Criteria & Scores

Diagnostic ECG criteria · risk stratification scores · pitfalls · teaching pearls

⚡

ECG Criteria

STEMI, BBB, arrhythmias, LVH, intervals, metabolic

📊

Clinical Scores

HEART, TIMI, GRACE, CHA₂DS₂-VASc, Wells, HAS-BLED

🏷️

Classifications

AFib types, HF staging, NYHA, Killip, CKD, TIMI flow

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Select a section above

Choose ECG Criteria or Clinical Scores to explore diagnostic thresholds and risk scores

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All Criteria

Show all diagnostic ECG criteria

🫀

Ischemia

STEMI, Wellens, de Winter, LBBB criteria

🔀

Bundle Branch

LBBB, RBBB, hemiblocks, fascicular blocks

⚡

Arrhythmia

AFib, flutter, VT, SVT, WPW criteria

📐

LVH / Morphology

Voltage criteria, RVH, P-wave changes

⏱

Intervals

QT, PR, QRS duration thresholds

🧪

Metabolic

Hyperkalemia, hypokalemia, drug toxicity

STEMI Criteria ▼

ST-Elevation MI — 2018 ESC / AHA Guidelines

Ischemia ACS STEMI-Equiv

Diagnostic Thresholds

Limb leads — I, II, III, aVF, aVL

STE ≥1 mm × ≥2 leads

Precordial — V1–V6 (men ≥40)

STE ≥2 mm × ≥2 leads

V2–V3 men <40 yrs

≥2.5 mm

V2–V3 women

≥1.5 mm

New LBBB + ischemic symptoms

STEMI-equiv

Posterior leads V7–V9

STE ≥0.5 mm

aVR STE ≥1 mm + diffuse STD → LM / proximal LAD

Territory Localization

Leads	Territory	Artery
V1–V4	Anterior	LAD
V1–V2	Septal	LAD septal
I, aVL, V5–V6	Lateral	LCx / Diagonal
II, III, aVF	Inferior	RCA 80%, LCx 20%
V1–V3 STD (mirror)	Posterior	PDA / LCx
V3R–V4R	RV infarct	Proximal RCA

⚠ Pitfalls

Early repolarization — concave ST, J-point notching, no reciprocal changes, young male
Pericarditis — saddle-shaped STE all leads, PR depression, no focal reciprocals
LVH — lateral strain pattern (ST↓ I/aVL/V5–V6) mimics lateral STEMI
LBBB — masks ischemia; always apply Sgarbossa criteria
Aortic dissection — retrograde extension to coronary ostium; thrombolytics are lethal
Takotsubo — women, emotional/physical stress, STE V1–V4, no culprit artery on angio

✦ Clinical Pearls

Reciprocal STD confirms STEMI — STE III/aVF + STD I/aVL raises specificity markedly
aVR STE ≥1 mm = LM or proximal LAD occlusion — highest-risk STEMI pattern
RV infarct complicates 40% inferior STEMIs — get V4R; avoid nitrates (preload-dependent)
Posterior MI is the most missed STEMI — unexplained V1–V3 STD = posterior leads mandatory

Sgarbossa Criteria ▼

MI diagnosis in LBBB — Sgarbossa 1996 NEJM · Modified Smith 2012

LBBB Ischemia

Original — Score ≥3 points = Positive

Concordant STE ≥1 mm (STE same direction as QRS)

+5 pts

Concordant STD ≥1 mm in V1–V3 (STD where QRS is negative)

+3 pts

Excessively discordant STE ≥5 mm

+2 pts

36%

Sensitivity

96%

Specificity

Modified (Smith) — Replaces Criterion 3

STD/STE ratio >0.25 in any discordant lead (absolute values)

Preferred

80%

Sensitivity

99%

Specificity

📍 When to Use

Any chest pain + LBBB — cannot clinically distinguish old from new LBBB; treat as ACS until proven otherwise
RV-paced rhythm — functional LBBB pattern; same criteria apply
Prefer Modified Sgarbossa — eliminates arbitrary 5 mm cutoff and is more sensitive

⚠ Pitfalls

Negative original Sgarbossa does NOT rule out STEMI — sensitivity only 36%
Hyperkalemia can create pseudo-LBBB pattern — check electrolytes
Rate-related LBBB at faster HRs complicates interpretation — serial ECGs at controlled rate

✦ Clinical Pearls

Any concordant change (STE or STD in same direction as QRS) is always abnormal in LBBB
Concordant changes = most specific finding; prompt cath lab activation even without full score

de Winter Pattern ▼

Proximal LAD occlusion without STE — de Winter, NEJM 2008

STEMI-Equivalent LAD Occlusion

⚡ All 3 criteria required — STEMI-equivalent, activate cath lab immediately

Upsloping STD at J-point in V1–V6

1–3 mm

Tall symmetric T-waves — hyperacute, in same leads

>6 mm

aVR STE — often present

0.5–1 mm

No STE anywhere — frequently triaged as NSTEMI

~2%

of LAD occlusions

⚠ Pitfalls

Often triaged as NSTEMI — delays door-to-balloon time significantly
Pattern may be transient — can evolve into classic STEMI; serial ECGs every 15–30 min
Upsloping STD distinguishes it from horizontal/downsloping STD of NSTEMI

✦ Clinical Pearls

Prevalence ~2% of LAD occlusions — rare but immediately life-threatening if missed
Mechanism: subendocardial ischemia from total proximal LAD occlusion without collateral flow

Wellens Syndrome ▼

Critical proximal LAD stenosis — Wellens, Am Heart J 1982

LAD Stenosis High Risk

🚫 Do NOT stress test — risk of massive anterior MI and sudden death

Type A — 25% of cases

Biphasic T-wave in V2–V3 (positive → negative deflection)

ST isoelectric or minimally elevated

Type B — 75% of cases

Deep symmetric T-wave inversions V2–V3 (may extend V1–V5)

Clinical Context Required

ECG obtained in pain-free period — prior episode of chest pain

Minimal or no enzyme elevation — often near-normal troponin

⚠ Pitfalls

Mistaken for non-specific T-wave changes — always check PR interval and clinical context
Normal or near-normal troponin does NOT rule out Wellens — lesion is still critical
Type A (biphasic) is less recognized and more commonly missed than Type B
Discharging without cardiology consult — requires urgent cath, not observation

✦ Clinical Pearls

Represents reperfusion pattern after transient proximal LAD occlusion — artery still critically stenosed
TIMI flow preserved at rest — enzymes underestimate culprit severity
Management: urgent cardiology consult → coronary angiography → PCI or CABG

Posterior MI ▼

Most commonly missed STEMI — LCx / PDA territory

STEMI-Equiv Often Missed

Standard 12-Lead Clues (V1–V3)

Horizontal STD V1–V3 (mirror of posterior STE)

≥1 mm

Tall broad R wave — R>S in V1–V2

Upright tall T-wave V1–V3 (normally inverted)

Confirm with Posterior Leads

STE in V7, V8, V9 (lower threshold than anterior leads)

≥0.5 mm

Common Associations

Inferior STEMI II, III, aVF → RCA occlusion

Lateral STD V5–V6 → LCx occlusion

⚠ Pitfalls

Posterior leads almost never applied routinely — must actively request when V1–V3 STD is unexplained
V1–V3 STD mistaken for NSTEMI or reciprocal change from anterior STEMI
Tall R in V1 also seen in RBBB, RVH, WPW type A, HCM — clinical context essential

