Over several recent ECMO orientation shifts, I was reminded of how much the role changes when you are helping someone else orient.

At the beginning, I stay close to the center of the action. I demonstrate procedures, explain decisions, and guide things step by step.

As the orientee gains experience, that starts to shift. I step back more. They lead the workflow, and I watch the patient and the circuit. Eventually, my role becomes supervision. They do the work, and I become the safety net. That part takes discipline. The natural urge is to jump in and do it yourself. Good orientation means resisting that urge while still keeping the patient safe.

In this case, the orientees were already experienced ICU nurses, and over several shifts, it was easy to see their confidence grow. What I appreciate about ECMO orientation is that it often becomes shared discovery. They asked good questions, and not every answer was obvious. That gave us a chance to pause, look things up, and learn together.

I’ve been fortunate to work with physicians, nurses, and ECMO specialists who take time to teach. Being on the receiving end of that makes it easier to pass something along. In critical care, the goal is not to know everything. It is to protect the patient, stay curious, and keep learning. Some of those questions also led us back to the lab signs of hemolysis in ECMO patients, which I wrote more about in “Hemolysis on ECMO: What It Means at the Bedside.”

Learn more

For a deeper dive into becoming an ECMO Specialist, visit my website: ECMO 143: AI-Assisted Journey.

I built a Custom GPT, AI ECMO Educator. It is free to use and provides evidence-based ECMO and ECPR guidance for ICU clinicians and trainees, covering physiology, cannulation, anticoagulation, circuit management, and troubleshooting. Built on sources like ELSO, PubMed, AmSECT, and leading centers. Version 5.2 | Supports 50+ languages.

Disclaimer

This content is for educational purposes only and does not replace clinical judgment, institutional protocols, or consultation with your ECMO team.

To understand how blood moves through the heart, we can number the valves in the order in which the blood passes through them as it travels from the venous to the pulmonary and then to the arterial side.

The Sequential Order of Heart Valves

1. Tricuspid Valve: The first valve. It allows deoxygenated blood to flow from the Right Atrium into the Right Ventricle. Tri=3 leaflets for the valve

2. Pulmonary Valve: The second valve in the sequence. It opens to allow blood to be pumped from the Right Ventricle into the Pulmonary Artery on its way to the lungs. There are 3 leaflets for the pulmonary valve.

3. Mitral Valve (also called the Bicuspid Valve): After the blood is oxygenated in the lungs, it returns to the Left Atrium and passes through this third valve into the Left Ventricle. Bi (cuspid) = 2 leaflets for the valve.

4. Aortic Valve: The final valve. It opens to allow oxygen-rich blood to leave the Left Ventricle and enter the Aorta, which distributes it to the rest of the body. 3 leaflets for the aortic valve.

Two Quick Memory Tricks

Here are a few solid memory tricks to help you remember the right-to-left valve sequence

(Tricuspid → Pulmonary → Mitral → Aortic):

Bonus Valve Information

The Rule of Three

3 valves have 3 leaflets:

• Tricuspid

• Pulmonary

• Aortic

This design allows a wide opening for flow and tight closure under pressure.

The Mitral Exception

The Mitral valve has 2 leaflets.

It sits on the left side of the heart and handles the highest pressures (transvalvular).

It is supported by chordae tendineae and papillary muscles, which prevent it from prolapsing back into the left atrium.

Why This Matters at the Bedside

If you understand the sequence, you can troubleshoot faster.

Example:

• Pulmonary edema? Think Mitral or left side problem

• High CVP and congestion? Think Tricuspid or right side problem

• No pulse pressure on VA ECMO? Think Aortic valve not opening

Start with flow. Then find where it’s blocked or leaking.

Learn more

If you want more ECMO breakdowns like this, make sure you are subscribed to this newsletter, ECMO 143: AI-Assisted Journey. I’ll keep sharing what I’m learning along the way.

