1. Causes of ACS
    • CAD
    • Cardiogenic shock/poor perfusion
    • Stimulants abuse(eg coccaine, amphetamine)
    • Embolus in left ventrcle/atrium
  2. Chronic stable angina...
    is chest pain on exertion/emotional stress related to a 70% narrowing of the lumen of epicardial artery or 50% of major artery
  3. Types of Angina
    • Classic/Stable 2/2 plaque
    • Vasospastic/variant/Prinzmetal's 2/2 reversible spasm of coronary arteries
    • Unstable angina/AC- incr feq/severity of attacks; combo of plaque rupture, plt aggregation and vasospasm (immediate precursor to MI). Leads to fibrin clot formation.
  4. Chronic stable angina tripped off by...
    • Imbalance in O2 supply/demand
    • Demand- HR, contractility, preload, afterload
  5. Heart's O2 demand determined by
    • HR
    • contractility
    • preload (diastolic )- blood volume/ venous tone
    • afterload (systolic)- arterial blood pressure/arterial tone
  6. ACS primarily results from
    partial or total occlusion of coronary artery by thrombus diminishing blood fflow and O2 supply.
  7. Types of ACS
    • Unstable angina (UA)
    • NSTEMI- UA w/ ischemia, usually limited to sub endocardial myocardium
    • STEMI (Q wave/ST elevation)- extensive transmural ischemia
  8. White clots contain and are associated with...

    Red clots contain and are associated with...
    Plts, cause incomplete occlusion and more associated w/ NSTEMI

    Fibrin which traps RBC, often complete occlusions and more w/ STEMI
  9. Hormones that promote plt aggregation include...
    epinephrine, serotonin and thrombin
  10. Ventricular remodelling in ACS
    Often occurs after MI (from activation of RAAS, catecholamines etc) and major cause of HF (systolic + diastolic)

    Slowed/reversed by ACE-I, BB, Aldosterone antagonist (decrease mortality)
  11. ACS complications
    • HF
    • cardiogenic shock
    • arrhythmias
    • VTE
    • bradycardia
    • heart block
  12. ACS Sx
    • Chest discomfort, lasts about 20mins (constant in STEMI; new onset, at rest or worsening in STEMI)
    • may radiate down left arm/back/jaw
    • N/V
    • SOB
    • Diaphoresis
  13. ECG Changes
    • ST elevation with STEMI
    • ST depression
    • T-wave inversion
    • No change
  14. LABS
    Troponin and CKMB rise within 6hrs ffg coranary artery occlusion and myocardail cell death

    • Troponin falls slowly (10 days)
    • CKMB rises and falls (48hrs) rapidly

    Must take at least 3 serial labs over 24hrs ffg presentation. +Ve MI w/ 1 elevated troponin or 2 CKMB
  15. STEMI- target time to reperfusion from hospital presentation
    • Fibrinolytics- 30mins
    • PCI-90mins

    Both at least <12hrs from Sx onsent to be eligible
  16. PPT factors of angina
    • 5 E’s of angina:
    • Exercise
    • Exposure to cold
    • Emotional stress
    • Eating large meals
    • severe anEmia
  17. Typical angina criteria
    • 1.Substernal chest pain with characteristic quality and duration
    • 2.Provoked by exertion or emotional stress 3 Relieved by rest or nitroglycerin

    Atypical meets only 2 of above; non-cardiac- 1 </= 1
  18. Cardiac cath
    Diagnostic to determine cause of angina; can determine presence of plaque, can also be treatment as per removing plaque
  19. ACS THx goals
    • Immediate relief of ischemia
    • Restoration of blood flow
    • Prevention of death/reinfarction
    • Secondary prevention of MIs
  20. ACS Thx guide
    Image Upload 1
  21. Initial ACS thx

    Relieve ischemia, decr O2 demand & incr supply, Halt thrombus formatn, Preserve myocardium
    • MONA + BB + anticoag
    • Morphine
    • Oxygen
    • Nitrates
    • Aspirin
    • Beta blockers
    • Heparin/lovenox
  22. Risk Stratification for NSTEMI
    Image Upload 2
  23. M: Morphine

    Anal gesic of choice
    • MOA: Blocks sympathetic efferent discharge at CNS level resulting in minimal peripheral venous and arterial dilation Established efficacy, quick onset of action, sedative• Give if ischemia is not relieved by NTG Dose: 2-4 mgIV q5 15min until pain relief or ADR
    • Monitor:– BP for hypotension HR for bradycardia
    • RR for reduced respiratory drive
    • Mental status for CNS depression
  24. O: Oxygen
    • Reduce demand on the heart by increasing oxygen delivery. Patients are often hypoxemic (SaO2 < 90% • Oxygen saturation is measured by continuous pulse‐ox
    • Dose:2‐4 L/min adminstered by nasal cannula (NC) or face mask
  25. N: NTG
    • IV- 10/10/5 x24hrs
    • oral- 0.4mg q 5min x 3 doses
    • Coronary and peripheral vasodilator– Decreases preload and O2demand, Increases Odelivery2
    • Avoid in Patients with initial SBP < 90 mmHg or Recent PDE‐5 inhibitors use
    • Monitoring– BP for hypotension – HR for reflex tachycardia
  26. A: Aspirin
    • Produces rapid clinical antithrombotic effect – Inhibits platelet aggregation, irreversible inhib. of COX‐1 pathway and decr production of thromboxane
    • Chew 325mg in the ER – not enteric coated ASAP
    • C/I– Aspirin allergy/Active or severe bleedingDosing
  27. BB: Beta blockers
    • Give promptly w/o C/I
    • Improves mortality
    • May give IV if BP high- metoprol 5mg q5min x 3 doses. Atenolol same x2doses.
    • May use CCB if BB C/I like coccaine induced MI, give PO, don't use if EF<40%
  28. ACE-I
    Decr mortality, remodelling, reinfarction, arrhythmias

    Use captopril, most flexible, transition to longer b4 d/c. Avoid IV use
  29. Statins
    • Pleiotropic effecrs, w/24hrs
    • Lipid profile also w/24hrs. high dose recce. Zocor 80 or atorvastatin 80
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