CAD 2 (ACS)

Question 1

acute coronary syndrome (ACS) - defined

Answer 1

*a range of conditions associated with sudden impairment of blood flow through the coronary arteries
*includes unstable angina & myocardial infarction

Question 2

classic physical exam consistent with acute coronary syndrome (ACS)

Answer 2

*general: well-developed male in moderate distress; diaphoretic and anxious-appearing
*vitals: HR normal, elevated RR, elevated BP, normal SaO2
*lungs: clear bilaterally
*cardiac: RRR, normal heart sounds, no murmurs, rubs, or abnormal sounds
*extremities: normal & equal pulses throughout; no edema

Question 3

classic HPI consistent with acute coronary syndrome (ACS)

Answer 3

*58 yo male with history of HTN presented after dinner to ED with a 45-minute history of chest pain
*pain is substernal & diffuse, “crushing” in nature, radiating to his jaw & left arm, and associated with SOB and diaphoresis; he feels anxious and a little nauseous

Question 4

initial treatment measures for acute coronary syndrome (ACS)

Answer 4

*comfort measures: oxygen, pain control
*aspirin
*clopidogrel
*initiation of IV nitroglycerin
*anticoagulation initiation with IV heparin
*emergent transfer to cardiac catheterization lab

Question 5

acute coronary syndrome (ACS) - defined clinical presentation

Answer 5

1. unstable cardiac symptoms:
   -new or changing anginal symptoms
   -anginal symptoms at rest

OR

2. any objective evidence of myocardial necrosis

Question 6

acute coronary syndrome (ACS): NEGATIVE TROPONIN

Answer 6

*negative troponin: diagnosis = unstable angina
*critical and acute under-perfusion that results in ischemia but NO INFARCTION (yet)

Question 7

acute coronary syndrome (ACS) - POSITIVE TROPONIN

Answer 7

*positive troponin: diagnosis is either: 1) non-ST elevation MI (NSTEMI; not transmural) or 2) ST elevation MI (STEMI; transmural)
*critical under-perfusion that results in tissue hypoxia & MYOCARDIAL NECROSIS
*accumulation of deleterious metabolites & potentially irreversible cardiac damage

Question 8

pathophysiology of acute coronary syndrome (ACS)

Answer 8

*atherosclerosis builds up over time, eventually the PLAQUE RUPTURES and causes acute coronary syndrome (ACS)
*plaque rupture → plaque interior exposed to blood → platelet activation & coagulation cascade → thrombus formation → acute coronary syndrome (ACS)

note - understand that any degree of coronary blockage can lead to ACS; the size of the atheroma is not the cause of the ACS; the RUPTURE of the atheroma causes the ACS

Question 9

progression of myocardial injury in ACS

Answer 9

*main biochemical consequence of ischemia is anaerobic glycolysis within seconds:
-inadequate production of high-energy products (ATP and creatine phosphate)
-accumulation of noxious breakdown products (lactic acid)

*necrosis starts subendocardially (~30 min) → necrosis extends toward subepicardium (~4 hrs) → completed infarct involving whole area, extending through myocardium (6-12 hrs)

Question 10

if sustained hypoxia occurs during an MI, the myocardium undergoes…

Answer 10

*undergoes COAGULATIVE NECROSIS
*hyperemic on gross pathology
*on microscopy: invasion of myocardium by neutrophils

Question 11

timeline of pathology findings in myocardial infarctions: 0-4 hours

Answer 11

*gross: none
*light microscopy: wave fibers
*complications: ventricular tachycardia, heart failure, cardiogenic shock

Question 12

timeline of pathology findings in myocardial infarctions: 4-12 hours

Answer 12

*gross: affected areas start to darken
*light microscopy: coagulative necrosis → cell contents released into blood & neutrophils invade; edema & hemorrhage
*complications: ventricular tachycardia, heart failure, cardiogenic shock

Question 13

timeline of pathology findings in myocardial infarctions: 12-24 hours

Answer 13

*gross: affected areas start to darken
*light microscopy: coagulative necrosis → cell contents released into blood & neutrophils invade; MORE NEUTROPHILS; edema & hemorrhage
*complications: ventricular tachycardia, heart failure, cardiogenic shock

Question 14

timeline of pathology findings in myocardial infarctions: 1-3 days

Answer 14

*gross: hyperemia
*light microscopy: extensive coagulative necrosis; tissues surrounding infarct (peri-infarct zone) shows acute inflammation with NEUTROPHILS
*complications: VT, post-infarction fibrinous PERICARDITIS