✦ Clinical Pearls

Tip: flip the paper and mirror V1–V3 — the STD pattern becomes a visible "STE" for posterior MI
Inferior + posterior = proximal RCA; lateral + posterior = LCx (circumflex)

LBBB Criteria ▼

Left Bundle Branch Block — AHA/ACC Standards

Bundle Branch Masks Ischemia

All 3 Required for Diagnosis

QRS duration

≥120 ms

Broad notched R in I, aVL, V5–V6 (RsR', M-shaped, or monophasic R)

Absent septal Q in I, V5–V6 (no normal septal q wave)

Secondary Features

Discordant ST-T (opposite direction to QRS)

rS or QS pattern V1–V3

Left axis deviation (common, not required)

⚠ Pitfalls

Masks anterior MI, LVH voltage, and primary repolarization abnormalities
Incomplete LBBB (100–119 ms) — same morphology but QRS <120 ms; still clinically significant
Rate-related LBBB — appears only at fast rates; disappears when HR normalizes; can mimic VT
New LBBB + chest pain = STEMI-equivalent — apply Sgarbossa criteria immediately

✦ Clinical Pearls

Depolarization travels right→left abnormally — explains absent septal Q in I/V5–V6
Any concordant ST change (STE or STD in same direction as QRS) is always abnormal in LBBB
Discordant ST-T is expected in LBBB — concordant = ischemia until proven otherwise

RBBB Criteria ▼

Right Bundle Branch Block — AHA/ACC Standards

Bundle Branch

All 3 Required for Diagnosis

QRS duration

≥120 ms

RSR' in V1–V2 ("rabbit ears" — R' taller than R)

Wide slurred S wave in I, aVL, V5–V6 (S >40 ms)

Secondary Features

ST depression + T inversion V1–V3 (normal secondary change)

Incomplete RBBB (QRS 100–119 ms, same morphology)

⚠ Pitfalls

New RBBB may indicate acute RV strain (PE, RV infarct), ACS, or structural disease — always investigate
RBBB + LAFB = bifascicular block; + prolonged PR = trifascicular block (risk of complete AV block)
Brugada syndrome can mimic RBBB in V1–V2 — look for coved (Brugada) vs RSR' (RBBB) morphology
RBBB alone does NOT mask ischemia as severely as LBBB — ST changes still interpretable

✦ Clinical Pearls

RBBB in acute PE: S1Q3T3 + incomplete RBBB + sinus tachycardia = classic triad (but low sensitivity)
New RBBB in anterior MI indicates septal involvement or proximal LAD occlusion — poor prognostic sign
Bifascicular block + syncope → EP study for HV interval; consider prophylactic pacing if HV >100 ms

Fascicular Blocks — LAFB & LPFB ▼

Left Anterior & Posterior Fascicular Block criteria

Bundle Branch

LAFB — Left Anterior Fascicular Block

Left axis deviation

−45° to −90°

rS pattern in II, III, aVF (small r, deep S)

qR pattern in I, aVL (small q, tall R)

QRS <120 ms — no wide QRS (fascicle block only)

LPFB — Left Posterior Fascicular Block

Right axis deviation

+90° to +180°

rS in I and qR in III (small r/large S in I; small q/tall R in III)

Must exclude RVH, lateral MI, vertical heart, pulmonary disease

⚠ Pitfalls

Isolated LAFB is common and usually benign — no specific treatment needed in isolation
LPFB is rare — always exclude RVH and lateral MI before diagnosing
RBBB + LAFB is the most common bifascicular combination (LAD + right bundle)

✦ Clinical Pearls

New bifascicular block in anterior MI → high risk of complete heart block → consider temporary pacing wire
LAFB can mask inferior MI Q waves in II/III/aVF — clinical context always required

Brugada Stepwise VT Criteria ▼

Wide-complex tachycardia differentiation — Brugada, Circulation 1991

VT vs SVT Arrhythmia

4-Step Algorithm — Stop at First YES = VT

Step 1: RS complex absent in ALL precordial leads?

Yes = VT

Step 2: RS interval >100 ms in any precordial lead?

Yes = VT

Step 3: AV dissociation present? (pathognomonic)

Yes = VT

Step 4: Morphology criteria met in V1 + V6? (RBBB/LBBB type)

Yes = VT

All steps NO → SVT with aberrancy

SVT-A

98.7%

Sensitivity

96.5%

Specificity

📍 Clinical Rule

Treat ALL wide-complex tachycardia as VT until proven otherwise — far safer clinical assumption
Fusion beats and capture beats (when visible) are pathognomonic for VT — no algorithm needed
Extreme northwest axis (−90° to ±180°) strongly suggests VT

⚠ Pitfalls

Antidromic AVRT (WPW) mimics VT — widened QRS with delta waves; adenosine can precipitate VF
NEVER use verapamil or diltiazem for undifferentiated wide-complex tachycardia — can cause VF if VT
Na-channel blocker toxicity (flecainide, TCA) makes criteria less reliable

✦ Clinical Pearls

AV dissociation is subtle — look for P waves marching at a different rate through the long rhythm strip
Morphology step 4 (RBBB-type VT): monophasic R or Rr' in V1; rS or QS in V6
Morphology step 4 (LBBB-type VT): r >30 ms or notched downstroke S in V1 or V2; any Q in V6

Brugada Syndrome Pattern ▼

Na-channel channelopathy — risk of sudden cardiac death

Channelopathy SCD Risk

Type 1 — Diagnostic: Coved STE ≥2 mm in ≥1 of V1–V3, followed by negative T ("shark fin")

Spontaneous

Type 2 — Suggestive: Saddle-back pattern ≥2 mm V1–V3, high takeoff with concave ST

Drug challenge

Type 3: Saddle-back <1 mm (not diagnostic)

Diagnosis = Type 1 Pattern + ≥1 of

VF or polymorphic VT documented

Syncope, nocturnal agonal breathing, or resuscitated SCA

Family history SCD <45 yrs OR Type 1 ECG in first-degree relative

SCN5A pathogenic variant (Na-channel gene mutation)

⚠ Pitfalls

Fever unmasks Type 1 pattern — any febrile patient with coved V1–V2 needs cardiac monitoring and antipyretics urgently
Drug-provoked: Na-channel blockers (flecainide, procainamide), cocaine, TCAs, lithium — check drug list
Electrode position critical — Type 1 more prominent with V1–V2 placed 1–2 intercostal spaces higher
Male sex 8:1 higher risk than female despite same SCN5A mutation

✦ Clinical Pearls

ICD is only proven therapy for symptomatic Brugada — quinidine for electrical storm adjunct
Asymptomatic Type 1: EP study to risk-stratify; inducible VF → higher-risk subgroup
Avoid competitive sports; treat fevers aggressively; wear MedicAlert ID

Atrial Fibrillation Criteria ▼

Most common sustained cardiac arrhythmia — ESC/AHA 2023

Arrhythmia

ECG Criteria

Irregularly irregular ventricular rhythm

Absent distinct P waves — fibrillatory baseline, best seen V1

Ventricular rate uncontrolled

110–160 bpm

Classification

Type	Duration	Management
Paroxysmal	<7 days	Self-terminating
Persistent	>7 days	Requires cardioversion
Long-standing	>12 months	Rhythm vs rate control
Permanent	Accepted	Rate control, no cardioversion

