Acute Coronary Syndromes Flashcards
1
Q
UA v NSETMI v STEMI
A
- ST Elev MI (STEMI)
- Transmural, see ST elevation and Q waves
- If total occlusion or occluded > 20 min
- Non ST Segment MI (NSTEMi)
- Sub-endocardial; may see ST depression
- If partial occlusion or occluded < 20 min
- Non ST Segment MI (NSTEMi)
- Unstable Angina (US) - threatening MI
* Usually represents wax/wane b/n thrombosis & thrombolysis- UA normally just white clot/ platelet plug that can be easily dispersed (unlike red cot that is more likely to cause MI)
2
Q
What is sudden cardiac death?
A
- Pt w/ severe CAD but NO thrombus occluding vessel and NO MI
- Death due to arrhythmia (usually VT) not acute change in underlying pathology
3
Q
Prinzmetal angina
A
- episodic, at rest, from coronary vasospasm NOT underlying pathology
4
Q
4 Factors That Determine Amount/Speed of Necrosis
A
1- Collateral vessels
2-Metabolic state/health of myocardium
3- Presence of anti-thrombotic therapy
4-Degree of arterial occlusion
5
Q
Early Changes in Pathology
A
(<24 hr)
- From no visible histology —> coagulative necrosis (wavy fibers w/o nuclei)
- “Contraction Band Necrosis” - cytoplasm clumps to form perpendicular bands
- May see neutrophils at very end of 24 hr period
6
Q
Middle Changes in Pathology
A
(1-3 days)
- NEUTROPHILS - blue dots
- Cell debris from dead myocytes
- Later macrophages arrive to phagocytose debris
7
Q
Later Changes in Pathology
A
(3-7 days)
- Lots of macrophages/ phagocytosis (most dead myocytes have been ingested now)
- Fibroblasts arrive but only form a loose granulation tissue
- VULNERABLE b/c old myocardium gone (dead and ingested) but no new fibers yet; greatest risk of myocardial rupture
8
Q
Healing 7 Days On
A
(7 days for wks or months)
- Fibroblasts
- New fiber = pink
- Neo-vascularization
- Collagen/fibrin —> myocardial scar
9
Q
3 Most Common Arteries Occluded & Results of Ea
A
- R Coronary Artery - RV, posterior LV and septum (if R dom), AV/SA nodes
- L Anterior Descending - anterior LV and septum, apex most common
- L Circumflex - Lateral LV, posterior LV and septum if L dom - minority
10
Q
4 Steps of Eval
A
1- Hx -
* New angina at rest/minimal exertion; change in angina pattern; angina in CAD pt that is unrelieved by rest or nitroglycerin * May have silent MI (no symptoms) but present w/ pulmonary edema or stroke
2- ECG - ST elevation (STEMI)? ST depression or inverted t waves? (ischemia) Q waves? (infarct)
* Which leads can tell location of infarct…
* Anterior wall - V1-V5 (septum — more lateral)
* Apex Only - V3 and/or V4
* Lateral wall - I, aVL, V6
* Inferior wall - II, III, aVF
3- Physical Exam - less helpful
* S3 if LV dysfunction and S4 if stiff L ventricle * Short systolic murmur (mitral regurg) may result from ischemia of papillary muscles
4- Biomarkers (**negative biomarkers are not sufficient to r/o MI)
* Cardiac troponins * CK-MB
11
Q
Specific Biomarkers
A
- Cardiac troponins - sensitive and specific (cardiac specific- not normally in circulation)
* Produced/out last but also gone last (can detect in circulation for 7-10 days after MI) - CK-MB - sensitive but not as specific (some CK-MB in skeletal muscle too)
* Produced earlier but gone earlier (gone after 48 hrs so good for detecting re-infarction days after acute MI)
12
Q
Therapy in UA/NSTEMI v STEMI
A
3 - CABG - coronary artery bypass graft (last b/c takes more time than others)
- NSTEMI/UA - anti-coagulation, (heparin), anti-platelet (aspirin), ADP receptor inhibitors, beta blockers, ACE inhibitors, statins
- Plus nitroglycerin and morphine for symptoms
- SEE anti-coag drug info below
* STEMI - goal is to re-perfuse w/in first few hours to restore salvageable myocardium
#1 choice = PCI - percutaneous coronary intervention
#2 choice = fibrinolysis (AKA use of drugs to breakdown clots- heparin, aspirin, ADP receptor inhibitors)
* Attach graft from base of aorta to somewhere past coronary artery stenosis
* Use saphenous vein, synthetic vein or internal mammary artery (BEST)
13
Q
Electrical Complications (7)
A
- Early VTs or V fib (first 2 days) - most common cause of sudden cardiac death post MI; use anti-arrhythmic meds; does not predict long-term prognosis
- Later VTs or V fib (after first 2 days) - does dec long-term prognosis; can be “scar VT” from re-entrant path formed b/n viable myocardium and infarct in LV (monomorphic)
- Usually treat w/ ICD esp if LVF < 35%
- AIVR - 50 to 120 BPM; may be due to reperfusion
- Sinus Brady- arrhythmias
- Often due to neurocardiac reflex
- Conduction delays —> brady
- Above His - may also be due to neurocardiac reflex; usually short-lived
- Below His - esp if anterior wall MI (AV node); less common now w/ new reperfusion therapy; more dangerous
- Sinus Tachy - due to pain, low CO, anxiety, hypovolemia, anemia, infection, etc (treat underlying cause)
- Atrial Tachy - a fib, flutter, SVTs - may use class III anti-arrhythmic in first 6-12 wks b/c common + rate and anti-thrombotic
14
Q
Neurocardiac Reflex
A
If post/inf wall infarct…mechano-receptors there are stimulated —> remove sympathetic tone so only parasympathetic
Can cause atypical cardiogenic shock
15
Q
Mechanical Complications (6)
A
- Cardiogenic Shock - LV muscle damage —> low CO —> hypotension
- Myocardial Rupture
- If free wall… hemopericardium & poss tamponade
- If septum…acute VSD w/ L—>R shunt
- If papillary muscles … acute mitral insufficiency/regurg
- Ventricular Aneurysm - Infarcted myocardium is thin so balloons out when nearby myocardium contracts (pressure); thrombus can form in aneurysm
- Mural Thrombus
- Since part of wall is not functioning, blood pools on endocardial surface (STASIS) —> thrombus –> can embolize —> stroke or gangrene
- Fibrinous pericarditis
* Can occur after 1-7 days (inflammation)
* Or weeks later (autoimmune) - Dressler’s Syndrome - Ventricular Remodeling
- Stiff L ventricle; zones of fibrosis then neighboring hypertrophy
