STEMI / NSTEMI Flashcards
STEMI
Occlusion of a coronary artery that is found with positive Cardiac marker labs (Troponin, CK-MB, and myoglobin) as well as ST-segment elevation on ECG.
Sudden interruption of blood flow to myocardium; most common cause is arteriosclerotic heard disease (ASHD); cocaine use associated with acute myocardial infarction (spasm); may lead to conduction abnormalities, ventricular aneurysms or decreased cardiac output; necrosis follows occlusion usually within 4 ‐ 6 hours
NSTEMI or Non-Stemi
Occlusion of a coronary artery that is found with positive Cardiac marker labs (Troponin, CK-MB, and myoglobin) with NO ST-segment elevation on ECG.
STEMI Pathophysiology
Sudden interruption of blood flow to myocardium; most common cause is arteriosclerotic heard disease (ASHD); cocaine use associated with acute myocardial infarction (spasm); may lead to conduction abnormalities, ventricular aneurysms or decreased cardiac output; necrosis follows occlusion usually within 4 ‐ 6 hours.
ST Segment Elevation occurs when there is insufficient collateral circulation to supply oxygen to the myocardium.
NSTEMI Pathophysiology
coronary arterial atherosclerotic plaque rupture or erosion & subsequent platelet aggregation/thrombus formation,
leads to subtotal occlusion of the involved artery. In an occasional patient, total thrombotic occlusion of the artery
leads to NSTE ACS rather than to ST segment elevation MI when extensive collateral blood supply perfuses the region of myocardium that is distal to the occluded artery.
STEMI/NSTEMI Epidemiology
Coronary heart disease causes about 1 of every 6 deaths in the United States or about 380,000 deaths per year.
635,000 Americans are diagnosed with a first MI,
230,000 have a recurrent MI,
150,000 more have a silent first MI.
1 American suffers a coronary event approximately every 30 seconds, and one dies from one every minute.
5 million+ people visit the ED in the US each year for evaluation of chest pain and related s/s
about 680,000 are dx with an acute coronary syndrome or NSTEMI
The presence of ST elevation or new left bundle branch block (LBBB) on the ECG distinguishes requiring consideration of immediate reperfusion (recanalization) CATH LAB
STEMIs accounts for about 30% of all MIs.
Key Symptoms of STEMI and NSTEMI
May have associated severe pain/pressure, SOB, diaphoresis, nausea. Caused by complete vessel occlusion, resulting in
transmural myocardial necrosis. ST-Segment. Elevation on ECG. Elevated cardiac biomarkers will usually follow, but are not necessary for diagnosis and initial treatment
Associated with anxiety, nausea, vomiting, restlessness, dyspnea, diaphoresis; occasionally painless (elderly, diabetics); S3 Or S4 gallop, new murmur. Chest pain Radiation to: left arm, jaw, back, and neck Mimics heartburn N & V Dyspnea Lightheadedness Diaphoresis Anxiousness Palpitation LOC *Women present with more unusual sx such as the nausea, indigestion, and vomiting. Some pts may be completely asymptomatic. This is known as a silent MI
Key Symptoms of NSTEMI
Associated with anxiety, nausea, vomiting, restlessness, dyspnea, diaphoresis; occasionally painless (elderly, diabetics); S3 Or S4 gallop, new murmur. Chest pain Radiation to: left arm, jaw, back, and neck Mimics heartburn N & V Dyspnea Lightheadedness Diaphoresis Anxiousness Palpitation LOC *Women present with more unusual sx such as the nausea, indigestion, and vomiting. Some pts may be completely asymptomatic. This is known as a silent MI
Physical exam findings in STEMI
NO physical exam findings are diagnostic or pathognomonic of an acute MI. Findings are typically normal or nonspecific. Watch for signs of L and R sided heart failure and signs of peripheral profusion.
Physical Exam Findings in NSTEMI
NO physical exam findings are diagnostic or pathognomonic of an acute MI. Findings are typically normal or nonspecific. Watch for signs of L and R sided heart failure and signs of peripheral profusion.
Acute vs. Chronic presentation of STEMI
Early Acute – begins minutes and lasts hours. T-wave will increase amplitude and widen over the area of the injury. ST segment line changes into the T-wave, which will look like a tombstone. Other causes of ST segment elevation must be included.
Evolved Acute Phase – the ST segment elevation begins to regress. T waves in leads w/ ST segment elevation will become inverted and the Q or QS waves become fully developed. (> 0.03s duration or depth)
Chronic Phase – Resolution of ST segment is variable. This normally resolves w/ in 2 weeks of an inferior infarction
U wave will be present on ECG
Acute vs. Chronic presentation of NSTEMI
Acute issue.
chronic issues may arise due to myocardial death
Differential Diagnosis of MI (both STEMI AND NSTEMI)
STEMI
- Acute Pericarditis
- Acute Myocarditis
- Stress Induced Syndrome (Takotsubo’s)
- Early Repolarization
NSTEMI
- aortic dissection
- pericarditis
- GI diseases
- The history
Diagnostics studies for MI (both)
- ECG – to differentiate between a STEMI and NSTEMI.
- Lab work including Troponin, CK-MB, and CBC.
