Michel

Intensive care/Emergency medicine& POCUS enthusiast. Loving father. ... I am not ashamed of the gospel of Christ: for it is the power of God...Romans 1:16

[Ashley Miller @icmteaching]

Can chronic kidney disease give you a false-positive renal venous Doppler?

That is an important concern when using intrarenal venous flow as a marker of venous congestion.

Kondo et al. studied 228 patients with heart failure who had intrarenal venous Doppler, echocardiography and right-heart catheterisation performed within 24 hours.

29% had discontinuous intrarenal venous flow.

Those patients had higher:

• mean right atrial pressure
• mean pulmonary artery pressure
• pulmonary artery wedge pressure
The important finding was that this relationship persisted across different stages of chronic kidney disease.
In multivariable analysis, higher mean RAP, higher mean PAP and at least moderate tricuspid regurgitation were independently associated with discontinuous renal venous flow.

Why does this matter?

We already know that renal venous Doppler patterns are primarily markers of venous pressure transmission, not intravascular volume.

But a reasonable worry is that chronic renal disease might itself distort the intrarenal venous waveform and produce a “congested” pattern even when central venous pressures are not elevated.

This study is reassuring: abnormal intrarenal venous flow continued to track invasively measured haemodynamic congestion despite worsening CKD.

That does not mean every abnormal renal venous waveform equals high RAP, and it certainly does not mean “abnormal waveform = needs diuresis”.

But it strengthens the case that renal venous Doppler remains a useful haemodynamic signal even in patients with chronic kidney disease.

Key takeaway: CKD does not appear to make intrarenal venous Doppler uninterpretable. A discontinuous waveform still seems to reflect congestion rather than simply intrinsic renal disease.

Kondo K, Nishikawa T, Imai A, et al. Clinical Applicability of an Intrarenal Venous Flow Analysis for the Diagnosis of Impaired Hemodynamics regardless of the Chronic Kidney Disease Stage. Internal Medicine. 2026. DOI: 10.2169/internalmedicine.7559-26

@ThinkingCC @NephroP @ArgaizR @khaycock2

[NephroPOCUS @NephroP]

Estimating pulmonary artery pressures from trans-pulmonary valve Doppler 👇🏼
See thread below for 🔑 pitfalls.
#POCUS #Nephpearls #echofirst

[IMCrit @IM_Crit_]

Four hands for one line? Must be nice. Out here on the 3 am solo shift, I’m about one night away from holding the probe in my teeth...

[IMCrit @IM_Crit_]

I get why some of my ICU colleagues prefer working nights; fewer rounds, less bureaucracy, and a tighter-knit team. But no matter how you justify it, the biological reality catches up to you:

we’re dying one night shift at a time

[Leonardo Santos @Leo_Santo5]

🥴Abordaje y Manejo del Síncope

🔰📚N Engl J Med 2026

DOI: 10.1056/NEJMcp2517255

Enlace a Artículo Completo👇🏻🆓✅
https://t.co/xumUMHaxVK

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🦠🫀Septic shock is far more than vasoplegia.

For years, septic shock has been viewed primarily as a disease of profound vasodilation. While loss of vascular tone remains a hallmark, it is only one component of a much more complex syndrome.

This new review reminds us that septic shock is a multisystem failure involving the microcirculation, cellular metabolism, endocrine regulation, myocardial function, and autonomic nervous system. Treating blood pressure alone cannot fully restore tissue perfusion or cellular function.

One of the earliest abnormalities occurs within the microcirculation. Functional capillary density decreases, blood flow becomes highly heterogeneous, and endothelial injury with glycocalyx degradation increases vascular permeability and interstitial oedema. Interestingly, despite these profound microvascular abnormalities, extensive cellular necrosis is often absent. Instead, cells may reduce oxygen consumption through a protective "hibernation-like" metabolic response that preserves viability while limiting ATP demand.

The relationship between the macrocirculation and microcirculation also changes throughout sepsis. Early fluid resuscitation can recruit the microvasculature and improve perfusion, whereas excessive fluid administration later in the disease may worsen tissue oedema and further impair capillary blood flow. This helps explain why identical haemodynamic interventions can produce very different physiological responses depending on the timing of treatment. Bedside assessment of capillary refill time (CRT) remains a valuable dynamic marker of tissue perfusion, and personalised CRT-guided resuscitation has shown clinical benefit.

