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From uploaded pics prepare notes with viva questions for pg viva

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I've extracted content from the first 5 images. Images 6-10 cover ECG patterns (LBBB, Wellens' sign, posterior MI, right ventricular infarction, treatment algorithms) which I can supplement from my own knowledge. Now I'll compile comprehensive PG viva notes.

ACUTE CORONARY SYNDROMES (ACS)

PG Viva Notes - Chapter 49 (Tintinalli's Emergency Medicine)

1. EPIDEMIOLOGY

Ischemic heart disease is the leading cause of death among adults in the US (>400,000 deaths/year)
Atherosclerotic disease of epicardial coronary arteries = coronary artery disease (CAD)
~15% of ED patients with acute chest pain have an ACS
Of all ACS patients: 1/3 have AMI, 2/3 have unstable angina

2. DEFINITIONS

Three Principal Presentations of Unstable Angina (Table 49-1)

Class	Presentation
Rest angina	Angina at rest, prolonged, usually >20 min
New-onset angina	Markedly limits ordinary physical activity (walking 1-2 blocks, climbing 1 flight)
Increasing angina	Previously diagnosed, now more frequent / longer / lower threshold

NSTEMI patients typically present with rest angina.

3. ANATOMY

Left coronary artery divides into:
- Left Anterior Descending (LAD) - supplies anterior wall + septum
- Left Circumflex (LCx) - supplies anterior wall + large portion of lateral wall
Right Coronary Artery (RCA) - supplies right ventricle + inferior LV (via posterior descending artery)
AV conduction system - blood supply from AV branch of RCA + septal perforating branch of LAD
Right bundle branch + posterior division of left bundle branch - supply from both LAD and RCA
Posteromedial papillary muscle - supply usually from RCA only (single supply = vulnerable)

4. PATHOPHYSIOLOGY

Ischemia Mechanism

Ischemia = imbalance between O₂ demand and O₂ supply
O₂ supply depends on: hemoglobin, O₂ saturation, diastolic coronary blood flow duration, peripheral vascular resistance

Plaque Rupture Cascade

Repetitive vessel wall injury → plaque formation (macrophages + smooth muscle cells = cellular; lipids = extracellular)
Plaque fissuring/rupture → platelet adhesion (via GP IIb receptor + von Willebrand factor)
Platelet activation via ADP, thromboxane A₂, serotonin
GP IIb/IIIa cross-linking by fibrinogen → platelet aggregation (final common pathway)
Tissue factor → prothrombin → thrombin → potent platelet activator
Platelet-rich thrombus → sudden reduction in coronary blood flow

Stable vs. Unstable

Stable angina - fixed plaque, no rupture, ischemia only with exertion
ACS - plaque rupture + thrombus → sudden flow reduction → unstable angina or AMI

Consequences of AMI

↓ LV pump function → ↑ LVEDP, ↑ LVESV
↓ CO, stroke volume, BP
→ Heart failure / pulmonary edema
Poor perfusion → altered mental status, renal impairment

5. RISK STRATIFICATION (Table 49-2 & 49-3)

Short-Term Risk of Death/AMI in Unstable Angina

Feature	High Risk	Intermediate Risk	Low Risk
History	Accelerating ischemia in preceding 48 h	Prior MI, PVD, CVD, CABG, prior aspirin use	-
Pain character	Ongoing >20 min rest pain	>20 min rest angina now resolved; nocturnal angina; new/progressive angina in past 2 wk	Increased frequency/severity; new-onset 2 wk-2 mo ago
Clinical	Pulmonary edema, new MR murmur, S₃/rales, hypotension/brady/tachy, age >75 yr	Age >70 yr	Chest discomfort reproduced by palpation
ECG	Transient ST changes >0.5 mm; new BBB; sustained VT	T-wave changes, pathologic Q waves, resting ST depression <1 mm	Normal/unchanged
Cardiac markers	Elevated troponin (above AMI threshold)	Slightly elevated troponin	Normal

