The duty doctor is NOT the night watchman for the hospital. If there are no patients waiting he will be asleep in his room. When a patient arrives, the nurse or the other Staff will knock or call and wake them up. That is the normal practice. Someone please tell this MLA.

World Heart Day (29/09/26) Today, let’s take a moment to prioritize the heart that keeps us going every day.🫀 #WorldHeartDay #HeartHealth #CardiovascularHealth #HealthyHeart

Fifth Universal Definition of Myocardial Infarction (2026) jacc.org/doi/10.1016/j.jacc.… 🫀 5th Universal Definition of MI is here! Types 1–5 are OUT ❌ IN: 3 clinical types 👉Primary, Secondary, and Procedure-related MI ⚖️ Sex-specific troponin cutoffs

Excellent video explaining cardiac axis determination

🫀 CardioNugget™: Before you push IV diltiazem for AF with RVR… Ask 3 questions: 1️⃣ Pre-excitation/WPW? → 🚫 AV nodal blockers → procainamide/ibutilide 2️⃣ Decompensated HFrEF/shock? → 🚫 negative inotropy → consider digoxin 3️⃣ Hypotension/AV block? → 🚫 diltiazem may make it worse Before dilt → ECG + EF + BP. #CardioNuggets #Cardiology #MedEd #CardioTwitter #FOAMed

Cardiac tamponade: ventricular interdependence Ventricular interdependence is the phenomenon in which the size, pressure, and filling of one ventricle influence the filling and function of the other because both ventricles share the interventricular septum and are enclosed within the relatively fixed pericardial space. In cardiac tamponade, this interdependence becomes exaggerated. During inspiration: - Increased venous return raises RV filling. - The RV expands and the interventricular septum shifts toward the LV. - LV filling falls, contributing to a marked inspiratory drop in systolic BP: pulsus paradoxus. During expiration, the septum shifts back toward the RV as LV filling increases. The pressure tracings demonstrate the same physiology: marked, reciprocal respiratory variation in right- and left-sided cardiac pressures. This exaggerated ventricular interdependence is a key hemodynamic feature of cardiac tamponade.

How different specialties act when called for a patient

People pay for what they do , and still more , for what they have allowed themselves to become and they pay for it simply by the lives they lead

Most Men: “I really want to retire my wife” Brothers, I’ve got some news for you. Wait for it…

ECG Diagnosis: Polymorphic Ventricular Tachycardia, consistent with Torsades de Pointes The ECG shows a wide-complex tachycardia with changing QRS morphology and a characteristic twisting appearance around the baseline, consistent with polymorphic ventricular tachycardia, specifically torsades de pointes. Torsades de pointes is associated with QT prolongation. Amiodarone can further prolong the QT interval and may worsen or perpetuate torsades. Acute management of torsades focuses on: 🟣 IV magnesium 🟣 Correction of hypokalemia and other electrolyte abnormalities 🟣 Withdrawal of QT-prolonging drugs 🟣 Defibrillation if the patient is unstable or the VT is sustained What about verapamil? This is where an important nuance exists. Verapamil is contraindicated in most forms of ventricular tachycardia and should not be given to an undifferentiated wide-complex tachycardia. It can cause profound hypotension and cardiovascular collapse. However, there is an important exception: fascicular ventricular tachycardia, also called idiopathic left ventricular VT or Belhassen VT. Fascicular VT is a rare idiopathic VT, usually occurring in younger patients without structural heart disease. It originates within the left ventricular fascicular system and can sometimes resemble supraventricular tachycardia with aberrancy. Unlike most VTs, fascicular VT is calcium-dependent and is characteristically responsive to intravenous verapamil. This led to the terms verapamil-responsive VT and Belhassen VT. Therefore, saying simply verapamil should never be used in VT would be incorrect. (Apologies for the poor formulation of the original question) 📸: Fascicular VT

Arrhythmias in pregnancy: what every clinician should know. A state-of-the-art review from JACC Clinical Electrophysiology highlights a growing challenge in maternal cardiovascular care. Thread 🧵

Elon Musk just measured your existence by how many times your atoms have been inside a dying star. Musk: “How many times have your atoms been at the center of a star? I think it’s like on average three or four times.” Every atom in your body has already survived the core of a star. Multiple times. Crushed under pressures that would flatten planets. Superheated to millions of degrees. Blown apart in explosions so violent they forged new elements. Then gravity pulled those scattered pieces back together. New stars formed. And the cycle repeated. For 13.8 billion years, your atoms have been fuel for the most violent process in the universe. And they are not done. Musk: “In terms of existence as measured by the number of times your atoms will be at the center of a star, we seem to be roughly halfway.” Halfway. Your atoms have been through the furnace three or four times. They will go through three or four more. But right now, in this impossibly thin sliver between cycles, those atoms are doing something they have never done before. They are conscious. For billions of years before you, they burned through stellar cores with no awareness. No memory. No sense of what they were or where they had been. After you, they will return to that state. Unconscious matter drifting through space until the next star claims them. This is the only moment in their entire journey where they can look back at the stars that made them and understand. Musk: “If you want to look at the big picture… that’s the really big picture.” The big picture is not that we are small. Everyone already knows that. The big picture is that we are temporary witnesses to a process that does not need witnesses. Stars do not need observers to burn. Atoms do not need anyone to understand where they have been. The universe ran for billions of years with no one in it. It will run for billions more after the last conscious thing disappears. But right now, matter is examining itself. That has never happened before in 13.8 billion years. You are not a person who happens to contain ancient atoms. You are ancient atoms that briefly figured out how to think. The universe did not design consciousness. It designed stars. Consciousness was the accident. And the accident is half over.

