The Basics
What Is it?
- Acute discrepancy b/tw myocardial demand and supply
- Acutely decreased supply (plaque rupture, Type 1)
- Increased Demand (Type 2 NSTEMI vs Ischemia)
Stable Angina
Unstable Angina
NSTEMI
STEMI
---------------------
Characterize Chest Pain
1) substernal
2) w/w exertion
3) A/w rest a/o nitroglycerin
Cardiac Chest Pain = 3/3
vs
Atypical Chest Pain = 2/3
vs
Non-Cardiac Chest pain 0-1/3
ANGINAL EQUIVALENTS: SOB, Diaphoresis, Extreme Fatigue
Other Assd Sxs: pain in neck, jaw, arm. N/V, chest PRESSURE, palps, dizziness/lightheadedness.
Diagnosis of ACS in General:
1. Physical Exam
•Ischemia: new S4, new MR murmur 2/2 pap muscle dysfunction, paradoxical S2, diaphoresis
•Heart Failure: JVP, Crackles, S3, hypotension, cool extremities (cardiogenic shock).
•Other areas of Atherosclerosis: bruits (fem/carotid), decreased distal pulses
2. Diagnostics
•EKG + Cardiac Markers (troponin Tn > CK-MB)
•Troponin rises 2-6 hours after BEGINNING of insult
Other Aids
•TTE – for new WMA
•CT Angio Coronary / perfusion /stress test (low prob)
•Coronary Angiography – Gold Standard
If non-diagnostic initially from trop/ekg, repeat 3-6h
If normal and clinical suspicion for ACS remains high:
r/o Unstable Angina – stress test (vs CT angio for CAD)
Inpt or outpt?
Inpt for HIGH RISK
- >70 YO
- prior CAD, CVD, PAD
- resting angina
Outpt (w/in 72 hours) for LOW RISK
NSTEMI
ONLY 1/3 HAVE 1+ MM ST DEPRESSIONS IN CONTINUOUS LEADS
Characterization: 5 types - Type 1 = plaque rupture, type 2 = ischemic balance (fixed disease but increased demand), types 3-5 are procedural/surgical
Stratification: TIMI Score:
If score is 3+, benefit from Early angiography (<24 hours)
If <3, intervene (if appropriate) any time within 72 hours
*If pain is REFRACTORY to medical management, OR HD instability -> angio w/in 2 hours!
Type 2 NSTEMI vs Demand Ischemia
The same pathophysiologic precipitant (increased demand with a stable coronary artery lesion).
The difference is, in T2 NSTEMI, myocardial tissue is irreversibly damaged (is not viable, heals by scar) vs Demand Ischemia where the tissue can heal and work well again if blood flow is restored.
STEMI
Complete Total Occlusion of a coronary artery causing FULL THICKNESS INFARCTION.
For dx You need:
>= 2 contiguous leads w/ >= 1mm* (1.5 mm+ in V2-V3)
OR
New/presumed new LBBB
WITH OR WITHOUT Trop elevation
and...SYMPTOMS!!
Treatment
Emergent REPERFUSION = 1st line therapy
Door->balloon goal time: 90 minutes
If you are at a Non-PCI capable facility: fibrinolytics w/in 30 min presentation. unless
you can get to PCI within 120 minutes
-------------------------------------------------------------------------
Prognosis in STEMI
Use the Killip and Forrester Classifications:
Medications in UA, T1 NSTEMI, and STEMI:
Antiplatelets
ASA
ADP blockers (clopid, ticagr)
GP 2b/3a – abciximab, eptifibatide, tirofiban
Anticoagulation
UFH, enox, bival, fondaparinux
BBs
Nitrates
Oxygen
Morphine
ACE-I = ARBs (NEJM 2003;349:20)
Additional Meds for STEMI that show benefit
Intensive Statin (decreases periprocedural myonecrosis, JACC 2007;49:1272)
Insulin for glucose >180
==========================================================
Some EKG Practice Resources:
www.litfl.com
============================================
Positive and Negative LRs in ACS
Commentaires