IHD and ACS Flashcards
ischemic heart disease
caused by stenosis in one or more of the major coronary arteries that supply blood to the heart
main symptom of IHD
angina (chest pain)
in IHD, oxygen demand is _____________ oxygen supply
why?
greater than
reduction in blood flow from atherosclerosis
manifestation of ischemic heart disease
stable ischemic heart disease
acute coronary syndrome
acute coronary syndrome
sudden obstruction in blood flow to the heart
from plaque rupture followed by clot formation
types of ACS
unable angina
NSTEMI
STEMI
low oxygen supply in IHD leads to
decreased arterial pressure
decreased diastolic filling time
decreased coronary blood flow
high oxygen demand in IHD leads to
increased HR
increased myocardial contractility
increased ventricular wall tension
many patients with IHD are
asymptomatic
tests for IHD
cardiac stress test
coronary catheterization with angiography
coronary CT angiography/ CT calcium scan
major goals of treatment for IHD
reduce ischemia/angina
prevent progression of the disease
control risk factors such as
smoking
hypertension
dyslipidemia
cardioprotection with aspirin
acute therapy to reduce ischemia/angina
sublingual nitrates
prn for episodes of angina
chronic therapy to reduce ischemia/angina
oral/transdermal nitrates
beta blockers
calcium channel blockers
ranolazine
(more for prevention)
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
unstable angina
markers of cardiac damage NOT present
ST segment NOT elevated
NSTEMI
markers of cardiac damage present
ST segment NOT elevated
STEMI
markers of cardiac damage present
ST segment elevated
what is the most severe type of ACS and what does it indicate?
STEMI
complete blockage
cardiac markers
creatine phosphokinase MB
troponins (1 and T)
why do ECG alterations occur?
ischemic myocardial tissue cannot depolarize/repolarize
when ACS is suspected, treat with
chewed aspirin and SL nitroglycerin
if ST segment is elevated,
urgent perfusion therapy is reguired
urgent perfusion therapy
angiography followed by percutaneous coronary intervention (PCI)
or
medication to break down clot (fibrolytic)
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)
