Myocardial Infarction (STEMI & Non-STEMI) Flashcards
Most MIs are caused by atherosclerosis; what are some other causes?
Vasospasm
Vasculitis
Dissection
Genetics
PE findings in AMI
May be normal
S4 gallop
BP is variable — in general, anterior MI is high catecholamine state meaning increased HR and BP are likely. In inferior MI, more likely to see bradycardia and decreased BP because of possible ischemia to SA and AV nodes
Heart failure possible — S3, crackles, JVD, new murmur
Define STEMI in terms of ECG findings in men vs. women
Men: ST elevation of 2+ mm at J point in V2-V3
Women: ST elevation 1.5+ mm in absence of LVH; or 1+ mm in at least 2 contiguous chest or limb leads
Another possible finding = New LBBB (proximal LAD injury —> anterior infarct) — LBBB may obscure ST elevation analysis
In the early acute phase of MI, there is an increase in amplitude of the ___ wave and _____ upward ST pattern
T; convex
Causes of ST segment elevation other than AMI
Pericarditis
LVH with J point elevation
Noraml variant early repolarization
Resolution of ST elevation is variable — roughly 2 weeks for inferior wall; later anterior wall.
Persistent ST elevation beyond 2 weeks is suggestive of possible _____ _____
Ventricular aneurysm (could also be persistent wall motion abnormalities as well)
1-2 mm, narrow, small Q waves are normal (non-pathologic) in what leads?
1, aVL, aVF, V5, V6
The ST segment is normally isoelectric. Sometimes it can be normally elevated, but not more than 1 mm in ______ leads and 2 mm in ______ leads
It is never normally depressed more than ____ mm.
Standard; chest
0.5
Normal T wave direction in all leads
Upright in 1, 2, V3-6
Inverted in aVR
Variable in 3, aVL, aVF, V1-V2
In terms of height, the T wave should not be greater than _____ in standard leads, and not greater than _____ in precordial leads
5 mm; 10 mm
What parts of the ECG are associated with myocardial ischemia vs. myocardial injury vs. myocardial infarct?
Ischemia = T wave inversion or tall, peaked T waves
Injury = ST elevation
Necrosis or infarct = Q wave or QS complex
What pathologic ECG pattern remains forever after MI occurs?
Q waves
Significant ___ waves and T wave _______ in leads II, III, and aVF are seen with inferior infarct. With ______ damage, changes may also be seen in V5 and V6
Q; inversion; lateral
ECG changes seen with posterior infarct
Since no ECG lead reflects posterior electrical forces, changes are reciprocal of those in anterior leads.
Lead V1 shows unusually large R wave (reciprocal of posterior Q wave) and upright T wave (reciprocal of posterior T wave inversion)
Lab findings in STEMI
Increased WBC 12,000-15,000 (hours to 2-4 days)
Increased CRP
BNP - increased ventricular wall stress and fluid overload
Cardiac biomarkers — troponin I or T detectable 1-4 hours after onset AMI and peak at 10-24 hrs; persist for 5-14 days
_____ _____ can cause false positive cTnT
Renal failure
What are non-myocardial infarction causes of elevated troponin level?
Cardiac: cardiac contusion, surgery, ablation, shocks, myocarditis, pericarditis, heart failure, cardiomyopathy, aortic dissection, severe aortic stenosis, tachycardia’s
Pulmonary: PE, pulmonary HTN, respiratory failure
Neurologic: stroke, intracranial hemorrhage
Other: shock, renal failure
ED standard of care in STEMI
12 lead ECG with continuous cardiac monitoring
IV lines inserted
Cardiac enzymes (cTnI), CBC, CMP, PT, PTT
Choices for reperfusion strategy
Primary percutaneous coronary intervention (PCI) with angioplasty and stenting (must get to cath lab within 90 minutes) — this is preferred choice for STEMI sx <12 hours
Fibrinolysis — fibrinolytic or thrombolytic; begin in ED within 30 mins (if unable to do PCI for any reason)
If patient needs PCI and hospital does not have capability, pt must be transferred within 120 minutes
Compared to fibrinolysis, reperfusion therapy has lower risk of _____ and ______
Death; intracranial hemorrhage
Contraindications to fibrinolytic therapy
Absolute: Active bleeding Prior hemorrhagic stroke Ischemic stroke w/i 3 months Intracranial or spinal cord neoplasm AV malformation Suspected aortic dissection Closed head or facial trauma w/i 3 months
Relative: Severe uncontrolled HTN Anticoagulation with INR >2-3 Recent major trauma or surgery Prolonged CPR (>10 mins) Active peptic ulcer Recent noncompressible vascular punctures Pregnancy Prior exposure or allergic reaction to streptokinase/anistreplase
Pharmacologic management of STEMI
ASA given on presentation unless contraindicated
IV heparin or Enoxaparin
Antiplatelet agent (clopidogrel, prasugrel, ticagrelor)
Nitroglycerin to relieve vasoconstriction, relieve pain, and reduce pre/afterload
Morphine for pain
Beta blocker (especially if increased BP or HR) — DONT use in decompensated HF, decreased HR, decreased BP, MCO2
Oxygen
Stool softener
ACEI (helpful if EF decreased or increased BP; prevent remodeling with statin)
What medications are used for 1 year after PCI for STEMI with stenting to prevent stent stenosis?
Dual antiplatelet therapy = ASA and clopidogrel/prasugrel/ticagrelor
A pt presenting 2-10 weeks after MI with chest pain different from their MI, dyspnea, and pain/sx improves with leaning forward is likely _______ syndrome. It is treated with ____
Dressler; ASA, NSAID
