Ischemic Heart Disease – ED

Ischemic Heart Disease

1. Given a patient with potential acute coronary syndrome (ACS), initiate diagnostic testing without delay and plan ongoing testing until diagnostic resolution (e.g., early and serial ECG, early biomarker testing, chest pain protocols).

2. In patients with potential ACS, accurately interpret ECGs, especially those with subtle changes and important rule-out diagnoses (e.g., pericarditis).

ECG: (up to 8% AMI have normal ECG)

  • Presence of reciprocal changes (large MI) increases specificity for true AMI
    • Reciprocal changes absent in ventricular aneurysm (chronic STE/ TWI) and benign early repoloarization
  • STD/TWI in at least 2 contiguous leads – Unstable angina
  • STEMI (diagnostic changes for AMI in <50% on initial ECG – serial ECG beneficial)
    • Hyperacute T waves (early)
    • TWI
    • Significant Q waves (1 square wide and 1/3 height of R wave) – may develop as quickly as 3-4 hours after infarct
    • STE (Transmural MI)
      • Anterior MI: LAD occlusion, STE V1-V6 (anterior-septal V1-V4)
        • inferior reciprocal changes
      • Anterolateral: LAD/anterior trunk occlusion, STE V3-V6, I, aVL
        • inferior reciprocal changes
      • Inferior: RCA occlusion, STE II, III, aVF
        • aVL reciprocal changes, consider posterior or RV involvement
      • Lateral: LC or diagonal branch occlusion, STE I, aVL, V5, V6
        • inferior reciprocal changes
      • Posterior: RCA/Circumflex, large R wave with STD V1-V3, STE posterior leads, associated with inferior MI, less common with lateral MI
        • V7-V9 elevation often subtle >0.5mm to make Dx
    • LBBB – scarbosa only needs 1 lead (STEMI equivalent)
      • STE in the same direction as the major QRS vector
      • STD at least 1mm in V1-V3
    • STEMI equivalents
      • STE in aVR with STD in multiple other leads – STE aVR>V1 increases specificity
        • Left main coronary artery occlusion
      • De Winter T wave – LAD occlusion; upsloping STD with tall hyperacute T waves (V1-V4)
      • Wellen’s (biphasic / deep TWI in V2-V3) – LAD

STEMI DDx:

  • Electrolytes: Hyperkalemia
  • LBB: (QRS >0.12; V1 – RSR’ terminal above = RBBB / Below baseline = LBBB)
  • Early repolarization – BER
  • Ventricular hypertrophy – LVH (can progress to LBBB)
  • Aneurysm (LV aneurysm – no reciprocal changes)
  • Treatments (needle advanced too far during pericardiocentesis)
  • Injury – Mycardial contusion
  • Osborn waves (hypothermia)
  • Non-occlusive vasospasm – Prinzmetal angina
  • Pericarditis
    • STE >6 and no reciprocal changes except aVR/V1,
    • PR depression- most specific finding
    • Stage 1- PR depression/STE; STage 2 – normal; Stage 3 – TWI, Stage 4 normal
    • Dx: typical chest pain, pericardial friction rub, ECG changes, new or worsening pericardial effusion
    • consider myopericarditis if + trop

3. Given a patient with a confirmed or possible ACS, stratify the risks for both typical and atypical presentations to direct management choices.

Stress test / MIBI / Coronary CT Angiograpny / Angiography for risk stratifications

4. In a patient with suspected ACS, do not rule out the diagnosis based on a single negative test result or based on findings of limited usefulness (e.g., response of pain to a “pink lady,” chest wall tenderness, resolution of pain).

5. Consider ACS as the possible cause of symptoms in atypical presentations. (e.g., fatigue, dizziness, dyspnea, atypical pain), especially in patients who may be at increased risk (e.g., elderly, cocaine users (young), females, diabetics).

Elderly, women, diabetic patients often have atypical presentation.

  • women have more frequent unrecognized AMI; atypical presentation more common
  • AMI symptoms: Dyspnea, Weakness, Fatigue (chest pain absent in 43% in women)

20% AMIs lack chest pain

  • pt may present with isolated abdominal pain, back pain, neck/jaw pain, arm parin
  • painless presentations: isolated dyspnea, malaise, weakness in 1/3 of patients

Young patients – consider cocaine use

  • 24x increased risk of MI during 1st hour after use
  • inc risk with chronic use (accelerated atherogenesis)
  • avoid use of beta-blockers

6. In a patient presenting with an STEMI, arrange for urgent reperfusion by the optimal available and appropriate means (e.g., PCI, thrombolysis).

