Bence Jonas @jonbenaa

Anticoagulation Cheat Sheet

@MrMikeZappulla @IM_Crit_ Well, I tried to emphasise the importance of checking and correcting electrolytes first. But yeah, I cannot argue with the original post. 🙂

@IM_Crit_ Magnesium is not magic, but it is a low-risk fix when levels are low and a reasonable adjunct in AF management.

@IM_Crit_ New-onset AF is not a ‘give diltiazem first, ask questions later’ diagnosis. Check potassium and magnesium, look for congestion, and use POCUS when you can, because a patient with systolic dysfunction may crash after AV nodal blockade.

🚨 Mechanical complications of post-AMI are rare but lethal: 💜 Free-wall rupture: 0.01–0.5% → mortality ~90% (conservative) 🟤 Pseudoaneurysm: 0.1–0.3% → mortality 50% 🟠 Papillary muscle rupture: 0.01–0.05% → mortality ~80% Shock/Heart Team decision is key.

Coronary artery segment diagram

🫀 Not all aortic regurgitation is the same — and repair strategy depends on the mechanism Mechanism-based classification = tailored repair. 🔧 #Cardiology #CardiacSurgery #AorticRegurgitation #ValvularHeartDisease #CardioTwitter

Beta blockers and their unique advantage in certain conditions 🙌 📍 Propranolol - Thyroid storm - non-selective β blockade controls adrenergic surge (tachycardia, tremor, anxiety) + uniquely blocks peripheral T4→T3 conversion (no other beta-blocker does this) - directly reduces the most active thyroid hormone; lipophilicity + non-selectivity makes it the only beta-blocker with dual sympatholytic + antithyroid action 📍 Labetalol - Preeclampsia - combined α1 + β1 blockade - α1 blockade reduces peripheral vascular resistance (addresses the vasospasm driving hypertension in preeclampsia) + β1 controls maternal tachycardia; does not reduce uteroplacental blood flow unlike pure beta-blockers (β2 blockade avoided - no uterine vasoconstriction); safe fetal profile - preferred over other antihypertensives in acute severe hypertension of pregnancy 📍 Landiolol - AF/AFL rate control - half-life 3–4 minutes - instantaneous titratability; extreme β1 selectivity (255:1) - rate control without hypotension - critical in AF with sepsis/LV dysfunction where haemodynamic compromise is already present; inactive metabolites - no accumulation; heart rate returns to baseline within 30 minutes if stopped - safety net unavailable with any other beta-blocker

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Reading transmitral Doppler The transmitral inflow pattern is one of the most fundamental windows into left ventricular diastolic function, filling pressures, and relaxation physiology. After aortic valve closure, the LV begins to relax, but both valves remain closed during the isovolumic relaxation time (IVRT). During this phase, LV pressure falls rapidly without any change in ventricular volume. Once LV pressure drops below left atrial (LA) pressure, the mitral valve opens and ventricular filling begins. The first peak is the E wave (early diastolic filling). This represents passive LV filling, driven by the pressure gradient between the LA and the relaxing LV. In healthy young adults, E velocity is typically dominant because ventricular relaxation is efficient and suction is preserved. After the E-wave peak, flow slows as the LA-LV pressure gradient declines. This creates the deceleration slope, and the time from peak E to baseline is the deceleration time (DT), an important marker of LV compliance and filling pressure. A brief phase of minimal flow may follow: diastasis, where LA and LV pressures nearly equalize. The second peak is the A wave, generated by atrial contraction (atrial kick), which contributes to late ventricular filling. Key quantitative parameters from transmitral Doppler: 🛑E velocity: peak early filling velocity 🛑A velocity: peak atrial filling velocity 🛑E/A ratio: quick assessment of diastolic filling pattern 🛑IVRT: time from aortic valve closure to mitral valve opening; reflects LV relaxation 🛑DT (deceleration time): reflects LV compliance and filling pressure 🛑VTI (velocity-time integral): total blood flow contribution during filling 🛑DFP (diastolic filling period): duration of ventricular filling Clinical interpretation: - A reduced E wave with dominant A wave (E/A <1) often suggests impaired relaxation. - A very tall E wave with short DT may indicate elevated LV filling pressures and restrictive physiology. - A seemingly normal E/A ratio can be deceptive (pseudonormal pattern), this is why tissue Doppler and LA assessment matter. Transmitral Doppler is not just a waveform, it is a hemodynamic conversation between the left atrium and left ventricle. Ref: Otto Catherine clinical textbook

