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VT vs SVT Brugada Algorithm

  VT vs SVT With Aberrancy Brugada Algorithm Explained --- Introduction Wide complex tachycardia (WCT) is defined as a tachycardia with QRS duration ≥120 ms. The two most common causes are: • Ventricular Tachycardia (VT) • Supraventricular Tachycardia with Aberrancy (SVT-A) Distinguishing between them is critical because misdiagnosing VT as SVT can lead to inappropriate therapy and clinical deterioration. The Brugada Algorithm, introduced by Brugada et al. (1991), is one of the most widely used ECG methods to differentiate VT from SVT with aberrant conduction. --- Brugada Algorithm (Stepwise Approach) The algorithm consists of 4 sequential ECG questions. If the answer to any step is YES → Diagnose VT. If NO → Move to the next step. --- Step 1: Absence of RS Complex in All Precordial Leads Look at V1–V6. Check whether any lead has an RS complex. RS complex = an R wave followed by an S wave. If no RS complex is present in all precordial leads → VT This means the QRS complexes are eit...

Sacubitril/Valsartan Reduces Mortality More Than ACE Inhibitors in HFrEF

Sacubitril/Valsartan Reduces Mortality More Than ACE Inhibitors in HFrEF Introduction Heart failure with reduced ejection fraction (HFrEF) remains a major cause of morbidity and mortality worldwide. For decades, ACE inhibitors were the cornerstone of therapy because they reduce mortality and hospitalization. However, the development of angiotensin receptor–neprilysin inhibitors (ARNIs), particularly sacubitril/valsartan, has significantly improved outcomes. Large randomized trials have demonstrated that sacubitril/valsartan reduces mortality and heart-failure hospitalizations more effectively than ACE inhibitors, leading to major changes in heart-failure guidelines. --- Mechanism of Action Sacubitril/valsartan combines two pharmacologic mechanisms: 1. Sacubitril (Neprilysin inhibitor) Inhibits neprilysin enzyme Prevents breakdown of natriuretic peptides Leads to: Vasodilation Natriuresis Reduced cardiac remodeling Decreased sympathetic activity 2. Valsartan (ARB) Blocks angiotensin II ...

SVT with Aberrancy - Wide Complex Tachycardia

SVT with Aberration SVT with aberration refers to a supraventricular tachycardia conducted through the ventricles with abnormal intraventricular conduction, resulting in a wide QRS complex (>120 ms) on ECG. Although the rhythm originates above the ventricles, conduction delay in the His–Purkinje system makes it appear similar to ventricular tachycardia. Correct identification is crucial because misdiagnosing SVT with aberrancy as VT (or vice versa) can lead to inappropriate management. --- Mechanisms Wide QRS during SVT occurs due to abnormalities in ventricular conduction. 1. Pre-existing Bundle Branch Block A patient with baseline right bundle branch block (RBBB) or left bundle branch block (LBBB) may develop SVT, which will naturally appear as a wide-complex tachycardia. 2. Rate-Dependent Aberrancy At very fast heart rates, one of the bundle branches may still be in its refractory period, leading to temporary conduction delay. This is commonly called functional bundle branch bloc...

Criteria for Left Anterior Fascicular Block (LAFB)

Left Anterior Fascicular Block (LAFB) Left Anterior Fascicular Block (LAFB), also called left anterior hemiblock, is a conduction abnormality involving the anterior fascicle of the left bundle branch. It is one of the most common intraventricular conduction disturbances seen on ECG. LAFB alters the normal sequence of ventricular depolarization and produces a characteristic pattern of left axis deviation on the electrocardiogram. Recognition of LAFB is important because it may occur in otherwise healthy individuals, but it can also be associated with structural heart disease such as ischemic heart disease, cardiomyopathy, or degenerative conduction system disease. --- Anatomy and Pathophysiology The left bundle branch divides into two main fascicles: 1. Left anterior fascicle 2. Left posterior fascicle The left anterior fascicle is thin and long, making it more vulnerable to damage from ischemia, fibrosis, or degeneration. In LAFB, conduction through the anterior fascicle is blocked. As...

Valvular Heart Disease Modifies Diastolic Assessment Parameters

Valvular Heart Disease Modifies Diastolic Assessment Parameters Diastolic function assessment by echocardiography is an essential component of cardiovascular evaluation, particularly in patients with dyspnea, heart failure, or structural heart disease. Standard diastolic indices such as E/A ratio, E/e′ ratio, left atrial volume, and tricuspid regurgitation velocity are widely used to estimate left ventricular filling pressures. However, the presence of valvular heart disease significantly alters these parameters and may lead to misinterpretation if standard algorithms are applied without modification. Understanding how specific valvular lesions affect diastolic indices is therefore crucial for accurate hemodynamic interpretation. --- Mitral Annular Calcification (MAC) Mitral annular calcification is a degenerative process characterized by calcium deposition at the mitral annulus. It is commonly seen in elderly patients and those with chronic kidney disease, hypertension, and diabetes. ...

When a Patient Dies in the Cath Lab

  When a Patient Dies in the Cath Lab.  Most people never see what happens after a patient dies in the cath lab. The room eventually gets cleaned. The equipment is reset. Another case may already be waiting. But for the team who was there, the moment does not just disappear. Cath lab physicians, nurses, and technologists are trained to stay focused and move forward quickly. Yet the emotional weight of losing a patient can stay with the people in that room long after the procedure ends. This side of cath lab work is rarely discussed, but it is part of the reality of high-acuity cardiovascular care. When a patient dies in the cath lab, what does real support for the team look like in your lab? Debriefing? Peer support? Or simply moving on to the next case?

Mavacamten in Hypertrophic Cardiomyopathy (HCM)

  Role of Mavacamten in Hypertrophic Cardiomyopathy (HCM) Mavacamten is a first-in-class cardiac myosin inhibitor used in the treatment of symptomatic obstructive hypertrophic cardiomyopathy (HCM). It targets the underlying pathophysiology of the disease rather than only treating symptoms. --- Mechanism of Action In HCM, excessive interaction between actin and myosin leads to hypercontractility and impaired relaxation of the myocardium. Mavacamten works by: • Inhibiting cardiac myosin ATPase activity • Reducing actin–myosin cross-bridge formation • Decreasing hypercontractility of the left ventricle This leads to: • Reduction in LV outflow tract (LVOT) obstruction • Improvement in diastolic relaxation • Decrease in myocardial energy consumption --- Clinical Effects Mavacamten has been shown to: • Reduce LVOT gradient • Improve NYHA functional class • Improve exercise capacity (peak VO₂) • Reduce symptoms such as dyspnea and chest pain --- Key Clinical Trial The EXPLORER‑HCM trial d...