You can also use my free Custom GPT, AI ECMO Educator, an evidence-based ECMO and ECPR educator for ICU clinicians and trainees, covering physiology, cannulation, anticoagulation, circuit management, and troubleshooting. Sources include ELSO, PubMed, AmSECT, and leading centers. Version 5.2 (2/21/26) | Supports 50+ languages.

Both nursing and respiratory therapy backgrounds provide distinct, highly valuable skill sets that uniquely prepare clinicians for the role of an ECMO Specialist. While both professions work in high-stakes critical care environments, they approach the therapy from different foundational strengths.

The Nurse’s Advantage: Holistic Patient Management. Critical care nurses excel at comprehensive patient management and bring a distinct advantage in treating the body as a whole system. Their unique contributions include:

• Holistic Assessment: Nurses are trained to perform thorough head-to-toe assessments, allowing them to notice subtle changes, such as decreased urine output, mottling, or pupillary asymmetry, that may indicate underlying circuit or perfusion issues.

• Complex Pharmacology: ECMO patients require careful combinations of sedatives, paralytics, vasopressors, and anticoagulants. Nurses already understand how these complex medications interact, how to safely titrate them, and how to monitor for side effects.

• Line and Wound Care: Nurses are highly experienced with invasive lines (central lines, arterial lines, chest tubes) and sterile techniques. This translates directly to monitoring ECMO cannulas, securing sites, preventing infection, and managing localized bleeding.

• Hemodynamic Management: Nurses, particularly those from cardiac ICUs, are adept at walking the tightrope of balancing blood pressure and perfusion, which is crucial when managing circuit flow alongside a patient’s native cardiac function.

• Care Plan Execution and Family Communication: Nurses are experts at integrating the multidisciplinary care plan, including nutrition, skin care, and mobility, and serve as a crucial, compassionate bridge for families who are overwhelmed by the ECMO machinery.

The Respiratory Therapist’s Edge: Mastering the Mechanics. Respiratory therapists (RTs) bring an unparalleled expertise in gas exchange and cardiopulmonary mechanics, which form the core of what ECMO actually does. Their unique contributions include:

• Gas Exchange and ABG Mastery: RTs deal with gas exchange physiology daily. They can swiftly interpret arterial blood gas (ABG) panels, including pre-oxygenator and post-oxygenator gases, and immediately determine the appropriate interventions.

• Sweep Gas Management: The tasks of adjusting sweep gas to clear carbon dioxide and adjusting FiO₂ to optimize oxygenation mirror what RTs already do with mechanical ventilators. This gives them a major head start in manipulating the ECMO circuit’s artificial lung.

• Mechanical Ventilation and ECMO Integration: In VV ECMO, the goal is often to “rest” the lungs. RTs are uniquely skilled at balancing extracorporeal support and protective mechanical ventilation (e.g., low tidal volumes or minimal PEEP) to prevent lung trauma.

• Oxygenator Troubleshooting: When a patient desaturates, RTs naturally follow a methodical sequence to diagnose the issue (e.g., checking gas flow, FiO₂, or looking for clotting), mirroring how they troubleshoot a deteriorating patient on a ventilator.

Ultimately, becoming an ECMO specialist requires both professions to bridge their knowledge gaps. Nurses must deepen their understanding of circuit physics and advanced gas exchange, while RTs must expand their scope to encompass total-body hemodynamics, broad-spectrum pharmacology, and comprehensive patient care.

Learn more

If you want more ECMO breakdowns like this, subscribe to this newsletter, ECMO 143: AI-Assisted Journey. I’ll keep sharing what I’m learning along the way.

You can also use my free Custom GPT, AI ECMO Educator.
An evidence-based ECMO and ECPR educator for ICU clinicians and trainees, covering physiology, cannulation, anticoagulation, circuit management, and troubleshooting.
Sources include ELSO, PubMed, AmSECT, and leading centers. Version 5.2 (2/21/26) | Supports 50+ languages.

