ECG LEARNING GUIDE

Systematic Interpretation • Acute Coronary Syndrome (ACS) • Arrhythmias •

Electrolyte Disturbances
Complete with Management, Doses, and Administration

A structured educational resource for healthcare workers & medical/nursing students

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 [!!] Important Disclaimer — Read First
This document is a learning resource and reference summary, not a substitute for official
guidelines, clinical judgment, or physician/consultant supervision.
The doses listed are general adult doses based on widely used guidelines (AHA/ACLS, ESC,
PERKI). Always adjust for body weight, renal/hepatic function, contraindications, drug interactions,
patient condition, and your facility's local protocols. Re-verify every dose before administration.
Emergency procedures (defibrillation, fibrinolysis, etc.) must follow official algorithms and be
performed by competent personnel.

Table of Contents
CHAPTER 1 ECG Fundamentals (conduction, paper, leads, waves)
CHAPTER 2 Reading an ECG Systematically (7 steps)
CHAPTER 3 Arrhythmias & Rhythm Disturbances + Management
CHAPTER 4 Acute Coronary Syndrome / ACS (STEMI, NSTEMI, UA) + Management
CHAPTER 5 Electrolyte Disturbances (Potassium, Calcium, Sodium, Magnesium) +
Management
CHAPTER 6 Other ECG Abnormalities (Hypertrophy, BBB, Pericarditis, PE, etc.)
APPENDIX Cardiovascular Emergency Drug Dose Summary

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 CHAPTER 1 · ECG Fundamentals
Understanding what the ECG records before assessing abnormalities

An electrocardiogram (ECG) is a recording of the heart's electrical activity from the body surface. Each
beat originates from an electrical impulse traveling through the conduction system, triggering
depolarization and repolarization of the atrial and ventricular muscle. It is this difference in electrical
potential that is recorded as waves.

1.1 The Cardiac Conduction System

• SA (sinoatrial) node — the natural pacemaker (~60–100/min), initiates the impulse.
• AV node — slows the impulse (physiologic delay → the PR interval) so the atria can fill the
ventricles.
• Bundle of His → right & left branches → Purkinje fibers — rapidly spread the impulse to the
ventricles.

[i] Waves ↔ electrical events

The P wave = atrial depolarization; the QRS complex = ventricular depolarization; the T wave =
ventricular repolarization. Atrial repolarization is hidden within the QRS.

1.2 ECG Paper & Calibration

Standard paper speed is 25 mm/s and calibration is 10 mm = 1 mV.

Figure 1. ECG paper calibration: small box 0.04 s and large box 0.20 s.

Size Time (horizontal) Amplitude (vertical)

Small box (1 mm) 0.04 s 0.1 mV

Large box (5 mm) 0.20 s 0.5 mV

5 large boxes 1.0 s 2.5 mV

1.3 The Twelve Leads & Cardiac Territories

The 12-lead ECG views the heart from 12 angles: 6 frontal-plane (limb) leads and 6 horizontal-plane
(precordial/chest) leads.

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 Group Leads Cardiac territory

Bipolar limb I, II, III General (Einthoven's triangle)

Augmented aVR, aVL, aVF aVL: high lateral; aVF: inferior

Inferior II, III, aVF Inferior wall (RCA)

Septal V1, V2 Septum (LAD)

Anterior V3, V4 Anterior wall (LAD)

Lateral I, aVL, V5, V6 Lateral wall (LCx)

Posterior* V7–V9 Posterior wall (RCA/LCx)

Right ventricle* V3R, V4R Right ventricular infarct

*Additional leads are placed when posterior or right ventricular infarction is suspected.

1.4 Waves, Segments, and Intervals

Figure 2. Anatomy of one normal ECG complex with the PR, QRS, and QT intervals.

Component Meaning Normal value

P wave Atrial depolarization Width <0.12 s; height <2.5 mm

PR interval Start of P → start of QRS 0.12–0.20 s

QRS complex Ventricular depolarization 0.06–0.10 s (<0.12 s)

ST segment J point → start of T Isoelectric

T wave Ventricular repolarization Same direction as QRS, asymmetric

QTc <0.44 s (men); <0.46 s

QT interval Start of QRS → end of T
(women)

U wave Late repolarization Small; prominent in hypokalemia

[*] Corrected QT (QTc)

Because QT depends on rate, use QTc = QT / √(RR in seconds) (Bazett). A prolonged QTc
increases the risk of Torsades de Pointes.

