Pharmacology of Angina and ACS Management Flashcards
How to reduce myocardial oxygen demand
- reduce afterload
- reduce preload
- reduce contractility
- reduce heart rate
How restore supply to ischemic tissue?
Prevent further thombosis:
- anti-thrombin (unfractionated heparin) + anti-platelet (ASA)
Reopen the occlusion
- percutaneous catheter intervention (angioplasty, stent)
- surgical (Coronary Artery Bypass Graft)
- pharmacological (fibrinolytics- activate the body’s clot- busting system)
Things that aggravate platelets
serotonin, epi, thromboxane A2, ADP, collagen, thrombin, tissue factor
What does UFH block?
How does it do this?
- Factor Xa and thrombin
- UFH binds endogenous antithrombin
What does ASA block?
ASA blocks thromboxane A2 production
What percentage of people do just fine on UFH+ASA therapy and how to guess who won’t?
~80%,
~20% need better intervention
Guess using risk stratification worksheet
What is a better alternative to UFH?
low molecular weight heparin (LMWH). It has had it’s sticky bits cleaved so it works better
What is the most important side-effect with anti-coagulants?
- you can bleed out
3 most important anti-platelets (besides ASA) and what they inhibit
clopidogrel
prasugrel
ticagrelor
**all block ADP mediated activation of platelets
What is the effect of bleeding during MI?
Who is most at risk to bleed?
- increases risk of mortality
- female, low BMI, increased age are all independent predictors of bleeding
How to stabilize plaques
- use cholesterol lowering drugs to prevent recurrent thrombosis
Which anti-cholesterols are known to reduce mortality?
-only statins
Effects of statins
- lower serum [LDL]
- increase LDL receptor –> uptake
- anti-inflammatory
- anti-oxidative
Vasodilatory drugs used in ACS
- CCB
- B-blocker (via decreased renin release)
- ACEi and ARBs
Drugs that reduce contractility in ACS
- CCB
- B-blocker
Drugs that reduce heart rate in ACS
- CCB
- B-blocker
Drugs that reduce preload in ACS
- diurectics
- nitroglycerin
Drugs that increase the fibrillatory threshold
-B-blockers
When to avoid the use of B-blockers/CCB?
- if in acute heart failure
- if bradycardic already
-could precipitate cardiogenic shock
Differences in AT1 and AT2 receptor actions
-which does ARB block?
AT1: vasoconstriction, cell growth, Na retention, SNS activation, oxidative stress
AT2: vasodilation, antiporliferative, anti-inflammatory, antithrombotic
**ARBs block AT1
The general treatment principles of ACS
1) relieve the obstruction
2) reduce inflammation to reduce recurrent events
3) reduce myocardial oxygen demand to limit the damage from ischemia
Symptom relief in ACS
- nitroglycerin
- analgesics (e.g. morphine)
Examples of fibrinolytics
- tissue plasminogen activator (t-Pa)
- tenecteplase (recombinant mutant of t-Pa)
The Canadian Cardiovascular Society (CCS) classification of angina
Grade I. Angina with extreme exertion
Grade II. Angina with more than two flight of stairs
Grade III. Angina with less than two flights of stairs
Grade IV. Angina at rest (unstable angina)
New York Heart Association Classification of Heart Failure (NYHA)
I. symptoms with extreme exertion
II. symptoms with moderate exertion
III. symptoms with mild exertion
IV. symptoms at rest
symptoms: shortness of breath
Management of stable angina (CCS I–>III)
- Management is conservative and medical
- Conservative includes lifestyle changes (diet, exercise, stress)
- Medical includes anti-hypertensives, anti-platelets (ASA), perhaps B-blockers and acute treatment of nitroglycerin
Is management of unstable angina (CCS IV), NSTEMI, STEMI conservative, medical or invasive/surgical?
Usually medical (see other cards) and invasive.
Percutaneous Catheter Intervention can result in angioplasty, drug-eluting stents, or subsequent CABG
DDx of chest pain
- Cardiovascular (acute MI, pericarditis, aortic dissection, aortic rupture)
- MSK (costochondral syndrome, cervical radiculitis)
- GI (GERD, peptic ulcer disease, esophageal spasm, biliary colic)
- Pulmonary (pulmonary thromboembolism, pneumothorax, pneumonia)
How to differentiate NSTEMI and unstable angina
- they cannot be distinguished on initial presentation
- UA will not have necrosis, so the cardiac enzymes will distinguish them
How to differentiate ACS from other forms of chest pain
History- may have previous history
Pain quality, location, length (pain will be tightness, pressure, squeezing, may radiate up to the jaw, down the arm, and to the epigastrium, MI pain lasts about 1/2 an hour)
ECG
Cardiac enzymes (troponin I or T, CK-MB, lactate dehydrogenase)
ACC/ AHA Staging of Heart Failure
Stage A: high risk
Stage B: structural heart disease, but no Sx
Stage C: structural heart disease with symptoms (previous or current)
Stage D: structural disease requiring special intervention
Mechanisms of nitroglycerin action
- decreased preload due to venodilation
- increased perfusion pressure due to decreased preload and therefore decreased LVEDP
- decreased afterload due to systemic vasodilation
- increased flow due to coronary vasodilation (at higher doses)
