Pharm-Angina Pectoris

Front 1

Typical Angina Treatment Strategies

Back 1

Decrease preload-reduce venous return with nitrates

Decrease sympathetic drive-B1 blocker, want HR at 50-60

Decrease Afterload-use vasodilators

Front 2

Typical Variant Angina treatment

Back 2

Vasodilators to suppress vasospasm and return flow-nitrates (reduce preload, coronary vasodilation)

CCB-slow smooth muscle activity

NOT BB-won't work on vasculature of heart

Front 3

Nitrates

Back 3

Nitroglycerides
Nitropresside

Hint 3

Nitrates-Works by increasing NO in smooth muscle which increases cGMP causing smooth muscle relaxation

Oral therapy has low bioavailability due to first pass effect thus sublingual and IV are more effect means for acute therapy

Can cause tachyphlaxis-depletes sulfa thus after time the same dose has less of an effect and dose needs to be increased. Same effect can be seen in albuterol and other BB. Can also cause reflex tachycardia but this may not be seen because often BB are used in conjunction. Toxicity causes orthastatic hypotention and methemoglobin formation-need to watch out for

Contraindicated when also taking PDE5 inhibitors

Front 4

CCB

Back 4

Verapamil
Diltiazem
"dipines"

Hint 4

block L type Ca channels. Verapamil is exclusive to the heart while diltiazem works on both the coronary and vasculature of arterioles. Are more targeted to arteries than veins meaning less orthastatic hypotension. Watch out for subarachnoid hemmhorage

Front 5

BB

Back 5

Used post AMI to bring HR to 50-60. WIth comorbid HF in chronic treatment BB is used to reduce the RAAS pathway, in acute treatment dopamine and DOButamine are used to increase CO. Caution with pations with asthma, COPD and history of bradycardia.