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 CHAPTER 2 · Reading an ECG Systematically
Seven steps so no abnormality is missed

Always read an ECG in the same order. A systematic approach prevents errors from fixating on a single
striking finding.

Step 1 — Check identity & recording quality

• Confirm name, date, and calibration (25 mm/s, 10 mm/mV) are correct.
• Watch for artifact, baseline wander, or reversed leads.

Step 2 — Rate (heart rate)

• The 300 method: 300 ÷ number of large boxes between R waves. Example: 4 boxes → 75/min.
• The 1500 method: 1500 ÷ number of small boxes between R waves.
• The 6-second method (AF/irregular): count QRS complexes in 30 large boxes × 10.

[*] Quick memory sequence (300 method)

If R waves fall on successive bold lines: 300 – 150 – 100 – 75 – 60 – 50 /min.

Step 3 — Rhythm
• Measure the R-R distance: regular or irregular?
• Is there a P before every QRS & is P positive in II? → sinus rhythm.
• Normal sinus: 60–100/min, P–QRS 1:1, normal PR.

Step 4 — Axis (frontal QRS axis)

Normal axis is −30° to +90°. Quick method: look at leads I and aVF:

Lead I Lead aVF Axis interpretation

Positive Positive Normal

Positive Negative Left axis deviation (LAD)

Negative Positive Right axis deviation (RAD)

Negative Negative Extreme deviation

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 Figure 3. The hexaxial reference system for determining axis.

Step 5 — Intervals & durations

• PR >0.20 s → first-degree AV block. PR <0.12 s + delta wave → WPW.
• QRS ≥0.12 s → wide (bundle branch block, ventricular rhythm, hyperkalemia).
• Long QT/QTc → Torsades risk; short → hypercalcemia.

Step 6 — Morphology (P, QRS, ST, T)

• Wide/notched P (left atrium), tall peaked P (right atrium).
• Pathological Q: width ≥0.04 s or >25% of R height → old infarct.
• ST segment: elevation (STEMI) or depression (ischemia).
• T: inversion (ischemia), peaked (hyperkalemia), flat + U (hypokalemia).

Step 7 — Hypertrophy & conclusion

Assess chamber enlargement (e.g. Sokolow-Lyon LVH: S in V1 + R in V5/V6 >35 mm), then summarize all
findings into a single conclusion (rhythm, rate, axis, abnormalities, clinical impression).

[i] Reading-flow summary

1) Quality → 2) Rate → 3) Rhythm → 4) Axis → 5) Intervals → 6) Morphology → 7) Hypertrophy
→ Conclusion.

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 CHAPTER 3 · Arrhythmias & Rhythm Disturbances
Recognizing patterns and principles of emergency management

Arrhythmias are classified by rate (brady/tachycardia), origin (supraventricular/ventricular), and QRS width.
Emergency principle: assess the patient's stability (BP, consciousness, chest pain, heart failure) before
choosing therapy.

3.1 Sinus Rhythm

• Normal sinus: 60–100/min.
• Sinus bradycardia: <60/min; if symptomatic, follow the bradycardia algorithm.
• Sinus tachycardia: >100/min; usually reactive → treat the cause.

3.2 Atrial Fibrillation (AF) & Atrial Flutter

Figure 4. Patterns of AF, atrial flutter, VT, and VF.

• AF: no P waves, undulating baseline, irregularly irregular ventricular rate.

• Atrial flutter: 'sawtooth' (F) waves, atrial rate ~250–350/min.

[Rx] AF/flutter management (overview)

Unstable: immediate synchronized cardioversion.
Stable – rate control: Diltiazem 0.25 mg/kg IV (± repeat 0.35 mg/kg), or Metoprolol 2.5–5 mg IV
every 5 min (max 15 mg), or Digoxin (if heart failure).
Anticoagulation per the CHA■DS■-VASc score to prevent stroke.

3.3 Supraventricular Tachycardia (SVT)

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 Narrow QRS, regular, ~150–250/min, often with no clear P waves.

