49 F ; HIV + , episodic dizziness : What’s the Mechanism ?@SergioPinski @KostekMilan @ecgrhythms @Frances98392343 @ecgandrhythmRoe @syamkumarmd

36 years old Male- Tobacco Chewer with episodes of chest pain ➖IRA ? @smithECGBlog @PendellM @amalmattu @DrRajeshG1 @ecgrhythms @The_Nanashi_O

Nothing special, but it keeps happening every now and then 🙂 This is a clip from a Holter ECG recording of an 84y/o woman with arterial hypertension. Would you mind taking a look and telling me what you see? What would you do in this situation?

Este es uno de los ECGs más peligrosos que podemos ver. Se trata de un varón de 60 años con molestia en el pecho y muy mal estado general de más de una hora de evolución. Qué prueba crees que no se puede retrasar?

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The IDSA recommendation is specifically a dilated ophthalmologic examination within the first week after diagnosis in nonneutropenic candidemia; it is a strong recommendation based on low-quality evidence. The guideline explicitly acknowledges that this was not based on randomized trials demonstrating benefit. The AAO reached the opposite conclusion: it does not recommend routine ophthalmology consultation solely because candidemia is present in an asymptomatic patient, citing the low frequency of definite endophthalmitis, inconsistent disease definitions, and lack of demonstrated outcome benefit from universal screening. The 2023 meta-analysis included 8,599 screened patients and estimated ocular candidiasis at 10.7% and concordant endophthalmitis-chorioretinitis with vitreous involvement at 1.8%. Importantly for our case, both TPN and C. albicans were associated with Candida endophthalmitis. And the controversy remains alive: a 2024 cohort found presumed chorioretinitis in 6% of examined patients, including asymptomatic patients, while a 2026 multicenter cohort found ocular candidiasis in 4.9% of examined patients; 60% of those cases were either asymptomatic or unable to report symptoms, and fundoscopy changed therapy in every identified case. However, that 2026 study was retrospective and explicitly notes that the clinical benefit of those treatment changes remains uncertain.

An elderly patient with dyspnea. Apical windows are technically difficult. A subcostal view is obtained. 1/2

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Pretty brave of ecgsource to code this as IVCD 🤦‍♂️

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ICU Controversies #001: A 68-year-old man with short bowel syndrome requiring chronic TPN is admitted to the ICU with septic shock. His central line is removed and antibiotic/antifungal therapy is started. Blood cultures grow Candida albicans. TTE shows preserved LV function, mild TR, and NO vegetations. He has no visual symptoms. Which consultation is most appropriate next? A. Cardiology for transesophageal echo B. Interventional radiology for tunneled central venous catheter C. Ophthalmology for dilated retinal examination D. Nothing else is needed What’s your answer? 👇 #FOAMed #FOAMcc #MedEd #medtwitter #idtwitter

What do you think about this rythm ⁉️⁉️⁉️ AVNRT AFL AT #ECG #Cardiology #MedicalEducation

A 37-year-old patient presents with abrupt onset of palpitations and marked tachycardia. The blood pressure is relatively preserved, and the following 12-lead ECG is obtained......ecgweekly.com/weekly-workout…

ECG Challenge: Regular wide-complex tachycardia at 150 bpm—is it VT or SVT with Aberrancy? 🫀 Comment your answer below and tell us which specific feature tipped you off! #draparnajaswal #cardiology #electrophysiology #fortisescorts #newdelhi #ECG #Quiz #Heart #Arrythmia

51F presents with acute chest pain & dyspnea (6h). Arrives in shock, hypotensive & hypoxemic. Provisional ED diagnosis: NSTEMI. ECG 1: Initial ECG 2: Post-treatment What’s your read, differential, and next management step? #CardioTwitter #MedTwitter #MedX

RT @Koichi16423232: SVTの鑑別とablation piped.video/_p-38tEO_y4?si=4lTp…

#ICU Visuals #001: Why does #thiamine deficiency cause lactate to rise? The entire physiology in one figure 👇

Answer: B. Cerebral arterial vasospasm, producing delayed cerebral ischemia (DCI). Neurologic deterioration occurs on day 6, the classic window for DCI after aneurysmal subarachnoid hemorrhage; it typically develops about 3–14 days after the bleed. New aphasia, gaze preference, facial weakness, and leg weakness indicate a focal ischemic deficit. Repeat CT shows no rebleeding, intraparenchymal hemorrhage, or hydrocephalus, making those alternative causes less likely. Nimodipine lowers the risk of DCI but does not eliminate it and does not reliably prevent angiographic vasospasm. Strictly, the clinical diagnosis is delayed cerebral ischemia due to symptomatic vasospasm; among the answer choices, cerebral arterial vasospasm is the best response.