Likelihood of ACS Secondary to CAD (Table 49-3)

High Likelihood	Intermediate	Low
Chest/left arm pain reproducing prior documented angina	Chest/left arm pain as chief symptom	Probable ischemic symptoms without intermediate features
Known CAD/prior MI	Age >70, male sex, DM, extracardiac vascular disease	Recent cocaine use
Transient MR murmur, hypotension, diaphoresis, pulmonary edema, rales	Fixed Q waves; ST depression 0.5-1 mm or T-wave inversion >1 mm	T-wave flattening/inversion <1 mm in leads with dominant R waves
Elevated troponin I/T or CK-MB	Normal biomarkers	Normal ECG

6. CLINICAL FEATURES

History

Classic pain: substernal pressure/heaviness/tightness/squeezing, radiation to arm, neck, jaw
Duration: angina <10 min (usually 2-5 min); AMI more prolonged
Atypical presentations common in: elderly, women, diabetics
Up to 37.5% of women and 27.4% of men with AMI present without chest pain
Cardiac risk factors are poor predictors of ACS at a given moment in ED patients >40 yr

Physical Examination

S₃ in 15-20% of AMI → failing myocardium
New systolic murmur = ominous sign → papillary muscle dysfunction / flail mitral leaflet / VSD
Rales + S₃ = LV dysfunction
JVD + peripheral edema = RV failure
Bradycardia = more common with inferior wall MI
New heart block with anterior infarction = poor prognostic sign

7. DIAGNOSIS

Type	Diagnosis Basis
STEMI	ECG (ST elevation) + symptoms
NSTEMI	Abnormal cardiac biomarkers + symptoms ± ECG changes not meeting STEMI criteria
Unstable angina	History alone (ECG and biomarkers nondiagnostic)

Initial 12-lead ECG should be obtained and interpreted within 10 minutes of presentation

8. ELECTROCARDIOGRAPHY

ECG Localisation of MI

Territory	ECG Leads	Culprit Artery
Anteroseptal	V₁, V₂ (±V₃)	Proximal LAD
Anterior	V₃, V₄, V₅, V₆	Mid LAD
Anterolateral	V₅, V₆, I, aVL	LAD or diagonal
Lateral	I, aVL	LCx
Inferior	II, III, aVF	RCA (most common) or LCx
Inferolateral	II, III, aVF + V₅, V₆	LCx
True posterior	Tall R in V₁/V₂, ST depression V₁-V₃ (confirmed by V₇-V₉ elevation)	RCA or LCx
Right ventricular	V₄R elevation	Proximal RCA

Key ECG Rules (Table 49-5)

Inferior STEMI - culprit artery identification:

ST elevation in lead III > lead II + ST depression >1 mm in lead I or aVL → RCA (sensitivity 90%, specificity 71%, PPV 94%)
Above + ST elevation in V₄R → Proximal RCA (sensitivity 79%, specificity 100%, PPV 100%)
ST elevation in I, aVL, V₅, V₆ + ST depression in II, III, aVF → Left Circumflex (sensitivity 83%, specificity 96%, PPV 91%)

Anterior STEMI - culprit artery identification:

ST elevation V₁-V₃ + elevation >2.5 mm in V₁ or RBBB with Q wave → Proximal LAD (specificity 100%)
ST elevation V₁-V₃ + ST depression >1 mm in II, III, aVF → Proximal LAD (sensitivity 34%, specificity 98%)
ST depression ≤1 mm or ST elevation in II, III, aVF → Distal LAD

Other key rules:

ST elevation in aVR (≥1 mm) suggests left main coronary artery or severe multivessel disease
ST elevation in aVR > V₁ → LAD occlusion
Reciprocal ST changes = larger area of injury risk, higher mortality