[Rx] SVT management (narrow QRS, stable)

1. Vagal maneuvers (modified Valsalva, carotid massage).
2. Adenosine 6 mg rapid IV + saline flush; if it fails, repeat 12 mg (may give 12 mg once more).
3. Alternatives: Diltiazem/Verapamil or a beta-blocker.
Unstable → synchronized cardioversion (start 50–100 J).

[!] How to give adenosine

Very short half-life (<10 s). Inject as fast as possible through a large vein, immediately followed by
a 20 mL saline flush and raise the arm. Warn the patient they will feel brief chest discomfort/flushing.

3.4 AV Block

Figure 5. AV block first-degree, second-degree (Mobitz I & II), and third-degree (complete).

Type ECG features Clinical approach

First-degree Constant PR >0.20 s, every P followed by QRS Usually observe

Mobitz I
PR lengthens progressively → 1 QRS dropped Often benign
(Wenckebach)

Mobitz II Constant PR, occasional P with no QRS Consider pacing

Third-degree
AV dissociation (P & QRS independent) Emergency → pacing
(complete)

3.5 Symptomatic Bradycardia — Algorithm

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 [Rx] Unstable bradycardia management (ACLS)
Atropine 1 mg IV (may repeat every 3–5 min, max 3 mg).
If no response: Transcutaneous pacing (TCP), and/or
Dopamine 5–20 mcg/kg/min or Epinephrine 2–10 mcg/min (titrated infusion).
High-grade block (Mobitz II / complete): prepare for pacing; atropine is often ineffective.

3.6 Ventricular Tachycardia (VT) & Ventricular Fibrillation (VF)

• VT: wide QRS (≥0.12 s), regular, fast.
• VF: chaotic waves with no QRS → cardiac arrest.

[Rx] VT with a pulse

Unstable → synchronized cardioversion (100 J, step up as needed).
Stable (monomorphic) → Amiodarone 150 mg IV over 10 min (may repeat); then infuse 1 mg/min
for 6 hours.
Torsades (polymorphic + long QT) → Magnesium sulfate 1–2 g IV.

[!!] Cardiac arrest VF / pulseless VT (ACLS)

Immediate defibrillation (biphasic ~120–200 J) + high-quality CPR.
Epinephrine 1 mg IV/IO every 3–5 min.
Amiodarone 300 mg IV bolus (second dose 150 mg) or Lidocaine 1–1.5 mg/kg if refractory.
Find & treat the 5 Hs & 5 Ts: hypoxia, hypovolemia, acidosis (H■), hypo/hyperkalemia, hypothermia;
toxins, tamponade, tension pneumothorax, coronary/pulmonary thrombosis.

[!] PEA & Asystole

Non-shockable rhythms. Focus: high-quality CPR, Epinephrine 1 mg IV every 3–5 min, correct
the cause (5 Hs/5 Ts). Do not defibrillate asystole.

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 CHAPTER 4 · Acute Coronary Syndrome (ACS)
STEMI, NSTEMI, and Unstable Angina

ACS results from rupture of an atherosclerotic plaque and coronary artery thrombosis, causing myocardial
ischemia/infarction. Diagnosis combines clinical symptoms, the ECG, and biomarkers (troponin).

4.1 The ACS Spectrum

Type ECG Troponin Pathophysiology

STEMI Persistent ST elevation / new LBBB Elevated Total coronary occlusion

ST depression / T inversion (no

NSTEMI Elevated Partial occlusion
persistent ST elevation)

UA ST depression / T inversion / normal Normal Ischemia without necrosis

4.2 ECG Changes in Ischemia & Infarction

Figure 6. STEMI — ST-segment elevation above the isoelectric line.

Figure 7. ST depression — subendocardial ischemia pattern (typical of NSTEMI/UA).

Figure 8. T-wave inversion — a sign of ischemia.

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 Figure 9. Pathological Q wave — marker of old infarct/necrosis.

[i] Criteria for significant ST elevation (STEMI)

ST elevation at the J point in ≥2 contiguous leads:
≥1 mm (0.1 mV) in most leads;
in V2–V3: ≥2 mm (men ≥40 y), ≥2.5 mm (men <40 y), ≥1.5 mm (women).
New LBBB + ischemic symptoms is treated as equivalent to STEMI.

