Pharm: some anti hypertensives & anti-anginals

Question 1

How do you treat HTN in CHF? Special considerations

Answer 1

use diuretics, ARBs/ACE-Is, beta blockers in compensated CHF, and aldosterone inhibitors. Beta blockers are contraindicated in cardiogenic shock and must be used very cautiously in decompensated CHF.

Question 2

How do calcium channel blockers work?

Answer 2

calcium channel blockers block the voltage-gated L-type calcium channels in heart and smooth musle. this reduces the contractility.

Question 3

How do different CCBs rank in terms of their effects on vascular smooth muscle?

Answer 3

amlodipine = nifidepine > diltiazem > verapamil

Question 4

Clinical uses of amlodipine and nifedipine

Answer 4

used to treat HTN and angina and vasospastic conditions, including Raynauds and Prinzmetal angina
both are dihydropyridines (plus nimodipine)

Question 5

Clinical use of nimodipine?

Answer 5

treats subarachnoid hemorrhage by preventing cerebral vasospasm.
dihydropyridine

Question 6

clinical use of diltiazem and verapamil

Answer 6

used to treat HTN, angina, and atrial fibrillation/flutter

Question 7

CCB toxicity

Answer 7

cardiac depression, AV node block, peripheral edema, constipation (relaxes smooth muscle), hyperprolactinemia

Question 8

How does hydralazine work?

Answer 8

hydralazine incr. cGMP, which causes smooth muscle relaxation. this will affect arterioles more than veins and reduces AFTERLOAD.

Question 9

When is hydralazine used? Special considerations?

Answer 9

hydralazine is the FIRST LINE for HTN in pregnancy. It can cause a reflex tachycardia as it drops blood pressure and thus is contraindicated in CAD/angina. We usually prescribe this with a beta blocker to reduce reflex tachycardia

Question 10

What are the toxicities of hydralazine?

Answer 10

causes a compensatory tachycardia and is contraindicated in CAD and angina. it can also cause a LUPUS-LIKE SYNDROME. May also cause fluid retention, nausea, headache, angina (won’t stress if I don’t get these last 4).

Question 11

What is a hypertensive emergency?

Answer 11

Systolic >210; diastolic > 120, esp. with end organ damage

Question 12

There are many drugs used to treat a hypertensive emergency. Which two will I know?

Answer 12

nitroprusside and fenoldopam

Question 13

How does nitroprusside work?

Answer 13

It increases cGMP via direct release of NO. this is short acting.

Question 14

How does fenoldopam work?

Answer 14

this is a D1 receptor agonist. It causes coronary, renal, and splanchnic vasodilation to decr. BP and incr. naturiesis

Question 15

How do different CCBs rank in terms of their effects on the heart?

Answer 15

verapamil > diltiazem > amlodipine/nifedipine (verapmil = ventricle). opposite order when compared with effects on vascular smooth muscle.

Question 16

How do does nitroglycerin work? What is another drug that works in the same way?

Answer 16

both nitroglycerin and isosorbide dinitrate incr. NO in vascular smooth muscle. This increases cGMP and causes smooth muscle relaxation. nitrates dilate veins&raquo_space;> arteries and reduce preload.

Question 17

What is “Monday disease?”

Answer 17

seen in patients who have industrial exposure to nitrates. these patients develop tolerance during the week and loose it on the weekend. At work again on Monday, they experience tachycardia, dizziness, and headache on re-exposure.

Question 18

Nitroglycerin toxicity

Answer 18

hypotension, reflex tachycardia that can be prevented with beta blockers, flushing, and headache.

Question 19

nitroglycerin use

Answer 19

angina, acute coronary syndrome, and pulmonary edema (to decr. preload?)

Question 20

Anti anginal therapy: look at nitrates, beta blockers, and combination wrt end-diastolic vol, BP, contractility, HR, ejection time, and myocardial O2 consumption

Answer 20

nitrates: decrease preload. end diastolic vol decr., BP decr. contractility incr (reflex), HR incr. (reflex), ejection time decr. (I think of this as a reflex), O2 consumption decr.
beta blockers: decr. afterload. end-diastolic vol incr. (more time to fill), BP decr, contractility decr., HR decr. ejection time incr., O2 consumption decr.
together:
no effect or decr. EDV, BP decr., little to no effect on contractility, decr. HR, little to no effect on ejection time, and more decreased myocardial O2 consumption.