CARDIAC DRUGS Flashcards
moa unfractionated heparin/
activates antithrombin III which inhibits thrombin, factor IXa, Xa, XIa and XIIa
concurrent use of which drugs can make clopidogrel less effective?
PPIs - definitely with omeprazole and esomeprazole
moa of LMWH?
activates antithrombin III which inhibitors factor Xa
examples of LMWH?
dalteparin sodium, enoxaparin sodium, and tinzaparin sodium
why are LMWHs often used over unfractionates heparins?
they are as effective and they have a lower risk of heparin-induced thrombocytopenia
MOA of fondaparinux?
this is a synthetic heparin that activates antithrombin III which inhibits factor Xa
moa of warfarin?
inhibits epoxide reductase which prevents reduction of vitamin K to its active form
this means there is not enough vitamin K to cofactor 2,7,9,10 and protein C
management of pts on warfarin undergoing emergency surgery?
stop warfarin & give four-factor prothrombin complex
management of pts on warfarin if surgery can wait for 6-8 hours?
stop warfarin and give 5mg IV vitamin K
4 examples of DOACs?
apixaban
rivaroxaban
dabigatran
edoxaban
MOA of apixaban?
direct factor Xa inhibitor
MOA of rivaroxaban?
direct factor Xa inhibitor
MOA of dabigatran?
direct thrombin inhibitor
MOA of edoxaban?
direct factor Xa inhibitor
reversing agents for apixavan?
andexanet alfa
reversing agents for rivaroxaban?
andexanet alfa
reversing agents for dabigatran?
idarucizumab
MOA of nicorandil? what is it used for?
K+ channel activator and vasodilator = drops BP = reduced myocardial oxygen demand
used as an anti-anginal
MOA of ivabradine? what is it used for?
acts on If (funny) ion currents which are highly expressed in the SAN which reduces cardiac pacemaker activity and decreases the HR
anti-anginal
MOA of ranalozine? what is it used for?
an inhibitor of late Na+ channels which reduces Ca2+ accumulation and lowers cardiac wall tension in the ventricles, reducing myocardial oxygen demand
anti-anginal
MOA of aspirin at low and high doses?
at low doses aspirin selectively inhibits COX1 whereas at higher doses it inhibits both isoenzymes
this reduces production of thromboxane A2 and therefore reduces platelet aggregation
examples of irreversible P2Y12 receptor antagonists?
clopidogrel
prasugrel
ticlodipine
examples of reversible P2Y12 receptor antagonists?
ticagrelor
cangrelor
examples of GPIIb/IIIa receptor antagonist?
tirofiban
eptifibatide
abciximab
MOA of dipyridamole?
inhibiting the function of phosphodiesterase and adenosine deaminase. this prevents the degradation of cAMP which is an inhibitor of platelet function
moa of alteplase and tenecteplase? how are they different?
they are recombinant tissue plasminogen antagonists that convert plasminogen to plasmin in a fibrin-dependant process
i..e they bind to fibrin-rich clots
tenecteplase has a longer half life and a higher binding specificity to fibrin
MOA of lidocaine?
1b - Na+ channel blocker
MOA of flecainide?
1c- Na+ channel blocker
MOA of sotalol?
III - K+ channel blocker
MOA of atropine on the heart?
antimuscuarininc that increases HR and improves AV condition by blocking parasympathetic Ach effects
MOA of amiodarine?
III - K+ channel blocker
how do beta blockers work to help angina
they decrease HR, reduce the force of cardiac contraction and lower bp by reducing CO
overall this reduces the myocardial oxygen demand
how do calcium channel blockers work to help angina
dihydropyridines - peripheral arterial dilation
non-dihydropyridines - negative chronotropic effect and reduces cardiac contractility
overall they reduce myocardial oxygen demand
outline the differences in moa of diydropyridines and non-dihydropyridines?
non- dihydropyridines exhibit frequency-dependant receptor bindings and gain access to Ca2+ channels when in its open state
dihydropyridines preferentially bind to the channel in its inactivated state. more Ca2+ channels are in the inactive state in relaxed vascular smooth muscle than in cardiac muscle so these CCBs selectively bid to vascular smooth muscle Ca2+ channels.
this is why non-dihydropyridines have anti arrhythmic properties and the dihydropyridines cause vasodilatation
initial drug therapy for all ACS?
aspirin 300mg
oxygen if sats <94%
morphine if severe pain
sublingual or IV nitrates
management of STEMI after initial drug Tx
if PCI is possible within 120mins then give another anti platelet (prasugrel or clopidogrel if already taking an oral anticoagulant) AND unfractionates heparin and bailout GPIIb/IIIa inhibitor f using radial access
if not possible within 120 mins then given a antithrombin (e.g. fondaparinux), fibrinolysis and following the procedure give ticagrelor
management of NSTEMI after initial drug Tx?
fondaparinux if no immediate PCI is planned
estimate 6 month mortality using GRACE.
if low risk give ticagrelor
if high risk then offer PCI within 72 hours. give prasugrel or ticagrelor and unfractional heparin
management of acute HF?