4.3 Infarct Localization by Lead

Location ST-elevation leads Artery Reciprocal changes

Inferior II, III, aVF RCA I, aVL

Anterior V3, V4 LAD –

Anteroseptal V1–V4 LAD –

Lateral I, aVL, V5, V6 LCx II, III, aVF

Extensive anterior V1–V6, I, aVL Proximal LAD II, III, aVF

ST depression V1–V3
Posterior RCA/LCx V1–V3
(mirror)

Right ventricle V4R elevation Proximal RCA –

[!] Watch for inferior + right ventricular infarct

In inferior infarction, record V4R. If there is right ventricular infarction, the patient is
preload-dependent — use nitrates cautiously/avoid them (risk of severe hypotension); give fluids if
hypotensive.

4.4 STEMI ECG Evolution

• Early minutes–hours: hyperacute (tall) T → ST elevation.
• Hours–days: ST elevation persists, Q waves appear, T begins to invert.
• Days–weeks: ST returns to baseline, pathological Q persists, T inversion.

4.5 ACS Management — Initial Therapy

[Rx] Early anti-ischemic & supportive therapy

Oxygen: only if SpO■ <90% or respiratory distress.
Nitroglycerin: SL 0.4 mg every 5 min (max 3 doses) if BP adequate; IV 5–10 mcg/min titrated.
Contraindications: hypotension, right ventricular infarct, PDE-5 inhibitors (sildenafil) in the last
24–48 h.
Morphine 2–4 mg IV for refractory pain (caution; may slow oral antiplatelet absorption).

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 4.6 Antiplatelet & Anticoagulant Therapy
Drug Loading Maintenance Notes

Aspirin 160–325 mg chewed 75–100 mg/day All ACS

Clopidogrel 300–600 mg 75 mg/day Fibrinolysis & >75 y: no loading

Ticagrelor 180 mg 90 mg twice daily Not with fibrinolysis

Prasugrel 60 mg 10 mg/day For PCI; avoid if prior stroke

Enoxaparin – 1 mg/kg SC every 12 h Adjust in renal impairment

bolus 60 U/kg (max

Heparin (UFH) 12 U/kg/h infusion Target aPTT
4000 U)

Fondaparinux – 2.5 mg SC/day Common in NSTEMI

[i] DAPT (Dual Antiplatelet Therapy)

The combination of aspirin + one P2Y■■ inhibitor (ticagrelor/prasugrel/clopidogrel) is the
backbone of ACS therapy; choice & duration follow the reperfusion strategy and bleeding risk.

4.7 Reperfusion Strategy in STEMI

[!!] The 'time is muscle' principle

Primary PCI = first choice when timely (door-to-balloon ≤90 min).
Fibrinolysis if PCI is unavailable within ~120 min & there are no contraindications, ideally
door-to-needle ≤30 min.

Fibrinolytic Dose & administration

Streptokinase 1.5 million units IV over 30–60 min

Alteplase (tPA) 15 mg bolus → 0.75 mg/kg (max 50 mg) /30 min → 0.5 mg/kg (max 35 mg) /60 min

Tenecteplase Single weight-based IV bolus (30–50 mg)

[!] Absolute contraindications to fibrinolysis (brief)

Any prior intracranial hemorrhage; ischemic stroke <3 months; intracranial neoplasm/vascular
malformation; active bleeding; severe head/facial trauma <3 months; suspected aortic dissection.
Check the full list before giving it.

4.8 Long-Term (Secondary) Therapy

• High-intensity statin: Atorvastatin 40–80 mg or Rosuvastatin 20–40 mg.
• Beta-blocker if no contraindication.
• ACE inhibitor/ARB, especially with left ventricular dysfunction, hypertension, or diabetes.
• Lifestyle modification, cardiac rehabilitation, risk-factor control.

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 CHAPTER 5 · Electrolyte Disturbances on ECG
Potassium, Calcium, Magnesium, and Sodium

Electrolytes set the membrane potential of cardiac cells, so their disturbances show characteristic ECG
patterns. Potassium and calcium are the most prominent; magnesium matters in Torsades; sodium
generally does not change the ECG directly.

5.1 Potassium (K■)

Figure 10. Hyperkalemia progression: peaked T → PR/QRS widening → sine wave.

Hyperkalemia (K■ >5.5 mmol/L) — progressive ECG changes:

• Mild: tall, narrow, peaked T (tented T).