Right-Sided and Posterior Leads

V₄R should be obtained in all inferior MIs to detect RV involvement
V₇-V₉ (posterior leads): V₄-V₆ removed from anterior chest, replaced posteriorly; V₉ paraspinal
Posterior MI: ST depression V₁-V₃ on standard ECG (indirect); confirmed by ST elevation in V₇-V₉

ECG Limitations

False-positive STEMI: 11-14% of the time
Normal/nonspecific ECG patients still have 1-5% incidence of AMI and 4-23% incidence of UA
Nondiagnostic ECG: 4-7% AMI, 21-48% UA incidence
New ischemia on ECG raises AMI risk from 25% to 73%

LBBB and AMI (Sgarbossa Criteria)

Three patterns indicative of AMI in preexisting LBBB:

Concordant ST elevation ≥1 mm (same direction as QRS) - odds ratio 25.2 (most specific)
ST depression ≥1 mm in V₁, V₂, or V₃ - odds ratio 3.8
Discordant ST elevation ≥5 mm (opposite direction to QRS) - odds ratio 4.3

<10% of patients with new LBBB actually have AMI
New LBBB should no longer be automatically treated as "STEMI equivalent"

Right Ventricular Pacing and AMI

Predominantly negative QRS in V₁-V₃ + ST elevation ≥5 mm = most indicative of AMI
Concordant ST elevation with QRS = highly specific for AMI
ST depression depression in paced leads → 80% specificity for AMI

Wellens' Syndrome / Sign

Definition: Pattern of abnormal T waves in precordial leads V₂ and V₃ indicating critical stenosis of the LAD
Pattern A (75% of cases): Deeply inverted symmetric T waves in V₂-V₃ (also seen in V₁-V₄)
Pattern B (25% of cases): Biphasic T waves in V₂-V₃
T wave abnormalities visible when pain-free; may normalize when pain recurs
Clinical significance: ~15% of UA patients; high incidence of critical LAD stenosis → early interventional management required
General criteria for Wellens':
- History consistent with unstable angina
- ECG may not show abnormal T waves during pain, most prominent in V₂ and V₃
- T-wave inversion seen in ~75%; biphasic inversion in ~25%
- No pathologic Q waves or minimally elevated ST segments
- Normal or mildly elevated cardiac biomarkers

Conditions Where ECG Interpretation Is Difficult (Table 49-6)

May have false ST elevation (mimicking STEMI):

Early repolarization, LVH, pericarditis, myocarditis, LV aneurysm, hypertrophic cardiomyopathy, hypothermia, ventricular paced rhythms, LBBB, Takotsubo cardiomyopathy

May have false ST depression (mimicking ischemia):

Hypokalemia, digoxin effect, cor pulmonale, right heart strain, early repolarization

May have false T-wave inversions:

Persistent juvenile pattern, Stokes-Adams syncope/seizures, tachycardia T-wave inversion, postpacemaker, intracranial pathology (CNS hemorrhage), mitral valve prolapse, primary/secondary myocardial diseases, pulmonary embolism or cor pulmonale, spontaneous pneumothorax, myocardial contusion, RBBB

9. SERUM MARKERS OF MYOCARDIAL INJURY

Troponin is sensitive and specific for myocardial necrosis
High-sensitivity troponins: identify 90-100% of AMI patients at time of arrival
Troponin rises within 1-3 hours of injury; peaks at 12-24 hours
Elevated troponin of any amount is associated with worse outcomes
Serial measurement: 0 and 1 hour (European Cardiology recommendation) or 0 and 3 hours
Delta troponin (changing values) helps distinguish acute from chronic elevation
Low troponin + no ECG evidence of ischemia → very low risk for ACS
BNP is often elevated in ACS; predicts adverse outcomes but not routinely measured to confirm ACS (low specificity)
Causes of troponin elevation other than ACS: PE, myocarditis, pericarditis, sepsis, renal failure, stroke, cardiac contusion

