Identify isoelectric lead on the ECG; the axis is perpendicular to this lead.
Use leads I and aVF for a quick estimation:
- Normal Axis: Positive QRS in both leads.
- LAD: Positive QRS in lead I and negative in aVF. Confirm with lead II (negative QRS indicates LAD).
- RAD: Negative QRS in lead I and positive in aVF, often due to right ventricular overload.

Definition for T-Wave Inversion (TWI):TWI is only clinically relevant if observed in leads with a positive QRS complex.

Normal:

TWI in leads with negative QRS complexes (III, aVR, V1).
TWI in V1–V3 is normal in children/young adults.

Pathological:

TWI >1mm deep in ≥2 contiguous leads, especially in V2–V6, indicates potential ischaemia, strain, or myocardial injury.
Persistent, deep TWI in precordial leads (e.g., V2–V4) can signify apical hypertrophy or previous ischaemia.

Additional Considerations:

Biphasic T waves: May indicate ischaemia or Wellens’ syndrome if seen in V2–V3.
Axis deviation or significant TWI should prompt further evaluation for underlying conditions (e.g., ischaemia, ventricular hypertrophy).

Sinus Tachy vs SVT

Sinus Tachy:

Often identifiable triggers like emotion, dehydration, fever
Gradual onset and offset
Usually slightly lower HR than SVT (<150 bpm but can exceed in younger pts: max HR = 220 – age)
P waves visible but depend on HR

SVT:

Sudden onset without obvious triggers
HR >150 bpm
Symptoms like palpitations or dizziness more prominent
P waves absent or inverted in inferior leads

MI Leads and Arterial Supply

V1–2: Anteroseptal (LAD)
V3–4: Anterior (LAD)
V5–6: Anterolateral (LCx; reciprocal STD in inferior leads)
I, aVL: Lateral (LCx)
II, III, aVF: Inferior (RCA > LCx; reciprocal STD in anterolateral leads)

Note: For exams, if ST elevation > ST depression in V5/V6, label as anteroseptal; otherwise say anterior or anterolateral

Digoxin Toxicity Symptoms

ECG:

Down-sloping ST depression (“scooped” or “mustache” appearance)
Possible arrhythmias: bradyarrhythmias or tachyarrhythmias (e.g., junctional tachycardia, AV block)

CNS:

Lethargy, confusion, headache

GI:

Anorexia, nausea/vomiting, diarrhoea

CVS:

Palpitations, syncope, dyspnoea

Ophthalmologic:

Yellow halos around lights (xanthopsia), blurred vision

Notes:

Consider alternative causes of tachycardia, especially dehydration or anaemia, before initiating treatment for SVT.
Elevated ST elevation in V1–V2 with concurrent reciprocal changes is highly suggestive of anterior MI (validate with troponins).

LVH

Voltage Criteria:

Sokolow-Lyon index: S wave in V1 + R wave in V5/6 >35mm
R wave in aVL >11mm (alternate voltage criteria)

Other findings:

LV strain pattern: STD, STE, and TWI (opposite direction of prominent R wave – termed "appropriate discordance")

Causes:

Aortic stenosis
Aortic regurgitation
HOCM
HTN
Aortic coarctation
Chronic mitral regurgitation (volume overload)
CKD

CHB (Complete Heart Block)

Characteristics:

Rate: ~40 bpm (ventricular or junctional escape rhythm, with 7–8 large squares between RR intervals)
Dissociation: Atrial rate ~100 bpm, ventricular rate ~40 bpm, with no atrial impulses conducted to ventricles
Regular PP and RR intervals, despite absence of conduction

Management:

Requires urgent admission and temporary pacing prior to permanent pacemaker (PPM) insertion

Causes:

Inferior MI (compromising AV node)
AV nodal blocking medications (e.g., CCBs, beta-blockers, digoxin)
Other causes:
- Lyme disease (early disseminated stage)
- Sarcoidosis (cardiac involvement)
- Amyloidosis

ECG

Axis Deviation

Identify the isoelectric lead (where the QRS is equally positive and negative), then the axis is perpendicular to that lead
Quick Estimation with Leads I and aVF
- Normal axis if QRS is positive in both leads (approximately −30° to +90°)
- Left Axis Deviation (LAD): QRS positive in I, negative in aVF. Confirm with lead II (if negative in II, strongly suggests LAD)
- Right Axis Deviation (RAD): QRS negative in I, positive in aVF, often due to conditions like right ventricular hypertrophy or chronic lung disease
Extreme Axis Deviation (aka Northwest axis) if negative in both leads I and aVF

Right Axis Deviation: leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE — **Right Axis Deviation**: leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE

T-Wave Inversion (TWI)

Clinically relevant if occurring in leads where the QRS is predominantly positive
Normal Variants
- TWI in leads with predominantly negative QRS (III, aVR, V1)
- TWI in V1–V3 can be normal in children or young adults
Pathological TWI
- 1mm deep in ≥2 contiguous leads (especially in V2–V6), suggesting possible ischaemia, strain, or injury
- Persistent, deep TWI in precordial leads (e.g. V2–V4) can indicate apical hypertrophy or prior ischaemia
- Biphasic T waves in V2–V3 may signify Wellens syndrome (critical LAD stenosis)