• Moderate: PR prolongs, P flattens/disappears, QRS widens.
• Severe: sine wave → risk of VF/asystole.

[Rx] Hyperkalemia management (with ECG changes / high K)

1. Stabilize the membrane — Calcium gluconate 10% 10 mL IV over 5–10 min (or Calcium
chloride 10% 5–10 mL via central access); repeat if the ECG has not improved. Onset <3 min,
duration ~30–60 min — does not lower the K level.
2. Shift K intracellularly: Regular insulin 10 units IV + Dextrose 25 g (e.g. D40% 62.5 mL) —
monitor blood glucose; Salbutamol nebulizer 10–20 mg; Sodium bicarbonate if acidosis.
3. Remove K from the body: Furosemide (if renal function adequate); potassium binders
(polystyrene sulfonate, patiromer, SZC); hemodialysis = definitive in renal failure/refractory cases.

Figure 11. Hypokalemia: flat T, prominent U wave, ST depression.

Hypokalemia (K■ <3.5 mmol/L): flat T, a U wave appears, ST depression, prolonged QT — increasing
arrhythmia risk.

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 [Rx] Hypokalemia management
Oral (mild): KCl 40–100 mEq/day in divided doses.
Intravenous (severe/symptomatic): KCl diluted, typically ≤10 mEq/h via a peripheral vein; ≤20
mEq/h via central access with ECG monitoring. Avoid rapid boluses.
Correct magnesium at the same time — hypomagnesemia makes hypokalemia hard to correct.

5.2 Calcium (Ca²■)

Figure 12. Hypercalcemia shortens the QT; hypocalcemia prolongs the QT.

Condition ECG change Brief management

IV hydration with 0.9% NaCl; calcitonin; IV

Shortened QT; bradycardia; arrhythmia
Hypercalcemia bisphosphonate (zoledronate/pamidronate);
risk
treat the cause

Prolonged QT (prolonged ST); Calcium gluconate 10% 10–20 mL slow IV

Hypocalcemia
Torsades risk; tetany (symptomatic); correct Mg; treat the cause

5.3 Magnesium (Mg²■)

• Hypomagnesemia: prolonged QT/PR, risk of Torsades de Pointes, worsens hypokalemia.
• Hypermagnesemia: prolonged PR, wide QRS, bradycardia; severe → cardiac arrest.

[Rx] Management
Torsades / symptomatic hypomagnesemia: Magnesium sulfate 1–2 g IV over 15 min (Torsades
may use 2 g IV).
Severe hypermagnesemia: stop the Mg source, IV calcium gluconate (antagonist), fluids +
diuretic, dialysis if needed.

5.4 Sodium (Na■)

[i] Important note on sodium & the ECG

Unlike potassium/calcium, sodium disturbances generally do not produce characteristic ECG
changes. The main clinical impact is neurological (confusion, seizures, coma), not
electrocardiographic.

Condition Main manifestations Correction principle (mind the rate!)

Severe symptomatic: 3% NaCl 100–150 mL IV

Hyponatremia (Na Nausea, headache, confusion,
(may repeat). Correct ≤8–10 mEq/L per 24 h
<135) seizures if severe/acute
(prevent ODS).

Hypernatremia (Na Thirst, lethargy, irritability, Replace the free-water deficit slowly; lower Na
>145) seizures ≤10–12 mEq/L per 24 h (prevent cerebral edema).

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 [!!] Sodium correction warning
The rate of correction is more dangerous than the absolute number. Too fast in hyponatremia →
osmotic demyelination; too fast in hypernatremia → cerebral edema. Calculate the correction rate
and monitor serial sodium.

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 CHAPTER 6 · Other Important ECG Abnormalities
Hypertrophy, bundle branch block, pericarditis, PE, and more

6.1 Hypertrophy / Chamber Enlargement

• LVH: Sokolow-Lyon S(V1)+R(V5/V6) >35 mm; often + strain (lateral ST depression/T inversion).
• RVH: right axis deviation, dominant R in V1.
• Left atrium: wide notched P in II (P-mitrale); right atrium: tall peaked P (P-pulmonale).

6.2 Bundle Branch Block

Figure 13. RBBB (rSR' pattern in V1) and LBBB (broad notched R in V6).

