Jj (@JjMDUS) profile picture

Trying to be a better doctor #FOAMed

Joined August 2023
Ever used the interfascial plane block (IPB) for shoulder pain? If not, you should consider it! 💉It targets the axillary nerve within the fascial plane between the deltoid and subscapularis muscles. Check out more via our newsletter! acep.org/emultrasound/newsro…
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EMCrit 437 - Massive Lithium Overdose with @NephroTox (tox + nephro in one human): -Gastric Decon -Who to dialyze -Why nephrologists are vampires and so much more! [#FOAMed for now} emcrit.org/437
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Wake up babe, there are now THREE types of delayed sequence intubation (DSI) Following the PREOXI trial, BiPAP preoxygenation has become standard in many ICUs. BiPAP allows patients to remain well recruited and oxygenated, even if they aren't awake and breathing hard. This opens up the door to a variety of types of delayed-sequence intubation. These techniques involve the same exact materials as a standard intubation, and similar medications. They represent ways to slow down the intubation process and proceed in a more stepwise fashion. This can be helpful for the physiologically challenging airway. [1] DSI-Oxygenation 🫁 Classic & most common type of DSI (what most people refer to when they say "DSI"). 🫁 This is fundamentally sedation to allow the patient to tolerate preoxygenation 🫁 Used for patients who are too agitated or anxious to tolerate BiPAP preoxygenation [2] DSI-Sedation 💉 Patient is placed on BiPAP and receives titrated doses of sedation to gradually promote unconsciousness. 💉 This is useful for patients who are hemodynamically tenuous, for two reasons. First, it minimizes the sedative dose to what you actually need (often very little, for sicker patients). Second, it allows you to observe how the patient responds to some sedation and positive-pressure ventilation. 💉 Sometimes BiPAP plus sedation will elicit severe hypotension! You have time to resuscitate the patient further before proceeding to paralysis and positive-pressure ventilation (which could make things worse). 💉 This could also be used for a patient with a history of being very difficult-to-sedate, because it allows you to be confident that the patient is unconscious prior to paralysis. [3] DSI-NPV (DSI to facilitate Negative Pressure Ventilation 🫀This is most often used for patients who are at the highest risk of hemodynamic collapse following positive pressure ventilation (e.g., severe PE, tamponade, refractory cardiogenic shock). It could also be useful in severe DKA (to maximize spontaneous minute ventilation post intubation). The goal is to preserve negative-pressure ventilation, which may improve hemodynamics and pCO2. 🫀You start out with DSI-Sedation as discussed above: initiate BiPAP and titrate sedatives to the point of unconsciousness. Follow hemodynamics and resuscitate further as needed. 🫀Then push rocuronium, intubate, then immediately give sugammadex to reverse the rocuronium. You end up with an intubated patient who is spontaneously breathing with negative pressure ventilation (e.g., on 5 cm of CPAP). 🫀This is one type of Hemodynamically Neutral Intubation as described by Weingart (the goal is intubation without perturbing hemodynamics). DSI-NPV is technically easier than an awake intubation. Unless you're insanely great at awake intubation, DSI-NPV will be easier and less likely to go sideways. #1/2, links in the next post.
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Pneumonia, hypotension, and large RV on bedside ultrasound. How to avoid the right sided death spiral? drsmithsecgblog.com/pneumoni…
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The following graphic illustrates four types of patient- ventilator interactions during the trigger phase. Can you identify them ?
