Acute Coronary Syndrome Flashcards
What is Acute Coronary Syndrome?
ACS is an array of clinical symptoms resulting from underlying acute myocardial ischemia: not meeting demand with enough supply of oxygen.
True or False: ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related coronary artery.
TRUE
What is the most common cause of ACS?
Atherosclerotic plaque rupture with thrombosis
What are 9 causes of ACS?
- Atherosclerotic plaque rupture with thrombus
- Vasculitic syndromes
- Coronary embolism
- Congenital anomalies (e.g. pinched artery)
- Coronary trauma or aneurysm
- Severe coronary artery spasm
- Increased blood viscosity
- Spontaneous coronary dissection
- Markedly increased myocardial O2 demand
What two effects are decreased by dysfunctional endothelium caused by atherosclerosis?
Decreased vasodilation effect, decreased anti-thrombotic effect
What two things are activated during plaque rupture?
Platelet activation, coagulation cascade activation
What are the two kinds of myocardial ischemia?
Transmural and subendocardial
What is transmural ischemia and what typically causes it?
Transmural ischemia spans the entire thickness of the myocardium. This is typically caused by an occlusion.
What is subendocardial ischemia and what typically causes it?
Subendocardial ischemia involves the innermost layers of myocardium. This is typically caused by partial occlusion.
If ischemia is prolonged, what results?
Myocardial infarction - Myocyte death and tissue necrosis.
What does ECG look like with subendocardial ischemia?
ST depression
What does ECG look like with transmural ischemia?
ST elevation
What is STEMI?
ST Elevation MI
What is NSTEMI?
Non ST Elevation MI
What are the 3 serum markers for diagnosing Myocardial Infarction?
Troponin I, Troponin T, Creatine Kinase - MB isoenzyme
Is Troponin or CK-MB a more specific and sensitive marker for myocardial infarction?
Troponin
When is the onset and peak of Troponin I and Troponin T for myocardial infarction?
Begins to rise 3-4 hours after onset of pain, peaks at 18-36 hours
When is the onset and peak of CK-MB for myocardial infarction?
Begins to rise 3-8 hours after onset of pain, peaks at 24 hours
Is stable angina or unstable angina easy for reproducing clinical symptoms with a predictable exertion?
Stable
Is stable or unstable angina new/acute onset?
Unstable
What are other symptoms, other than angina, for myocardial ischemia? (name 6)
Shortness of breath, diaphoresis, nausea, vomiting, weakness, sometimes referred pain up to jaw/back/neck/arm
Is there partial or total occlusion in unstable angina?
Partial
Is there partial or total occlusion in NSTEMI?
Partial
Is there partial or total occlusion in STEMI?
Total
Are serum biomarkers present in unstable angina?
No
Are serum biomarkers present in NSTEMI?
Yes
Are serum biomarkers present in STEMI?
Yes
What is the ECG finding in unstable angina?
Normal or there could be ST depression depending on how the patient is or if the patient is getting stress test etc.
What is the ECG finding in NSTEMI?
ST Depression
What is the ECG finding in STEMI?
ST Elevation
Is stable angina ACS?
No
What 3 things are considered to be ACS?
Unstable angina, NSTEMI, STEMI
There is an increase of _____, ____, or _____ of angina in Unstable Angina.
duration, intensity, or frequency
How do you treat STEMI?
Free up the occlusion as fast as possible. If you can, open it within 90 minutes (cath lab). If resources not available, give fibrinolytic drugs and transfer to nearest center that can perform the operation. Also, give beta blockers and nitrates.
Why are beta blockers and nitrates given in STEMI treatment?
Beta blockers will reduce the heart rate which reduces the oxygen demand of the heart. The nitrates cause vasodilation in hope of allowing some blood flow through obstruction. It’s important to give these medications to help improve prognosis while you ate trying to get patient to cath lab as fast as possible.
How do you treat unstable angina and NSTEMI?
Treatment of unstable angina and NSTEMI is similar to treatment of STEMI. You want to halt the progression of the clot (anti-coagulation and anti-platelet activation) and you also want to give beta blockers and nitrates in order to reduce the myocardial oxygen demand of the heart and also to try to cause more blood flow with vasodilation. For UA and NSTEMI, you also need to bring the patient to the cath lab for percutaneous intervention however it’s not as urgent–try to do within 24 hours.
What is the most common anti platelet agent?
Aspirin. This is used in all UA/NSTEMI patients.
What is dual anti-platelet therapy?
Aspirin + P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor)
What is given in conjunction with Aspirin to provide “dual anti-platelet therapy”?
P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor)
Name 3 P2Y12 inhibitors (anti platelet agents).
- Clopidogrel
- Prasugrel
- Ticagrelor
In addition to “dual anti-platelet therapy”, what is the 3rd kind of anti platelet agent you can give if a patient is high risk or proceeding to catheterization?
Glycoprotein IIa/IIIb inhibitor (eptifibatide, tirofiban, abciximab)
Name 3 Glycoprotein IIa/IIIb inhibitors
- Eptifibatide
- Tirofiban
- Abciximab
Name 3 anticoagulant agents
- Unfractionated heparin
- Enoxaparin
- Fondaparinux
Name the “direct” anticoagulant agent that you can give if the patient is proceeding to catheterization.
Bivalirudin
