Dr. Usman's Cardiology Notes

  Diagnosis of Diabetes Mellitus: A Practical, Guideline-Based Approach for Clinicians Diabetes mellitus is a chronic metabolic disorder defined by persistent hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Accurate diagnosis is essential because early identification and timely intervention significantly reduce microvascular and macrovascular complications. This post outlines the diagnostic criteria, tests, and practical clinical considerations based on international guidelines. --- Diagnostic Criteria for Diabetes Mellitus According to widely accepted criteria from American Diabetes Association (ADA) and World Health Organization (WHO), diabetes can be diagnosed by any one of the following (confirmed on a separate day unless unequivocal hyperglycemia is present): 1. Fasting Plasma Glucose (FPG) Diabetes: ≥ 126 mg/dL (≥ 7.0 mmol/L) Prediabetes (Impaired Fasting Glucose): 100–125 mg/dL (5.6–6.9 mmol/L) Normal: < 100 mg/dL (< 5.6 mmol/L) Fast...

Hyperkalemia ECG changes (progressive with rising serum K⁺) Mild hyperkalemia (≈ 5.5–6.5 mmol/L) • Tall, narrow, peaked T waves (“tented” T) • Shortened QT interval • ST segment may appear flattened or absent Moderate hyperkalemia (≈ 6.5–7.5 mmol/L) • Progressive PR prolongation • P wave flattening → low amplitude P • Widening of QRS complex • Bradycardia may appear Severe hyperkalemia (≥ 7.5 mmol/L) • Disappearance of P waves • Markedly wide QRS • Sine-wave pattern (fusion of QRS and T) • Ventricular arrhythmias: VT, VF • Asystole / cardiac arrest Key electrophysiologic concept • Hyperkalemia reduces resting membrane potential → slows atrial, AV nodal, and ventricular conduction • Atrial myocardium is affected earlier than ventricular myocardium (early P-wave loss) Clinical pearls • ECG changes may not correlate perfectly with serum K⁺ level • Rapidly rising potassium is more dangerous than chronic elevation • Any ECG change = medical emergency → treat immediately, do not wait for lab...

  Brugada ECG Patterns: A Comprehensive, Clinically Oriented Guide Overview Brugada syndrome is an inherited cardiac ion-channel disorder characterized by distinctive ECG patterns in the right precordial leads and an increased risk of malignant ventricular arrhythmias and sudden cardiac death (SCD), often in structurally normal hearts. The ECG phenotype is dynamic and may be concealed, unmasked, or modulated by fever, drugs, and autonomic tone. --- ECG Patterns of Brugada Syndrome Type 1 (Diagnostic Pattern) Key features Coved ST-segment elevation ≥2 mm in ≥1 right precordial lead (V1–V3) Followed by a negative T wave J-point elevation with downsloping ST segment Clinical significance Only ECG pattern diagnostic of Brugada syndrome (when present spontaneously or induced by sodium-channel blocker) High arrhythmic risk, especially if spontaneous and associated with symptoms --- Type 2 (Suggestive Pattern) Key features Saddleback ST elevation ≥2 mm ST segment remains elevated ≥1 mm Po...

  Factors Affecting BNP Levels B-type natriuretic peptide (BNP) is released predominantly from ventricular myocardium in response to increased wall stress. Although widely used for diagnosis, prognosis, and treatment guidance in heart failure, BNP levels are influenced by multiple cardiac and non-cardiac factors. Understanding these modifiers is essential to avoid misinterpretation. Physiological and Demographic Factors Age BNP levels rise progressively with age, even in the absence of heart failure. Elderly patients may have “false-positive” elevations. Sex Women have higher baseline BNP levels than men, likely related to hormonal influences and myocardial gene expression. Body Mass Index Obesity is associated with lower BNP levels due to increased clearance by adipose tissue and reduced myocardial secretion. Normal BNP does not exclude heart failure in obese patients. Genetic Variability Inter-individual genetic differences affect natriuretic peptide synthesis, secretion, and deg...

PROPAFENONE — KEY POINTS (Class IC Antiarrhythmic) Mechanism Potent fast Na⁺ channel blocker Marked slowing of atrial & ventricular conduction Use-dependent effect (stronger at higher heart rates) Mild β-blocking activity Effect on Atrial Fibrillation Reduces multiple chaotic atrial wavelets Organizes AF → atrial flutter / atrial tachycardia Facilitates pharmacologic or electrical cardioversion ECG Effects ↑ PR interval ↑ QRS duration (rate-dependent) Little effect on QT (no significant AP prolongation) Aberrancy / Wide QRS Due to use-dependent Na⁺ channel block Causes functional bundle branch block at high rates QRS widens during tachycardia, narrows when rate slows Clinical Use Rhythm control in AF / SVT “Pill-in-the-pocket” strategy (selected patients) Important Precautions ❌ Avoid in structural heart disease ❌ Avoid in ischemic heart disease / LV dysfunction Always combine with AV-nodal blocker (β-blocker or diltiazem/verapamil) One-Line Memory Propafenone slows conduction, org...

 Pericardial Fat Pad Mimicking Cardiomegaly: Cause of Increased Cardiothoracic Ratio on Chest X-Ray Introduction An increased cardiothoracic ratio (CTR) on chest X-ray (CXR) is commonly interpreted as cardiomegaly. However, not all apparent cardiac enlargement reflects true cardiac pathology. One important and often overlooked cause is a pericardial fat pad, which can enlarge the cardiac silhouette without any increase in actual heart size. Recognizing this entity is essential to avoid misdiagnosis and unnecessary investigations. --- What Is a Pericardial Fat Pad? Pericardial fat refers to adipose tissue located: Epicardial fat: between the myocardium and visceral pericardium Paracardial (mediastinal) fat: outside the parietal pericardium When excessive, this fat can project over the cardiac borders on CXR, producing a falsely increased CTR. --- Why It Increases CTR on Chest X-Ray CTR is calculated as the ratio of maximal transverse cardiac diameter to maximal thoracic diameter (no...

Adenosine Response in Regular Narrow Complex Tachycardia (NCT) 🫀⚡ Regular narrow complex tachycardia (QRS < 120 ms) is most commonly due to supraventricular tachycardias (SVTs). Adenosine is both a diagnostic and therapeutic agent in this setting because of its transient AV nodal block. Understanding the ECG response to adenosine is crucial for accurate rhythm diagnosis at the bedside, emergency department, and EP lab. --- Mechanism of Action of Adenosine Adenosine acts primarily on A1 receptors in the AV node, leading to: Hyperpolarization of AV nodal tissue Transient complete AV block Very short half-life (≈ 10 seconds) This makes adenosine ideal for unmasking atrial activity or terminating AV node–dependent tachycardias. --- Why Adenosine Is Useful in Regular NCT In regular NCT, the differential diagnosis includes: AV nodal–dependent tachycardias Atrial tachyarrhythmias with rapid ventricular response Adenosine helps by answering one key question: Is the AV node essential for ma...