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Increasing ST Elevation. MI ruled out. Must be pericarditis, right? drsmithsecgblog.com/increasi… @willyhfrick @PMcardioApp
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Read the latest Educational Pearl on The One CT You Should Get in Children!? at umem.org/educational_pearls/…
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Echo From Scratch | Post #36 Mitral Valve M-Mode: Learn the E and A Points At the mitral valve level, M-mode captures the rapid motion of the mitral leaflets with exceptionally high temporal resolution. The tracing typically includes the RV, interventricular septum, anterior and posterior mitral leaflets, posterior LV wall, and pericardium. The key landmarks 🟫E point The maximum early-diastolic opening of the anterior mitral leaflet. 🟨A point The late-diastolic opening produced by atrial contraction. 🟪C point Mitral leaflet coaptation during systole. Between E and A, the leaflets move toward each other during diastasis. ⭕EPSS: E-point to septal separation EPSS is the distance between the anterior mitral leaflet at its E point and the interventricular septum. In the appropriate clinical context, an increased EPSS can suggest: - LV dilatation - Reduced LV systolic function - Significant aortic regurgitation But EPSS is not a standalone measure of LV function. Modern echocardiography relies primarily on 2D/3D assessment and other validated measures for LV systolic function. ⭕ The A-C segment Normally, anterior leaflet motion from A toward C is relatively linear. A B bump / A-C shoulder may appear when LV filling dynamics are abnormal, including elevated LV end-diastolic pressure. A high-yield clue Fine fluttering of the anterior mitral leaflet during diastole is not considered normal. A classic cause is aortic regurgitation, where the regurgitant jet strikes the anterior mitral leaflet. The pattern to remember E = early filling A = atrial contraction C = closure EPSS = E-point to septal separation M-mode is particularly valuable here because it shows exactly when and how rapidly the mitral valve moves. Current echocardiography practice uses M-mode selectively and in conjunction with 2D imaging rather than as the primary method for routine chamber quantification.
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Replying to @argulian
Here is how I see it
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Read the latest Educational Pearl on Red flag symptoms after strangulation at umem.org/educational_pearls/…
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Is this OMI, Subendocardial ischemia, LVH, or some combination? You can see the results of an experimental PMcardio Queen of Hearts model for OMI mimics. drsmithsecgblog.com/is-this-… @PMcardioApp
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Critical Physiology Series #93 Catastrophic Antiphospholipid Syndrome A patient develops acute kidney injury, respiratory failure, neurological dysfunction and thrombocytopenia within days. Sepsis? DIC? TTP? Consider also catastrophic antiphospholipid syndrome (CAPS). Pathophysiology CAPS is a rare, life-threatening manifestation of antiphospholipid syndrome characterized by rapidly progressive thrombosis, predominantly affecting the microcirculation. Antiphospholipid antibodies, particularly those targeting β2-glycoprotein I, activate endothelial cells, monocytes and platelets. Antibody binding → complement activation → endothelial dysfunction → tissue-factor expression → thrombin generation Neutrophil extracellular traps and inflammatory mediators amplify thrombosis. The result: microvascular occlusion → tissue ischemia → organ dysfunction Unlike isolated venous thromboembolism, CAPS may simultaneously damage kidneys, lungs, brain, heart and other organs. Risk factors and triggers CAPS may develop in established APS or be its first manifestation. Important associations include: systemic lupus erythematosus, previous thrombosis and high-risk antiphospholipid antibody profiles. Common triggers: infection, surgery, trauma, pregnancy complications and interruption of anticoagulation. Diagnosis Suspect CAPS when thrombosis and organ dysfunction develop rapidly across multiple systems. Classical classification criteria include: ≥3 organs involved manifestations within approximately one week small-vessel thrombosis on histology positive antiphospholipid antibodies However, incomplete criteria do not exclude probable CAPS. Request: lupus anticoagulant anticardiolipin IgG/IgM anti-β2-glycoprotein I IgG/IgM Interpret testing cautiously during acute illness and anticoagulation. Differentiate CAPS from DIC, TTP/HUS, HIT and sepsis-associated microangiopathy. Monitoring Follow: platelets and hemolysis markers PT/aPTT, fibrinogen creatinine/urine output lactate and organ perfusion ECG/troponin/echocardiography neurological and respiratory function Management CAPS requires urgent multidisciplinary treatment, often before complete diagnostic confirmation. The conventional approach combines: Therapeutic heparin → suppress ongoing thrombosis High-dose corticosteroids → suppress inflammation Plasma exchange and/or IVIG → modulate pathogenic immune activity Treat the precipitating infection or other trigger. In SLE-associated CAPS, cyclophosphamide may be indicated. Refractory cases may require rituximab or complement inhibition with eculizumab in selected circumstances. Evidence remains largely observational because randomized trials are lacking. Recommended lectures 📚 Jacobs, 2024. doi.org/10.3390/antib1301002… Raschi, 2024. doi.org/10.1093/rheumatology… Legault, 2018. doi.org/10.1111/jth.14192 Kazzaz, 2016. doi.org/10.1097/BOR.00000000…
