my liking! Link to comment Share on other sites More sharing options...
leviathan Posted July 4, 2012 Report Share Posted July 4, 2012 It's odd that your course teaches the wrong mechanism for why nitro helps (dilating coronary vessels) but then teaches the right reason for why it works (decreasing myocardial demand). The coronary vasodilation is actually thought to be harmful because ischemic areas of the heart already are maximally vasodilated. Dilating up the other coronary vessels will then steal/redirect bloodflow away from ischemic myocardium. Link to comment Share on other sites More sharing options...
cheech10 Posted July 4, 2012 Report Share Posted July 4, 2012 Not harmful exactly: you'd have to have *extremely* low cardiac output for bloodflow to actually be redirected away from ischemic heart muscle in absolute terms (there is a relative change as you describe, which is the basis for myocardial perfusion scanning, but the bloodflow to potentially ischemic areas doesn't drop in absolute terms). Link to comment Share on other sites More sharing options...
doctorbetty Posted July 4, 2012 Author Report Share Posted July 4, 2012 It's odd that your course teaches the wrong mechanism for why nitro helps (dilating coronary vessels) but then teaches the right reason for why it works (decreasing myocardial demand). The coronary vasodilation is actually thought to be harmful because ischemic areas of the heart already are maximally vasodilated. Dilating up the other coronary vessels will then steal/redirect bloodflow away from ischemic myocardium. So the venodilation is most helpful? And the reduction in preload and wall stress leads to reduced myocardial oxygen demand and myocardial O2 cons? Vasodilation of the coronary arteries is not the best explanation in terms of nitro's pharmacodynamics? Thanks Link to comment Share on other sites More sharing options...
doctorbetty Posted July 4, 2012 Author Report Share Posted July 4, 2012 So the venodilation is most helpful? And the reduction in preload and wall stress leads to reduced myocardial oxygen demand and myocardial O2 cons? Vasodilation of the coronary arteries is not the best explanation in terms of nitro's pharmacodynamics? Thanks Link to comment Share on other sites More sharing options...
cheech10 Posted July 4, 2012 Report Share Posted July 4, 2012 Yes, the reduction in afterload (LV wall tension) is the major determinant of myocardial oxygen consumption. Reduction in preload (LV end diastolic volume) also reduces myocardial oxygen consumption, but to a lesser degree. Coronary vasodilation is of limited benefit to increasing oxygen supply (locally) to areas supplied by diseased coronaries; as already stated, these are typically maximally dilated already. Link to comment Share on other sites More sharing options...
doctorbetty Posted July 4, 2012 Author Report Share Posted July 4, 2012 Yes, the reduction in afterload (LV wall tension) is the major determinant of myocardial oxygen consumption. Reduction in preload (LV end diastolic volume) also reduces myocardial oxygen consumption, but to a lesser degree. Coronary vasodilation is of limited benefit to increasing oxygen supply (locally) to areas supplied by diseased coronaries; as already stated, these are typically maximally dilated already. Great - thanks for the clarification ) Link to comment Share on other sites More sharing options...
leviathan Posted July 4, 2012 Report Share Posted July 4, 2012 Not harmful exactly: you'd have to have *extremely* low cardiac output for bloodflow to actually be redirected away from ischemic heart muscle in absolute terms (there is a relative change as you describe, which is the basis for myocardial perfusion scanning, but the bloodflow to potentially ischemic areas doesn't drop in absolute terms). Thanks for your input. So it's not harmful, but not helpful either. Do you know any articles or studies that show the afterload drop is more important than preload drop? I was taught preload was the most important determinant as it's primarily a vENOdilator, and while afterload is helpful it is often offset by the reflex tachycardia (which also decreases diastolic filling times). Link to comment Share on other sites More sharing options...
cheech10 Posted July 4, 2012 Report Share Posted July 4, 2012 Sorry, I wasn't clear. NTG is in fact mainly a venodilator, and predominantly affects preload, as you correctly stated, but afterload is in general a more important factor in determining myocardial oxygen consumption, albeit less affected by NTG. Link to comment Share on other sites More sharing options...
leviathan Posted July 4, 2012 Report Share Posted July 4, 2012 Sorry, I wasn't clear. NTG is in fact mainly a venodilator, and predominantly affects preload, as you correctly stated, but afterload is in general a more important factor in determining myocardial oxygen consumption, albeit less affected by NTG. Makes sense, thanks. Link to comment Share on other sites More sharing options...
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