@Info_SerieA Kalau post ga julid gini enak bgt dibaca min sekaligus nambah wawasan, sering-sering min posting kayak gini, selang-seling sama postingan julid gapapa
@atleticos_indo@Qiqicampjamaica@Info_SerieA Ini lah sebenernya argumen ttg pakde carlo dan taktiknya yg paling baik yg menggambarkan dia bukan tipe manajer yg terlalu taktikal, jauh lebih bagus daripada argumen koci. Sampe @Info_SerieA cuma bales “Y” doang yg mungkin artinya setuju dgn argumen anda, good job bro 👍🏻
@mk_anam@NgLelang@SiaranBolaLive Paling bener kalau ngikutin usulan wenger, pemain baru dianggap offside kalau dia memiliki keuntungan mekanis akibat posisinya, misal sudah lebih dari separuh badan didepan bek atau seluruh telapak kaki sudah didepan bek. Kalau cuma kukunya doang yg didepan ga dpt keuntungan apa2
@garistengah_id@Info_SerieA Turki mainnya sama aja kayak sebelumnya, bedanya lawannya main lebih terbuka, dan pemain high profile turki lebih lepas juga, 2 match awal mainnya kayak sambil bawa beban berat harus main bagus
@AndikaNugroho_@JCIndonesia Setuju, sekarang kalau ketemu temen fans inter diajak adu banter saya langsung kicep iya iya aja malah temen saya jadi kasian kapok ngebanter juve lagi 🥹
🫀In cardiogenic shock, we still focus heavily on MACROcirculation:
📉 blood pressure
📉 cardiac output
📉 LVEF
📉 vasopressor dose
But what if the real battle is happening deeper?
🩸 At the microcirculatory level.
This excellent ATS viewpoint highlights one of the most important evolving concepts in shock physiology:
⚠️ normalization of macrocirculation does not necessarily mean restoration of tissue perfusion.
Despite advances in cardiogenic shock management, mortality remains >40%.
Even more striking, up to 45% of deaths occur in patients with normalized cardiac index.
That disconnect may be explained by persistent:
🩸 microvascular dysfunction
🩸 impaired capillary perfusion
🩸 endothelial dysfunction
🩸 tissue hypoxia despite “acceptable” hemodynamics
The review reinforces that: Microcirculation is not a passive bystander.
It may be a central driver of:
• organ dysfunction
• lactate persistence
• shock progression
• mortality
Particularly interesting is the emphasis on simple bedside tools.
We often think microcirculation requires advanced devices, yet:
📌 capillary refill time (CRT)
📌 mottling
📌 ΔPCO₂
📌 lactate trends
still carry strong prognostic value.
A CRT >3 seconds at ICU admission was associated with worse outcomes, and combining CRT with the CardShock score achieved an impressive AUC of 0.93 for outcome prediction.
The article also reviews modern technologies:
🔬 handheld vital microscopy
🔬 sublingual microcirculation imaging
🔬 NIRS
🔬 laser Doppler assessment
bringing “real time” bedside microcirculatory monitoring closer to clinical practice.
One of the strongest physiological messages:
⚠️ Shock is not only about flow. It is about effective tissue level oxygen delivery.
The review beautifully summarizes the four major mechanisms of microvascular dysfunction:
• heterogeneity
• hemodilution
• congestion
• edema
Particularly relevant for intensivists:
📌 venous congestion itself may worsen microvascular flow
📌 elevated filling pressures impair driving pressure
📌 edema increases oxygen diffusion distance
This is highly relevant in:
• advanced heart failure
• VA ECMO
• mixed shock states
• fluid overloaded patients
Another important takeaway: Persistent microcirculatory dysfunction after VA ECMO initiation was associated with increased mortality, even when macrocirculation improved.
Perhaps the key message of this paper is:
🩸 Microcirculation should no longer be considered a secondary endpoint in cardiogenic shock.
It may become one of the most important physiological targets of the next decade.
📖 Merdji H, American Journal of Respiratory and Critical Care Medicine. 2026, 212(3), 410–413 https://t.co/81Zp3aj274.
This state-of-the-art review provides a comprehensive overview of the pathophysiological mechanisms underlying the no-reflow/slow-flow phenomenon, covering invasive and non-invasive diagnostic tools, pharmacological and interventional treatment strategies, and the key clinical gaps that still need to be addressed in the field. https://t.co/glYW3u2X2z
🚨 ¿Cómo tratar la congestión en Insuficiencia Cardíaca Aguda (ICA)?
Un nuevo meta-análisis en el @EHJ_CardioPharma analiza 25 ensayos clínicos (7,149 pacientes) para darnos respuestas claras sobre las estrategias diuréticas. 🏥💊
🫀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. https://t.co/T4MVjK0vGd