- Lipid Panels to determine need for medications to reduce cholesterol
- Percutaneous Coronary Intervention via catheterization lab for the pt w/ recurrent anginal sx (for STEMIs - NSTEMIs will have further evaluation and labs on the floor to determine the necessity of a Cath and/or stent placement.
Genetics in diagnosis and management
Strong family hx of heart disease and MI increase risk of MIs
Signs and symptoms of MI
Associated with anxiety, nausea, vomiting, restlessness, dyspnea, diaphoresis; occasionally painless (elderly, diabetics); S3 Or S4 gallop, new murmur. Chest pain Radiation to: left arm, jaw, back, and neck Mimics heartburn N & V Dyspnea Lightheadedness Diaphoresis Anxiousness Palpitation LOC *Women present with more unusual sx such as the nausea, indigestion, and vomiting. Some pts may be completely asymptomatic. This is known as a silent MI
Diagnosis of MI (both)
STEMI
Using hx, and EKGs in an acute setting. Lab work and CXR will aid diagnosis as well.
Pt will have :
1. ST elevation seen on EKG
2. Positive cardiac marker labs (Troponin, CK-MB)
NSTEMI
Hx given by patient w/ positive findings and family hx, AND Positive Cardiac Marker Lab results (Troponin, CK-MB, BNPs)
Management of STEMI
Regardless of the level of risk, should promptly receive antiplatelet/antianginal medications and a statin.
Should Give:
A – antianginal (plasugrel, clopidigrel) &/or antiplatelet therapy (Nitro)
B – Beta Blocker (Metoprolol)*
C – Ca2+ Channel Blocker and Cholesterol – statin (atorvastatin)
D – diet modification
*unless contraindicated During a STEMI.
Revascularization is preformed asap on STEMI pts to return profusion to the area
Management of NSTEMI
Every NSTE ACS patient, regardless of the level of risk, should promptly receive antiplatelet/antianginal medications and a statin.
Should Give:
A – antianginal (plasugrel, clopidigrel) &/or antiplatelet therapy (Nitro)
B – Beta Blocker (Metoprolol)
C – Ca2+ Channel Blocker and Cholesterol – statin (atorvastatin)
D – diet modification
unless contraindicated
Cath and revascularization may be necessary if pts sx are not managed with medications or there is an ECG change.
Key points to remember in MIs
Key Points to Remember
- ASA Should be administered ASAP & continued indefinitely in those who can tolerate it.
- A Loading dose of P2Y12 Receptor inhibitor is recommended for UA/NSTEMI in whom Percutaneous Coronary Intervention (PCI) is planned.
- Prasugrel should not be administered routinely to patient with UA/NSTEMI Before Angiography, Or used in patients who are being medically treated.
- Patients With definite UA/NSTEMI Whom invasive strategy is selected should receive dual antiplatelet therapy on presentation (clopidogrel or ticagrelor only with ASA)
- For patients on P2Y12 receptor inhibitors hold 5-7 Days prior to CABG
- Early Invasive strategy is indicated in UA/NSTEMI Patients that have refractory Angina or hemodynamic or electrical instability.
- For patients with plans for conservative therapy that have recurrent symptomatic ischemia, heart failure, serious arrhythmias than diagnostic angiography should be planned.
- Use Of Warfarin, ASA And or P2Y12 Receptor inhibitor should be cautious secondary to increased risk of bleeding
- Creatinine clearance Should be estimated in UA/NSTEMI Patients and doses of renally cleared medications adjusted accordingly
- Development Of a regional system of UA/NSTEMI Care is a matter of utmost importance to standardize performance and quality.
Considerations in MI situations
It is important to inquire about cocaine and methamphetamines use in the patient with suspected ACS, esp. pts younger than 40 years or have few traditional risk factors for atherosclerosis. Urine drug screen should be considered when substance abuse is suspected as a cause of ACS.
These drugs can increase myocardial oxygen demand and concomitantly decrease oxygen supply by causing vasospasm and thrombosis.
Referrals in STEMI/NSTEMI
STEMI - immediate cardiology consult and activation of the Cath lab/team for immediate revascularization procedure.
Non-pharmacologic tx of MIs
Cath lab for revacularization.
Lifestyle modifications including increased exercise and diet changes.
Pharmacologic treatment of MI
Antiplatelet/Antianginal
Beta-Blocker
Calcium Channel Blocker/ Cholesterol control
Diagnostic studies to use in MI
- History– find out what symptoms they have had and for how long. Anything more than 20 min means that irreversible damage has occurred.
- ECG – ST-Segment elevation or LBBB is a cause for immediate revascularization
- Labs for Cardiac markers including Troponin (T & I), the most specific, and CKMB. A CBC and platelet count (to look for polymorphonuclear leukocytosis), standard blood chemistry studies (CMB – check electrolytes, glucose and renal function), a lipid panel (to determine need for lipid lowering therapy if any), and coagulation tests (establish a baseline before anticoagulation therapy).
- Percutaneous Coronary Intervention with Cardiac Catheterization.
If 2/3 tests are positive, you have probably had a heart attack. If 3/3 of these tests are positive, you have had a heart attack.