⚠ Pitfalls

MAT (multifocal atrial tachycardia) — 3+ distinct P morphologies, irregular; often COPD; not AF
Frequent PACs — irregular but discrete P waves before each beat
AF + WPW — irregular, very fast (>250 bpm), wide complex; DO NOT give AV nodal blockers → VF risk

✦ Clinical Pearls

Early rhythm control preferred within first year of AF — reduces hospitalizations and adverse outcomes
Rate control target: resting HR <110 bpm (lenient rate control acceptable if asymptomatic)
DC cardioversion safe <48 h onset OR ≥3 weeks anticoagulation; TEE-guided shortcut if urgent
Valvular AF (mechanical valve/mitral stenosis): warfarin only — DOACs not validated

WPW / Pre-excitation Criteria ▼

Wolff-Parkinson-White syndrome — accessory pathway

Pre-excitation SCD Risk if AFib

Classic Triad

Short PR interval

<120 ms

Delta wave — slurred QRS upstroke (pre-excitation of ventricle)

Wide QRS

>110 ms

Accessory Pathway Localization

Delta in V1	Pathway
Positive (upright)	Left-sided AP
Negative (inverted)	Right-sided AP
Neg in II/III/aVF	Posteroseptal AP

⚠ Pitfalls

AF + WPW: very fast (>250 bpm), wide, irregular — DO NOT give adenosine, beta-blockers, CCBs, or digoxin → VF
WPW mimics anterior MI — negative delta waves in precordial leads create pseudo-Q waves
Intermittent pre-excitation — delta wave absent on some beats; short PR may be the only clue

✦ Clinical Pearls

AF + WPW: treat with IV procainamide (preferred) or DC cardioversion — blocks accessory pathway
Highest risk: shortest RR interval <250 ms during AF, history of syncope or resuscitated SCA
Ablation is curative — gold standard for symptomatic WPW or high-risk features

LVH Voltage Criteria ▼

Left Ventricular Hypertrophy — multiple validated criteria

LVH

Criterion	Threshold	Sn / Sp
Sokolow-Lyon	SV1 + RV5 or RV6 ≥35 mm; or RaVL ≥11 mm	~50% / 85%
Cornell Voltage (men)	RaVL + SV3 ≥28 mm	~42% / 96%
Cornell Voltage (women)	RaVL + SV3 ≥20 mm	~42% / 96%
Cornell Product	Cornell voltage × QRS duration ≥2440 mm·ms	Higher

LV Strain Pattern

Asymmetric ST depression + T-wave inversion in lateral leads I, aVL, V5–V6 (opposite to QRS)

Romhilt-Estes score ≥5 — includes voltage + P wave + ST-T + axis

⚠ Pitfalls

ECG sensitivity is low (~40–50%) — many LVH cases on echo are missed by ECG voltage criteria
Body habitus affects voltage: thin young men → high voltage without true LVH; obese → low voltage despite LVH
LVH strain pattern can mimic lateral ischemia — echo and clinical context essential
LBBB invalidates all LVH voltage criteria

✦ Clinical Pearls

LVH on ECG carries independent cardiovascular risk regardless of echo findings
Cornell product is the best ECG predictor of outcomes in hypertensive patients (LIFE trial)

Right Heart Strain Pattern ▼

Acute PE / Pulmonary Hypertension ECG findings

RV Strain PE

ECG Findings (in descending frequency)

Sinus tachycardia — most common finding in PE

~40%

T-wave inversions V1–V4 — RV wall tension

Incomplete or complete RBBB — acute RV pressure overload

S1Q3T3 pattern — S in I, Q in III, T inversion in III

P pulmonale — tall P ≥2.5 mm in II (RA enlargement)

Right axis deviation

12–50%

S1Q3T3 Sn

85%

S1Q3T3 Sp

⚠ Pitfalls

Normal ECG does NOT exclude PE — occurs in ~6% of massive PE cases
S1Q3T3 has low sensitivity — never use to rule out PE; use Wells + D-dimer + CTPA algorithm
RV infarct from inferior STEMI also causes RV strain pattern — context is critical

✦ Clinical Pearls

New RBBB + sinus tachycardia in a dyspneic patient = PE until proven otherwise
T inversions V1–V4 in PE resolve with treatment — markers of RV pressure load, not ischemia
McGinn-White pattern: S1Q3T3 + RBBB — more specific than S1Q3T3 alone

QTc Prolongation Criteria ▼

Long QT — Torsades de Pointes risk stratification

Intervals TdP Risk

Correction Formulas

Bazett — QTc = QT / √RR (overcorrects at fast rates; most common)

Fridericia — QTc = QT / RR^(1/3) (preferred at extreme heart rates)

Thresholds

Category	Men	Women
Normal	≤440 ms	≤460 ms
Borderline	441–470 ms	461–480 ms
Prolonged	>470 ms	>480 ms
High TdP Risk	≥500 ms (either sex)
Short QT	<340 ms (SCD risk)

📍 Common QT-Prolonging Drugs

Antiarrhythmics: sotalol, amiodarone, quinidine, dofetilide, ibutilide
Antibiotics: azithromycin, ciprofloxacin, moxifloxacin, clarithromycin
Antipsychotics: haloperidol, quetiapine, ziprasidone, clozapine
Antiemetics: ondansetron (esp. high-dose IV), droperidol
Antifungals: fluconazole, voriconazole

⚠ Pitfalls

Measure QT in lead II or V5 — from Q onset to T-wave end (not peak); avoid leads with U waves
Bazett overcorrects at HR >100 — may falsely diagnose prolonged QTc; switch to Fridericia
Hypokalemia + hypomagnesemia potentiate drug-induced QT prolongation — always correct electrolytes first
Congenital LQTS subtypes: LQT1 (exercise), LQT2 (sudden noise), LQT3 (sleep) — different triggers

✦ Clinical Pearls

TdP management: IV magnesium 2 g even if serum Mg is normal — first-line treatment
Refractory TdP: overdrive pacing at 90–110 bpm or isoproterenol to shorten QT dynamically

Hyperkalemia ECG Progression ▼

Sequential ECG changes with rising serum potassium

Metabolic

K⁺ Level	ECG Change
5.5–6.0 mEq/L	Peaked T waves — narrow base, tall, symmetric, "tented"; best in V2–V4, II
6.0–6.5 mEq/L	PR prolongation and QRS widening begin
6.5–7.0 mEq/L	P wave flattening / loss — sinoventricular rhythm
7.0–7.5 mEq/L	Wide bizarre QRS — sine-wave pattern
>8.0 mEq/L	Ventricular fibrillation or asystole

⚠ Pitfalls

Peaked T-waves alone are non-specific — early repolarization, LBBB, ischemia all cause similar findings
ECG changes are not linear — patients can deteriorate rapidly with small K⁺ increments
Pseudo-LBBB at high K⁺ levels can mimic structural LBBB — check labs before attributing

✦ Clinical Pearls

Calcium gluconate 1g IV stabilizes myocardium within 2–3 min — does NOT lower K⁺, buys time for other treatments
Any wide-complex rhythm in ESRD or AKI = hyperkalemia until proven otherwise
Treatment ladder: Ca²⁺ → insulin+dextrose → albuterol → kayexalate/patiromer → dialysis

