Acute coronary syndrome Flashcards
What is the definition of STEMI?
Clinical syndrome defined by characteristic symptoms of myocardia ischemia in association with persistent ECG changes and subsequent release of biomarkers of myocardial necrosis
- new ST elevation at the J point in at least 2 contiguous leads of >2mm in men or >1.5mm in women in leads V2- V3
- and/ or of >1mm in other contiguous chest leads or limb leads
Acute, often complete occlusion of a coronary artery, typically by a ruptured atherosclerotic plaque
Contiguous leads
- Anterior: V1-V4
- Lateral: V5, V6, Lead I, aVL
- Inferior: Leads II, III, aVF
- R Sided Leads: V4R – V6R
- Posterior Leads: 15-Lead ECG
What are the ECG changes in STEMI?
[Within minutes]
Hyperacute T waves
- T waves more prominent, symmetrical and pointed
- most evident in anterior chest leads
- usually present only for 5- 30 minutes from onset
ST segment changes
- ST segment straightens, followed by loss of ST, T wave angle
- T wave becomes broad and ST segment elevates, loss of normal concavity
- Segment tends to become convex upwards
- ST segment and T wave fuse to form single monomorphic deflection “tomb stones”
Reciprocal ST segment depression
• ST segment depression in leads remote from site of acute infarct
• Very useful if in doubt about clinical significance of ST elevation
[Hours- days]
Pathological Q waves
- loss of R wave height
- due to loss of viable myocardium beneath recording electrode
- may develop within 1-2 hours from onset of symptoms
- usually take 12- 24 hours
[Days]
Resolution of changes in ST segment
• ST segment elevation diminishes and T waves invert
• T wave inversion may persist for many months; may be permanent
What is DeWinter T waves?
Seen in 2% of LAD occlusions, in young pt who have hypercholesterolaemia
- Upsloping ST depression (> 1mm at J-point) in the precordial leads V2-6, leads I & II
- Peaked anterior T waves, with the ascending limb of the T wave commencing below the isoelectric baseline
Differentiate from HyperK b/c latter does not have preceding ST depression
What is the most sensitive lead for right ventricular infarction?
Most sensitive lead: V4R
• ST segment elevation in RV infarct may be short lived
Right Ventricular Infarction
• Associated with 40% of __________
• May also complicate some anterior infarctions
• Rarely occurs as an isolated phenomenon
• Do right sided chest leads for __________ immediately
• Most sensitive lead: _______
• ST segment elevation in RV infarct may be short lived
• Patients with RV infarction are very preload sensitive due to ____________
• ________ are contraindicated: Can develop severe hypotension in response to nitrates and other preload reducing agents
• Hypotension in RV infarct is treated with __________
inferior infarctions;
ALL inferior STEMI ;
V4R;
poor RV contractility;
Nitrates;
fluid loading
Posterior MI
• Occurs in 15-20% of STEMIs in context of an ____________
• Posterior extension implies _____________
• Increased risk of _____________
• Isolated posterior MI less
common (3-11%)
• Do __________ to confirm presence of ST elevations
Look at leads V1-3 (which face the endocardial surface of posterior wall of LV) for clues: • Tall, broad R waves • Dominant R wave (R/S > 1) in V2 • Horizontal \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ • \_\_\_\_\_\_\_ T waves
inferior or lateral infarct:
larger area of myocardial damage;
LV dysfunction and death
leads V7-9;
ST depression;
Upright
What is Wellen’s syndrome?
• Pattern of T wave changes associated with critical, _________________
Criteria
• ___________________ in V2-3
• Isoelectric or minimally elevated ST segment
• No ______________
• History of _________
• Presence of ECG pattern even in __________
• ____________ serum cardiac markers
Proximal LAD artery stenosis
Deeply inverted or biphasic T waves;
precordial Q waves
angina;
pain free state;
Normal or minimally elevated
What is the Diamond and Forrester classification of angina to determine whether chest pain is cardiac in origin?
Typical angina (Definite)
- Substernal chest discomfort with a characteristic quality & duration: Central crushing / squeezing chest pain >20min, Radiation down the left arm / L shoulder or Jaw
- Worse w/ exertion or emotional stress
- Relieved by rest or GTN (Glyceryl Trinitrate)
Atypical angina (Probable): Meets 2 of the above characteristics
Non-cardiac chest pain
- Meets one or none of the typical anginal characteristics
What is the difference between stable and unstable angina?
Stable angina: Chest pain characteristics unchanged over the preceding 60 days (>2 months)
Unstable angina
- Resting angina
- New-onset angina (<2 months)
- Prior angina increasing in severity, duration and frequency
What is Prinzmetal’s Angina?
- Due to coronary artery vasospasm
- Presents with angina at rest, usually in early morning hours
- Patients are generally younger with few CVS risk factors
- Treat with GTN and CCB
What are the different types of MI based on aetiology?
- Type 1: Plaque Rupture
- Type 2: PE, anemia, arrhythmia, HTN, HypoTN, Sepsis, Tachycardia
- Type 3 = sudden cardiac death before ECG can be done to understand Dx (can any cause)
- Type 4a = MI in patients with percutaneous coronary intervention (aka angioplasty)
- Type 4b = MI in patients with thrombosis within stent
- Type 5 = MI in patients with CABG
What are the risk factors for ACS?
