Patrick Sullivan @PSullivan000 - Twitter Profile

17 days ago

Can we predict right heart failure in #LVAD patients before it happens? New publication below! 🌟 #PVloop #Hemodynamics #PVloops #Heartfailure #MCS #Cardiology #Cardiotwitter #ICU #PeoplesVentricle #RHF #AHF

Steven Hsu @stevenhsu_md

17 days ago

Newly published: Low RV Ees/Ea predicts subsequent development of late right heart failure post LVAD better than basic RHC. Congrats to first author @OslerResidency SAR @lexiem515! And many thanks to our co-authors @Js08Paul & @RyanTedfordMD. https://t.co/iE06HbLWYE

stevenhsu_md's tweet photo. Newly published: Low RV Ees/Ea predicts subsequent development of late right heart failure post LVAD better than basic RHC. Congrats to first author @OslerResidency SAR @lexiem515! And many thanks to our co-authors @Js08Paul & @RyanTedfordMD.

https://t.co/iE06HbLWYE https://t.co/0C1GJIErCN

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Sara Inglis @SaraInglisMBBCh

about 1 month ago

#PVLoops to dive deep into hemodynamic biventricular interactions in #LVAD patients Thankful for opportunities to partake in this exciting work @MayoCVFellows

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Dr. Chacón-Lozsán F .'.

@franciscojlk

2 months ago

🫀Invasive monitoring is not dead. It was misunderstood For years Pulmonary artery catheters were abandoned “Too invasive” “No outcome benefit” But maybe the problem was not the tool...It was how we used it 🧐 *Hemodynamics is not a number. It is a trajectory This review reframes the concept Not a snapshot But a dynamic evolution After initial therapy The hemodynamic trajectory predicts outcomes 🫀 Clinical implication If you are not reassessing You are treating blindly *Phenotyping shock. The real power of invasive monitoring Cardiogenic shock is not one entity Cold and wet Cold and dry Warm and wet (SIRS-driven) Mixed shock 🫀 Clinical implication Same blood pressure Different physiology Different treatment *Normotensive shock. The silent killer One of the most important concepts Patients can have: Normal BP Normal lactate But low cardiac output 🫀 Clinical implication SvO₂ ↓ is often more sensitive than lactate Perfusion can be impaired before hypotension appears *PAC is not for everyone. But essential for some Routine use? No Targeted use? Absolutely Indications: • Overt cardiogenic shock • Unclear hemodynamics • Failure of initial therapy • Mechanical circulatory support 🫀 Clinical implication Use PAC when decisions matter most *Cardiac power output. The strongest prognostic marker CPO = MAP × CO / 451 It integrates pressure + flow 🫀 Clinical implication Low CPO = high mortality Better than CO alone *Right ventricle. The forgotten determinant RV failure changes everything Key markers: • CVP/PAWP ratio • PAPi • Pulmonary compliance 🫀 Clinical implication If you treat LV and ignore RV You will fail *Monitoring during mechanical support tMCS is not “set and forget” You need continuous adjustment Flow Preload Afterload RV-LV interaction 🫀 Clinical implication PAC transforms tMCS from support Into precision therapy *AI is coming. But physiology remains the foundation Hypotension prediction Shock phenotyping Outcome prediction But Garbage data → garbage AI 🫀 Clinical implication Good monitoring is the prerequisite for good AI 🤓Final reflection We moved from: Clinical exam → Non-invasive tools Now we must integrate Invasive + non-invasive + physiology Because monitoring does not save patients, Understanding does 🤓 📚 Baldetti L et al. Rev. Cardiovasc. Med. 2025; 26(6): 27034 https://t.co/tcTmhBNKC1

franciscojlk's tweet photo. 🫀Invasive monitoring is not dead. It was misunderstood

For years
Pulmonary artery catheters were abandoned

“Too invasive”
“No outcome benefit”

But maybe the problem was not the tool...It was how we used it 🧐

*Hemodynamics is not a number. It is a trajectory

This review reframes the concept

Not a snapshot
But a dynamic evolution

After initial therapy
The hemodynamic trajectory predicts outcomes

🫀 Clinical implication
If you are not reassessing You are treating blindly

*Phenotyping shock. The real power of invasive monitoring

Cardiogenic shock is not one entity

Cold and wet
Cold and dry
Warm and wet (SIRS-driven)
Mixed shock

🫀 Clinical implication
Same blood pressure
Different physiology
Different treatment

*Normotensive shock. The silent killer

One of the most important concepts

Patients can have:
Normal BP
Normal lactate

But low cardiac output

🫀 Clinical implication
SvO₂ ↓ is often more sensitive than lactate
Perfusion can be impaired before hypotension appears

*PAC is not for everyone. But essential for some

Routine use? No

Targeted use? Absolutely

Indications:
• Overt cardiogenic shock
• Unclear hemodynamics
• Failure of initial therapy
• Mechanical circulatory support

🫀 Clinical implication
Use PAC when decisions matter most

*Cardiac power output. The strongest prognostic marker

CPO = MAP × CO / 451

It integrates pressure + flow

🫀 Clinical implication
Low CPO = high mortality
Better than CO alone

*Right ventricle. The forgotten determinant

RV failure changes everything

Key markers:
• CVP/PAWP ratio
• PAPi
• Pulmonary compliance

🫀 Clinical implication
If you treat LV and ignore RV
You will fail

*Monitoring during mechanical support

tMCS is not “set and forget”

You need continuous adjustment

Flow
Preload
Afterload
RV-LV interaction

🫀 Clinical implication
PAC transforms tMCS from support
Into precision therapy

*AI is coming. But physiology remains the foundation

Hypotension prediction
Shock phenotyping
Outcome prediction

But Garbage data → garbage AI

🫀 Clinical implication
Good monitoring is the prerequisite for good AI

🤓Final reflection

We moved from:
Clinical exam → Non-invasive tools

Now we must integrate Invasive + non-invasive + physiology

Because monitoring does not save patients, Understanding does 🤓

📚 Baldetti L et al. Rev. Cardiovasc. Med. 2025; 26(6): 27034 https://t.co/tcTmhBNKC1

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Patrick Sullivan

@PSullivan000

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