Pericarditis ECG Stages ▼

4 stages — must differentiate from STEMI

Morphology

Stage	Timing	ECG Finding
1	Hours–days	Diffuse concave STE (all leads except aVR, V1) + PR depression + PR elevation aVR
2	Days	ST normalizes, T-waves begin to flatten
3	Weeks	Diffuse T-wave inversions develop
4	Months	ECG normalizes completely

Key Differentiators from STEMI

Diffuse STE — all leads except aVR and V1 (not regional)

Concave (saddle-shaped) ST elevation — not convex/domed

PR depression in most leads — absent in STEMI

No reciprocal STD — except aVR; no Q waves developing

⚠ Pitfalls

Focal pericarditis can mimic regional STEMI — especially if only inferolateral leads are affected
Myopericarditis — troponin elevation + regional wall motion abnormality; cardiac MRI needed
Spodick's sign (downsloping TP segment) is specific but difficult to see at fast heart rates

✦ Clinical Pearls

V6 STE/T ratio >0.25 favors pericarditis over early repolarization (Ginzton-Laks criterion)
NSAIDs + colchicine for 3 months reduces recurrence by 50% — avoid steroids (↑ recurrence risk)

📋

All Scores

Show all clinical risk scores

💔

Chest Pain / ACS

HEART, TIMI, GRACE, PURSUIT scores

🔥

AF & Stroke

CHA₂DS₂-VASc, EHRA symptom classification

🫁

PE / DVT

Wells PE, Wells DVT, PERC, Geneva scores

⚠️

Post-MI / Severity

Killip class, TIMI risk index, Sgarbossa

🩸

Bleeding

HAS-BLED, CRUSADE bleeding risk scores

HEART Score ▼

Chest pain risk stratification — Backus 2010 · HEART Pathway trial

Chest Pain Widely Validated

Component	0 pts	1 pt	2 pts
History	Slightly suspicious	Moderately suspicious	Highly suspicious
ECG	Normal	Non-specific repol	Significant ST deviation
Age	<45 yrs	45–64 yrs	≥65 yrs
Risk factors	No known RF	1–2 RFs	≥3 or known CAD
Troponin	≤Normal limit	1–3× ULN	>3× ULN

0–3 · Low · ~2% MACE → Discharge

4–6 · Moderate · ~12% → Observe

≥7 · High · ~65% → Admit / Cath

📍 When to Use

ED chest pain triage: first presentation, deciding between observation vs safe early discharge
HEART Pathway: score 0–3 + two negative troponins (0 h and 3 h) → safe discharge (misses <1% MACE)
Not for: known ACS, ST elevation, or hemodynamically unstable patients

⚠ Pitfalls

Subjective components (History, ECG interpretation) — significant inter-rater variability
Less accurate in atypical presentations: women, elderly, diabetics — may underestimate risk
High-sensitivity troponin assays change thresholds and timing — validate locally which cutoffs to use

✦ Clinical Pearls

Most widely used ED chest pain score in the US — good balance of sensitivity and specificity
Outperforms TIMI and GRACE for safe low-risk discharge decisions in undifferentiated chest pain

🧮 Quick Calculate — HEART Score

H History

E ECG

A Age

R Risk Factors

T Troponin

TIMI Score — UA / NSTEMI ▼

Thrombolysis in MI for unstable angina/NSTEMI — Antman, JAMA 2000

Chest Pain NSTEMI

1 Point Each — Maximum 7

Age ≥65 years

1 pt

≥3 CAD risk factors (HTN, DM, hyperlipidemia, smoking, family Hx)

1 pt

Prior coronary stenosis ≥50%

1 pt

ST deviation ≥0.5 mm on presenting ECG

1 pt

≥2 anginal events in prior 24 hours

1 pt

Aspirin use in prior 7 days (suggests aspirin resistance)

1 pt

Elevated serum cardiac markers (troponin or CK-MB)

1 pt

0–2 · Low · 5% MACE

3–4 · Intermediate · 13%

5–7 · High · 26–41%

14-day all-cause mortality / MI / urgent revascularization

⚠ Pitfalls

Aspirin-use criterion is counterintuitive — signals resistance/non-response, not protective effect
TIMI UA/NSTEMI ≠ TIMI STEMI — completely different scoring systems with different variables
Performance inferior to GRACE for predicting mortality in large meta-analyses

✦ Clinical Pearls

TIMI ≥5: early invasive strategy within 24 h is guideline-recommended (ESC, AHA)
Validated the benefit of enoxaparin, GP IIb/IIIa inhibitors, and early cath in high-risk UA/NSTEMI

TIMI Score — STEMI ▼

30-day mortality in STEMI — Morrow, Circulation 2000

STEMI Mortality

Variable	Points
Age 65–74 years	2
Age ≥75 years	3
DM / Hypertension / Angina	1
SBP <100 mmHg	3
Heart rate >100 bpm	2
Killip class II–IV	2
Weight <67 kg	1
Anterior STE or new LBBB	1
Time to treatment >4 hours	1

0–4 · <5% mortality

5–7 · ~12%

≥8 · >20%

⚠ Pitfalls

Developed in thrombolytic era — less validated for primary PCI outcomes in modern practice
GRACE score outperforms TIMI STEMI for mortality prediction in contemporary PCI-era cohorts

✦ Clinical Pearls

Score ≥8: 30-day mortality >20% — consider aggressive hemodynamic support (IABP, Impella)
SBP <100 and Killip ≥III contribute most heavily — cardiogenic shock dominates prognosis

GRACE Score ▼

Global Registry of ACS — Fox 2006 · ESC preferred ACS risk tool

ACS ESC Guidelines

8 Continuous Variables (Calculator Required)

Age (years — continuous)

Heart rate (bpm)

Systolic blood pressure (mmHg)

Serum creatinine (mg/dL)

Killip classification (I–IV)

ST-segment deviation (yes / no)

Elevated cardiac enzymes (yes / no)

Cardiac arrest at admission (yes / no)

<108 · Low · <1% in-hosp

109–140 · Intermediate · 1–3%

>140 · High · >3%

0.83

C-statistic

GRACE 2.0

Updated version

📍 When to Use

ESC NSTE-ACS guidelines: GRACE >140 = high risk → invasive strategy within 24 hours
Superior to TIMI for mortality discrimination (C-statistic 0.83 vs ~0.74)
Incorporates hemodynamics (BP, HR) and renal function — better captures physiologic severity

⚠ Pitfalls

Requires calculator — not computable at bedside; reduces real-world clinical uptake
GRACE 2.0 recalibrated for modern PCI era; prefer over original GRACE when available

CHA₂DS₂-VASc Score ▼

AF stroke risk — Lip 2010 · 2023 ESC / AHA AF Guidelines

AF Stroke Risk

Factor	Points
CHF / LV dysfunction	1
Hypertension	1
Age ≥75 years	2
Diabetes mellitus	1
Stroke / TIA / thromboembolism history	2
Vascular disease (MI, PAD, aortic plaque)	1
Age 65–74 years	1
Sex category — Female	1

Anticoagulate if score ≥2 (men) or ≥3 (women)

DOAC preferred

Score 1 (men) — individualize; consider anticoagulation

Score 0 (men) or 1 female-only — no anticoagulation needed

⚠ Pitfalls

Female sex is a risk modifier, NOT an independent risk factor — score 1 (female sex only) does not warrant anticoagulation
Valvular AF (mechanical valve, moderate-severe mitral stenosis) — warfarin required regardless of score; DOACs contraindicated
Score doesn't adjust for renal function or liver disease — affects DOAC dosing, not eligibility