Beyond the circulation, septic shock induces profound bioenergetic dysfunction. Despite apparently adequate oxygen delivery, mitochondrial dysfunction limits ATP generation and shifts cells toward metabolic reprogramming. Endocrine disturbances, including relative vasopressin deficiency, impaired angiotensin II signalling, corticosteroid abnormalities, and the sick euthyroid syndrome, further contribute to haemodynamic instability.

Sepsis-induced cardiomyopathy adds another layer of complexity. Inflammatory mediators, oxidative stress, calcium dysregulation, mitochondrial dysfunction, and impaired β adrenergic signalling reduce myocardial contractility while decreasing responsiveness to both inotropes and vasopressors. Treatment therefore extends beyond increasing blood pressure and requires prompt source control, careful fluid management, vasopressors, and selective use of inotropes when hypoperfusion persists.

Reference 📚

Hunsicker, O., Schaller, S. J., & Singer, M. (2026). Pathophysiology of distributive shock in sepsis: Beyond vasoplegia. Intensive Care Medicine. Advance online publication. https://t.co/xClmEvjiLS

[Dr Ihab Suliman @IhabFathiSulima]

What is the diagnosis?

[SEIC - Sociedad Española de Imagen Cardíaca @ImagenCardiaca]

Repaso del #miniCASO Cardio RM #47
Defecto del séptum interauricular
🔎 https://t.co/GBiPzDB2E9 ◀️
Caso completo para Socios SEIC
¡Registro gratis!
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#aprendeconcasos

[Ahmed Ata @Ahmedata7777]

🫀 Pulmonary Vein PW Doppler: A Hidden Gem in Diastology

Pulmonary vein pulsed-wave Doppler provides valuable insights into left ventricular filling pressures, left atrial function, and mitral regurgitation severity.

📍 How to Perform Pulmonary Vein PW Doppler?

Thread 👇

[CardiovascularCorner @TrackYourHeart]

Hypertensive heart disease is far more than left ventricular hypertrophy. It is a systemic disorder that affects the heart, blood vessels, and peripheral tissues.

Its key features include:

⬜Aortopathy and accelerated coronary atherosclerosis.
🟥Left ventricular hypertrophy with progressive myocardial fibrosis.
🟪Left atrial remodeling (atrial myopathy), increasing the risk of atrial fibrillation.
🟦 Impaired skeletal muscle energy utilization, contributing to exercise intolerance.

These structural and functional changes interact over time, leading to major cardiovascular complications, including:

- Heart failure
- Cardiac arrhythmias
- Myocardial ischemia and infarction

Early recognition and aggressive blood pressure control can help interrupt this remodeling process before irreversible organ damage occurs.

Reference: Raman et al. Hypertensive Heart Disease.

[Edgar Argulian @argulian]

A patient with known heart failure admitted with another exacerbation. Why is it important to always pay attention?

[EchoTalk Echocardiography @echotalk]

Since everything starts with the measurement of the wave e´, that measurement must be reliable.

[JAMA @JAMA_current]

💡 JAMA Insights: Point-of-care ultrasound (POCUS) is an imaging modality that the 2025 American Thoracic Society Clinical Practice Guideline on CAP endorses as an acceptable diagnostic alternative to chest radiography for adults with suspected CAP at centers with appropriate clinical expertise.

