Myocardial Oxygen Demand/Supply and Nitrates

Question 1

Angina Pectoris

Answer 1

Chest pain or “tightness” that originates from the heart muscle due to lack of oxygen

Question 2

stable angina

Answer 2

if I stay still I don’t have any chest pain but every time I walk up the hill, I have this type of intensity of chest pain
- predictible
- medication can help prevent heart attack

Question 3

unstable angina

Answer 3

• unpredictible pain that can happen at rest
• more frequent attacks and more at rest
• a clot can be formed, blocking the blood that goes to the heart, leading to an MI
• use Heparin to maintain heart flow going to the heart
• emergency

Question 4

Non-Stemi

Answer 4

there is so much oxygen deprevation that the whole thickness of the heart wall is affected

Question 5

STEMI

Answer 5

• urgent

Question 6

strategies to fix the angina

Answer 6

• increase O2 delivery through Coronary artery bypass surgery, Percutaneous transluminal angioplasty, Stenting
• decrease O2 demand by medications

Question 7

How do we decrease O2 demand through pharmacology?

Answer 7

• contractility and heart rate because if you squeeze less frequent, less oxygen is needed (afterload)
• preload meaning if you bring less blood back to the heart, the heart is less stretched out (the higher the stretch the more it has to squeeze)

Question 8

Less venous return = Less

Answer 8

wall tension

Question 9

Less wall tension = Less

Answer 9

O2 use

Question 10

Nitrates Toxicities

Answer 10

• Tachycardia
• Headache
• Orthostatic hypotension
• Interaction with PDE-5 inhibitors (risk: severe hypotension when combined within 24 hrs)

Question 11

Smooth muscle

Answer 11

• Increased cGMP
• Relaxes smooth muscle in
• Bronchi
• GI
• GU (erectile effect reason for “abuse”)

Question 12

Platelets

Answer 12

Increased cGMP
* inhibits platelet aggregation (@ high doses)
* no survival benefit when used in acute MI