Acute cardiology

This article builds on the fundamental concepts of right-sided heart failure, including clinical features and diagnostic approach, which are covered in detail, available for further reading here : Right-Sided Heart Failure: Clinical Features, Causes, and Diagnosis Acute right ventricular (RV) failure is not just a diagnosis—it’s a rapidly evolving hemodynamic state where rising pulmonary resistance can lead to circulatory collapse within hours. Introduction Acute right ventr

Right-sided heart failure is a clinical condition in which the right ventricle fails to pump blood effectively through the pulmonary circulation, leading to systemic venous congestion and elevated central venous pressure (CVP). It is frequently under-recognized, yet it can result in significant hemodynamic compromise and multi-organ dysfunction if not identified early. Unlike left-sided heart failure, where pulmonary congestion dominates, right-sided failure is characterized

Cardiogenic shock is primarily a low-flow state . Critically reduced cardiac output may be present even when blood pressure appears normal due to compensatory vasoconstriction. In these situations, clinical assessment and echocardiography alone may not fully explain the physiology. Selective use of invasive hemodynamic monitoring with a pulmonary artery catheter (Swan–Ganz) or PiCCO can clarify the dominant mechanism and guide targeted therapy. Key principle:  In cardiogenic

A Practical, Physiology-Based Guide for Clinical Decision-Making In cardiogenic shock  and advanced heart failure , due to practical reasons, treatment often has to be guided without access to advanced invasive hemodynamic monitoring. In everyday clinical practice, central venous oxygen saturation (SvO₂/ScvO₂)  and central venous pressure (CVP) (apart from echocardiography and arterial line) are among the most readily available and frequently used clinical tools and parameter

How low cardiac output, elevated central venous pressure, and compensatory vasoconstriction shape treatment decisions in cardiogenic shock. (Part 2 in the Cardiogenic Shock series) Why This Article Is Necessary In Part 1 , we demonstrated how cardiogenic shock is frequently overlooked - particularly when blood pressure and early warning scores provide false reassurance. Many patients are already severely circulatory compromised long before hypotension develops. The goal of th

The shark-fin sign on ECG  is a rare but extremely high-risk electrocardiographic pattern seen in acute myocardial infarction. It is most commonly associated with left main coronary artery occlusion  or proximal LAD occlusion  and carries a very high risk of cardiogenic shock, malignant arrhythmias, and cardiac arrest. Because the ECG appears to show an extremely wide QRS complex , the pattern is frequently misinterpreted by automated ECG algorithms and clinicians , leading t

Acute occlusion of the left circumflex coronary artery (LCx) frequently causes transmural myocardial infarction without meeting classic STEMI criteria on the standard 12-lead ECG. This article explains why LCx infarctions are often misclassified as NSTEMI, illustrates a typical ECG pattern, and highlights key anatomical and electrophysiological principles that can prevent delayed revascularization. Prehospital ECG - standard leads Prehospital ECG - precordial leads Circumflex

Introduction Electrical storm and incessant ventricular tachycardia are life-threatening ventricular arrhythmias that require rapid, structured, and mechanism-based management. This practical clinical guide outlines a step-by-step approach to the assessment and treatment of electrical storm and incessant VT, based on current ESC, EHRA and AHA/ACC/HRS recommendations and real-world critical care experience. The article is written in collaboration with Dr Njord Nordstrand, Cons

Introduction Electrical storm and incessant ventricular tachycardia are among the most challenging conditions in acute cardiology, particularly in patients with structural heart disease and implanted cardiac devices. Rhythm diagnosis and selection of the correct treatment strategy can be difficult, and misclassification of arrhythmia may have serious clinical consequences. This case report describes the clinical course of a patient with ischemic cardiomyopathy and CRT-D, in w

Case Presentation An 80-year-old man was found confused and somnolent at home. On EMS arrival, his blood pressure was 73/46 mmHg and heart rate fluctuated between 25 and 50 beats per minute. The ECG demonstrated a wide-complex bradycardia (rate 26). Atropine had no effect. He received intravenous adrenaline. On hospital arrival, the patient appeared pale, cold and hypotensive, with clinical signs of pulmonary edema and acute kidney injury. His creatinine was 260 µmol/L with