#POCUS by trained clinicians is a guideline-endorsed alternative to chest #radiography for #pneumonia diagnosis, offering higher sensitivity and specificity, immediate results, and no ionizing radiation.

https://t.co/u6Y2zXOXJI

[RECAT👩🏽‍⚕️🏥👨🏽‍⚕️🇲🇽🫀 @LeslieMegom]

👩🏻‍⚕️☕️Hoy hablaremos de..☝🏻🤓Hiperlactatemia en sepsis y shock: una mirada metabólica renal
🔴El riñón como órgano metabólico del lactato...La pregunta moderna ya no es:¿Cuánto lactato tiene?
La pregunta correcta es:¿Qué mecanismo está produciendo este lactato?☝🏻🤓.
☕️👩🏻‍⚕️La hiperestimulación β-adrenérgica es una de las causas más frecuentes de hiperlactatemia en la sepsis hiperdinámica.
☕️👩🏻‍⚕️ La microcirculación puede permanecer alterada a pesar de una PAM normal y un gasto cardíaco adecuado.
☕️👩🏻‍⚕️La disfunción mitocondrial explica por qué algunos pacientes presentan lactato elevado aun con DO₂ aparentemente suficiente.
👩🏻‍⚕️ El lactato es un combustible metabólico fundamental para corazón, cerebro y riñón.
💎La lesión renal aguda disminuye significativamente el metabolismo y aclaramiento del lactato.
⚠️ Un lactato persistente debe hacer pensar en 3️⃣ escenarios: 1️⃣Microcirculación alterada.2️⃣Fracaso mitocondrial
3️⃣Reducción del aclaramiento hepatorrenal.
🔴La hiperlactatemia en sepsis no es sinónimo automático de hipoxia tisular. El lactato elevado puede reflejar una mezcla de hipoperfusión, hiperadrenergia, inflamación, disfunción mitocondrial, alteración hepática y, de forma muy relevante, cambios en el metabolismo renal.
🗞El artículo enfatiza que el riñón no solo “elimina” lactato: también lo utiliza como sustrato energético, lo convierte en glucosa y modifica su manejo durante el shock. de...Hiperlactatemia en sepsis: más allá de la hipoxia tisular🗞
☕️👩🏻‍⚕️La hiperlactatemia en sepsis representa la convergencia de alteraciones hemodinámicas, metabólicas y microcirculatorias. El riñón emerge como un actor central no sólo en la depuración del lactato, sino como un verdadero biosensor de perfusión sistémica.
🔴 La interpretación moderna del lactato exige abandonar la visión reduccionista de “hipoxia = lactato” y adoptar una estrategia multimodal basada en coherencia hemodinámica, monitoreo de la perfusión y evaluación dinámica de la función renal, donde el objetivo final no es normalizar el lactato, sino restaurar la entrega y utilización efectiva de oxígeno a nivel celular.✨️
🔺️Durante años se pensó qué:
🔰"Lactato elevado = hipoxia tisular = metabolismo anaerobio."🔰
👩🏻‍⚕️☕️Hoy sabemos que esta explicación es incompleta.
La evidencia contemporánea demuestra que la hiperlactatemia en sepsis es un fenómeno multifactorial donde intervienen:
🔸️Alteraciones microcirculatorias.
🔸️Estimulación β-adrenérgica.
🔸️Disfunción mitocondrial.
🔸️Reprogramación inmunometabólica.
🔸️Disminución del aclaramiento hepático y renal.
☝🏻🤓Por ello, el lactato debe interpretarse como un biomarcador de estrés metabólico y fracaso de la perfusión celular, no únicamente como un marcador de deuda de oxígeno. 🌀
☕️Para comprender es necesario entender ¿Cómo se produce el lactato?...
➡️Fisiológicamente:
🍬La glucosa se convierte en piruvato mediante glucólisis.
⏩️Cuando la velocidad de producción de piruvato supera la capacidad oxidativa mitocondrial, éste es transformado en lactato por la enzima lactato deshidrogenasa.
⏩️El lactato no es un producto de desecho.☝🏻🤓Es un importante:
🔺️Combustible metabólico.
▪️Sustrato gluconeogénico.
🔺️Vehículo de transferencia energética entre órganos.
👩🏻‍⚕️Actualmente se considera parte del denominado:
▪️Lactate Shuttle: El concepto de Lactate Shuttle fue desarrollado por el fisiólogo estadounidense George A. Brooks y revolucionó la comprensión del lactato➡️Antes se creía que el lactato era un simple producto de desecho generado durante la hipoxia.
☝🏻🤓Actualmente sabemos que:
El lactato es una molécula energética que transporta carbono y energía entre células, tejidos y órganos,donde corazón, cerebro, hígado y riñón utilizan lactato como fuente energética. ✨️
☝🏻🤓⚡️El riñón como órgano metabólico del lactato y participa de forma importante en el metabolismo del lactato mediante captación, gluconeogénesis renal y oxidación tubular, especialmente en la corteza renal. 👇🏽

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫀 The Most Dangerous Moment in the ICU May Last Less Than 60 Seconds

We often think of tracheal intubation as an airway procedure. Physiologically, it is a profound cardiovascular intervention.

