FELIquis ❤️👨🏻⚕️ retweeted
The most common causes of chronic AR include age-related degenerative changes and primary cusp pathology.
The RCC is frequently involved in cusp prolapse - possibly related to its anatomical support, being less closely associated with the fibrous central skeleton of the 🫀.
FELIquis ❤️👨🏻⚕️ retweeted
Pneumonia, hypotension, and large RV on bedside ultrasound. How to avoid the right sided death spiral?
drsmithsecgblog.com/pneumoni…
FELIquis ❤️👨🏻⚕️ retweeted
Wissen Sie, meine Frau und ich glauben nicht an Medikamente.
Deshalb hat sie das Amlodipin und Candesartan abgesetzt.
Der Körper heilt sich selbst.
Neurologe:
Ihre Frau hat eine Hirnblutung, ausgelöst durch einen nicht behandelten Bluthochdruck mit schweren Symptomen
FELIquis ❤️👨🏻⚕️ retweeted
FELIquis ❤️👨🏻⚕️ retweeted
Acute pulmonary edema. Why?
With a 2nd case also
drsmithsecgblog.com/acute-pu…
@PMcardioApp
FELIquis ❤️👨🏻⚕️ retweeted
SEVERE AORTIC STENOSIS: THE GRADIENT CAN BE MISLEADING
An aortic valve area ≤1.0 cm² suggests severe aortic stenosis (AS), but the mean gradient may be below 40 mmHg.
The gradient depends on blood flow, not just valve narrowing.
1. High-gradient AS
- AVA ≤1.0 cm²
- Mean gradient ≥40 mmHg
- Usually preserved or reduced LVEF
2. Classical low-flow, low-gradient AS
- AVA ≤1.0 cm²
- Mean gradient <40 mmHg
- LVEF <50%
- Stroke volume index ≤35 mL/m²
3. Paradoxical low-flow, low-gradient AS
- AVA ≤1.0 cm²
- Mean gradient <40 mmHg
- LVEF ≥50%
- Stroke volume index ≤35 mL/m²
4. Normal-flow, low-gradient AS
- AVA ≤1.0 cm²
- Mean gradient <40 mmHg
- LVEF ≥50%
- Stroke volume index >35 mL/m²
Why this matters: Low flow can conceal the hemodynamic severity of a stenotic valve. Discordant findings require careful assessment of Doppler measurements, blood pressure, flow state and valve anatomy.
In classical low-flow AS, dobutamine stress echocardiography can help distinguish true severe from pseudo-severe AS. CT aortic valve calcium scoring can help when severity remains uncertain.
Clinical pearl: Never grade AS using the valve area or gradient alone. Integrate AVA, mean gradient, peak velocity, stroke volume, LVEF and clinical context.
Reference: 2025 ESC/EACTS Guidelines for the Management of Valvular Heart Disease.
FELIquis ❤️👨🏻⚕️ retweeted
Intermittierende Dialyse oder CRRT zum Start auf der ITS?
ICRAKI (NEJM): abgebrochen.
Tod bis Tag 90: 63,1 % unter intermittierender Dialyse, 53,5 % unter CRRT. HR 1,30.
Der Abbruch kann die Größe überschätzen. Die Richtung gilt als belastbar.
#Intensivmedizin #Nephrologie
FELIquis ❤️👨🏻⚕️ retweeted
Bicaval view in a patient with ischemic heart disease. What is the structure in RAA? #echofirst
FELIquis ❤️👨🏻⚕️ retweeted
🫀 CardioNugget™:
WPW Risk Stratification:
Asymptomatic WPW pattern on ECG—what’s next? ⚡️
➡️ Exercise stress testing can non-invasively risk-stratify the accessory pathway.
🟢 Abrupt + complete loss of the delta wave with exercise = LOW-risk pathway
→ pathway cannot conduct rapidly at higher HRs
🔴 Persistent pre-excitation (or only gradual loss) = HIGHER-risk pathway
→ capable of rapid conduction → ↑ risk of malignant arrhythmias/VF
#CardioNugget #Cardiology #EP #WPW #MedEd
FELIquis ❤️👨🏻⚕️ retweeted
Patient with severe shock, what is the regionality of LV dysfunction shown here?
FELIquis ❤️👨🏻⚕️ retweeted
A known HTN found unconscious. Died just after 10mins of Hospital stay🥺🪦
What's the cause if death from EKG!?🚫💔
@TrackYourHeart @docakx @IhabFathiSulima @lacor_hospital @HeartAssociatn @kisubi_hospital
FELIquis ❤️👨🏻⚕️ retweeted
A patient with exertional dyspnea and a normal coronary angiogram.
