IHD and ACS Flashcards by Emily Andrle

ischemic heart disease

caused by stenosis in one or more of the major coronary arteries that supply blood to the heart

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main symptom of IHD

angina (chest pain)

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in IHD, oxygen demand is _____________ oxygen supply

why?

greater than

reduction in blood flow from atherosclerosis

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manifestation of ischemic heart disease

stable ischemic heart disease
acute coronary syndrome

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acute coronary syndrome

sudden obstruction in blood flow to the heart
from plaque rupture followed by clot formation

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types of ACS

unable angina
NSTEMI
STEMI

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low oxygen supply in IHD leads to

decreased arterial pressure
decreased diastolic filling time
decreased coronary blood flow

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high oxygen demand in IHD leads to

increased HR
increased myocardial contractility
increased ventricular wall tension

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many patients with IHD are

asymptomatic

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tests for IHD

cardiac stress test
coronary catheterization with angiography
coronary CT angiography/ CT calcium scan

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major goals of treatment for IHD

reduce ischemia/angina
prevent progression of the disease

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control risk factors such as

smoking
hypertension
dyslipidemia
cardioprotection with aspirin

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acute therapy to reduce ischemia/angina

sublingual nitrates
prn for episodes of angina

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chronic therapy to reduce ischemia/angina

oral/transdermal nitrates
beta blockers
calcium channel blockers
ranolazine
(more for prevention)

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what type of medications can be used to reduce ischemia/angina?

acute therapy
chronic therapy
medications that cause vasodilation
medication that work on the heart to reduce oxygen demand

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unstable angina

markers of cardiac damage NOT present
ST segment NOT elevated

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NSTEMI

markers of cardiac damage present
ST segment NOT elevated

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STEMI

markers of cardiac damage present
ST segment elevated

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what is the most severe type of ACS and what does it indicate?

STEMI

complete blockage

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cardiac markers

creatine phosphokinase MB
troponins (1 and T)

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why do ECG alterations occur?

ischemic myocardial tissue cannot depolarize/repolarize

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when ACS is suspected, treat with

chewed aspirin and SL nitroglycerin

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if ST segment is elevated,

urgent perfusion therapy is reguired

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urgent perfusion therapy

angiography followed by percutaneous coronary intervention (PCI)
or
medication to break down clot (fibrolytic)

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if no ST segment elevation and there is higher risk

early invasive strategy (angiography with PCI)

if no ST segment elevation and there is lower risk

ischemia driven strategy (stress test)

following a MI, patients should receive treatment of

aspirin, a beta blocker, ACE inhibitor and statin

when do troponin levels elevate after MI?

3-6 hours

nitrates examples

nitroglycerin (nitrostat, nitro-dur) isosorbide dinitrate (isordil) isosorbide mononitrate (imdur)

cardioselective beta blockers examples

atenolol bisoprolol (zebeta) metoprolol (lopressor) esmolol (brevibloc) nebivolol (Bystolic)

nonselective beta blockers examples

nadolol (corgard) propranolol (inderal) timolol (blocadren)

mixed alpha/beta beta blockers examples

carvedilol (coreg) labetalol (trandate)

dihydropyridine calcium channel blockers

amlodipine felodipine (plendil) nicardipine (cardene) nifedipine (Procardia)

nondihydropyridines calcium channel blockers

diltiazem (cardizem) verapamil (calan)

nitrates MOA

converted to nitric oxide --> vasodilation and increases oxygen supply to myocardium

nitric oxide increases ____________ which leads to __________________ leading to relaxation of ________________ muscle

cGMP dephosphorylation vascular smooth

for nitrates, vasodilation occurs in

venous and arterial system (more in venous)

nitroglycerin is ___________ and must be kept in __________________ container

chemically unstable light protected, tightly sealed

duration of action of nitrates

ISMN > ISDN > NG

what is the issue with long acting nitrates for daily use? how is this resolved?

there is tolerance to vasodilatory effects within 24 hours of consistent exposure therapeutic effects for only 16 hours a day, nitrate free overnight

ADRs of nitrates

headache reflux tachycardia orthostatic hypotension facial flushing

reflux tachycardia can be a problem since it

increases myocardial oxygen demand

to decrease reflux tachycardia, nitrates can be used in combination with

drugs that decrease HR, like beta blockers

PK of nitrates

high first pass metabolism low oral bioavailability SL dose smaller than oral

drug interactions with nitrates what happens if both of these drugs are used?

PDE5 inhibitors (sildenafil, tadalafil, etc) synergistic effect on vasodilation

doses of nitrates and PDE5 inhibitors must be

separated by 24-48 hours to prevent life threatening hypotension

beta blockers MOA

antagonism at b1 receptors reduces HR and contractility which reduces myocardial oxygen demand

beta blockers that cause vasodilation also

increase myocardial oxygen supply

beta blockers are typically the

preferred agents for chronic therapy in IHD

MOA of DHPs

block calcium channels on arterial smooth muscle --> vasodilation increases myocardial oxygen supply

MOA of non-DHP verapamil

blocks calcium channels on myocardial tissue --> reduction in HR and contractility decreases myocardial oxygen demand

MOA of non-DHP diltiazem

blocks claim channels on arterial smooth muscle and myocardial tissue vasodilation, reduction in HR and contractility

diltiazem increases _____________________ and decreases _________________

myocardial oxygen supply oxygen demand

which calcium channel blockers are more effective?

non-DHPs

why are DHPs combined with beta blockers?

DHP causes reflux tachycardia --> combo decreases this

can non-DHP and beta blockers be combined?

yes but avoid there is additive bradycardia

ranolazine (ranexa) MOA

reduces myocardial oxygen demand inhibits late sodium channels --> reduces intracelluylar calcium concentrations --> reduce tension in myocardium

ranolazine is effective in

prevention of angina with only minimal effects on HR

ADRs of ranolazine

dizziness constipation headache nausea

ranolazine can prolong

the QT interval

PK of ranolazine

substrate of CYP3A4 renal elimination by OCT2 inhibits P-glycoprotein pumps

ranolazine may be beneficial in patients

at risk for bradycardia

ranolazine is effective at mono therapy but used as

2nd line or add on treatment due to cost

which enzyme converts nitrates into nitric oxide?

mitochondrial aldehyde dehydrogenase 2 (mtALDH2)

IHD and ACS Flashcards

(64 cards)