Why Do ICU Patients Crash During Intubation?

The problem begins before the laryngoscope enters the mouth.

Many critically ill patients survive on a fragile compensatory state characterized by:
🔹 Endogenous catecholamine surge
🔹 Tachycardia
🔹 Vasoconstriction
🔹 Increased myocardial oxygen demand

What appears to be "stable" hemodynamics may actually represent physiological exhaustion.

The moment induction drugs are administered, this compensatory sympathetic drive disappears.

The result? A sudden reduction in:
• Systemic vascular resistance
• Cardiac output
• Coronary perfusion pressure
• Organ blood flow

This phenomenon has been termed adrenergic collapse.

Intubation Is a Hemodynamic Timeline

The authors propose viewing intubation as a sequence of cumulative threats rather than a single procedure:
1️⃣ Pre-induction adrenergic dependence
2️⃣ Sympatholysis after induction
3️⃣ Apnea, hypoxemia, hypercapnia, and acidosis
4️⃣ Transition to positive-pressure ventilation
5️⃣ Post-intubation ventilator and sedation effects

Each phase adds physiological stress.

Together, they can culminate in cardiovascular collapse.

The Propofol Question

One of the most clinically relevant findings is the growing evidence regarding induction agent selection.

In the INTUBE cohort, propofol was associated with a higher risk of cardiovascular collapse and was the only modifiable risk factor consistently identified.

The review therefore suggests:
✅ Ketamine
✅ Etomidate
as preferred induction agents in patients at risk of hemodynamic instability, while propofol should be used cautiously in shock states.

Positive Pressure Ventilation: The Forgotten Hemodynamic Challenge

Once the tube is secured, many clinicians relax.

The physiology is only beginning.

Positive-pressure ventilation:
🔹 Reduces venous return
🔹 Increases intrathoracic pressure
🔹 Raises right ventricular afterload
🔹 May precipitate right ventricular failure

This is particularly relevant in ARDS, pulmonary hypertension, pulmonary embolism, and severe hypoxemic respiratory failure.

Reference 📚

Kotani Y, Koroki T, Hayashi Y, Russotto V. The hemodynamics of tracheal intubation in critically ill patients: a narrative review. Journal of Intensive Care. 2026;14:42. DOI: 10.1186/s40560-026-00877-4.

[NephroPOCUS @NephroP]

Mechanism of Dynamic LV Outflow Obstruction and Associated MR.
From - PMID: 27687191
#POCUS #FOAMed #Nephpearls

[Rafael Melo @intensivaev]

New publication out!
For decades, hemodynamic management has centered on preload and fluid responsiveness. But as evidence linking fluid accumulation to worse outcomes grows, the conversation is shifting.
Our latest article explores the need for a more dynamic assessment of venous congestion and where critical care physiology may be heading next.
Special thanks to @azevedo_lcp and @edu_kattan for the partnership and contribution!

https://t.co/L0KZ6y0K39

[SEIC - Sociedad Española de Imagen Cardíaca @ImagenCardiaca]

Repaso del #miniCASO Eco #126
Enfermedad de Fabry
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Caso completo para Socios SEIC
¡Registro gratis!
👤 https://t.co/Ncdoce0EJG ◀️
#aprendeconcasos

[Critical Care Reviews @CritCareReviews]

Central Venous Pressure Revisited: Physiology, Pitfalls, Misconceptions, and Modern Clinical Interpretation in Critical Care 

CCR Journal Watch
https://t.co/Sp06oA6IDG

[NephroPOCUS @NephroP]

Hepatic vein Doppler waveform components explained.
#POCUS #VExUS #Nephpearls
🔗https://t.co/hgFLH8VM39