When your patient gets cold, hemoglobin holds onto oxygen tighter. Cooling shifts the oxyhemoglobin curve to the left, so at a given PaO2, you may see a higher SaO2, but less oxygen gets unloaded to the tissues. On ECMO, that means the “numbers” can look reassuring while perfusion and tissue oxygenation are not. If you’re fighting hypothermia, it’s worth thinking beyond the saturation and watching the whole picture: temperature, lactate trend, perfusion, and venous oxygen data if you have it.

Merry Christ-mas

• Cardiac stun is a reversible myocardial dysfunction. The heart is alive but temporarily unable to contract.

• It shows up on VA-ECMO as low EF, no pulsatility, poor MAP, and rising lactate.

• It happens because of ischemia–reperfusion, severe hypoxia, prolonged shock, and sudden afterload spikes when starting VA flows too fast.

• Cold prime and metabolic instability can worsen the picture — the problem isn’t Plasmalyte, it’s temperature and how fast I increase the ECMO flow.

• You resolve it by slow-controlled ECMO initiation, correcting metabolic problems, supporting perfusion, and letting the myocardium recover.

• The heart isn’t dead. It just needs time. ECMO gives it that time.

A few days ago, someone asked me a simple question:

“Hey Jon, what exactly is cardiac stun?”

I knew the usual bedside signs — weak squeeze, low stroke volume, almost no pulse pressure, lactate creeping up even with “good” circuit flow. But when I tried to give a clear, confident explanation, I realized I was only describing what it looks like, not what it is or why it happens.

So I went back, reviewed the physiology, double-checked the ECMO guidance, and asked my AI ECMO Educator GPT to help me tighten the concept. What came out is the version I wish I had ready in the moment, and the version I think early ECMO clinicians deserve: something practical, accurate, and actually usable at the bedside.

Here it is.

1. What Cardiac Stun Is

Cardiac stun is a temporary myocardial dysfunction after a major physiologic insult.
The myocardium is alive and well-perfused, but the muscle can’t generate an effective squeeze. It’s not infarction, it’s not permanent damage — it’s a ventricle recovering from shock, hypoxia, or reperfusion.

On VA-ECMO, it typically looks like:

• Very low EF on echo

• Minimal or absent pulsatility on the arterial line

• Tiny stroke volume, even with full coronary perfusion

• MAPs are completely dependent on ECMO flow and vasoactive support

• Lactate that rises or clears slowly because forward flow is insufficient

The key idea:
The heart has oxygen. It has perfusion. It just doesn’t have the contractile strength yet.

ECMO doesn’t fix the heart — it carries the circulation while the heart repairs itself.

2. Why Cardiac Stun Happens

Several pathways lead to cardiac stun, and most ICU clinicians have seen at least one of them. The physiology is straightforward once you look at the sequence.

Ischemia–Reperfusion After Arrest

After downtime, the heart gets blood flow back — but the myocytes aren’t ready to contract. They need time to recover, redistribute calcium, normalize pH, and restore ATP levels.

Severe Hypoxia or Prolonged Shock

A ventricle exposed to prolonged underperfusion loses contractile reserve. Even after restoring oxygen delivery, mechanical output lags behind.

Abrupt Hemodynamic Shifts During VA-ECMO Initiation

This one is under-taught but very real:

When you start VA flows too fast, you instantly increase LV afterload.
A stunned or borderline heart may not be able to open the aortic valve against that pressure.

The result is:

• No pulsatility

• No forward stroke volume

• A ventricle that looks even worse after ECMO is started

This isn’t ECMO “hurting” the heart — it’s ECMO exposing how little native output was left.

Systemic Inflammation and Vasoplegia

Post-arrest and septic physiology depress contractility globally. ECMO restores perfusion, but it doesn’t instantly reverse the inflammatory myocardial depression.

What About the Prime? (The Accurate Version)

I’ve heard (and once believed) the idea that:

“Plasmalyte doesn’t carry oxygen, so it can stun the heart if you start VA too fast.”

Here’s the fact-checked version:

• Crystalloid prime doesn’t carry oxygen, but it mixes immediately with circulating blood.

• The heart is not perfused with pure crystalloid in isolation.

• ELSO does not list crystalloid prime as a cause of stunning.

