Professional Documents
Culture Documents
Coronary Syndrome
No ST Elevation ST Elevation
Unstable Angina Myocardial Infarction
NSTEMI (Trop pos.)
ECG assessment
ST Depression or dynamic
T wave inversions
NSTEMI
Non-specific ECG
Unstable Angina
Unstable angina/NSTEMI
cardiac care
Evaluate for conservative vs. invasive
therapy based upon:
• Risk of actual ACS
• TIMI risk score
• ACS risk categories per AHA guidelines
Low High
Intermediate
ACS risk criteria
Low Risk ACS Intermediate Risk
No intermediate or high ACS
risk factors Moderate to high likelihood
of CAD
<10 minutes rest pain
>10 minutes rest pain,
Non-diagnositic ECG now resolved
Conservative strategy
High-risk patients
Patients with recurrent ischemia
Recurrent chest pain
Dynamic ST-segment changes (ST- depression
or transient ST elevation)
Early post infarction unstable angina
Elevated troponin levels
Diabetes
Hemodynamic instability
Major arrhythmias (VF, VT)
Acute Coronary Syndromes
Cognitive
Education, cardiac rehab program
Secondary Prevention
disease management
Blood Pressure
Goals < 140/90 or <130/80 in DM /CKD
Maximize use of beta-blockers & ACE-I
Lipids
LDL < 100 (70) ; TG < 200
Maximize use of statins; consider fibrates/niacin
first line for TG>500; consider omega-3 fatty acids
Diabetes
HbA1c < 7%
Secondary prevention
behavioral intervention
Smoking cessation
Cessation-class, meds, counseling
Physical Activity
Goal 30 - 60 minutes daily
Risk assessment prior to initiation
Diet
DASH diet, fiber, omega-3 fatty acids
<7% total calories from saturated fats
Medication Checklist
after ACS
Antiplatelet agent
Aspirin* and/or Clopidorgrel
Lipid lowering agent
Statin*
Fibrate / Niacin / Omega-3
Antihypertensive agent
Beta blocker*
ACE-I*/ARB
Aldactone (as appropriate)
LAD Stenosis, Wellens Syndrome
Positive Troponin-Non-cardiac
conditions
Sepsis
Aortic dissection
SAH, ICH, seizure, stroke, preeclampsia
Exacerbation COPD, Pulmonary Hypertension, PE
Chemotherapy: Antracycline, Cyclophosphamide, 5-
FU, Cisplatin (toxic effect)
GI-Bleeding (mismatch between oxygen demand
and supply of the myocardium)
ESKD, rhabdomyelisis
It is important to note that cardiac troponins are a marker of all heart
muscle damage, not just myocardial infarction. Other conditions that
directly or indirectly lead to heart muscle damage can also increase
troponin levels. Severe tachycardia (SVT, FAF) in an individual with
normal coronary arteries can also lead to increased troponins for
example, presumably due to increased oxygen demand and
inadequate supply to the heart muscle.