HTN (functions)

ACE-I action

blocks conversion of angiotensin I to II

effects of ACE-I

• reduces SVR by arteriolar and venous dilation

  • suppresses aldosterone and decreases blood volume

what effect does ACE-I have on diabetes

slows diabetic nephropathy

what effect does ACE-I have on CHF

slows progression of LV systolic dysfunction

what effect does ACE-I have on Post-MI

reduced mortality

what effect does ACE-I have on mitral regurgitation

afterload reduction and promotes forward flow

ACE-I are first line agents in patients that are

• <55

• left ventricular dysfunction

• diabetes

• chronic kidney disease

what are contraindications for ACE-I

• pregnancy (2nd and 2rd trimesters)

• renal artery stenosis

• hyperkalemia

  • angioedema

what are side effects of ACE-I

• capoten cough

• hyperkalemia

• fatigue

• headache

• angioedema

ARBs action

blocks effects of angiotensin II on specific receptors

what are indications for ARB use

< 55, LV dysfunction, DM, CKD, pts that developed cough or angioedema from ACE-I

beta blockers decrease

heart rate, force of contraction, renin secretion (decreased RAAS)

Cardioselective beta blockers have

• greater affinity for beta 1 receptors (reduces bronchospasm)

• less vasoconstriction

  • less interference with insulin therapy

alpha-beta blockers have

additional benefit of vasodilation by blocking alpha 1 receptors

beta blockers with ISA (intrinsic sympathomimetic activity) reduce

reduce resting HR and CO (but less than traditional blockers) (dont use in CAD or MI pts)

cardiac condition that favors beta blocker use

CAD, MI, tachyarrhythmia (AFib/flutter, VT), PVCs/PACs, dissecting aortic aneurysms

non-cardiac conditions that favor beta blocker use

migraine prophylaxis, anxiety, hyperthyroidism, senile tremor

contraindications for beta blockers

overt CHF (fluid overload), severe bradycardia, 2nd or 3rd degree heart block, asthma, depression, active peripheral artery disease

side effects of beta blockers

fatigue, impotence, nightmares, depression

T/F: it is bad to stop beta blockers abruptly

true

Calcium channel blockers action

blocks intracellular entry of calcium in cardiac and smooth muscle, leads to smooth muscle relaxation

use a combo of CCB and ACE or ARB in

patients with higher initial BP (stage 2)

Dihydropyridine CCBs are potent

vasodilators, with some negative inotropic effect

non-dihydropyridines are

negative inotropes — decrease sinus rate, AV node conduction

• also vasodilators

use of CCBs is indicated in

pts with increased peripheral vascular resistance

CCBs are 1st line treatments in

• pts >55

• for black/african american pts (+thiazide diuretcs)

for CAD/angina pts that cannot use beta blockers (asthma, COPD), use

CCBs

pts with HTN and atrial tachyarrhythmias (A FIb/flutter, SVT) can use

non-dihydropyridine CCBs

which CCB do we avoid in 2nd and 3rd degree heart block

non-dihydrophyridines

which medications do we avoid in 2nd and 3rd degree heart block

non-dihydropyridines, beta blockers

T/F: we dont used CCBs in CHF/heart failure except for amlodipine

true

what are side effects of CCBs

peripheral edema, constipation, headache, flushing, palpitations

alpha 1 blockers are good for pts with

BPH

what is the main side effect if Alpha-1 blockers

1st dose syncope/orthstatic hypotension

what diuretic is ofthen 1st or 2nd line for HTN in monotherapy or combo with ACE-I

thiazides

what are side effects of diuretics

• hypokalemia/hyponatremia

• hyperuricemia

• hypercalcemia (thiazide)

• glucose intolerance

  • hypercholesterolemia/ hyperglyceridemia

what labs do we monitor with diuretics

potassium, blood sugar, lipids

do vasopressin receptor antagonists incresae or decrease free water excretion?

increase