Anti-Anginal Drugs Flashcards
what results in myocardial ischemia?
imbalance between oxygen supply and demand
what are 2 things that can cause decrease of oxygen/blood supply?
- plaques obstruct perfusion
- coronary artery spasm
what can coronary artery spasm cause?
prinzmetal / vasospastic / rest angina
what can cause an increase in oxygen/blood demand?
exertion/stress
what is stable/typical angina also called?
coronary artery disease
how is typical angina usually managed?
lifestyle changes and medications
what is unstable angina also called?
acute coronary syndrome (ACS)
what is unstable angina caused by?
ruptured plaque with platelet aggregation and thrombi formation
what does angina with increased pain severity, frequency, duration, and occurrence at a lower exercise level indicate?
patient is progressing from stable to unstable angina
what is used to prevent ischemic heart disease?
statins
what two variables determine oxygen supply?
- arterial oxygen content
- coronary blood flow
what four variables determine oxygen demand?
- increased HR
- increased contractility
- increased preload
- increased afterload
amount of blood in the ventricle during diastole
preload
resistance the heart has to pump against to push blood into systemic circulation
afterload
what will an increase in one or all of HR, contractility, preload, and/or afterload cause?
increased demand
what is the cardinal symptom of angina?
squeezing pain in center of chest that lasts more than a few minutes
what are the classic symptoms of angina? (7)
- pain to arms, neck, jaw, shoulder or back
- SOB
- diaphoresis
- dizziness, fainting
- anxiety
- nausea
- fatigue
what is the primary function of nitric oxide?
dilates blood vessels
what does nitrate combine with to be reduced to nitric oxide?
sulfhydryl (SH)
where is sulfhydryl found?
endogenously
what is myocardial oxygen consumption (MVO2)?
the amount of oxygen used by the heart
when active nitric oxide dilates coronary arteries and veins at low doses, what does is cause?
decreased preload
when active nitric oxide dilates large arteries and arterioles at high doses, what does it causes?
decreased TPR, afterload, and MVO2
how does cGMP affect contractility?
it does not let calcium into the muscle = decreases contractility
what does the activation of nitrate to nitric oxide lead to?
activation of guanylyl cyclase to create cGMP
how can nitroglycerine be administered? (2)
- sublingual
- buccal
what is the onset of sublingual or buccal nitroglycerine?
2-4 mins
what is the duration of action of sublingual or buccal nitroglycerine?
1 hour
if a patient with chest pain is given NTG SL x1 and pain is not relieved within 5 minutes, what does this suggest?
unstable angina
how should NTG be administered for acute MI?
IV infusion
what is the duration of action for prophylactic NTG administered via ointment?
4-8 hours
what is the duration of action for prophylactic NTG administered via patch?
24 hours
how should isosorbides be administered?
PO
which isosorbide is the active form?
isosorbide mononitrate
how does tolerance to nitrate develop?
chronic exposure
in the tolerance to nitrate, how is there a decreased capacity of vascular smooth muscle to convert nitrates to nitric oxide?
used up sulphydryl groups in the body
how can tolerance to nitrate be overcome?
short periods (8-12hrs/day) of nitrate absence from the body
what causes the adverse effect of SL NTG of postural hypotension?
rapid drop in BP and sudden movement
what causes reflex tachycardia as an adverse effect of NTG?
compensation of drop in BP - heart pumps quicker
what causes the flushing and headaches as an adverse effect of NTG?
vasodilation of all vessels in the body
what administration route of NTG is most likely to cause a rash?
transdermal NTG
why is it important to give NTG sublingual?
avoid extensive first-pass effect by hepatic nitrate reductase
which type of nitrite is less effected by first pass effect and is therefore given PO?
isosorbide dinitrate
what does PDE V do?
inactivates cGMP
what does PDE V inhibitor do?
inhibits the inactivation of cGMP, which leads to increased cGMP
what does cGMP do?
stimulates smooth muscle relaxation = decreased BP
why shouldn’t sildenafil (PDE V inhibitor) be given to a patient taking an organic nitrate?
can cause prolonged hypotension
what do beta 1 and beta 2 blockers do?
block sympathetic nervous system
where are beta 1 receptors present on? (2)
juxtaglomerular cells in kidney
heart
what would a beta 1 blocker do? (3)
- block renin release
- decrease angiotensin II
- decrease afterload
what are beta 1 blockers typically used for? (2)
- hypertension
- heart failure
where are beta 2 receptors typically located?
smooth muscle cells on heart, lungs, and liver
what does activation of beta 1 receptor cause? (5)
- increased HR
- increased contractility
- increased CO
- increased renin
5 increased angiotensin II
what does blocking of the beta 1 receptor cause? (4)
- decreased HR
- decreased CO
- decreased afterload
- decreased angiotensin II
what does blocking of beta 1 receptors mask?
hypoglycemia
what does activation of beta 2 receptors cause? (5)
- bronchodilation
- vasodilation
- skeletal m tremor
- hepatic glycogenolysis
- gluconeogenesis (increased BG)
what does blocking of beta 2 receptors cause? (2)
- bronchoconstriction
- hypoglycemia
if a patient comes in to the clinic to reverse the blockade of beta 2 receptors, what are they at risk for?
acute hypertension with too much vasopressors
what does it mean when some beta blockers have membrane stabilizing activity?
they can inhibit action potential in cardiac cells
what can beta blockers with intrinsic sympathomimetic activity (ISA) do?
partially activate receptor
what is not a good choice for patients with angina?
beta blockers with intrinsic sympathomimetic activity (ISA)
which organ metabolizes and eliminates lipid soluble medications?
liver
which two beta blockers are generation 1 (nonselective)?
propranolol
sotalol
what receptors do generation 1 (propranolol) beta blockers work on?
beta 1 and beta 2 receptors
which receptors do generation 2 beta blockers work on?
beta 1 (selective)
which 3 beta blockers are generation 2? (beta 1 selective)
atenolol
metoprolol
acebutolol
what are bad effects of generation 1 and 2 beta blockers? (2)
increase triglycerides
decrease HDL
what receptors do generation 3 beta blockers work on?
alpha 1 receptors
what 3 alpha blockers are generation 3?
carvedilol
labetalol
nebivolol
which medication is used in hypertensive emergency?
labetalol
what is the main function of generation 3 alpha 1 blockers? (2)
peripheral vasodilation
better decrease in BP
what are beta blockers not effective for? (2)
- coronary artery spasm
- exertion-induced angina
why are beta blockers combines with nitrates?
antagonize SNS activity
what should be avoided in beta blockers?
those with intrinsic sympathomimetic activity
what can abrupt withdrawal of long-term beta blockers lead to? (2)
unstable angina
MI
what do calcium channel blockers bind to?
L-type Ca channels
what do CCBs cause?
peripheral and coronary vasodilation
what do CCBs decrease? (2)
afterload
MVO2
what are 2 non-dihydropyridines CCBs?
verapamil
ditiazem
what do NDHP CCBs decrease?
HR
CO
(myocardial contractility)
conduction in SA and AV nodes
what do NDHP CCBs work on?
the heart
what are NDHP CCBs used for? (2)
angina and arrhythmias
what type of antianginal is contraindicated in patients with heart failure?
NDHP CCBs
what are 5 dihydropyridines CCBs?
Nifedipine
Isradipine
Nicardipine
Felodipine
Amlodipine
what do DHP CCBs cause?
peripheral vasodilation
what is a side effect of DHP CCBs?
reflex tachycardia
what are DHP CCBs used for?
hypertension