Your "normal" magnesium lab range was set in 1974. Updated data in the Journal of Nutrition estimates how many US adults fall below the magnesium threshold linked to chronic disease risk (serum Mg <2.06 mg/dL): - 67.8% of all adults - 66.6% of metabolically healthy adults - 68.5% with hypertension - 71.1% with CKD - 78.3% with diabetes The reference range hasn't been updated in 50 years.

📝Entendiendo el Acoplamiento Ventrículo-Arterial 🫀. 📜Notas cafeteras ☕️ 🔰El acoplamiento ventrículo-arterial es la traducción fisiológica entre contractilidad y perfusión: cuando se pierde, el corazón puede latir, la presión puede existir, pero la circulación deja de ser eficiente. 🫀El acoplamiento ventrículo-arterial (AVA) describe qué tan bien el ventrículo transforma su contractilidad en flujo efectivo frente a la carga arterial.📝La contractilidad del corazon está acoplada a una vasculatura capaz de recibir y distribuir el volumen sistólico con eficiencia.🫀 🔎La forma clásica de expresarlo es: 🫀VAC = Ea / Ees 📍➡️ Ea es la elastancia arterial efectiva ⏭️una aproximación de poscarga global. ➡️ Ees es la elastancia telesistólica ventricular ⏭️marcador de contractilidad relativamente menos dependiente de carga. ➡️Un acoplamiento cercano a 1 suele interpretarse como eficiente; cuando Ea/Ees aumenta, el ventrículo está trabajando contra una carga desproporcionada o con contractilidad deprimida. ⚠️ El AVA integra tres mundos que muchas veces evaluamos por separado: ●1. Corazón: contractilidad, volumen sistólico, fracción de eyección, reserva inotrópica. ●2. Arterias: resistencia vascular, compliance arterial, presión arterial, tono vasomotor. ●3. Perfusión: entrega de oxígeno, presión de perfusión, eficiencia energética y coherencia hemodinámica. ☝🏻🤓Debemos tener en cuenta que fracción de eyección puede engañar: en vasoplejía séptica puede verse “normal” o hiperdinámica aunque la contractilidad real esté deprimida; en poscarga alta puede verse reducida aunque el miocardio no esté primariamente fallando. ‼️ 🔰En choque séptico: ⚠️En sepsis suele haber desacoplamiento ventrículo-arterial por combinación de vasoplejía, cambios bruscos de poscarga, disfunción miocárdica séptica y alteración de la eficiencia energética. ☝🏻🤓El paciente puede tener gasto cardíaco aparentemente aceptable, pero con mala transferencia de energía, mala presión efectiva y perfusión tisular incoherente. ☝🏻🤓La pregunta que debemos hacernos no es solo: ¿Tiene buen gasto cardíaco? Sino: ¿Ese gasto cardíaco se genera con eficiencia y logra perfusión útil? 🔰En ventilación mecánica: ⏭️La presión positiva modifica el AVA al alterar retorno venoso, poscarga del VD, presión transpulmonar, poscarga del VI y gradientes de perfusión.☢️ Un PEEP excesivo puede mejorar oxigenación pero desacoplar el sistema cardiopulmonar si aumenta carga del VD o reduce precarga efectiva.‼️ ☝🏻🤓La ventilación protectora no debe evaluarse solo por PaO₂/FiO₂; debe integrarse con VTI, presión arterial, lactato, diuresis, VExUS y función VD-VI. 🔰AVA izquierdo vs derecho🫀 🫀El AVA izquierdo se centra en VI–sistema arterial sistémico. El VAC derecho, o acoplamiento VD–arteria pulmonar, evalúa si el VD puede adaptarse a la carga pulmonar. 🫁Es especialmente importante en SDRA, hipertensión pulmonar, embolia pulmonar, ventilación mecánica, shock séptico y posoperatorio cardiovascular. ☝🏻🤓Revisiones recientes destacan que el eje VD–arteria pulmonar es un marco fisiológico sólido para valorar pronóstico y falla circulatoria derecha. 🔰Evaluación práctica a pie de cama En clínica avanzada, el AVA puede estimarse con: 🫀Ecocardiografía: VTI del TSVI, volúmenes, FEVI, strain, TAPSE, S’, FAC, RV/LV ratio. 🫀Presión arterial invasiva: presión sistólica, diastólica, pulso, elastancia arterial dinámica. ⏭️Marcadores de perfusión: lactato, ScvO₂/SvO₂, diuresis, piel, ΔCO₂, mottling. ⏭️Congestión venosa: VExUS, presión venosa central contextualizada, Doppler hepático/portal/renal. 💎Perlas CAFETERAS ☕️ 💎1. La presión arterial no es perfusión. 🔎Un paciente puede tener PAM “aceptable” y AVA ineficiente, con bajo volumen sistólico y mala perfusión tisular. 💎2. La FEVI no equivale a contractilidad. 🔎La FEVI es altamente dependiente de carga. En vasoplejía, una FEVI alta puede esconder disfunción miocárdica. 👇🏽👇🏽👇🏽 continúa:

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That's pretty striking Reversal of amyloidosis cardiomyopathy in 3 individuals who had developed anti-ATTR amyloid antibodies nejm.org/doi/full/10.10… @NEJM @MariannaFonta11

Most people take melatonin right before bed. That might be one of the worst times to take it. Melatonin isn't a sedative, it's a chronobiotic. It doesn't knock you out. It signals to your circadian clock that it's dark. And the effect it has on your sleep timing depends entirely on WHEN you take it. There's a concept called the Phase Response Curve. It shows that melatonin taken ~3 hours before your usual bedtime produces the largest phase advance, meaning it shifts your internal clock earlier, so you fall asleep sooner and wake up easier. But take it AT bedtime? You can actually push your clock in the wrong direction. That's a phase delay. You end up falling asleep later over time, not earlier. The sweet spot sits just before dim light melatonin onset, the point when your brain would naturally start releasing melatonin. For most people, that's roughly 3 hours before habitual bedtime. Timing > dose. Lewy et al. (1998), Burgess et al. (2010), and Challet et al., J Pineal Res (2024).

Vitamin B12 is absorbed through two pathways. The first is intrinsic factor, a protein produced by parietal cells in the stomach. IF binds B12 in the small intestine and carries it across the gut wall via a receptor called cubilin in the distal ileum. This pathway is efficient but has a hard ceiling: it saturates at roughly 1.5 µg per dose. No matter how much B12 you swallow beyond that, IF cannot carry any more. The second pathway is passive diffusion. About 1 to 2% of any oral dose diffuses across the intestinal lining without IF, and this occurs along the entire length of the gut. At dietary doses, this pathway is negligible. At supplement doses, it becomes the primary route of absorption. Adams et al. (1971, Scand J Gastroenterol) measured whole body retention of radiolabeled cyanocobalamin at different doses. At 1 µg, roughly 50% was retained. At 5 µg, about 20%. At 25 µg, just over 5%. The NIH Office of Dietary Supplements reports approximately 2% absorption at 500 µg and 1.3% at 1,000 µg. The fraction drops dramatically. But the total amount absorbed keeps rising. At 1 µg you absorb about 0.5 µg. At 1,000 µg you absorb roughly 13 µg total, of which approximately 10 µg comes from passive diffusion alone. The RDA is 2.4 µg. Even the backup pathway, working at 1% efficiency, delivers more than four times your daily requirement from a single pill. This is the basis for high-dose oral B12 as an alternative to injections in patients who lack intrinsic factor. The NIH notes that high-dose oral supplementation "may be another treatment option" for pernicious anemia, though injections remain standard first-line therapy and the available randomized controlled trials comparing the two approaches are considered limited in quality. One important nuance: absorbing B12 into your bloodstream is only the first step. After absorption, B12 must bind to a transport protein called transcobalamin to reach your cells. This complex, holotranscobalamin, is the biologically active fraction. It represents only about 20 to 30% of the total B12 circulating in your blood. The remaining 70 to 80% rides on a separate protein called haptocorrin, which does not deliver B12 to most tissues. This is why serum B12 can be misleading as a status marker. A person can have a "normal" total serum B12 level while their holotranscobalamin, the fraction that actually delivers B12 to cells, is low. Methylmalonic acid is a more sensitive functional marker because it rises when cellular B12 is genuinely insufficient, regardless of what total serum B12 shows. Absorption determines how much B12 enters your blood. Transport determines how much reaches your cells. Testing only total serum B12 measures neither of these processes accurately. Adams et al., Scand J Gastroenterol, 1971 NIH Office of Dietary Supplements, 2024 Allen et al., J Nutr, 2018