Age & male gender
- Ethnic origin
- Family Hx of premature CAD (premature = <55 for males, <65 for females)
- This is due to cardioprotective hormones in females
Modifiable
- Smoking (increases risk by 50%)
- Hypertension & hyperlipidemia
- Diabetes
- Obesity & metabolic syndrome
- Sedentary lifestyle
- Psychological stresses
What is the approach to acute coronary syndrome?
1) Take history and physical examinations
2) Do initial investigations + ECG findings + Cardiac Enzymes
3) TIMI Scoring for STEMI / NSTEMI / UA
4) Medication w/ AAABS (DAPT, ACE-I, Anticoagulation, Beta Blockers, Statins)
+/- Nitrates, +/- Morphine, +/- Oxygen
- Remove ACE-I and BB if hypotensive from cardiogenic shock
- Nitrates are C/I in R Sided AMI
- Morphine only given if severe pain
- Oxygen only given if desaturating
- Note: A stands for Aspirin -> think DAPT
5) Coronary Angiogram to elucidate level of clot + severity of occlusion
6) Revascularization Therapy
7) Discharge advice + Meds
i. e. DAPT for 1-year, lifelong Aspirin, BB, ACE-I, Statins
- Control Risk Factors and Metabolic Co-morbids
- Lifestyle Management
What are the symptoms of unstable angina?
Features of Typical angina
- Substernal chest discomfort with a characteristic quality & duration
- Central crushing / squeezing chest pain >20min
- Radiation down the left arm / L shoulder or Jaw
- Worse w/ exertion or emotional stress
- Relieved by rest or GTN (Glyceryl Trinitrate)
Associated w/: N&V, Diaphoresis, Palpitations, Dyspnoea
Atypical presentation in elderly & diabetics (due to peripheral neuropathy):
- syncope, pulmonary oedema
- epigastric pain, vomiting, confusion, diabetic
- hyperglycaemic states
- Numbness in the arm (instead of pain),
- Cough (esp in patients w/ DM)
R Sided AMI can lead to BRADYCARDIA / Heart Blocks instead of Tachycardia
- Due to SA node dysfunction / AV blocks
- Such nodal dysfunction are transient and due to edema not ischaemia
Complications – to ask in history + look out for in PE
- Syncope
- Features of Heart Failure: Pedal Edema, Dyspnoea, Orthopnoea, PND
What are the ECG changes found in NSTEMI i.e. Sub-endocardial ischemia Ischaemia, <100% CA Occlusion? What sort of monitoring is required?
Classical Findings: T wave inversion OR ST depression
HOWEVER: Any non-STEMI changes (incl. Normal ECG) w/ ↑ Cardiac Enzymes = NSTEMI!
SERIAL ECG & CARDIAC MARKERS for NSTEMI w/o intervention or UNSTABLE ANGINA
- q8h (every 8 hours) for 1 day, then daily
- In the event that NSTEMI / UA converts into a STEMI!
What are the other initial investigations in acute coronary syndrome
[Cardiac Enzymes – look at both ABSOLUTE value & TRENDING]
Cardiac troponin I – most sensitive and specific
- ↑ within 4 hrs from onset of chest pain
- Peak at 24-48 hrs
- Decrease to baseline over 5-14 days
Creatine kinase Muscle-Brain subtype (CKMB)
- 1st to rise & peak – rises within 2 hours
- CKMB – peaks at 24hours, lasts 3 days
- Levels twice the upper limit consider abnormal
- Useful for evaluation of re-infarction (esp if pt may have had 2 MIs within 14 days, because troponins take 10-14 days to decrease after a cardiac event)
Blood Tests
- FBC, Renal panel, Glucose, Lipids
- FBC will see a slightly raised TW
- Renal panel b/c of contrast used in CA Angiogram
CXR – to screen for Heart Failure (if suspected)
- Cardiomegaly
- Pulmonary oedema
- Widened mediastinum (aortic rupture)
What are the goals of therapy in ACS?
Rapid initiation of therapy to limit myocardial damage and minimize complications
And we do that by
1) Restoring normal coronary blood flow
2) Decreasing myocardial oxygen consumption.
What is medical therapy for immediate stabilisation of STEMI?
[Antithrombotic therapies]
1) DAPT (Aspirin + Plavix [Clopidogrel] / Ticagrelor)
- Comprises: PO Aspirin (300mg loading dose then 100mg om)
- AND a P2Y12 Inhibitor: PO Plavix ie Clopidogrel (300mg loading dose then 75mg om) OR PO Ticagrelor (180mg Loading Dose then 90mg BD)
2) Anticoagulation: Unfractionated Heparin and Low Molecular weight Heparin
[Anti- ischemic therapies]
3) Beta Blockers – remove if Hypotensive (Cardiogenic Shock)
- Cardioselective BB: 1st dose Atenolol 5mg IV, followed by oral
- C/I: ABCD – Asthma, COPD, Heart Block, Decompensated HF
4) Nitrates: C/I in RV Infarct as RV STEMI is Preload.
• Recall: Nitrates = Venodilator; Hydralazine = Arteriodilator
5) Ca Channel Blockers
[Adjunctive therapies]
6) ACE-Inhibitors – remove if Hypotensive (Cardiogenic Shock)
7) Statins – should be started ASAP as it has mortality benefit
[Other anti anginals]
- Ivabradine
- Trimetazidine
[Others]
8) IV Morphine: ONLY if severe pain, as opioids can limit drug absorption. No longer routinely used! For pain / anxiety relief; given w/ Maxalon (Metoclopramide) for N&V
9) Oxygen: ONLY if desaturated, as excessive O2 can limit drug absorption
