MI Flashcards
STEMI ECG
- ST segment elevation of 2 mm or more at J point in V2-V3 in men; 1.5 mm or more in women in absence of LVH or 1 mm or more in 2 or more contiguous chest or limb leads
- T wave ischemic pattern – inverted T waves or tall, peaked T waves
- “transmural” – large Q wave
- New LBBB (obscures ST elevation analysis)
- May need serial tracings
STEMI causes
atherosclerosis, vasospasm, vasculitis, dissection, genetics
STEMI hx
- Chest discomfort, more severe than angina
- Heavy, pressure, crushing, etc
- Retrosternal, left, across chest; neck, jaw, left arm, epigastrium
- N/V, diaphoresis, dyspnea
- Not reliably relieved by Nitro or rest
- 20% painless – DM, elderly women
Physical exam findings for STEMI
• Normal
• S4 Gallop – atrial beating forcefully against less compliant, stiffened ventricle
• BP variable
• Sympathetic hyperactivity (increased HR, increased BP) seen in anterior MI
• Parasympathetic hyperactivity (bradycardia, decreased BP) in inferior MI
o GI manifestations
• Heart failure – S3, crackles, increased JVD, new murmur
Early Acute phase for MI
- T wave increased amplitude
- Hyper-acute pattern
- Convex upward ST pattern
Chronic phase for MI
- Resolution of ST elevation is variable (2 weeks for inferior wall, later for anterior wall)
- Persistent ST elevation (after 2 weeks) think ventricular aneurysm
Zones of Infraction
o Infarction – dead tissue, lacks depolarization
• Q waves
o Injury – deficient blood supply, inability to fully polarize
• ST Segment shifts
o Ischemia – deficient blood supply, impaired repolarization
• T wave changes
Posterior wall infarctions
reciprocal changes in anterior leads
o V1 and V2
• Prominent R wave (reciprocal of posterior Q wave)
• Upright T waves (reciprocal of inverted T wave)
• ST depression (reciprocal of ST elevation)
Labs in MI
o Increased WBC 12,000-15,000 (hours to 2-4 days)
o Increased CRP
o BNP – increased in ventricular wall stress and fluid overload
Troponin I
- 1-4 hrs detectable after onset AMI
- 10-24 hour peak
- Persists 5-14 days
- Renal failure can cause false positive cTnT (clearance route)
non-MI cardiac causes for elevated troponin level
- Myocardial injury, inflammation
- Heart Failure
- Cardiomyopathies
- Aortic dissection
- Severe aortic stenosis
- Tachycardia
Pulmonary causes for elevated troponin
• PE, pulmonary HTN, respiratory failure
Neurologic causes for elevated troponin
stroke, intracranial hemorrhage
Other causes of elevated troponin
- Shock: septic, hypovolemic, cardiogenic
* Renal failure
Standard of care STEMI
o 12 lead ECG with continuous cardiac monitoring
o IV lines inserted
o Cardiac enzymes (cTnI), CBC, CMP, PT, PTT
Primary percutaneous coronary intervention (PCI)
with angioplasty and stenting
• Within 12 hours
• Lower mortality rate and intracerebral hemorrhage
Cath lab
within 90 minutes
• Transport to other hospital if needed within 120 min
Fibrinolysis (clot busters)
- Fibrinolytic or Thrombolytic
- Begun in ED within 30 minutes
- Useful for STEMI or new LBBB within 12 hours of onset of symptoms
- Major risk is intracerebral hemorrhage
- Contraindication with active bleeding at any site (ex. GI, GU (except menses))
Reperfusion therapy
- Accelerates changes over minutes to hours
* Failure of ST elevation to resolve by >50-70% within 1-2 hours, suggests failure of fibrinolysis
Initial medical management of STEMI
o ASA (162-325 mg) PO – given on presentation – unless contraindicated • Helps prevent platelet aggregation
o IV Heparin or Enoxaparin
• Adenosine diphosphate receptor (p2Y12) inhibitor
• Antiplatelet agent
• Use for 1 year after PCI for STEMI with stenting to prevent stent stenosis
Treatment of STEMI
o Nitroglycerin – relieve vasoconstriction, relieve pain, reduce pre and afterload
o Morphine – persistent pain
o Beta blocker – esp if increased BP or increased HR
• Don’t use in decompensated HF, decreased HR or BP, MCO2
o Oxygen
o Stool softener (avoid valsalva)
o ACEI – helpful if low EF, increased BP – prevent remodeling
o Coronary ICU – AHA diet
Complications of MI - pericarditis
- 2-4 days post MI
- 2-10 weeks after MI could be Dressler syndrome (immune mediated)
- Hurts to breathe, feels better leaning forward
- Friction rub
- Tx: ASA, NSAID
Complications of MI - Arrhythmias
o Ventricular rhythm disturbance • Occur early • VF in 1st 4 hours – treat via elective cardioversion • VT • VT (polymorphic VT) • VF
o Accelerated Idioventricular Rhythm
• Slow VT (60-100/min)
• After fibrinolytic therapy
• Benign, still irritable
o Atrial fibrillation - First 24 hours (5-10%)
o Sinus Bradycardia
• Included parasympathetic tone
• Associated with inferior MI (up to 40%)
o Second degree AV Block (Wenckebach)
• Associated with inferior wall MI
Complications of MI - HF
leading cause of death after AMI
• LV dysfunction – S3, S4 crackles
• RV infarction – 10-30% of inferior STEMI
• Decreased BP, clear lungs, increased JVP
• Kussmaul sign (distention of jugular vein on inspiration)
• Treat with IV fluids
• Cardiogenic shock – decreased BP, decreased CI (>1.8 L/min/m2)
• Increased Pulmonary capillary wedge pressure (PCWP) >18 mmHg
• Mortality 70-80%
Mechanical complications of MI
- Acute mitral valve regurgitation – infarction related rupture or dysfunction of papillary muscle
- New holosystolic murmur associated with inferior wall MI
- Treatment – surgery
Complications of MI - VSD
o Septal Rupture with Ventricular Septal Defect (VSD) – associated with anterior wall MI
• LV free wall rupture – causes tamponade
• LV aneurysm- associated with anterior MI
• Treat with surgery
Thromboembolic complications of MI
- Arterial emboli from LV aneurysm
* Cause stroke, ischemic bowel
RV infarction
o Proximal occlusion of RCA before acute marginal branch
• Cause acute inferior wall MI in 30% of cases
o Use right chest leads
o ST elevation of 1 mm or more in V4-V6 R
o Pericarditis, myocarditis, stress induced (takotsubo) syndrome, early repolarization
DDX for STEMI
pericarditis, myocarditis, stress induced (takotsubo) syndrome, early repolarization
Echocardiogram
o Global and RWM abnormalities
o Murmur, Papillary muscle dysfunction, VSD
o LV free wall rupture, LV aneurysm
o Mural thrombosis