#Thiamine in the ICU: 10 high-yield pearls 1. Unexplained lactate? Think thiamine. Thiamine is required for pyruvate dehydrogenase. Deficiency blocks conversion of pyruvate to acetyl-CoA, shunting pyruvate toward lactate and impairing mitochondrial aerobic metabolism. Thus, thiamine deficiency belongs in the differential diagnosis for otherwise unexplained lactic acidosis. 2. Thiamine deficiency in the ICU is not rare. ~30-70% of critically ill patients are thiamine-deficient. Many arrive deficient; others develop deficiency during critical illness because of increased metabolic demand, inadequate intake, or losses. 3. The bedside phenotype is more important than waiting for a thiamine level. High-risk situations include malnutrition, alcohol-related liver disease, bariatric surgery, renal replacement therapy, polyuria/DKA, chronic diuretic therapy, unexplained encephalopathy, unexplained lactate elevation, and sepsis. 4. Starting nutrition can unmask the deficiency. Glucose administration increases carbohydrate metabolism and thiamine utilization. A malnourished patient may therefore develop rising lactate after initiation of enteral/parenteral nutrition. Refeeding syndrome is not simply a phosphorus/potassium problem; thiamine deficiency can be central to its pathophysiology. 5. Dialysis and polyuria are major clues. Thiamine can be lost during continuous RRT, hemodialysis, and peritoneal dialysis. Renal losses also rise with polyuria, including the diuretic phase of AKI, post-transplant polyuria, DKA, and chronic diuretic therapy in heart failure. 6. Do not wait for the classic Wernicke's triad. Altered mental status, ocular abnormalities, and gait ataxia are rarely all present together. I think I have seen it only a few times. In an at-risk ICU patient with otherwise unexplained encephalopathy, absence of the complete triad should not reassure you. 7. A plasma thiamine concentration is not a great “rule-out” test. Testing is often unavailable and expensive, and blood concentration does not necessarily reflect tissue thiamine status. I don't even remember when I last ordered the test (if ever...). Erythrocyte transketolase activity is physiologically more informative, but its cutoffs are poorly defined. Just recognize the risk population and consider a therapeutic trial rather than wait for laboratory confirmation. 8. The sepsis data are more nuanced than “thiamine works” or “thiamine doesn't work.” Thiamine is not expected to improve hard outcomes in the overall septic-shock population. Some subgroup analyses and meta-analyses suggest signals for improved lactate clearance and organ function, particularly renal outcomes. I don't consider it a magic drug... 9. Thiamine alone ≠ HAT (hydrocortisone + ascorbic acid +thiamine) therapy. Do not interpret negative trials of HAT as proof that correcting thiamine deficiency is useless. Large HAT RCTs failed to demonstrate the dramatic clinical benefit initially claimed, and a VICTAS secondary analysis raised concerns about longer-term outcomes. That is a different question from replacing thiamine in a patient likely to be deficient. 10. The kidney may be an important target organ. Renal tubular cells are highly energy dependent. Across secondary analyses, observational data, and meta-analytic evidence, thiamine supplementation -particularly in deficient patients- shows a signal toward less AKI progression, better renal recovery, and less need for RRT, although individual RCTs have not consistently demonstrated significant benefit in unselected populations. Rule of thumb: “⬆️ lactate + risk factor + no good explanation" → think B1 deficiency” Especially think about it when you see malnutrition/refeeding, alcoholism/cirrhosis, dialysis, polyuria/DKA, chronic diuretics, unexplained encephalopathy, sepsis, or otherwise unexplained persistent hyperlactatemia. I usually include it in the admission orders for most of my ICU patients along with DVT and GI prophylaxis...! Thiamine deficiency behaves less like an obscure vitamin deficiency and more like a potentially reversible form of mitochondrial energy failure. Or that's how I like to think about it. #foamed #foamcc #meded

Severe CP with this EKG, What’d you do next? What’s the culprit? #OMI