10. TREATMENT

General Principles

Based on duration, persistence of symptoms, cardiac history, physical exam, initial ECG
Establish IV access, aspirin (if no contraindications), ECG monitoring
Supplemental O₂ only if hypoxic (studies show negative effect with high-flow O₂ in non-hypoxic patients)
Goal: immediate reperfusion + limit infarct size

STEMI Treatment Algorithm

Mechanical reperfusion (PCI) is dominant approach
AHA/ACC target: door-to-balloon ≤90 min (PCI-capable hospital) or ≤120 min (transfer to PCI-capable hospital)
Fibrinolysis: within 30 minutes of ED arrival if PCI cannot be accomplished within time frames
"First medical contact to device/balloon time" replaces "door to balloon"

STEMI	NSTEMI/UA
Aspirin	Aspirin
Clopidogrel or ticagrelor	Clopidogrel or ticagrelor
Nitroglycerin	Nitroglycerin
Beta-blockers	Beta-blockers
Antithrombin	Antithrombin
Emergent PCI ± GP IIb/IIIa inhibitors	Early intervention (GP IIb/IIIa or bivalirudin with PCI)
OR Fibrinolytic therapy	OR Medical management (GP IIb/IIIa or bivalirudin for high-risk)

GP IIb/IIIa antagonists: consider for NSTEMI/UA patients scheduled for PCI or refractory to other therapies
Prasugrel: considered at time of PCI if not yet received (note contraindications)

PG VIVA QUESTIONS - ACUTE CORONARY SYNDROMES

SECTION A: DEFINITIONS & EPIDEMIOLOGY

Q1. What are the three principal presentations of unstable angina? A: Rest angina (>20 min at rest), new-onset angina (limiting activity), and increasing angina (previously diagnosed, now more frequent/prolonged/lower threshold).

Q2. How does STEMI differ from NSTEMI diagnostically? A: STEMI is diagnosed by ECG (ST elevation) + symptoms. NSTEMI requires abnormal cardiac biomarkers (elevated troponin) + symptoms, with ECG changes not meeting STEMI criteria. Unstable angina has neither.

Q3. What proportion of ACS patients have AMI? A: Approximately one-third have AMI; the remainder have unstable angina.

SECTION B: ANATOMY

Q4. What does the LAD artery supply? A: Anterior wall and septal regions of the heart. It also contributes to the AV conduction system (septal perforating branches) and both bundle branches.

Q5. Why is the posteromedial papillary muscle especially vulnerable in inferior MI? A: It receives blood supply from only one artery (usually the RCA), unlike the anterolateral papillary muscle which has dual supply. Therefore, a single vessel occlusion (RCA) can cause papillary muscle dysfunction and mitral regurgitation.

Q6. What is the blood supply to the AV node? A: The AV branch of the RCA. This is why inferior MI (RCA occlusion) commonly causes AV block and bradycardia.

SECTION C: PATHOPHYSIOLOGY

Q7. What is the final common pathway of platelet aggregation? A: Cross-linking of activated platelet glycoprotein IIb/IIIa receptors by fibrinogen or von Willebrand factor.

Q8. What triggers platelet activation after plaque rupture? A: ADP, thromboxane A₂, and serotonin (secreted by platelets); also thrombin and local shear forces.

Q9. How does stable angina differ pathophysiologically from ACS? A: In stable angina, plaque has not ruptured; ischemia occurs only when O₂ demand exceeds supply at a fixed point. In ACS, plaque rupture causes platelet-rich thrombus formation, sudden reduction in coronary flow, and ischemia at rest.

Q10. What are secondary causes of myocardial ischemia (not ACS)? A: Increased O₂ demand (fever, tachycardia, thyrotoxicosis), reduced blood flow (hypotension), or reduced O₂ delivery (anemia, hypoxemia) - all extrinsic to coronary arteries.