• RBBB: QRS ≥0.12 s, rSR' pattern ('rabbit ears') in V1, wide S in I & V6.
• LBBB: QRS ≥0.12 s, broad notched R in I/V6. New LBBB + ischemic symptoms ≈ STEMI.

6.3 Pericarditis & Long QT

Figure 14. Pericarditis (diffuse concave ST elevation + PR depression) and Long QT.

• Acute pericarditis: diffuse concave ST elevation in many leads + PR depression; distinct from
STEMI, which is localized with reciprocal changes.
• Long QT: congenital/acquired (drugs, hypokalemia/hypomagnesemia/hypocalcemia) → Torsades
risk.

6.4 Pulmonary Embolism

[i] ECG patterns in pulmonary embolism

Most often just sinus tachycardia. The classic S1Q3T3 pattern is not sensitive. There may also be
new RBBB, anterior T inversion, and signs of right ventricular strain. The ECG helps but does not
rule out pulmonary embolism.

6.5 Digoxin Effect, WPW, and Brugada

• Digoxin effect: 'scooped' ST depression, shortened QT. Distinguish this from digoxin toxicity.
• WPW: short PR (<0.12 s) + delta wave + wide QRS; risk of tachyarrhythmia.

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• Brugada: 'coved' ST elevation in V1–V2 + partial RBBB; risk of sudden cardiac arrest — refer to a
cardiologist.

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 CHAPTER A · Appendix — Emergency Drug Dose Summary
Quick reference; always verify against local protocols

A. Cardiac Arrest & Arrhythmia (ACLS)

Drug Indication Dose & administration

Epinephrine VF/pVT, PEA, asystole 1 mg IV/IO every 3–5 min

Refractory VF/pVT; Arrest: 300 mg IV bolus (repeat 150 mg). Stable VT: 150
Amiodarone
stable VT mg /10 min

Lidocaine Amiodarone alternative 1–1.5 mg/kg IV; repeat 0.5–0.75 mg/kg (max 3 mg/kg)

Symptomatic
Atropine 1 mg IV every 3–5 min (max 3 mg)
bradycardia

Adenosine SVT (narrow QRS) 6 mg rapid IV → 12 mg → 12 mg, each with a saline flush

Magnesium
Torsades de Pointes 1–2 g IV over 15 min
sulfate

Dopamine Refractory bradycardia 5–20 mcg/kg/min titrated infusion

B. Acute Coronary Syndrome

Drug Dose Administration/notes

Aspirin 160–325 mg loading; 75–100 mg/day Chewed at onset

Clopidogrel 300–600 mg; 75 mg/day Oral

Ticagrelor 180 mg; 90 mg twice daily Not with fibrinolysis

SL 0.4 mg every 5 min (max 3×); IV 5–10

Nitroglycerin Avoid in hypotension/RV infarct/PDE-5
mcg/min

Enoxaparin 1 mg/kg SC every 12 h Adjust for renal function

Morphine 2–4 mg IV for refractory pain Monitor breathing/BP

Atorvastatin 40–80 mg/day High-intensity statin

C. Electrolyte Disturbances
Condition Key therapy Dose

Hyperkalemia Calcium gluconate 10% 10 mL IV /5–10 min (membrane stabilization)

Insulin + dextrose 10 U regular insulin IV + 25 g dextrose

Salbutamol nebulizer 10–20 mg

Oral 40–100 mEq/day; IV ≤10 mEq/h peripheral

Hypokalemia KCl
(monitor)

Hypocalcemia Calcium gluconate 10% 10–20 mL slow IV (symptomatic)

Hypomagnesemia/To
Magnesium sulfate 1–2 g IV over 15 min
rsades

Severe hyponatremia 3% NaCl 100–150 mL IV; correct ≤8–10 mEq/L/24 h

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 [*] Closing
Skill in reading ECGs grows from repeated practice with a systematic approach, always linking
findings to the patient's clinical condition. Use this guide as a framework, then enrich it with
hands-on mentoring and ECG practice banks. Verify every dose and intervention against the latest
official guidelines and your institution's protocols.

Prepared as a self-study learning resource. Principles follow the generally accepted AHA/ACLS, ESC, and PERKI guidelines. Not a
substitute for official guidelines.

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