Anti-Anginal/STEMI meds Flashcards
Organic Nitrates indications (short vs long acting)
If short: acute treatment for symptomatic relief of angina pectoris
if long: prevents recurrent anginal episodes; NOT for acute episode
Nitrate (short acting) meds/route/use
- Nitroglycerin (NTG)
- route: sublingual (SL) tablet/spray/powder
- use: short onset/duration; PRN
Nitrate (long acting) meds/route/use
- Isosorbide DInitrate or MONOnitrate
- route: PO
- use: slow onset/long duration; preventative
Nitroglycerin MoA
- Nitrates converted to nitric oxide (NO) –> vessel relaxation/vasodilation
- less work, less O2 demand/afterload
Nitroglycerin pharmacodynamic effects
- reduced left ventricular volume/tension (preload)
- reduced vascular resistance (afterload)
- reduces spasms and improves O2 delivery
Nitrates adverse effects
- headache
- hypotension, flushing, orthostasis
- reflex tachycardia
- dizziness
- tolerance/tachyphylaxis (reversible)
Nitrates D-D interactions
avoid combo with:
- PDE-5 inhibitors
- HTN/pulmonary HTN drugs
(all lead to major drop in BP)
Beta-blocker indication/outcome
- long-term treatment of stable angina pectoris
- reduced risk of death
- will suppress reflex tachycardia (happens with nitrate use)
Beta-blocker meds/selectivity
- metoprolol & atenolol (beta-1 cardioselective)
- nadolol & propranolol (beta-1/beta-2 non selective)
Beta-blockers MoA/effects
block B1 receptors
- decreases cAMP
- no Ca2+ influx
- reduced HR/contractility/oxygen demand
- also B2 receptors –> broncho/vaso-dilation (increase in oxygen delivery)
Beta-blocker AEs
- Common: bradyarrhythmia, hypotension, bronchospasm
- Less: N/V/D
- Sig: heart block
BB contraindications
- asthma
- severe bradycardia
- AV block
- severe LV failure
BB D-D interactions
- with other drugs of similar affects (ex. CCBs): bradycardia, hypotension, AV block
- antagonistic effects: albuterol/catecholamine
- CYP2D6 inhibitors ex. some SSRIs
- CYP2D6 inducers ex. rifampin
Calcium channel blockers indication/outcomes
- Treatment of angina at rest (chronic, vasospastic, unstable)
- no proven mortality benefit
CCBs meds/type
- Nifedipine XL (dihydropyridine aka in arterioles)
- verapamil & diltiazem (non-dihydropyridine aka in cardiac cells)
CCBs MoA
- Ca2+ channels get blocked –> vascular relaxation
- reduce O2 demand (decrease HR/contractility) & increased O2 delivery
CCBs AEs
- Dihydropyridine: peripheral edema as arterioles get dilated
- Non-Dihydros: AV-block, bradycardia, cardiac failure, constipation
calcium channel blockers D-D interactions
- additive effects (increased hypotension)
- hepatic metabolism interactions (CYP inducers/inhibitors)
Sodium channel blocker indication/outcomes
- treatment of chronic angina
- leads to decreased frequency of anginal episodes and increased exercise tolerance
Sodium channel blocker med
- ranolazine
**contraindicated in hepatic cirrhosis, pre-existing prolonged QT interval
sodium channel blocker MoA
- blocks sodium influx into cell
- less contractility, vasoconstriction, SA pacemaker rate/AV conduction velocity
- overall decreased O2 demand
Ranolazine D-D interactions
- CYP3A4 inducers/inhibitors (ex. rifampin, ketocanazole)
- interaction w/ p-glycoprotein inhibitors/some -statins/SSRIs/antibiotics
- all either increase ranolazine concentration in body or lead to QT prolongation –> cardiac dysrhythmia, death!
Ranolazine AEs
- prolonged QT interval
- N/V, constipation
- headache/dizziness
Morphine MoA/Pharm effect
- bind opioid receptors to inhibit pain pathways
- reduced response to pain –> decreases O2 demand, afterload, and preload
- no mortality reduction
Morphine AEs
- respiratory depression
- hypotension
- bradycardia
- pruritis
- hypersensitivity
Morphine D-D interactions
- PDE-5 inhibitors combo and other antihypertensive meds use leads to hypotension
Oxygen outcomes
- theoretically increases O2 delivery
- no mortality reduction
- caution in COPD
Aspirin outcomes in STEMI
- inhibit platelet aggregation/clot forming
- mortality reduction when in combo with fibronlytics
- reduced risk of re-infarction, death, and stroke
Aspirin AEs
- dyspepsia, N/V
- bleeding
- increased liver enzymes
- increased SCr
Aspirin D-D interactions
- high bleed risk when in combo with other anti-coags
- increased nephrotoxicity w/ ACE-Is
- decreased cardioprotective effect with NSAIDS**
P2Y12 (ADP) inhibitors in STEMI
- clopidoGREL & prasuGREL
- used with aspirin
- reduce platelet aggregation
IV antiplatelet therapy in STEMI (GII/IIIb inhibtors)
- eptifibatide & tirofiban
- inhibits platelet aggregation
- alternative to oral anti-platelet therapy
STEMI drugs used to inactivate thrombin
- Bivalirudin –> direct thrombin inhibitor
- LMWH aka enoxaparin
- unfractioned heparin
thrombolytic therapy meds in STEMI
- alteplASE & tenecteplASE
- lyse coronary artery thrombi
- activate plasminogen to plasmin (initiates fibrinolysis)
ACE inhibitors in STEMI
- lisinopril & ramipril
- admin w/in first 24 hours
- reduce major CV events and prevent LV remodeling