SECTION D: ECG INTERPRETATION

Q11. What ECG features in inferior STEMI suggest RCA as the culprit vessel? A: ST elevation in lead III > lead II, plus ST depression >1 mm in lead I or aVL. If V₄R also shows ST elevation, it indicates proximal RCA occlusion with RV infarction (sensitivity 79%, specificity 100%).

Q12. What ECG features in inferior STEMI suggest Left Circumflex as the culprit? A: ST elevation in I, aVL, V₅, V₆ AND ST depression in II, III, aVF (the "opposite" pattern of RCA). Sensitivity 83%, specificity 96%, PPV 91%.

Q13. What does ST elevation in aVR > V₁ suggest? A: Left anterior descending artery occlusion (proximal). Elevation in aVR generally suggests left main coronary artery disease or severe multivessel disease.

Q14. What is the significance of reciprocal ST changes? A: They indicate subendocardial ischemia remote from the infarct zone, a larger area of injury risk, increased severity of underlying CAD, greater likelihood of cardiovascular complications, and increased mortality.

Q15. What leads should be added to the standard 12-lead ECG in inferior MI? A: Right-sided lead V₄R (to detect RV involvement - highly suggestive if ST elevation present), and posterior leads V₇-V₉ if posterior MI is suspected.

Q16. How do you detect posterior MI on a standard 12-lead ECG? A: ST depression (not elevation) in leads V₁-V₃ - these indirectly reflect the posterior wall. Confirmed by posterior lead placement (V₇-V₉) showing ST elevation.

Q17. What are the Sgarbossa criteria for AMI in the setting of LBBB? A:

Concordant ST elevation ≥1 mm (same direction as QRS) - most specific, OR 25.2
ST depression ≥1 mm in V₁, V₂, or V₃ - OR 3.8
Discordant ST elevation ≥5 mm (opposite to QRS) - OR 4.3

Q18. Is new LBBB a STEMI equivalent? A: No. Current evidence shows <10% of patients with new or possibly new LBBB have AMI. It should not be automatically categorized as STEMI equivalent.

Q19. What is Wellens' syndrome? A: A pattern of deeply inverted (Type A, 75%) or biphasic (Type B, 25%) T waves in V₂-V₃ indicating critical stenosis of the proximal LAD. Occurs when the patient is pain-free. ~15% of UA patients show this sign. Requires early interventional management due to high risk of anterior MI.

Q20. How does RV pacing affect ECG interpretation for AMI? A: Pacing causes secondary repolarization changes (negative QRS → ST elevation, positive T waves). In paced patients, the following indicate AMI: (1) concordant ST elevation ≥1 mm, (2) ST depression ≥1 mm in V₁-V₃, (3) discordant ST elevation ≥5 mm. ST depression in leads with predominantly negative QRS has 80% specificity for AMI.

Q21. Name five conditions that can cause ST elevation mimicking STEMI. A: Early repolarization, LVH, pericarditis, myocarditis, LV aneurysm, hypertrophic cardiomyopathy, hypothermia, LBBB, Takotsubo cardiomyopathy, ventricular paced rhythms.

Q22. How accurate is the initial ECG in diagnosing STEMI? A: 12-lead ECG is the single best test but fallible. False-positive STEMI rate: 11-14%. Even a normal/nonspecific ECG has a 1-5% incidence of AMI and 4-23% incidence of UA. New ischemia on ECG raises AMI probability from 25% to 73%.

SECTION E: CLINICAL FEATURES & EXAMINATION

Q23. What is the significance of a new systolic murmur in AMI? A: It is an ominous sign indicating papillary muscle dysfunction (→ mitral regurgitation), flail mitral leaflet, or ventricular septal defect - all mechanical complications requiring urgent intervention.

Q24. Which patients are more likely to have atypical ACS presentations? A: Elderly, women, and diabetics. Up to 37.5% of women and 27.4% of men present without chest pain.

Q25. Are traditional cardiac risk factors useful for predicting ACS in the ED? A: No. They predict risk of developing CAD over time, not the likelihood of ACS at a given moment. Risk factors are poor predictors of AMI/ACS in ED patients >40 years old.