Another surprisingly common 💊 medication side effect in the ICU: dexmetomidine (precedex) associated fever. - Occurs in 3-10% of patients on Precedex - higher risk with longer duration. - Most importantly it resolves within hours of stopping precedex journals.sagepub.com/doi/pdf/10.117…

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Your valves

@tmnaseem @IM_Crit_ However, yeah, prospective validation is favourable. I think we use dexme far more than we should. It’s good in masking the symptoms but the processes still running…

@tmnaseem @IM_Crit_ Retrospective studies are good. Every study is just as good as the data used. It’s a great option for hypothesis generation. Fast data collection, kind of high case numbers.

🚨 Cardio pearls you should never miss 6️⃣ The T wave in the ECG is a story about repolarisation not a random squiggle. When it inverts, something changed in the direction or timing of ventricular recovery. Let’s clear the confusion once for all & understand in depth. 1️⃣ Why is the normal T wave upright? ✔ Purkinje fibers are subendocardial in location. So: Depolarization → Endocardium → Epicardium Repolarization → Epicardium → Endocardium Epicardial cells: 🔻Shorter action potential duration 🔻Larger transient outward K⁺ current (Ito) 🔻Faster phase 3 repolarization Repolarization is a negative wave moving opposite depolarization → vector aligns with QRS. 👉 Upright T wave. 2️⃣ Subendocardial ischemia (early) Inner myocardium + Purkinje network suffer first. Ischemia causes: 🔻ATP depletion 🔻KATP channel opening 🔻Extracellular K⁺ accumulation 🔻Shortened action potential in ischemic zone 🔻Slowed Purkinje conduction ECG: → Tall, symmetric, broad-based T waves (Hyperacute phase) 3️⃣ Transmural ischemia Repolarization sequence reverses abnormally. Vector flips. → Deep, symmetric T-wave inversion Seen in: 🔻Evolving MI 🔻Wellens pattern 🔻Reperfusion Deep + symmetric + territorial + dynamic = ischemia until proven otherwise. 4️⃣ Hyperkalemia Global extracellular K⁺ elevation. ECG: 🔻Narrow, tented T waves 🔻Short QT Sharp, narrow spikes ≠ broad ischemic T waves. 5️⃣ Hypokalemia Delayed repolarization. ECG: 🔻Flat T waves 🔻ST depression 🔻Prominent U waves U waves help differentiate from ischemia. 6️⃣ CNS / Neurogenic T waves Catecholamine surge → myocardial stunning. ECG: 🔻Deep, diffuse T inversions 🔻QT prolongation 🔻Not vascular territory specific Distribution matters. 7️⃣ LVH & Strain Pattern This is not primary ischemia. It’s repolarization abnormality secondary to abnormal depolarization. In LVH: 🔻Increased myocardial mass 🔻Prolonged depolarization 🔻Delayed repolarization in hypertrophied wall ECG: ✔ High-voltage QRS ✔ Downsloping ST depression ✔ Asymmetric T-wave inversion (Usually lateral leads: I, aVL, V5–V6) Key point: Strain T waves are asymmetric, gradual downstroke + rapid return. Ischemic T waves are symmetric. 8️⃣ Cardiomyopathies Hypertrophic cardiomyopathy (HCM) 🔻Deep T inversions (often in precordial leads) 🔻May mimic ischemia 🔻Often associated with large voltages Apical HCM 🔻Giant negative T waves in precordial leads Dilated cardiomyopathy 🔻Nonspecific ST-T changes 🔻Often diffuse Mechanism: Structural remodeling alters repolarization gradients. Not vascular. Not dynamic like ACS. 9️⃣ Final Differentiation Framework ✔ Symmetric + territorial + dynamic → Ischemia ✔ Narrow tented + short QT → Hyperkalemia ✔ Flat T + U waves → Hypokalemia ✔ Diffuse deep T + long QT + neuro event → CNS ✔ High voltage + asymmetric lateral T inversion → LVH strain ✔ Giant precordial inversions + echo changes → HCM ✔ Stable V1–V3 inversion in young → Benign variant T waves reflect: • Repolarization timing • Potassium currents • Myocardial thickness • Conduction sequence • Autonomic tone If you understand vectors + ionic physiology, the ECG becomes logical. Electrophysiology > memorized patterns. (Ref: Marriott’s Practical Electrocardiography; Surawicz & Knilans) #MedTwitter #MedX #ECG #Cardiology

