Chest Pain Flashcards
Dx tests for acute MI:
Physical Exam
ECG
Cardiac Markers
Pros and cons of the different cardiac markers:
CK-MB = >90% sensitive for MI 5-6h after symptom onset, but only 50% sensitive shortly after presentation, elevate @ 3-12 hours, peak @ 18-24 hours, duration 2 days
Troponin = Tn-I similar to CK-MB but duration is 5-10 days; TN-T is less sensitive, but is an independent marker of CV risk
Treatment for patient with ACS:
“OH BATMAN Mneumonic:
Oxygen heparin beta-blocker aspirin thrombolytic morphine anti-platelet agent nitrates
Examples of common anti-platelet agents:
Plavix
MOA of Aspirin
Irreversibe antiplatelet agent
Inhibits thomboxane A2 and therefore blocks platelet aggregation
MOA of nitrates:
Decrease preload + afterload through massive vasodilation
Increases coronary perfusion
Role of ß-blocker in ACS
decrease infarct size, CV complications, and mortality
When fibrinolytics are indicated in AMI:
if ST elevation > 0.1mV in 2+ continguous leads
Or There is a new LBBB
Time to therapy < 12 hours (class I), 12-24 hours (class IIb)
Types of cardiac issues associated with cocaine:
6% of patients w/ cocaine-associated chest pain have an AMI (often atypical chest pain)
20-60% have transient myocardial ischemia
Onset of cardiac symptoms in cocaine use:
Can be delayed hours to days after most recent use
Etiology of cardiac issues with cocaine:
spasm
inc. myocardial O2 demand
clot formation
accelerated atherosclerosis w/ LVH
Diagnosis of cocaine related chest pain:
History
Tn-I useful
ECG is less sens/spec than for MI
CK-MB less sens
Prognosis for cocaine related chest pain:
Favorable short term
Higher 1 year mortality due to associated comorbidities or cont. cocaine use
Treatment for cocaine related chest pain:
Benzos
AVOID ß-blockers (unopposed alpha agonism can result in vasospasm)
What is an aortic dissection?
intimal tear w/ entry of blood into media, dissecting btw. intima and adventitia