Increase NO which increases c-GMP that relaxes smooth muscle (ateries and veins)

Most prominent effect on veins, decreases venous return/preload

Decreases pulmonary pressures and reduces heart size significantly due to reduced cardiac muscle fiber length/tension.

Decreases afterload via arterial relaxtion (lower TPR)

Reduces cardiac work/demand for Oxygen and increase collateral flow in ischemic area

Decreases platelet aggregation

Stable, unstable and variant (prinzmetal) angina

acute attacks use sublingual

Nitroglycerin

Given sublingual, IV and oral spray

Used in an acute attack

Nitroglycering Ointment

Nitroglcyerine Transdermal Patch

Isosorbide Dinitrate

Given to prevent attacks of angina, can be used orally and topically

-excessive dilation can cause:

hypotension

reflex tachychardia

orthostatic hypotension (dizziness)

vasomotor flushing

headache (meningeal artery dilation)

Block slow voltage-dependant, L-type Ca channels to preveent influx of Ca in smoot muscle, cardiac nodal and muscle cells

Results in:

-decreased myocardial contractility = reduced O₂ requ

-decreased arterial tone = lowered TPR

-Relief of Coronary Artery Spasm

-used as a prophylactic, not acute treatment

CI:

variant and stable angina

fast atrial/nodal arrhythmias

slow HR/AV conduction

ADR:

vasodilation & dec after load

dec HR & AV conduction (Verapmil>Diltazem)

dec myocardial contractility (V>D)

high dose can cause CHF

Caution with beta blocker, too much red. contractility

Dihydropyridine class = arteriolar dilator

Excess dilation can trigger reflexive HR increase

Used in stable angina AND ESPECIALLY VASOSPASTIC (prinzmetal's)

ADR:

all related to excess vasodilation

nausea, tachycardia, lightheadedness, dizziness, headache, tachychardia and peripheral edema

Nifedipine, amlodipine, nicardipine

arteriolar dilators used in treating prinzmetal angina

Effective = unstable and stable

Ineffective = vasospastic (prinzmetal)

Beta 1 receptors, when stimulated, cause increased cardiac outpout as follows:

-heart rate in SA node, increased atrial contractility, increased AV node conduction velocity and increased contractility and automaticity in the ventricles

Other areas effected are increased lipolysis and increased Renin release.

Decreased HR

Decreased Arterial Pressure (TPR)

No change in EDV, Contractility or Ejection Time