✦ Clinical Pearls

Prior stroke/TIA scores 2 — single most powerful predictor; anticoagulate regardless of other factors
DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin for non-valvular AF
Apixaban preferred in CKD and elderly — lowest bleeding profile across multiple trials

🧮 Quick Calculate — CHA₂DS₂-VASc

C — CHF or LV dysfunction +1 H — Hypertension +1 A — Age ≥75 years +2 D — Diabetes mellitus +1 S₂ — Stroke / TIA / thromboembolism +2 V — Vascular disease (MI, PAD, aortic plaque) +1 A — Age 65–74 years +1 Sc — Sex category: Female +1

Score: 0 — No anticoagulation needed (0 male / female sex only)

HAS-BLED Score ▼

Bleeding risk on anticoagulation — Pisters, Chest 2010

Bleeding Risk AF

Factor	Pts
Hypertension — uncontrolled SBP >160	1
Abnormal renal function (dialysis, Cr>2.3, transplant)	1
Abnormal liver function (cirrhosis, bilirubin>2×, AST/ALT>3×)	1
Stroke history	1
Bleeding history or predisposition	1
Labile INR (TTR <60% on warfarin)	1
Elderly — age >65	1
Drugs (antiplatelets, NSAIDs)	1
Drink — alcohol ≥8 drinks/week	1

⚠ Score ≥3 = high bleeding risk (~3.7%/yr major bleeding)

⚠ Critical Pitfalls

NEVER withhold anticoagulation solely because of high HAS-BLED — stroke risk almost always outweighs bleeding risk
High HAS-BLED = address modifiable risk factors (control BP, stop NSAIDs, reduce alcohol, fix INR)
Elderly patients often score high on both CHA₂DS₂-VASc and HAS-BLED — net benefit still favors OAC

✦ Clinical Pearls

Labile INR is modifiable — switching from warfarin to a DOAC resolves this criterion entirely
Document shared decision-making discussion of stroke vs bleeding risk in high HAS-BLED patients

Wells Score — Pulmonary Embolism ▼

Pre-test probability for PE — Wells 2000 · Simplified 2010

PE Pre-test Probability

Criterion	Pts
Clinical signs of DVT (leg swelling, tenderness)	3.0
PE most likely diagnosis (vs alternatives)	3.0
Heart rate >100 bpm	1.5
Immobilization ≥3 days OR surgery in 4 weeks	1.5
Prior DVT or PE	1.5
Hemoptysis	1.0
Malignancy (on treatment or within 6 months)	1.0

≤4 · Low / Unlikely → D-dimer first

>4 · High / Likely → CT-PA directly

⚠ Pitfalls

"PE most likely" criterion is subjective — accounts for 3 points and significantly skews the score
Apply PERC rule first in very low PTP patients — if all 8 PERC criteria met, no further testing needed
Age-adjusted D-dimer: age × 10 µg/L for age >50 — improves specificity without losing sensitivity
Massive PE with hemodynamic instability: skip scoring, go directly to bedside echo or CTPA

✦ Clinical Pearls

YEARS algorithm (3 items + D-dimer threshold) is an alternative that reduces CT-PA rate by ~14%
Negative D-dimer in low PTP rules out PE with >99% NPV — no imaging needed

PESI / Simplified PESI ▼

PE Severity Index — guides disposition after PE diagnosis

PE Severity Disposition

Simplified PESI — 1 Point Each

Age >80 years

Active cancer

Chronic cardiopulmonary disease (CHF, COPD)

Heart rate ≥110 bpm

SBP <100 mmHg

O₂ saturation <90%

sPESI = 0 · 1% mortality → Outpatient

sPESI ≥1 · 10.9% mortality → Hospitalize

📍 ESC 2019 PE Risk Stratification

Hemodynamically unstable → High risk → Systemic thrombolytics / surgical embolectomy
Stable + sPESI ≥1 + RV dysfunction on echo/CT + positive troponin → Intermediate-high → Monitor ± reperfusion
Stable + sPESI = 0 → Low risk → Early discharge with DOAC (rivaroxaban or apixaban)

⚠ Pitfalls

sPESI doesn't include troponin or BNP — ESC adds these + echo to further risk-stratify intermediate group
Outpatient treatment requires: reliable follow-up, no anticoagulation contraindication, adequate social support

Killip Classification ▼

Post-MI heart failure severity — Killip, Am J Cardiol 1967

Post-MI Cardiogenic Shock

Class	Definition	Original Mortality
I	No HF signs — clear lungs, no S3	~6%
II	Mild HF — rales <50% lungs, S3 gallop, ↑JVP	~17%
III	Frank pulmonary edema — rales >50% lungs	~38%
IV	Cardiogenic shock — SBP <90 + tissue hypoperfusion	~81%

Modern PCI era: Killip IV mortality 40–60% despite revascularization

📍 Clinical Application

Killip is a component of TIMI STEMI score — class II–IV contributes 2 points
Cardiogenic shock (Killip IV): immediate PCI of culprit artery + MCS consideration (IABP, Impella, TandemHeart)
Forrester classification is the hemodynamic variant — uses PCWP and cardiac index for ICU precision

⚠ Pitfalls

Killip assigned at admission only — does not capture dynamic deterioration or improvement
Original mortality data from pre-PCI, pre-thrombolytic era — absolute numbers lower today but ranking preserved

SYNTAX Score ▼

Coronary complexity — PCI vs CABG decision tool

Revascularization CAD Complexity

Angiographic Score — Lesion Complexity Modifiers

Lesion characteristics: total occlusion, bifurcation, trifurcation, calcification, thrombus, diffuse disease, tortuosity

Risk Stratification

Score	Risk	Recommendation
≤22	Low	PCI noninferior to CABG — PCI preferred if anatomy suitable
23–32	Intermediate	Individualize — Heart Team decision; consider SYNTAX II
≥33	High	CABG preferred — lower 5-yr MACE and mortality

📍 When to Use

Heart Team meetings for multivessel CAD or unprotected LM disease — guides PCI vs CABG
SYNTAX II adds age, CrCl, EF, sex, COPD, LM disease — better individualization than anatomy alone
EXCEL trial: PCI of LM with low-intermediate SYNTAX showed similar 5-yr outcomes to CABG in experienced centers

⚠ Pitfalls

Inter-observer variability moderate without specialized training — requires experienced operators
Does not incorporate functional significance — FFR-guided SYNTAX score reduces unnecessary revascularization
Not applicable for acute STEMI PCI — culprit-only intervention first; multivessel staged later

CRUSADE Bleeding Score ▼

In-hospital major bleeding after NSTEMI — Subherwal, Circulation 2009

Bleeding Risk NSTEMI

8 Variables (0–100 Point Scale)

Baseline hematocrit (continuous — lower = higher risk)

Creatinine clearance (lower = higher risk)

Heart rate (higher = higher risk)

Female sex (independent predictor)

Signs of CHF at presentation

Prior vascular disease

Diabetes mellitus

Systolic BP (U-shaped: very low or very high = risk)

≤20 · 3.1%

21–30 · 5.5%

31–40 · 8.6%

41–50 · 11.9%

>50 · 19.5%

✦ Clinical Pearls

High CRUSADE: prefer radial access for PCI — reduces major access-site bleeding by 30–40% vs femoral
Weight-based anticoagulant dosing critical — renal dose-adjustment of enoxaparin for CrCl <30