IV loop diuretics
oxygen if sats <94%
if concomitant MI, severe hypertension or regurgitant aortic/mitral valvular heart disease then give nitrates
first line therapy for chronic HF?
ACEi and BB - start 1 drug at a time!
second line therapy for chronic HF?
aldosterone antagonist
(remember to monitor K+ due to ACEi and aldosterone antagonist use)
SGLT2 inhibitor
third line therapy for chronic HF?
initiate by specialist…
ivabradine
sacbitril-valsartan
hydralazine and nitrate
digoxin
cardiac resynchronisation therapy
which drugs can be used for pharmacological cardioversion in AF?
amiodarone
flecainide
less commonly - quinidine, dofetilide, ibutilide, propafenone
CI to flecainide?
structural heart disease
which anticoagulants should be used I AF?
DOACs
(second line is warfarin)
what drugs can be used for rate-control in AF?
BB
rate-limiting CCB such as verapamil monotherapy
digoxin monotherapy
monitoring f amiodarne?
TFT, LFT, U&E, CXR prior to treatment
TFT and LFTs every 6 months
which drugs can be used to maintain sinus rhythm in pts with AF?
BB
dronedarone
amiodarine - particularly if coexisting HF
adverse effect of amiodarone?
thyroid dysfunction
corneal deposits
pulmonary fibrosis
liver fibrosis or hepatitis
peripheral neuropathy and myopathy
photosensitivity
slate-grey appearance
thrmbophlebitis
bradycardia
QT prolongation
management of VT?
if adverse signs -> immediate cardioversion
otherwise…
amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours
other choices include lidocaine and procainamide
(VERAPAMIL SHOULD NOT BE USED)
when is warfarin still used in preference to DOACs for AF?
if the pt has a mechanical heart valve
management of regular SVT i.e. not AF!?
vasalva manoeuvre
adenosine 6mg rapid IV bolus. if not effective give 12mg and then a further 12mg
electrical car diversion
drugs given in ALS non-shockable rhythm?
adrenaline 1mg
repeat every 3-5 minutes
drugs given in ALS when pts are in VF or pulseless VT after 3 shocks have been administered?
amiodarine 300mg
further dose of amiodarine 150mg after 5 shocks administered
(if not available use lidocaine)
drug management of life-threatening adult bradycardia?
give 500mcg IV atropine.
You can repeat this to a maximum of 3mg, or you could try transcutaneous pacing or isoprenaline/adrenaline infusion
if nothing works seek expert help and arrange transvenous pacing
most common adverse effects of statins?
myalgia (measure CK and if concentration is >5 ULN discontinue)
headache and GI disturbances
sleep disorders
arthralgia
dizziness
potentially serious SE of statins?
myopathy/myositis
rhabdomyolysis
raise liver enzymes/drug-induced hepatitis
very influent reports of new-set myasthenia graves
when should statins be avoided?
caution with hepatic impairment
reduce dose in renal disease as excreted by the kidneys
discontinue 3 months before trying to conceive and 1 month after - congenital anomalies
avoid in breastfeeding
in inadequately managed hypothyroidism
what affects the metabolism of statins?
CYP450 inhibitors
leads to an accumulation of statins in the body putting pt at increased risk of adverse effects. most worryingly this is induced muscle injury - most common with simvastatin
e.g. pts should avoid grapefruit juice and some drugs
monitoring of statins?
before stating - 1 full lipid profile, TSH, U&Es, eGFR, LFTs, CK, HbA1c or fasting BG if high risk of diabetes
LFTs should be repeated at 3 months and 12 months. as long as serum transaminases are less than 3x ULN then continue
recheck diabetes at 3 months
only check CK if muscle pain
when should a patient take simvastatin?
before bed as its short acting and this maximises their effect as HMG-CoA reductase is more active at night
(longer acting statins e.g. atorvastatin can be taken at night or morning)
