CAD 2 (ACS) Flashcards
acute coronary syndrome (ACS) - defined
*a range of conditions associated with sudden impairment of blood flow through the coronary arteries
*includes unstable angina & myocardial infarction
classic physical exam consistent with acute coronary syndrome (ACS)
*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
classic HPI consistent with acute coronary syndrome (ACS)
*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
initial treatment measures for acute coronary syndrome (ACS)
*comfort measures: oxygen, pain control
*aspirin
*clopidogrel
*initiation of IV nitroglycerin
*anticoagulation initiation with IV heparin
*emergent transfer to cardiac catheterization lab
acute coronary syndrome (ACS) - defined clinical presentation
- unstable cardiac symptoms:
-new or changing anginal symptoms
-anginal symptoms at rest
OR
- any objective evidence of myocardial necrosis
acute coronary syndrome (ACS): NEGATIVE TROPONIN
*negative troponin: diagnosis = unstable angina
*critical and acute under-perfusion that results in ischemia but NO INFARCTION (yet)
acute coronary syndrome (ACS) - POSITIVE TROPONIN
*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
pathophysiology of acute coronary syndrome (ACS)
*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
progression of myocardial injury in ACS
*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)
if sustained hypoxia occurs during an MI, the myocardium undergoes…
*undergoes COAGULATIVE NECROSIS
*hyperemic on gross pathology
*on microscopy: invasion of myocardium by neutrophils
timeline of pathology findings in myocardial infarctions: 0-4 hours
*gross: none
*light microscopy: wave fibers
*complications: ventricular tachycardia, heart failure, cardiogenic shock
timeline of pathology findings in myocardial infarctions: 4-12 hours
*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
timeline of pathology findings in myocardial infarctions: 12-24 hours
*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
timeline of pathology findings in myocardial infarctions: 1-3 days
*gross: hyperemia
*light microscopy: extensive coagulative necrosis; tissues surrounding infarct (peri-infarct zone) shows acute inflammation with NEUTROPHILS
*complications: VT, post-infarction fibrinous PERICARDITIS
timeline of pathology findings in myocardial infarctions: 3-14 days
*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
timeline of pathology findings in myocardial infarctions: 2 weeks to several months
*gross: gray-white scar
*light microscopy: contracted scar complete
*complications:
-Dressler’s syndrome
-heart failure
-VT
-true LV aneurysm (risk of mural thrombus)
main determinants of size of myocardia infarction
*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
diagnosis of ACS: clinical presentation
*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
diagnosis of ACS: physical exam
*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)
diagnosis of ACS: EKG
*ST segment changes:
-depressions = ischemia or nontransmural stenosis (critical coronary stenosis)
-elevations = TRANSMURAL INJURY (likely coronary occlusion)
*Q waves: suggest prior or evolving infarct
EKG findings correlated to LV infarct zones
*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
diagnosis of ACS: biomarkers
*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)
treatment of ACS: immediate
- antiplatelets (aspirin, P2Y12 antagonist)
- anticoagulant (heparin/enoxaparin)
- nitro for pain
treatment of ACS: urgent
*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
treatment of ACS: long-term
*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
complications of acute MI
*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
during what time frame are mechanical complications of MI most likely to happen?
*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
right ventricular infarcts
*RV infarcts can accompany an RCA infarct
*RV infarcts are PRELOAD DEPENDENT: nitroglycerin causes hypotension (BAD); may require aggressive IV fluids