⚠ Pitfalls

Predicts in-hospital bleeding only — not validated for outpatient long-term anticoagulation risk
Developed in NSTEMI cohort — less validated for STEMI or purely medically managed patients

EuroSCORE II ▼

Cardiac surgery operative mortality — Nashef, Eur J Cardiothorac Surg 2012

Surgery Risk CABG / Valve

Key Input Variables

Patient factors: age, sex, CrCl, extracardiac arteriopathy, poor mobility, prior cardiac surgery, active endocarditis, critical preop state, DM on insulin

Cardiac factors: NYHA class, CCS angina class 4, LV function (EF), recent MI (<90 days), pulmonary HTN

Operation factors: urgency (elective/urgent/emergency/salvage), weight of procedure (isolated CABG vs combined)

<2% · Low risk

2–5% · Moderate

>5% · High — consider TAVR/TAVI

📍 Clinical Application

Used in Heart Team meetings — if EuroSCORE II >4% + high SYNTAX score → TAVR preferred over SAVR/CABG for aortic stenosis
STS score preferred in North American guidelines; EuroSCORE II more common in Europe

⚠ Pitfalls

Frailty and cognitive decline not captured — major predictors of poor surgical outcome especially in elderly
EuroSCORE II may overestimate risk in high-volume experienced centers with better outcomes than registry average
Porcelain aorta, prior CABG, and hostile chest are procedural considerations not captured in score

Atrial Fibrillation — Types & Classification ▼

ESC 2020 AFib Guideline · AHA/ACC/HRS 2023

Arrhythmia ESC 2020

Type	Duration	Key Feature
Paroxysmal	≤7 days	Self-terminates; may recur; most episodes <48 h
Persistent	>7 days	Does not self-terminate; cardioversion required to restore SR
Long-standing Persistent	>12 months	Continuous AF for >1 year; rhythm control still being pursued
Permanent	Accepted indefinitely	Rhythm control abandoned; rate control only — a clinical decision, not irreversibility

ESC 2020 additional subcategories: First-diagnosed AFib (first presentation, any duration) · Silent AFib (asymptomatic, found on Holter/ILR) · Valvular AFib (mechanical prosthetic valve or moderate-severe MS → warfarin mandatory) vs Non-valvular AFib (DOAC preferred).
Key principle: Paroxysmal AFib carries the same stroke risk as persistent — anticoagulation decisions use CHA₂DS₂-VASc regardless of type.

⚠ Pitfalls

"Permanent" is a treatment decision (rhythm control abandoned), NOT an electrophysiological state — it can be reclassified if cardioversion is later attempted
Paroxysmal AFib has the same stroke risk as persistent — do not under-anticoagulate because episodes are short or infrequent
Valvular AF (mechanical valve / severe MS) requires warfarin — DOACs are contraindicated; DOAC trials excluded these patients
Sub-clinical AF detected on implantable devices (AHRE) carries stroke risk but optimal anticoagulation threshold is still debated (ARTESIA/NOAH trials)
Lone AFib is a historical term — no longer used in ESC 2020 guidelines; do not document it as it implies no further investigation is needed

✦ Clinical Pearls

Cardioversion >48 h of AF duration or unknown onset → anticoagulate ≥3 weeks before or perform TOE to exclude LAA thrombus
Rate control target: resting HR <110 bpm is acceptable in most (RACE II); <80 bpm if symptomatic or LV dysfunction
Rhythm control may reduce cardiovascular events in high-risk early AF (EAST-AFNET 4, NEJM 2020)

🔗 Related Calculators

📊 CHA₂DS₂-VASc — Stroke Risk 📊 HAS-BLED — Bleeding Risk

AHA/ACC Heart Failure Staging (A–D) ▼

2022 AHA/ACC/HFSA Guideline · Emphasises prevention and progression

Heart Failure ACC/AHA 2022

Stage	Definition	Examples	Management Focus
Stage A At Risk	Risk factors for HF; no structural disease; no symptoms	HTN, DM, obesity, family Hx HCM, prior cardiotoxic therapy	Risk factor modification; ACE-I/ARB if HTN + DM (Class IIa)
Stage B Pre-HF	Structural heart disease OR ↑ filling pressures; no HF symptoms	Reduced LVEF, LVH, prior MI, elevated BNP, diastolic dysfunction	ACE-I/ARB/ARNI + β-blocker (HFrEF Stage B); statin; ICD if LVEF ≤30% (MADIT-II)
Stage C Symptomatic HF	Structural heart disease + current or prior HF symptoms	Dyspnoea, fatigue, oedema; HFrEF or HFpEF	4-pillar GDMT (HFrEF): ARNI + β-blocker + MRA + SGLT2i; diuresis; ICD/CRT as indicated
Stage D Advanced HF	Severe symptoms at rest or with minimal activity; refractory to GDMT	Recurrent HF hospitalisations, inotrope-dependence, severely reduced QoL	LVAD, cardiac transplantation, palliative care; TPVAD in selected centres

2022 rename: Stage A → "At Risk for HF"; Stage B → "Pre-HF" — emphasises that disease begins before symptoms. SGLT2 inhibitors (dapagliflozin, empagliflozin) added as Class I GDMT for HFrEF (DAPA-HF, EMPEROR-Reduced, NEJM 2019/2020). Staging is unidirectional (does not improve); NYHA class can fluctuate with treatment.

⚠ Pitfalls

AHA/ACC staging is not reversible — a patient who improves from Stage C does not return to Stage B; document the highest stage achieved
Do not confuse AHA/ACC stages with NYHA classes — staging reflects structural/biomarker progression; NYHA reflects current symptoms (can improve)
Stage B patients have no symptoms but may already need ICD (LVEF ≤30%, MADIT-II) or GDMT — do not defer treatment
Stage D diagnosis requires documentation that maximal GDMT has truly been optimised, not just that symptoms are severe
BNP/NT-proBNP elevation alone (without structural disease) does not qualify as Stage B unless reproducibly elevated

✦ Clinical Pearls

4 pillars of HFrEF GDMT: ARNI (sacubitril/valsartan) + β-blocker + MRA (spironolactone/eplerenone) + SGLT2i — titrate all 4 before adding others
Stage C HFpEF (LVEF ≥50%): empagliflozin now Class IIa for symptom improvement (EMPEROR-Preserved); treat underlying HTN, AF, and volume overload
Stage D referral criteria: ≥2 HF hospitalisations in 12 months, persistent NYHA III–IV despite GDMT, inotrope dependence

🔗 Related Calculators

📊 HEART Score — Chest Pain Triage 📊 GRACE Score — ACS Risk

NYHA Functional Classification ▼

New York Heart Association · Symptom-based functional classification

Heart Failure Universal

Class	Symptom Threshold	Functional Capacity
Class I	No limitation; no symptoms with ordinary activity	Ordinary exertion does not cause fatigue, dyspnoea, or palpitations
Class II	Slight limitation; comfortable at rest; ordinary activity → symptoms	Walking >2 blocks or >1 flight of stairs provokes symptoms
Class III	Marked limitation; comfortable at rest; less-than-ordinary activity → symptoms	Walking <1 block or 1 flight causes symptoms; ADLs limited
Class IV	Unable to carry on any activity; symptoms at rest possible	Dyspnoea/fatigue at rest or with any exertion; chairbound or bedridden

Device therapy thresholds: CRT indicated for NYHA II–III (or ambulatory IV) + LBBB + QRS ≥150 ms + LVEF ≤35%. ICD for NYHA I–III + LVEF ≤35% on GDMT ≥90 days. NYHA complements AHA/ACC staging — staging is structural/progressive (irreversible), NYHA is functional (can improve with treatment).