Question 15

timeline of pathology findings in myocardial infarctions: 3-14 days

Answer 15

*gross: hyperemic border/yellow core
*light microscopy: MACROPHAGES/GRANULATION TISSUE; coagulative necrosis
*complications:
-free wall rupture → tamponade
-papillary muscle rupture → mitral regurgitation
-ventricular septal rupture (due to macrophage-mediated structural degradation) → left-to-right shunt
-LV pseudoaneurysm

Question 16

timeline of pathology findings in myocardial infarctions: 2 weeks to several months

Answer 16

*gross: gray-white scar
*light microscopy: contracted scar complete
*complications:
-Dressler’s syndrome
-heart failure
-VT
-true LV aneurysm (risk of mural thrombus)

Question 17

main determinants of size of myocardia infarction

Answer 17

*duration & extent of coronary arterial occlusion
*size of the vascular bed supplied by the obstructed vessel (proximal vs. distal)
*extent of collateral vessels
*alterations in BP, HR, and cardiac rhythm

Question 18

diagnosis of ACS: clinical presentation

Answer 18

*classically, ACUTE ONSET of TIGHT/CRUSHING CHEST PAIN radiating to arm and jaw, associated with dyspnea, nausea, and diaphoresis
*atypical chest or epigastric pain more likely in women
*may be clinically silent
*may present with catastrophic arrhythmia
*CHF or cardiogenic shock

Question 19

diagnosis of ACS: physical exam

Answer 19

*tachycardia
*tachypnea
*diaphoresis
*distended jugular veins, lung crackles, or edema if severe MI and resultant heart failure
*new murmur if valvular disturbance or complication of MI (myocardial rupture)

Question 20

diagnosis of ACS: EKG

Answer 20

*ST segment changes:
-depressions = ischemia or nontransmural stenosis (critical coronary stenosis)
-elevations = TRANSMURAL INJURY (likely coronary occlusion)

*Q waves: suggest prior or evolving infarct

Question 21

EKG findings correlated to LV infarct zones

Answer 21

*ST elevations localize (not ST depressions)

*LAD infarct zones:
-anterior = V1 - V4
-septum & anteroseptum = V1 - V3
-anterolateral = V4 - V6

*left circumflex infarct zones:
-lateral = lead I & aVL

*RCA infarct zones:
-inferior = leads II, III, & aVF
-posterior = depressions anteriorly

Question 22

diagnosis of ACS: biomarkers

Answer 22

*TROPONIN (troponin I and troponin T) are most common and by far the most specific for myocardial necrosis
*creatinine kinase (CK) elevation is proportional to SIZE of infarct

*note - NEITHER rises IMMEDIATELY and can be negative early in an infarct (usually troponin rises after 3-5 hours)

Question 23

treatment of ACS: immediate

Answer 23

1. antiplatelets (aspirin, P2Y12 antagonist)
2. anticoagulant (heparin/enoxaparin)
3. nitro for pain

Question 24

treatment of ACS: urgent

Answer 24

*send to CATH LAB (to stabilize the plaque with a stent)
*if no cath lab within 120 minutes (from presentation of chest pain), can consider thrombolytics

Question 25

treatment of ACS: long-term

Answer 25

*indefinite aspirin for secondary prevention
*12 months of additional antiplatelets
*statin therapy to prevent progression of atherosclerosis and recurrent events
*beta-blocker for at least 3 years to prevent dangerous arrhythmias

Question 26

complications of acute MI

Answer 26

*arrhythmias: heart block, bradycardia, or ventricular arrhythmias
*CHF, pulmonary edema
*cardiogenic shock
*pericarditis
*mechanical complications: VSD, papillary muscle rupture with development of severe mitral regurgitation, rupture of LV free wall
*development of scar or ventricular aneurysm

Question 27

during what time frame are mechanical complications of MI most likely to happen?

Answer 27

*mechanical complications (VSD, papillary muscle rupture with development of severe mitral regurgitation, rupture of LV free wall) are most likely THREE TO FOURTEEN DAYS AFTER MI

Question 28

right ventricular infarcts

Answer 28

*RV infarcts can accompany an RCA infarct
*RV infarcts are PRELOAD DEPENDENT: nitroglycerin causes hypotension (BAD); may require aggressive IV fluids