Treatments

  1. oxygen if hypoxic
  2. Nitrates (if not inferior/posteiror/RV)
  3. ASA – reduces reinfarction and mortality
  4. Morphine for intractable pain
  5. Heparin / LMWH
  6. Beta-blocker – give orally within 24hr; avoid IV unless intractable HTN/A Fib (increase long term survivability)
  7. Clopidogrel or Ticagrelor
    1. if TPA – load with clopidogrel 300mg po
    2. if PCI – load with clopidogrel 600mg po
  8. PCI – Angioplasty or Stent
    1. Post-arreat STEMI with ROSC but unresponsive needs therapeutic hypothermia & rapid PCI
    2. NSTEMI who are unstable, intractable ischemic symptoms, post-arrest NSTEMI
  9. Thrombolytics / TPA – if PCI n/a within 90min to balloon inflation
    1. if pt presents to non-PCI hospital, transfer protocols can be employed that allow up to 120min to balloon inflation
    2. Chest pain / symptoms >30min and <12hr
    3. PCI not immediately available
    4. Complication
      1. bleeding / serious bleeding / intracranial hemorrhage
      2. REperfusion arrhymia – transient

7. In a patient with ACS, assess risks and benefits of the possible specific interventions (thrombolytics, pacing, PCI, beta blockers) prior to initiating treatment.

contraindications of TPA:

    1. Active GI/GU bleed, bleeding diathesis (high INR),
    2. hx of hemorrhagic CVA,
    3. ischemic CVA <6mo,
    4. hx of intracranial neoplasm, AVM, aneurysm,
    5. recent Sx or trauma <2mo,
    6. Severe uncontrolled HTN >200/120

cocain related – no beta-blocker

Cardiac pacemaker

  • hemodynamically unstable bradycardia in which atropine is unsuccessful or not indicated (mobitz 2, 3rd degree AV block)
  • Bradycardia due to malignant ventricular escape rhythm unresponsive to drug Tx
  • Termination of malignant tachydysrhythmias (overdrive pacing in torsades de pointes) – rate at 120bpm dec QTc
  • Standby pacing if pt decompensation is probable

8. Given a patient with potential ACS stratified as low risk, ensure appropriate follow-up and investigation (e.g., provocative testing) until the diagnosis is eliminated or confirmed.

Early Complications of AMI

  1. Dysrhythmias
    1. Tachycardia (anteroseptal)
    2. Bradycardia (inferior)
    3. PVS
    4. VT – preceded by PVCs / V Fib usually within 12hr
  2. Recurrent ischemic chest pain vs re-infarction – if post TPA, needs PCI (can’t repeat TPA)
  3. Papillary muscle dysfunction (loud systolic murmur from acute MR)
    1. within first few days post MI
    2. often causes acute pulmonary edema / HoTN
  4. Cardiogenic shock (loss >40% LV muscle) – Tx with inotropes
    1. HoTN
    2. systemic hypoperfusion (dec U/O, AMS)
    3. Pulmonary edema
  5. RV infarct – preload depended – needs lots of IVF (not inotropes) & caution with nitrates
    1. HoTN, JVD, clear lungs 
    2. associated with inferior MI, rarely with lateral MI
    3. high incidence of 2nd / 3rd AV block
    4. RV3-4 STE
  6. Conduction block
    1. first degree or Wenckeback (mobitz 1) – seen in inferior MI
    2. mobitz 2 or 3rd degree AV block in anterior MI – needs pacing
    3. LBBB/ RBBB in the setting of acute Anterior MI will likely progress to complete block

Late AMI complications

  1. Acute MR – ruptured papillary muscle; dx w/ echo
    1. 3-5d post MI; associated with inferior MI
    2. acute CHF & new systolic murmur
  2. Ruptured ventricular septum – dx w/ echo
    1. acute ventricular septal defect (loud harsh systolic murmur)
    2. CHF
  3. Pericarditis (1-7d post MI)
  4. Dressler’s syndrome – autoimmune
    1. 2-8wk post MI
    2. Tx with steroids and NSAIDs
Posted in CCFP EM, Uncategorized

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CCFP ExamApril 30th, 2015
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August 2020
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