⚠ Pitfalls

NYHA class is highly subjective — interobserver variability is significant; a patient may report Class II while objective testing shows Class III capacity
Elderly, deconditioned patients may limit activity to avoid symptoms — artificially appearing as Class I/II while having severe disease
NYHA Class IV does not require symptoms at rest — inability to perform any activity without symptoms qualifies, even if resting symptoms are absent
Do not use NYHA alone to decide device therapy — combine with LVEF, QRS morphology (LBBB), and duration of optimised GDMT
Class can fluctuate day-to-day — document based on the patient's usual state over the past 2 weeks, not their best or worst day

✦ Clinical Pearls

6-Minute Walk Test (6MWT) provides objective functional correlate: <300 m ≈ NYHA III–IV; >450 m ≈ NYHA I–II
CPET (peak VO₂) is the most objective measure: <12 mL/kg/min supports transplant listing; <14 mL/kg/min = advanced HF
Improvement from NYHA III → I with GDMT does not change AHA/ACC stage (still Stage C)

🔗 Related Calculators

📊 GRACE Score — ACS/HF Risk 📊 HEART Score — Chest Pain

Killip Classification (Acute MI) ▼

Killip & Kimball 1967 · Clinical HF severity at time of MI

Ischemia / MI Prognostic

Class	Clinical Features	Original Mortality	Modern PCI Era
Class I	No HF; no rales, no S3	~6%	~2–3%
Class II	Mild-moderate HF: basilar rales ≤50% fields, S3 gallop, JVD	~17%	~5–8%
Class III	Frank pulmonary oedema: rales >50% lung fields	~38%	~10–15%
Class IV	Cardiogenic shock: SBP <90, peripheral vasoconstriction, cyanosis, altered mentation	~67–81%	30–50%

Incorporated into TIMI STEMI score (Class II–IV = 2 points) and GRACE score. Killip IV (cardiogenic shock) still carries 30–50% mortality despite primary PCI and MCS (IABP-SHOCK II, CULPRIT-SHOCK). Assign Killip class at presentation only — it does not update with clinical changes.

⚠ Pitfalls

Killip assigned at admission only — it does not capture dynamic deterioration or improvement during hospitalisation
Killip III and IV can be easily confused — Killip III requires frank pulmonary oedema (>50% fields), not just signs of fluid overload
Not validated in non-MI settings — applying Killip to decompensated chronic HF or non-ischaemic cardiomyopathy may be misleading
Cardiogenic shock (Class IV) is a clinical diagnosis — do not rely solely on SBP <90; end-organ hypoperfusion (lactate, cool extremities, oliguria) is required even with BP "maintained" on vasopressors
Original mortality figures are from the pre-PCI, pre-GDMT era — use for risk stratification context only, not for quoting to patients

✦ Clinical Pearls

Killip IV (cardiogenic shock) STEMI: primary PCI of culprit artery only (CULPRIT-SHOCK trial) — complete revascularisation upfront increases renal failure and mortality
Avoid nitrates and morphine in Killip III–IV (reduce preload, potentially worsen shock); use diuretics carefully and consider mechanical unloading early
IABP does not improve mortality in cardiogenic shock (IABP-SHOCK II, NEJM 2012) — Impella CP is now preferred for haemodynamic support

🔗 Related Calculators

📊 TIMI Score — UA/NSTEMI 📊 GRACE Score — ACS Risk

CKD Staging (KDIGO) ▼

KDIGO 2012 CKD Guideline · eGFR + albuminuria-based classification

Renal KDIGO 2012

Stage	eGFR (mL/min/1.73m²)	Description	Cardiology Action
G1	≥90	Normal or high (CKD if kidney damage markers present)	No DOAC adjustment
G2	60–89	Mildly decreased	No DOAC adjustment
G3a	45–59	Mildly to moderately decreased	Check DOAC dose thresholds
G3b	30–44	Moderately to severely decreased	Dose-reduce most DOACs; avoid dabigatran
G4	15–29	Severely decreased — plan for RRT	Apixaban 2.5 mg BID; avoid dabigatran/edoxaban/rivaroxaban
G5	<15 / Dialysis	Kidney failure (ESRD)	Warfarin preferred for AFib; apixaban in selected dialysis patients (AXADIA)

KDIGO requires ≥3 months of abnormal eGFR or kidney damage markers for CKD diagnosis — a single low eGFR may be AKI. Albuminuria (ACR) adds independent prognostic value: A1 (<30 mg/g) / A2 (30–300) / A3 (>300). Contrast nephropathy risk: Hold metformin ≥48 h if eGFR <30 before contrast PCI; IV hydration peri-procedure.

⚠ Pitfalls

A single low eGFR is NOT CKD — KDIGO requires abnormality persisting for >3 months; document dates of first and confirming measurements
Creatinine-based eGFR underestimates renal function in sarcopenic/elderly patients and overestimates it in muscular young patients — cystatin C-based eGFR is more reliable in these groups
Dabigatran is renally cleared — avoid if eGFR <30; rivaroxaban 20 mg OD → 15 mg OD if eGFR 15–49 (for AF); edoxaban contraindicated if eGFR >95 (paradoxical ↓ efficacy)
Hyperkalaemia risk with MRA (spironolactone/eplerenone) increases substantially at eGFR <30 — monitor K+ closely; consider finerenone (FIDELIO-DKD) in CKD + DM
ACE-I/ARB may cause transient rise in creatinine (<30% acceptable) — do not discontinue unless K+ >5.5 or creatinine rises >30%

✦ Clinical Pearls

SGLT2 inhibitors (dapagliflozin, empagliflozin) reduce CKD progression independent of diabetes — now guideline-recommended for CKD G3–G4 + proteinuria (DAPA-CKD, CREDENCE)
Cardiorenal syndrome: worsening renal function during HF treatment may reflect over-diuresis — check urine sodium; if <20 mEq/L, consider diuretic resistance, not true AKI
eGFR <30 at time of PCi: NAC + pre-hydration + iso-osmolar contrast + minimise volume — KDIGO CIN prevention bundle

🔗 Related Calculators

📊 CHA₂DS₂-VASc — AFib Stroke Risk 📊 HAS-BLED — Bleeding Risk

TIMI Flow Grades (Coronary Angiography) ▼

TIMI Study Group · Angiographic grading of coronary perfusion

Ischemia / PCI Angiographic

Grade	Angiographic Appearance	Clinical Significance
TIMI 0	No antegrade flow beyond obstruction	Complete occlusion; maximal myocardial risk
TIMI 1	Contrast penetrates obstruction; fails to opacify distal vessel	Near-complete obstruction; minimal myocardial perfusion
TIMI 2	Partial perfusion — distal vessel opacifies but fills/clears slower than normal	Incomplete reperfusion; mortality ↑ vs TIMI 3 even if vessel is "open"
TIMI 3	Normal flow — fills and clears as rapidly as a non-culprit reference vessel	Target of PCI; strongest independent predictor of ↓ STEMI mortality

TIMI 3 is the target — not just patency. TIMI 2 post-PCI approaches failed-reperfusion mortality in some registries. TIMI Frame Count (cTFC): cine frames for contrast to reach distal landmark; cTFC <27 correlates with TIMI 3. MBG (Myocardial Blush Grade) assesses tissue-level perfusion even when epicardial TIMI 3 is achieved.