Based on this intraoperative TEE, can you guess which cardiac surgical procedure is being performed? #echofirst #TEE #CardiacSurgery
FELIquis ❤️👨🏻⚕️ retweeted
19 yo man suddenly collapses while playing soccer and is found to be in ventricular fibrillation.
After resuscitation, the ECG shown below.
What's your take
FELIquis ❤️👨🏻⚕️ retweeted
"Zoom out" views commonly provide important complimentary information. Which effusions do you see in this apical 4-chamber view?
FELIquis ❤️👨🏻⚕️ retweeted
Meinungen? Opinions?
@MergencyFe darf nicht
@ecgandrhythmRoe @doc_ecmo @fbalex19071 @bordistef etc
No cardiac history. No specific cardiac complaints. 40y female. PMH Hypertension
🧵 10 HIGH-YIELD ICU PEARLS #002
Temporary Mechanical Circulatory Support in Cardiogenic Shock:
I’ve seen patients die despite temporary Mechanical Circulatory Support (tMCS). I’ve seen others die from complications related to it. And I’ve seen several who, in my opinion, are alive today because of it.
That has made me a believer in temporary MCS devices but deeply respectful of what happens when we get them wrong.
The first rule:
Define the shock phenotype before choosing the device.
Don’t put the cart before the horse.
1️⃣ Phenotype first
LV failure? RV failure? Bi-ventricular failure? Mechanical complication? Obstructive physiology?
The “strongest” device isn’t necessarily the right one.
PHENOTYPE → DEVICE
Not the other way around.
2️⃣ Impella = direct LV unloading
Impella moves blood: LV → ascending aorta
It reduces LV filling while providing forward flow.
The key concept isn’t simply: “More cardiac output.”
It’s: "Unload the failing LV".
3️⃣ Think in pressure-volume loops
As Impella support increases, the pump assumes more of the work of moving blood forward.
The LV PV loop generally shifts leftward:
↓ LV filling pressure/volume
↓ native LV stroke work
↓ pressure-volume area
↓ wall stress
A smaller native LV PV loop ≠ less systemic flow.
The LV does less work because the pump is doing part of it.
That’s LV unloading.
4️⃣ VA-ECMO is different
VA-ECMO provides powerful circulatory + respiratory support.
But peripheral VA-ECMO can bite you:
↑ LV afterload
↑ LV distension
↑ pulmonary congestion
Hemodynamic support ≠ LV unloading.
5️⃣ More support ≠ better support
Temporary MCS trades hemodynamic benefit for potential harm:
Bleeding. Vascular injury. Hemolysis. Thrombosis. Device complications. And I may be missing some...
The goal isn’t the biggest pump. It’s the right level of support for the shock phenotype.
6️⃣ Know DanGer Shock
In selected patients with STEMI-related cardiogenic shock, Impella CP + standard care reduced 180-day mortality: 45.8% vs 58.5% (the number needed to treat was 8)
But:
⚠️ Safety events: 24.0% vs 6.2% (the number needed to harm was 6)
⚠️ Renal replacement therapy: 41.9% vs 26.7%
The lesson isn’t: “Impella saves lives.”
It’s: Benefit comes with complications. Patient selection matters. A lot.
7️⃣ Don’t forget the RV
An LV support device cannot directly support an isolated failing RV. Impella also needs adequate blood reaching the LV.
Ask:
Can the RV provide enough preload for effective LV support? Ignore the RV and you may choose the wrong device.
8️⃣ Find the lesion
Think beyond “low EF.”
Before initiating LV support, ask whether the underlying lesion or physiology makes unloading ineffective or potentially harmful.
Find the lesion → understand the physiology → choose the support.
Cardiogenic shock is a hemodynamic syndrome, not an EF diagnosis.
9️⃣ Timing matters
Escalating vasoactives. Persistent hypoperfusion. Failure to clear lactate. Evolving end-organ dysfunction.
Ask: “Is the support actually working?”
A better cardiac index ≠ reversal of shock. If lactate isn’t clearing and end-organ dysfunction keeps worsening despite apparently adequate support, ongoing hypoperfusion may still be present.
The transition from hemodynamic → hemometabolic shock is ominous and increasingly difficult to reverse.
🔟 Have an EXIT strategy
Where are we going?
Recovery? Bridge to decision? Durable LVAD Transplant? Another temporary support strategy?
Temporary MCS should have a destination.
If none is realistic, that matters before support is initiated.
After years of watching temporary MCS succeed spectacularly -and fail miserably- my framework has become pretty simple:
SHOCK → PHENOTYPE → DEVICE → EXIT STRATEGY
Not:
SHOCK → BIGGER PUMP
#FOAMcc #FOAMed #MedEd



