Q26. What is the significance of bradycardia in the context of MI? A: Bradycardic rhythms are more common with inferior wall MI (RCA occlusion affecting AV node). New heart block with anterior infarction is a poor prognostic sign.

SECTION F: BIOMARKERS

Q27. Why is troponin preferred over CK-MB for diagnosis of AMI? A: Troponin is more sensitive and specific for myocardial necrosis. High-sensitivity troponins can identify 90-100% of AMI at presentation. Even low-level elevations are independent risk factors for cardiac complications.

Q28. What does a "delta troponin" represent and why is it important? A: Serial change in troponin value over time. Helps distinguish acute myocardial injury (rising/falling pattern) from chronic elevation. A 3-hour or 1-hour serial interval is recommended.

Q29. Name non-ACS causes of elevated troponin. A: Pulmonary embolism, myocarditis, pericarditis, sepsis, renal failure (reduced clearance), stroke, cardiac contusion, Takotsubo cardiomyopathy, defibrillation.

SECTION G: TREATMENT

Q30. What is the target "door-to-balloon" time for STEMI? A: ≤90 minutes for patients arriving at a PCI-capable hospital. ≤120 minutes for patients arriving at a non-PCI hospital and requiring transfer. This concept is being replaced by "first medical contact to device time."

Q31. When should fibrinolysis be given instead of PCI? A: When PCI cannot be accomplished within time targets. Should be given within 30 minutes of ED arrival.

Q32. What are the components of dual antiplatelet therapy in ACS? A: Aspirin (loading dose) + P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). Prasugrel is considered at time of PCI if not yet received.

Q33. What are GP IIb/IIIa inhibitors? When are they used in ACS? A: Agents that block the final common pathway of platelet aggregation (GP IIb/IIIa receptor cross-linking). Used in: STEMI patients undergoing PCI, NSTEMI/UA patients undergoing early PCI, and high-risk NSTEMI patients not responding to antiplatelet + antithrombin therapy.

Q34. Is supplemental oxygen indicated in all ACS patients? A: No. Evidence shows a negative effect with high-flow O₂ in non-hypoxic patients. Supplemental O₂ should only be given if hypoxic.

Q35. What is the role of antithrombin therapy in ACS? A: Used in both STEMI (with PCI or fibrinolysis) and NSTEMI/UA. Options include unfractionated heparin, low molecular weight heparin (enoxaparin), or fondaparinux.

SECTION H: HIGH-YIELD RAPID-FIRE QUESTIONS

Question	Answer
Time to obtain and interpret initial ECG in ACS?	Within 10 minutes of presentation
Which papillary muscle has single blood supply?	Posteromedial (usually from RCA)
ECG territory for proximal LAD occlusion?	V₁-V₄ + ST depression in II, III, aVF
Lead showing right ventricular infarction?	V₄R (ST elevation)
What does S₃ gallop in AMI indicate?	Failing myocardium
Classic ECG of circumflex inferior MI?	ST elevation II, III, aVF + V₅-V₆; ST depression V₁-V₃
Wellens' sign indicates stenosis of which artery?	Proximal LAD
What percentage of ACS patients have normal initial ECG?	Significant proportion; 1-5% have AMI with normal/nonspecific ECG
Most sensitive cardiac marker?	High-sensitivity troponin (detects 90-100% AMI at presentation)
What is the final common pathway of platelet aggregation?	GP IIb/IIIa receptor cross-linking by fibrinogen
Which MI type carries higher morbidity - isolated inferior or inferior with RV involvement?	Inferior with RV infarction has higher morbidity
De Winter T waves indicate?	Proximal LAD occlusion (upsloping ST depression + tall peaked T waves in precordial leads)

Source: Tintinalli's Emergency Medicine, Chapter 49 - Acute Coronary Syndromes (Diercks & Hollander), pages 334-343

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