⚠ Pitfalls

TIMI 3 epicardial flow does not guarantee myocardial reperfusion — "no-reflow" phenomenon: microvascular obstruction despite patent culprit artery (occurs in ~25% primary PCI)
TIMI 2 is often incorrectly called "success" — TIMI 2 vs 3 post-PCI carries significantly different prognosis; do not stop at TIMI 2
Collateral-dependent flow in chronic total occlusion (CTO) does not score as TIMI 3 even if the territory is viable — graded separately
TIMI grading is subjective — experienced operators required; digital quantitative coronary angiography (QCA) is more reproducible
Do not confuse TIMI Flow Grade (angiographic classification) with TIMI Risk Score (clinical risk stratification) — entirely different systems

✦ Clinical Pearls

No-reflow treatment: adenosine IC (100–200 mcg), verapamil IC, nitroprusside IC — aspiration thrombectomy not routinely recommended (TASTE, TOTAL trials)
MBG 0–1 despite TIMI 3 = microvascular obstruction; associated with larger infarct, worse LV recovery, and higher mortality
ST-resolution ≥70% in culprit lead within 90 min of PCI is the best ECG surrogate of successful myocardial reperfusion

🔗 Related Calculators

📊 TIMI Risk Score — UA/NSTEMI 📊 GRACE Score — ACS Mortality

ACC/AHA Valve Disease Stages (A–D) ▼

2021 ACC/AHA Valvular Heart Disease Guideline

Structural ACC/AHA 2021

Stage	Definition	Haemodynamics / Example	Action
Stage A At Risk	Risk factors present; no structural change yet	Normal morphology; bicuspid AoV, rheumatic fever history	Risk factor modification; surveillance echo
Stage B Progressive	Mild-moderate valve disease; asymptomatic; no haemodynamic compromise	Mild AS (Vmax 2–3 m/s); mild-moderate MR; normal LV	Periodic surveillance; no intervention
Stage C Severe Asymptomatic	Severe valve disease; asymptomatic	C1: LVEF ≥60% (watch); C2: LVEF <60% (AS/AR intervention)	C1: monitor closely; C2: AVR/MVR indicated (Class I)
Stage D Severe Symptomatic	Severe valve disease + symptoms attributable to the lesion	Severe AS + angina/syncope/dyspnoea; severe MR + dyspnoea	Class I indication for intervention in most cases

Severe AS thresholds: Vmax ≥4 m/s · mean gradient ≥40 mmHg · AVA ≤1.0 cm² (or ≤0.6 cm²/m² indexed). Stage D symptomatic severe AS: median survival 2–3 years without intervention. Low-flow, low-gradient AS (LVEF <50%, AVA <1 cm², mean gradient <40 mmHg) — dobutamine stress echo or CT calcium scoring to confirm severity.

⚠ Pitfalls

Preserved LVEF does not rule out severe haemodynamic compromise in MR — LVEF 60% with severe chronic MR may already represent LV dysfunction (normal LVEF in MR is 70%+); surgery indicated at LVEF <60%
Low-flow low-gradient severe AS (LVEF <50%, AVA <1.0 cm², gradient <40 mmHg) — may represent pseudo-severe AS (reduced flow reduces calculated gradient); dobutamine stress echo differentiates
Asymptomatic ≠ safe — Stage C patients with LVEF <60% have a Class I indication for AVR even without symptoms; waiting for symptoms leads to irreversible LV damage
Symptoms must be attributable to the valve lesion for Stage D — HF symptoms from concomitant CAD or cardiomyopathy should not automatically upgrade to Stage D

✦ Clinical Pearls

TAVI (TAVR) is non-inferior to SAVR for severe symptomatic AS in low-, intermediate-, and high-risk patients (PARTNER 3, Evolut Low Risk) — discuss multidisciplinary heart team approach
Severe AS + AFib: cardioversion before AVR may reduce volume overload; anticoagulation strategy depends on valve type post-procedure
TR is increasingly recognised as not "benign" — isolated severe TR has poor prognosis; tricuspid intervention gaining Class IIa evidence in 2021 guidelines

🔗 Related Calculators

📊 HEART Score — Pre-op Risk 📊 CHA₂DS₂-VASc — AF Anticoagulation

HF Classification by Ejection Fraction ▼

ESC 2021 · AHA/ACC/HFSA 2022 · EF-based subtype classification

Heart Failure ESC 2021

Subtype	LVEF	GDMT	Key Trials
HFrEF Reduced EF	<40%	4 pillars: ARNI + β-blocker + MRA + SGLT2i; ICD/CRT as indicated	PARADIGM-HF, MERIT-HF, RALES, DAPA-HF
HFmrEF Mildly Reduced EF	40–49%	Emerging evidence: SGLT2i (Class IIa), ARNI, MRA may benefit	EMPEROR-Preserved sub-group, TOPCAT
HFpEF Preserved EF	≥50%	SGLT2i Class IIa (empagliflozin); diuretics; treat HTN, AF, DM	EMPEROR-Preserved (NEJM 2021)
HFrecEF Recovered EF	Was <40%, now ≥40%	Continue all GDMT — high relapse on withdrawal; serial echo monitoring	TRED-HF (Lancet 2019)

4 Pillars of HFrEF GDMT (titrate all 4 concurrently):
1. ARNI — sacubitril/valsartan (PARADIGM-HF: superior to enalapril, NEJM 2014)
2. β-blocker — carvedilol, bisoprolol, or metoprolol succinate (MERIT-HF, COPERNICUS)
3. MRA — spironolactone (RALES) / eplerenone (EPHESUS); monitor K+ and eGFR
4. SGLT2i — dapagliflozin (DAPA-HF, NEJM 2019) / empagliflozin (EMPEROR-Reduced)

⚠ Pitfalls

LVEF is dynamic and operator-dependent — EF measured during acute decompensation may not reflect true underlying subtype; repeat echo after 3 months of GDMT before classifying as HFpEF
HFpEF is a diagnosis of exclusion — other causes of dyspnoea (PE, COPD, obesity hypoventilation, anaemia) must be excluded before attributing to preserved-EF HF
HFrecEF is NOT cured HF — TRED-HF trial: 40% relapsed within 6 months of stopping GDMT; continue all medications even with normalised EF
Do not switch ARNI to ACE-I after EF recovers — maintain ARNI for continued benefit; switching is associated with higher relapse rates
HFmrEF patients often started as HFrEF and improved — their evidence base overlaps; treat with HFrEF GDMT if any uncertainty

✦ Clinical Pearls

Titrate GDMT simultaneously (not sequentially) — starting all 4 medications at low doses and up-titrating is safer and more effective than sequential addition (STRONG-HF trial)
Iron deficiency (ferritin <100 or 100–300 with transferrin sat <20%) should be treated with IV iron (AFFIRM-AHF) — reduces HF hospitalisations regardless of anaemia
Vericiguat (sGC stimulator) and omecamtiv mecarbil (myosin activator) are newer agents for high-risk HFrEF; not yet universal GDMT but Class IIb options

🔗 Related Calculators

📊 HEART Score — ACS vs HF 📊 GRACE Score — ACS Risk