on 21.1.09 with 0 comments

Coronary insufficiency is when there is an O2 demand higher than the supply to the myocardium. Ca++ antagonists can increase myocardial blood supply by producing coronary arterial vasodilation (only if there isn’t too much arteriosclerotic plaque, otherwise you can’t dilate the arteries), increasing blood flow, and prevention of coronary spasms.

How is this accomplished?
  1. The myocardium contractility is reduced, both when you’re at rest and during exercise—here’s the catch, if you are healthy and have plenty of residual contractility reduced contractility may be beneficial, but if someone is borderline cardiac failure there’s a problem. Normally you can stand a little reduction in contractility, but if your heart is failing it’s a problem.

  2. Heart rate is also reduced. Coronary blood flow occurs primarily during diastole, so you don’t want the heart to go too fast or else there is no time for filling. But if a person doesn’t have a high diastolic BP and you give them a Ca++ antagonist, their heart rate can be reduced and damage the oxygen supply.

  3. Blood pressure is reduced. Arterioles relax so resistance is reduced and the work of the heart is reduced. Because the work is less, the oxygen demand is reduced.

“You must balance between beneficial effects and deleterious effects of the cardiology drugs. This is something that with cardiac drugs has been a damnation. Sometimes I think that the cardiologists go on a spree of thinking that this drug is great, but when you see over a period of ten years, you find that the death rate of people taking the drugs is higher than those not taking the drugs.”

Ca++ antagonists, in addition to having classic calcium blocking effects, there are electrophysiological effects. These are most evident in SA and AV nodes because the calcium currents that were producing depolarization are antagonized. Ca++ antagonists slow nodal discharge, and lengthen AV conduction time. The overall effects of calcium antagonism are the result of complex interactions between the depressant effects on slow Ca++ channel fibers, nonspecific sympathetic antagonism, and reflex sympathetic activation caused by peripheral vasodilation. The dentist must be wary of these cardiac drugs because they are very complicated, and can be dangerous to the patient. We must manage our own health as well, so know to be careful with the cardiac drugs.


Nifedipine: dizziness, flushing, hyotension, skin rash, peripheral edema, tachycardia

Verapamil/ Diltiazem (less used than nifedipine due to problems): bradycardia, hyptension, congestive heart failure, heart block, skin rash, constipation

Category: Pharmacology Notes



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