Sinus Tachycardia vs SVT

Sinus Tachycardia

Usually triggered by pain, fever, anxiety, hypovolaemia
Gradual onset/offset
Heart rate often <150 bpm (though can exceed this in younger patients)
P waves visible before each QRS, but may blend with preceding T wave if rate very high

SVT (Supraventricular Tachycardia)

Sudden onset/offset
Often HR >150 bpm
P waves typically absent, hidden within QRS, or inverted in inferior leads
Patients may report palpitations or dizziness without an obvious precipitant

Supraventricular tachycardia (SVT): Rhythm strip demonstrating a regular, narrow-complex tachycardia — **Supraventricular tachycardia (SVT):** Rhythm strip demonstrating a regular, narrow-complex tachycardia

MI Leads and Arterial Supply

V1–V2: Anteroseptal (LAD)
V3–V4: Anterior (LAD)
V5–V6: Anterolateral (often LCx, can be diagonal branch of LAD)
I, aVL: Lateral (LCx or diagonal branch of LAD)
II, III, aVF: Inferior (RCA > LCx in most individuals)
Reciprocal changes often appear in opposite leads (e.g. ST depression in II, III, aVF when lateral leads are elevated)
Compare ST elevation magnitude in V1–V2 to the remainder of the precordial leads to differentiate anteroseptal from anterolateral involvement

Digoxin Toxicity

ECG Findings

Down-sloping ST depression (Salvador Dali moustache or “scooped” appearance)
Arrhythmias: junctional tachycardia, AV block, bidirectional VT in severe cases

Clinical

Neurological: confusion, headache
Gastrointestinal: anorexia, nausea, vomiting, diarrhoea
Visual: yellow halos (xanthopsia), blurred vision
Risk Factors: advanced age, renal impairment, electrolyte imbalances (hypokalaemia, hypomagnesaemia)

Digoxin effect: Sagging ST segments resemble a “reverse tick” — **Digoxin effect:** Sagging ST segments resemble a “reverse tick”

LVH (Left Ventricular Hypertrophy)

Voltage Criteria

Sokolow-Lyon: S wave in V1 + R wave in V5 or V6 >35mm
R wave in aVL >11mm

Strain Patterns

ST depression and T-wave inversion in left-sided leads (I, aVL, V5–V6) with a prominent R wave

Causes

Hypertension, aortic stenosis/regurgitation, hypertrophic cardiomyopathy, coarctation of the aorta

LVH can elevate risk of arrhythmias and ischaemic events

Left ventricular hypertrophy (LVH): Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm); R-wave peak time > 50 ms in V5-6 with associated QRS broadening; LV strain pattern with ST depression and T-wave inversions in I, aVL and V5-6; ST elevation in V1-3; Prominent U waves in V1-3; Left axis deviation — **Left ventricular hypertrophy (LVH):** Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm); R-wave peak time > 50 ms in V5-6 with associated QRS broadening; LV strain pattern with ST depression and T-wave inversions in I, aVL and V5-6; ST elevation in V1-3; Prominent U waves in V1-3; Left axis deviation

Complete Heart Block (CHB)

Characteristics

Atrial rate ~100 bpm with regular P waves
Ventricular rate ~40 bpm (escape rhythm), no conduction from atria to ventricles
PP and RR intervals are regular but dissociated

Causes

Inferior MI compromising the AV node
AV nodal blocking medications (beta-blockers, non-DHP CCBs, digoxin)
Structural diseases (Lyme carditis, sarcoidosis, amyloidosis)

Management

Urgent admission, potential need for temporary pacing if symptomatic or haemodynamically unstable
Consider permanent pacemaker if not resolved after the acute cause is addressed

Complete heart block: There is AV dissociation, with the atrial rate (~100 bpm) independent of the ventricular rate (~40 bpm) — **Complete heart block:** There is AV dissociation, with the atrial rate (~100 bpm) independent of the ventricular rate (~40 bpm)

Additional Considerations

Alternative Tachycardia Causes

Dehydration, anaemia, hyperthyroidism can mimic or exacerbate sinus tachycardia

Reciprocal Changes in MI

ST depression in leads opposite the region of ST elevation may help confirm the diagnosis

Identifying Infarct Location

Detailed correlation of ECG changes in multiple leads enhances diagnostic accuracy

LVH and Hypertension

LVH on ECG significantly increases cardiovascular risk, warranting aggressive BP management

Digoxin Caution

Close monitoring of renal function and electrolytes to avoid toxicity

Wellens Syndrome

Biphasic or deeply inverted T waves in V2–V3 suggest critical LAD stenosis, high risk for anterior MI

All suspicious ECG changes should be correlated clinically and, if necessary, investigated further with echocardiography, troponin assays, or advanced imaging. Early recognition and management of ECG abnormalities can prevent significant morbidity and mortality.

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