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Hemiblocks (Fascicular Blocks) on ECG

Hemiblocks (Fascicular Blocks): A Practical ECG-Based Guide Hemiblocks refer to conduction delays or blocks in one of the fascicles of the left bundle branch. The left bundle divides into two main fascicles—anterior and posterior—so involvement of one results in a left anterior hemiblock (LAHB) or left posterior hemiblock (LPHB). When two conduction pathways are involved simultaneously, the pattern is termed a bifascicular block. Recognition of these patterns on ECG is clinically important because they often reflect underlying structural heart disease and may predict progression to higher-degree atrioventricular (AV) block. Left Anterior Hemiblock (LAHB) Left anterior hemiblock is the most common fascicular block. It occurs due to delayed conduction through the left anterior fascicle, with impulses traveling preferentially down the posterior fascicle and then upward and leftward through the myocardium. Key ECG features Left axis deviation (usually −45° to −90°) Small q waves in leads I...

Acute Treatment of Hyperkalemia

Acute Treatment of Hyperkalemia – A Practical, Bedside-Oriented Guide Hyperkalemia is a potentially life-threatening electrolyte abnormality that demands prompt recognition and decisive management. The danger lies not only in the absolute potassium value but in its effects on cardiac conduction, which can rapidly progress to fatal arrhythmias. Acute treatment focuses on three parallel goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing excess potassium from the body. Understanding this stepwise approach helps clinicians act quickly and rationally in emergency settings. Why Hyperkalemia Is Dangerous Potassium plays a key role in maintaining the resting membrane potential of cardiac myocytes. Elevated serum potassium reduces the transmembrane gradient, leading to slowed conduction, ECG changes, ventricular arrhythmias, and asystole. Importantly, ECG changes do not always correlate with potassium levels, so treatment decisions should be based on clinical c...

Myocardial Infarction Locations and ECG Leads

  Understanding Myocardial Infarction Locations and ECG Leads Myocardial infarction (MI) occurs when blood flow to a part of the heart muscle is abruptly reduced or completely blocked, leading to myocardial ischemia and necrosis. The 12-lead electrocardiogram (ECG) remains the fastest, most accessible, and most important initial investigation for localizing the infarct territory, identifying the culprit coronary artery, and guiding urgent management. Correct interpretation of ECG leads in relation to myocardial anatomy is therefore a core clinical skill for doctors and medical students. Basic Concept: ECG Leads and Myocardial Walls Each ECG lead views the heart from a specific electrical angle. ST-segment elevation, T-wave inversion, or pathological Q waves in a group of contiguous leads indicate injury to the myocardial wall “seen” by those leads. The left ventricle is conventionally divided into anterior, septal, lateral, inferior, and posterior walls, each supplied by characteri...

2025 AHA Guidelines for Primary PCI in STEMI

  Indications of Primary PCI in STEMI Patients (2025 ACC/AHA Guideline) Primary percutaneous coronary intervention (PCI) remains the preferred reperfusion strategy for patients presenting with ST-elevation myocardial infarction (STEMI), provided it can be performed in a timely and appropriate setting. The 2025 ACC/AHA guidelines classify indications for primary PCI based on symptom duration, hemodynamic status, and ongoing ischemic risk. Understanding these classes helps clinicians make rapid, evidence-based decisions in acute coronary care. CLASS I INDICATIONS (Procedure Recommended) Primary PCI is strongly recommended when clear benefit outweighs risk. STEMI with symptom onset less than 12 hours Patients presenting within 12 hours of symptom onset derive the greatest mortality and morbidity benefit from immediate reperfusion. Primary PCI should be performed as soon as possible, ideally within guideline-recommended door-to-balloon times. Acute coronary syndrome with cardiogenic sh...

ECG and Left Ventricular Aneurysm

ECG and Left Ventricular Aneurysm Left ventricular (LV) aneurysm is a late mechanical complication of transmural myocardial infarction, most commonly following an anterior wall STEMI. Recognizing its characteristic ECG pattern is crucial because it can closely mimic acute STEMI and may lead to unnecessary thrombolysis or cath lab activation if misinterpreted. What Is a Left Ventricular Aneurysm A left ventricular aneurysm is a thin, scarred, dyskinetic segment of myocardium that bulges outward during systole. It usually develops weeks after a full-thickness myocardial infarction due to replacement of necrotic myocardium with fibrous tissue. ECG Changes in Left Ventricular Aneurysm The ECG findings are distinctive and relatively stable over time. Distribution of ECG Changes ECG abnormalities are most commonly seen in the precordial leads, especially V1 to V6, reflecting involvement of the anterior wall. Inferior lead involvement (II, III, aVF) is uncommon unless the aneurysm involves th...

Indications of left atrial appendage (LAA) device closure

Indications of left atrial appendage (LAA) device closure: Patients with non-valvular atrial fibrillation who have an increased risk of stroke (CHA₂DS₂-VASc score ≥2 in men or ≥3 in women) and are not suitable for long-term oral anticoagulation. Absolute contraindication to long-term oral anticoagulants: History of major or life-threatening bleeding (e.g., intracranial hemorrhage). Active bleeding disorder or high-risk bleeding lesion. Severe thrombocytopenia or advanced liver disease with coagulopathy. Relative contraindication or intolerance to oral anticoagulation: Recurrent clinically significant bleeding while on adequate anticoagulation. Poor tolerance or allergy to anticoagulants. Inability to maintain stable INR on warfarin. Poor adherence or inability to take long-term anticoagulant therapy. High bleeding risk despite indication for anticoagulation: HAS-BLED score ≥3 with anticipated long-term bleeding risk. Elderly patients with frequent falls or frailty where bleeding risk o...

Dilated Pulmonary Artery in Marfan syndrome

Dilated Pulmonary Artery in Marfan syndrome Overview Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the FBN1 gene, leading to abnormal fibrillin-1 and weakness of elastic tissues. Cardiovascular involvement classically affects the aorta, but dilation of the pulmonary artery (PA) is a recognized, though under-discussed, manifestation. Pulmonary artery dilation in Marfan syndrome reflects the same underlying medial degeneration that affects the aorta and can have diagnostic and prognostic significance. Pathophysiology The pulmonary artery wall, like the aorta, is rich in elastic fibers. In Marfan syndrome, defective fibrillin-1 results in: • Fragmentation of elastic fibers • Medial degeneration and cystic medial necrosis • Reduced tensile strength of the vessel wall Although pulmonary artery pressures are normally much lower than systemic pressures, chronic exposure to abnormal wall stress can still lead to progressive dilation. This explains w...