Calcium Channel Blockers - DHP/nonDHPs

Question 1

Calcium entry into L-type calcium channels

Answer 1

Fast response cardiac tissue (atria/ventricles) - contraction, positive ionotropic

Slow-response cardiac tissue (SA/AV node) - increase conduction = increased rate = positive chronotropic.
Increase conduction of electrical activity -> positive dromotrope

Vascular smooth muscle (arteries/arterioles -> NOT venous) - contraction, vasoconstriction of arteries and arterioles -> increase BP -> increase afterload -> DEC coronary blood flow

Adrenal cortex - increase aldosterone production -> Na retention -> increase BP

Question 2

Blocked Ca Channel

Answer 2

Fast response cardiac tissue (atria/ventricles) - reduce FOC -> negative ionotrope

Slow-response cardiac tissue (SA/AV node) - decrease heart rate = negative chronotropic.
Decrease conduction of electrical activity -> negative dromotrope

Vascular smooth muscle (arteries/arterioles -> NOT venous) - relaxation, vasodilation of arteries and arterioles -> reduced BP -> reduced afterload -> INC coronary blood flow

Adrenal cortex - decrease aldosterone production -> reduced BP

Question 3

Non-DHPs drugs, physiologic and cardiac effects

Answer 3

“Nonselective” vasodilator

Negative chronotropic/ionotropic effects - work on AV node

Drug examples: verapamil, diltizem

physiologic effects: vasodilation of arteries and arterioles - inhibits Ca channels in cardiac muscle

Cardiac effects: block Ca channels in slow response tissue to slow AV nodal conductivity - negative ionotrope/chronotropic

Question 4

Non DHPs therapeutic uses, Adverse effects, precautions

Answer 4

Therapeutic uses:

Angina:
less reflex tachy -> less demand for O2 with reduction in HR
Increase O2 supply -> vasodilation -> increase coronary blood flow
Decrease O2 demand -> vasodilation -> reduce systemic vascular resistance -> reduce afterload

Arrythmia (afib, aflutter, PVST)
Class IV antiarrythmic - prolong phase 2 of cardiac AP

adverse effects: constipation,
hypotension, sinus bradycardia, arrythmia, flushing, headache, peripheral edema, rhinitis, AV block

Precautions:
avoid use in patients with HF - negative cardiac effects exacerbate HF
Avoid use in AV block
Avoid combined use with beta blocker - both work on AV node

Question 5

DHPs drugs, physiologic and cardiac effects

Answer 5

“Selective” - more potent vasodilator

Drug examples: “-ipine” amlodipine, nifedipine, nicaradipine, felodipine etc

Physiologic effects: vasodilation
Block VGCC in blood vessels -> arterial relaxation and reduction in peripheral resistance

Cardiac effects: little to no cardiac effects

Question 6

DHPs Theraputic uses, adverse effects, precautions

Answer 6

Therapeutic uses: HTN
vasodilation -> reduced systemic vascular resistance -> reduce BP

Adverse effects: peripheral edema, reflex tachycardia
Flushing, palpitations, hypotension, dizziness, fatigue

Precautions: risk of exacerbating angina second to reflec tachycardia
Increase Hr -> increase O2 demand = exacerbate angina

OK in HF
OK w beta-blocker

Question 7

DHP vs NonDHP

HR
SA/AV node conduction 
Contractibility
Vasodilation
Coronary flow

Answer 7

DHPs. Non DHPs

HR. Increase (reflex tachy). Decrease - negative chronotropic

SA/AV N/a. Decrease - work on AV node
node conduction

Contractibility. N/a. Decrease - work on AV node (neg ionotropic)

Vasodilation. More potent increase. Increase

Coronary flow. Increase. Increase