Benign early repolarisation (BER). A classic ECG masquerader, producing ST elevation that can look alarming, yet not necessarily indicating acute MI. BER is a usually benign ECG pattern, commonly seen in young, healthy individuals under 50, and is also known as high take-off or J-point elevation. Classic ECG features include: - Widespread concave ST elevation, most prominent in V2–V5 - J-point notching or slurring - Prominent concordant T waves - ST/T ratio in V6 < 0.25 (helpful in distinguishing from pericarditis) - No reciprocal ST depression, which argues against occlusive MI The diagnostic challenge is that BER can mimic acute MI or pericarditis, especially in emergency settings. However, caution is essential: in patients >50 years, particularly those with ischemic risk factors, ST elevation should not be casually labeled as BER until ischemia is excluded. Read more: litfl.com/benign-early-repol…

What is the procedure? What type of arrhythmia? Was it effective? What medication was put beside the patient?

TAPSE ● Measure of RV longitudinal systolic function (tricuspid annulus motion) ● Method: M-mode in apical 4-chamber at lateral tricuspid annulus. ● Key Cutoff > 17 mm → Normal ≤ 17 mm → RV dysfunction ● Severity 13–17 mm → Mild 10–13 mm → Moderate ≤ 10 mm → Severe 》Clinical pearl ● Always interpret TAPSE with other RV parameters, especially: ▪︎ RV S’ (TDI) ▪︎ FAC (Fractional Area Change) ▪︎ TAPSE/PASP ratio → useful for RV–pulmonary artery coupling

🫀Heart failure in 2026: we are no longer treating symptoms. We are redesigning the disease. The latest evidence update reminds us of something profound: Heart failure is no longer a single entity. It is a spectrum, and now, finally, we are treating it as one. Several paradigm shifts stand out. 1. SGLT2 inhibitors are no longer “add-on” therapy. They are foundational across the entire EF spectrum. From HFrEF to HFpEF, the data are now consistent. Not just symptom improvement, but hard outcomes. This may be the most important unifying therapy in modern HF. 2. HFpEF is no longer a therapeutic desert. For the first time, we have real disease-modifying options: Finerenone → outcome reduction across EF ranges GLP-1 / dual incretin therapies → targeting the obesity phenotype Structural and metabolic mechanisms are finally being addressed We are moving from “HFpEF frustration” → HFpEF phenotyping. 3. Acute heart failure is no longer about stabilization. It is about early transformation. The new paradigm: Start GDMT in-hospital Optimize rapidly Treat beyond congestion Decongestion is still important, but it is no longer the goal. Disease modification starts on day 1. 4. Decongestion is becoming precision medicine Urine sodium-guided therapy Early escalation of loop diuretics Sequential nephron blockade Not just “give furosemide”, but measure, adjust, and target response. 5. Devices are no longer rescue therapy, they are integrated care TEER expanding from mitral → tricuspid Pulmonary artery pressure monitoring reducing hospitalizations Remote hemodynamics shaping outpatient management The boundary between ICU, ward, and home is dissolving. 6. The biggest problem is no longer evidence. It is implementation. We already have: Quadruple therapy Proven outcome benefits Yet many patients never reach target doses. The gap is no longer science. It is execution. 🤓Final message Heart failure care has entered a new era: Mechanism-based therapy Early aggressive optimization Phenotype-driven treatment And perhaps most importantly: We are no longer chasing symptoms. We are altering the trajectory of the disease. 📃Reference Liori S, et al. Heart failure evidence update 2026. Heart Failure Reviews. 2026. doi.org/10.1007/s10741-026-1…

A heart being shocked back into regular sinus rhythm from ventricular fibrillation

The most likely diagnosis: VT. A wide QRS complex tachycardia (WCT) (rate >100 bpm, QRS >120 ms) should be treated as Ventricular Tachycardia (VT) until proven otherwise, as VT accounts for roughly 80% of cases and >90% in patients with structural heart disease. Misdiagnosing VT as Supraventricular Tachycardia (SVT) can lead to inappropriate, fatal treatments; hence, immediate assessment for hemodynamic instability and potential ACLS management is crucial Ventricular tachycardia signs😍 1. Fusion beat 2. Capture beat 3. Josephson's sign 4. Brugada sign 5. +Ve or -Ve Concordance 6. AV dissociation

Coronary Artery Branches on Angiogram Credit: medicalsnippet

The typical IV dose of fentanyl for cardiac chest pain is: A. 5–10 μg B. 10–20 μg C. 25–50 μg D. 100–200 μg