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Dr. Shiv_Kumar @Dr_Shiv_kumar_

5 months ago

🚨 Cardio pearls you should never miss 5️⃣ 1️⃣ Confused whether it’s VT or wide-complex SVT? Before jumping to algorithms, remember this: Some ECG findings are exclusively seen in Ventricular Tachycardia. If you spot them the debate ends.👇 2️⃣ 🔴 Features classically seen in VT

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Sunday ECG Academics Site of Origin in Ventricular Tachycardia : ECG Perspective DR. D.P. KHAITAN,MD (MEDICINE) FCGP(IND) FIAMS(MEDICINE) FICP FICCMD FIACM, Gayajee, Bharat @ecgandrhythmRoe @smithECGBlog @ecgchallenge @EcgOxford @medflutter_ Geographical mapping translates complex spatial data into understandable visuals , acting as a crucial tool for navigating how to reach to a particular place. It provides a path to arrive at the point of destination at a glance. A map is not the territory it represents , but if accurate , it maintains a point-to-point structural correspondence with the territory, whichaccounts for its usefulness. In a similar way , 12-lead surface ECG helps to localize the site of ventricular tachycardia (VT) , thereby enabling clinicians to guide its management. In ventricular tachycardia, the impulse writes its autobiography in the form of the QRS complex, and the ECG allows us to read the story of its origin. The ECG serves as a non-invasive electrophysiologic map, enabling clinicians to identify the anatomical origin of VT, guide management, assess prognosis, and plan catheter ablation when a necessity arises. Thus, the ECG functions as a non-invasive electrophysiologic mapping tool that helps localize the site of origin in ventricular tachycardia, directs therapeutic strategy, aids prognostic assessment, and facilitates procedural planning when intervention is required. 💢keypoints o Ventricular tachycardia (VT) represents an abnormal rapid rhythm arising from the ventricular myocardium, where electrical activation proceeds outside the normal His–Purkinje conduction system. As a result, ventricular depolarization follows an altered and slower pathway, producing characteristic changes in QRS morphology. o The shape, axis, and pattern of the QRS complex during VT are not random phenomena. Rather, they reflect the direction of impulse propagation as it spreads away from its site of origin. Since electrical activation moves centrifugally from its source, the surface ECG provides valuable spatial information regarding the location of the arrhythmic focus. o This principle forms the fundamental basis of ECG localization of VT. By careful analysis of bundle branch block morphology, frontal plane axis, precordial transition, and concordance patterns, one can determine whether the tachycardia originates from  Right ventricle or left ventricle  Septum or free wall  Apex or base  Outflow tract or inflow region o Understanding this relationship between electrical morphology and myocardial origin transforms the ECG from a simple recording tool into a powerful instrument VT localization Next.....

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