ACS
I.
II.
III.
ACS includes
a. Non ST segment elevation ACS (NSTE-ACS)
i. Unstable angina
ii. Non-st segment MI (NSTEMI)
b. ST segment elevation MI (STEMI)
Oxygen supply ≠ oxygen demand
Symptoms
a. Chest pain
i. Take SL nitroglycerin
1. If it helps chest pain they probably have stable angina
2. If pain doesn’t go away after 1 tablet then call 911, then can take
another one in 5 mins
b. Dyspnea
c. Syncope or lightheadedness
d. Diaphoresis
UA
-
Cardiac Enzymes (TnT,
TnI)
ECG Changes
None or transient
Blockage
Partial
Note: Cardiac enzymes include troponin T and I
IV.
Drug Treatment for ACS
a. MONA-GAP-BA
i. MONA (Get these early)
1. Morphine
NSTEMI
+
STEMI
+
ST elevation
Complete
V.
a. Vasodilator of coronary arteries
b. Relieves pain
2. Oxygen
a. Given if O2 sat less than 90%
b. Calms them down
3. Nitrates
a. Dilates coronary arteries
4. Aspirin
a. Anti-platelet given to everyone
b. Chew a non-enteric coated aspirin (325mg mostly)
i. Get absorption faster
c. Don’t use extended or delayed release aspirin
ii. GAP (management dependent)
1. GP IIb/IIIa Inhibitors
a. IV only
2. Anticoagulants
a. Mainly heparin and LMWH
b. Fondaparinux or bivalirudin can be used if putting a stent in
cath lab
3. P2Y12 Inhibitors
a. Clopidogrel
iii. BA (get within 24 hours)
1. Should both be given orally
2. Both prevent cardiac remodeling and help long term picture
3. Vasodilate
4. Beta blockers
a. Should be beta-1 selective (AMEBBA) since beta 1 receptors are
in the heart
b. Metoprolol commonly used
c. Don’t use ISA beta blockers
5. ACE Inhibitors
Platelet Activation (4 ways to block it)
a. When plaque breaks off from endothelium then platelets activate to fix where plaque
broke off in blood vessel
b. Arachidonic acid is converted to thromboxane A2
i. TXA2 stimulates platelets and activates it more
ii. Aspirin works here to block COX which converts AA to TXA2 (1)
c. Adenosine diphosphate (ADP) get released and activates the platelets
i. ADP binds to receptor on platelet to activate it
1. Receptor is P2Y12 receptor
2. P2Y12 receptors antagonist are also called ADP antagonists (2)
d. GP IIb and IIIa receptor undergoes conformational change to bind fibrinogen which is
critical in crosslinking platelets to bind making a big plug/clot
i. GPIIb and IIIa inhibitors block this (3)
ii. Contraindications deal with bleeding
iii. Abciximab not recommended for medical management, only for those going to
PCI
1. Only one with reversible blockade the others have irreversible blockade
iv. Cause thrombocytopenia
v. Focus more on mechanism because you won’t end up choosing if they get one
or not
e. Coagulation cascade is activated causing thrombin generation
i. Anticoagulants helps stop this step (4)
Clopidogrel (Plavix)
Prodrug (2C19)
-given once daily
Irreversible binding
Prasugrel (Effient)
Do not use in patients with
history of stroke/TIA (worse
outcomes in clinical trials)
Ticagrelor (Brilinta)
Keep maintenance ASA dose
<100mg (first dose of aspirin
will still typically be 325mg)
-given once daily
Reversible binding
Irreversible binding
Avoid omeprazole (Prilosec)
Only for ACS patients receiving 90mg BID x 1 year, then 60mg
and esomeprazole (Nexium)
PCI
BID
(2C19 inhibitors)
Dispense in original container
Tablets can be crushed
Note: Cangrelor is an injectable P2Y12, not used much but good outcomes in clinical trials.
VI.
Fibrinolytics
a. Only used in STEMI
b. MOA: Bind to fibrin in the clot and convert plasminogen to plasmin
c. Timing
VII.
VIII.
IX.
i. PCI preferred (door to balloon time: 90 minutes)
1. Get them to PCI capable hospital
ii. If not able to receive PCI within 120 minutes of FMC (first medical contact), use
fibrinolytic
1. Can’t get them to cath lab then decide whether or not to use fibrinolytic
iii. Door to needle time=30 minutes (as soon as possible)
1. This means time patient hits door the time to make fibrinolytic and
inject patient must be done in 30 minutes
iv. TNKase
1. Most popular for STEMI ACS
2. Single bolus
v. Alteplase
1. Harder to use but only thrombolytic approved for acute ischemic stroke
vi. Cathflo activase
1. Used to restore function in devices that might be clotted to declot them
Long-term management after ACS (secondary prevention)
a. Aspirin
i. Indefinitely 81mg daily (81-325mg)
b. P2Y12 inhibitor
i. Medical management: Clopidogrel or ticagrelor + ASA for at least 12 months
1. DAPT therapy
ii. PCI-treated patients: any oral P2Y12 inhibitor + ASA for at least 12 months
1. If patient doing well, has a stent, no bleeding, can extended beyond 12
months
c. NTG (tabs or spray) as needed
d. Beta blocker daily (target HR 50-60BPM) for 3 years
i. Can be used longer if they have another indication (HF, HTN)
e. ACE inhibitor=reduced EF, HTN, CKD or DM
i. Used indefintely
f. Aldosterone antagonist-reduced LVEF and symptomatic HF or DM
i. On it forever
ii. Don’t use if Scr>2.5mg/dL in men, Scr>2mg/dL in women, or hyperkalemia K>5
g. Statin
i. <75 use high intensity
ii. >75 use moderate intensity stain
Pain management
a. Try acetaminophen, tramadol, or small dose narcotics before trying NSAIDs
Warfarin therapy
a. If using triple therapy lower goal INR to 2-2.5 and use for shortest time possible
b. Give PPI if person has history of GI bleed