Dr. Usman's Cardiology Notes

  ECG Predictors of Atrial Fibrillation Early Electrical Clues Before the First Episode Atrial fibrillation (AF) is often preceded by subtle electrical changes on the surface electrocardiogram. Recognizing these predictors helps clinicians identify high-risk patients, guide closer monitoring, and initiate early preventive strategies. --- 1. P-Wave Abnormalities The P wave reflects atrial depolarization. Structural and electrical atrial remodeling alters its morphology and duration. • Prolonged P-wave duration (>120 ms) suggests atrial conduction delay • Notched or bifid P wave (P mitrale) indicates left atrial enlargement • Low-amplitude or flattened P waves reflect atrial fibrosis Clinical relevance: Prolonged P-wave duration is a strong, noninvasive predictor of future AF. --- 2. P-Wave Dispersion P-wave dispersion is the difference between maximum and minimum P-wave duration across ECG leads. • Normal: <40 ms • Increased dispersion (>40–50 ms) indicates heterogeneous at...

Cornell Duration Product in ECG: Detailed, Practical Guide for Clinicians Left ventricular hypertrophy (LVH) is a key marker of chronic pressure overload and adverse cardiovascular outcomes. Among ECG-based criteria, the Cornell Duration Product (CDP) improves diagnostic accuracy by combining voltage with QRS duration, making it superior to voltage-only criteria in many clinical settings. Concept and Rationale Traditional ECG criteria for LVH rely mainly on QRS voltage, which is influenced by body habitus, age, and sex. The Cornell Duration Product incorporates QRS duration, reflecting both myocardial mass and conduction time. This integration enhances sensitivity for detecting true anatomical LVH. What Is the Cornell Duration Product The Cornell Duration Product is calculated by multiplying the Cornell voltage by the QRS duration. Cornell voltage is defined as: • S wave amplitude in lead V3 • Plus R wave amplitude in lead aVL Cornell Duration Product = [S(V3) + R(aVL)] × QRS duration ...

Evaluation of Syncope With Electrocardiographic Monitoring Syncope is a common clinical problem encountered in cardiology and general medicine, ranging from benign reflex causes to potentially life-threatening cardiac arrhythmias. Electrocardiographic (ECG) monitoring plays a central role in identifying arrhythmic causes of syncope, particularly when initial history, examination, and baseline ECG are non-diagnostic. The choice of monitoring strategy depends largely on the patient’s clinical risk profile and the frequency of syncopal episodes. Role of ECG Monitoring in Syncope The primary objective of ECG monitoring in syncope is to establish a symptom–rhythm correlation. Detecting bradyarrhythmias, tachyarrhythmias, pauses, or advanced conduction disease during a syncopal or pre-syncopal event can directly guide definitive management, including pacemaker implantation, catheter ablation, or antiarrhythmic therapy. Types of ECG Monitoring and Their Indications In-hospital (Telemetric) Mo...

AHA 2025 Guidelines – Acute Coronary Syndrome (ACS) Management – Key Points The 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes represents a major update to how clinicians diagnose and treat acute coronary syndromes, unifying previous STEMI and NSTEMI guideline documents into a single comprehensive evidence-based resource.  1. Unified ACS Guideline (STEMI + NSTEMI + UA) The 2025 guideline consolidates separate STEMI and NSTEMI guidance from 2013 and 2014 into one framework covering all presentations of ACS — unstable angina (UA), non-ST-elevation ACS (NSTE-ACS), and ST-elevation myocardial infarction (STEMI).  2. Early Evaluation and Initial Management Rapid assessment remains paramount: Immediate ECG and clinical risk stratification for patients with suspected ACS. Early initiation of appropriate antithrombotic therapy unless contraindicated.  3. Antiplatelet and Antithrombotic Therapy (DAPT) Dual antiplatelet therapy ...

  Brugada Syndrome – A Practical Clinical Review Definition Brugada syndrome is an inherited cardiac channelopathy characterized by a distinctive ECG pattern in the right precordial leads (V1–V3) and an increased risk of polymorphic ventricular tachycardia and sudden cardiac death, often in the absence of structural heart disease. --- Epidemiology More common in males (≈8–10:1) Higher prevalence in Southeast Asia Often presents in young to middle-aged adults Sudden cardiac death may be the first manifestation --- Genetic and Pathophysiology Most commonly linked to loss-of-function mutations in SCN5A Reduced inward sodium current (INa) Creates transmural voltage gradients in the right ventricular outflow tract Predisposes to phase 2 reentry and malignant ventricular arrhythmias --- ECG Patterns (Cornerstone of Diagnosis) Type 1 (Diagnostic) Coved ST-segment elevation ≥2 mm in V1–V3 Followed by a negative T wave Can be spontaneous or drug-induced Type 2 Saddleback ST elevation ST ele...

Normal ECG Changes During Pregnancy Pregnancy induces profound physiological changes in the cardiovascular system to meet the increased metabolic demands of the mother and fetus. These changes are reflected on the electrocardiogram (ECG) and are considered normal variants rather than pathological findings. Understanding these expected ECG changes is essential to avoid unnecessary investigations and misdiagnosis. Sinus Tachycardia An increase in resting heart rate is one of the most common ECG changes during pregnancy. Plasma volume expansion, increased cardiac output, and heightened sympathetic tone lead to sinus tachycardia. Heart rate may increase by 10–20 beats per minute, especially in the second and third trimesters, while maintaining normal P-wave morphology and sinus rhythm. Short PR Interval Pregnancy is associated with enhanced atrioventricular (AV) nodal conduction due to increased sympathetic activity. This may result in a mildly shortened PR interval on ECG. Importantly, th...

  Constrictive Pericarditis vs Restrictive Cardiomyopathy A Practical, Clinically Oriented Comparison Constrictive pericarditis (CP) and restrictive cardiomyopathy (RCM) present with remarkably similar clinical features—predominantly right-sided heart failure with preserved or near-preserved systolic function. Despite this overlap, the underlying pathology, diagnostic clues, and management strategies differ fundamentally. Accurate distinction is critical because constrictive pericarditis is potentially curable, while restrictive cardiomyopathy usually requires long-term medical therapy or advanced heart failure interventions. --- Pathophysiologic Basis Constrictive pericarditis is caused by a rigid, often thickened or calcified pericardium that limits diastolic expansion of the heart. Ventricular filling becomes abruptly halted in mid-diastole, leading to exaggerated ventricular interdependence and marked respiratory variation in intracardiac flows. Restrictive cardiomyopathy, in c...