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EMCrit Explosion Wee - F/u with the 2026 ACEP Sedation Guidelines Authors -- A follow-up episode on the @ACEP sedation guidelines. [#FOAMed for Now] emcrit.org/emcrit/wee-sedati…
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Echo From Scratch | Post #40 Atrial Filling: Understanding the a, x, v and y Waves The atria act as conduits, transferring blood from the venous circulation to the ventricles. Doppler assessment of pulmonary venous and systemic venous flow provides insight into atrial function and cardiac hemodynamics. 1. Left atrial filling Pulmonary venous Doppler normally shows two forward-flow phases: - S wave: Predominantly during ventricular systole, when atrial relaxation and downward mitral annular motion promote LA filling. - D wave: During early ventricular diastole, as blood flows from the LA into the LV. - A-wave reversal: Brief backward flow into the pulmonary veins during atrial contraction. - V-wave effects: LA pressure rises during ventricular systole as the atrium fills. The pattern is influenced by mitral regurgitation and LA compliance. In healthy individuals, systolic and diastolic forward flow may be similar in magnitude, but their relative contributions vary with age, heart rate and loading conditions. 2. Right atrial filling Systemic venous Doppler, especially hepatic vein flow, reflects changes in RA pressure. - a-wave reversal: Associated with atrial contraction. - S wave: Forward flow toward the RA during ventricular systole, supported by atrial relaxation and downward tricuspid annular motion. - v-wave reversal: May occur as RA pressure rises late in systole. - D wave: Forward flow during early ventricular diastole as blood continues toward the RA and RV. These waveforms correspond broadly to the a, x, v and y components of the jugular venous pressure waveform. 3. What alters these patterns? - Atrial fibrillation: Loss of effective atrial contraction changes or abolishes the normal atrial reversal wave. - Mitral regurgitation: Can reduce systolic pulmonary venous forward flow or produce systolic flow reversal when severe. - Tricuspid regurgitation: Can cause prominent systolic hepatic venous flow reversal. - Ventricular diastolic dysfunction: Alters atrial pressure and venous filling patterns. - Elevated atrial pressure or reduced compliance: Changes the relative timing and magnitude of the waves. 4. Where do we record them? - Pulmonary venous flow: Apical four-chamber TTE, often targeting the right upper pulmonary vein. TEE can provide better visualization of multiple pulmonary veins. - Systemic venous flow: Hepatic veins from the subcostal window or SVC from the suprasternal notch. Key takeaway: Atrial filling Doppler is not just about identifying waves. Interpret the waveform alongside rhythm, valve regurgitation, ventricular function and filling pressures.
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Welcome to Short Clip Challenge week #117 What dynamic abnormality of the anterior mitral valve leaflet is shown obstructing the left ventricular outflow tract (LVOT) during systole? Click here to take the challenge pulmonarypocus.com/short-cli…
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Read the latest Educational Pearl on Tenecteplase Before Thrombectomy at 4.5 to 24 Hours for Basilar Artery Occlusion (ATTENTION LATE) at umem.org/educational_pearls/…
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50 something male with acute chest pain drsmithsecgblog.com/50-somet… @MagnusNossen @PMcardioApp
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Correct diagnosis: Sick sinus syndrome (sinus node dysfunction). ECG interpretation 1. Marked sinus bradycardia: Sinus P waves are present, but the atrial rate is very slow. 2. Junctional escape rhythm: When sinus impulses fail to arrive in time, impulses from the AV junction maintain ventricular activation. 3. AV dissociation: Sinus P waves and junctional QRS complexes occur independently, without a consistent P-QRS relationship. 4. RBBB: Abnormal ventricular depolarization due to delayed right ventricular activation. 5. LAFB: Left-axis deviation with a characteristic pattern in the limb leads. 6. Occasional conducted sinus beat: One P wave conducts to the ventricles, producing a ventricular capture complex. Why does this matter? Sinus node dysfunction is often caused by age-related fibrosis of the sinus node and surrounding atrial tissue. It can produce persistent bradycardia, sinus pauses, escape rhythms, dizziness, presyncope, or syncope. Clinical pearl: In an older patient with dizziness and profound sinus bradycardia, consider sinus node dysfunction. The combination of RBBB and LAFB also raises concern for significant conduction-system disease.
78 yo female with dizziness. What's your diagnosis?
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