The real factors are:

• Cold prime: can transiently depress myocardial function

• Rapid flow initiation: spikes afterload

• Metabolic instability: acidosis, hypothermia, low calcium

So the teaching point is this:

Temperature and how fast you increase your ECMO flow matter far more than whether the prime is Plasmalyte.

3. How Cardiac Stun Resolves

You can’t “treat” stun directly — the myocardium simply needs time to recover. But you can create the conditions for recovery.

Controlled Flow Initiation

Start VA-ECMO gradually. Build flow slowly, allowing the LV to adjust and preventing an abrupt afterload hit.

Correct Metabolic Problems

The stunned ventricle won’t recover if the environment is hostile:

• Normalize calcium

• Correct acidosis

• Maintain temperature

• Optimize electrolytes

Many centers give calcium at initiation for this reason.

Support Perfusion

While the heart rests:

• Maintain appropriate ECMO flow

• Use vasoactive support judiciously

• Monitor lactate and regional perfusion

• Avoid unnecessary LV distention

Unload the LV When Needed

If the aortic valve isn’t opening and the LV begins to distend, intervene early:

• Reduce afterload

• Consider inotropes, IABP, Impella, or surgical venting, depending on your program

Watch for Signs of Recovery

You’ll know the heart is coming back online when you see:

• The aortic valve opens intermittently

• Pulse pressure returning

• Stroke volume rising

• Improved lactate clearance

Once you see pulsatility, the heart is re-engaging.

Closing Thoughts

Cardiac stun used to feel vague to me — something people mentioned, assumed, and moved past without a clear explanation. Being asked directly forced me to clarify what it actually is and why it shows up the way it does, especially during VA-ECMO initiation.

Here’s where I landed:

Cardiac stun is the myocardium saying, “I’m viable — I just need time.”
Our job is to protect the patient while the heart rebuilds its ability to generate mechanical work.

VA-ECMO gives the heart the chance to recover, and when it does, it’s unmistakable:
Pulsatility returns, the aortic valve opens, and the circulation begins to shift back toward native output.

That moment never gets old.

Key Points (Before You Dive In)

• HIT is a prothrombotic immune complication triggered by heparin.

• Use the 4T score to assess likelihood of HIT before testing.

• Confirm with PF4 ELISA and SRA if HIT is suspected.

• If HIT is likely, stop heparin and switch to a direct thrombin inhibitor like bivalirudin.

• Match the anticoagulant to the right test: Anti-Xa for heparin, aPTT for bivalirudin/argatroban.

• Monitor closely, especially in unstable ECMO patients.

Introduction

I remember the first time I heard someone say, “The patient’s platelets just dropped by half—could be HIT.” At the time, I nodded, pretending to understand. I had no idea what they meant. It wasn’t covered in any of the ECMO training I’d gone through. It wasn’t until later that I realized how dangerous—and how commonly overlooked—this complication is.

What is HIT?

Heparin-Induced Thrombocytopenia (HIT) is a life-threatening immune complication of heparin therapy. HIT occurs when antibodies form against complexes of heparin and platelet factor 4 (PF4), leading to platelet activation, thrombocytopenia, and an increased risk of thromboembolic events such as DVT, stroke, and ECMO circuit clotting.

This prothrombotic state—despite falling platelets—is one of the most dangerous complications of anticoagulation on ECMO and must not be confused with typical circuit-related thrombocytopenia.

According to the ELSO Red Book, HIT is more common in adult VA ECMO patients, and its diagnosis should trigger immediate anticoagulant reassessment. The ECMO Specialist Training Manual further highlights that circuit thrombus or oxygenator failure should always prompt a review of the patient’s platelet count and coagulation profile.

Diagnosing HIT: The 4T Score

The 4T Score is a clinical tool to estimate the pretest probability of HIT and guide further testing. It includes four components:

In ECMO, a 50% platelet drop occurring on or after Day 5, especially with new thrombosis or oxygenator dysfunction, should never be dismissed as routine. It demands immediate investigation.

Confirmatory Testing

• PF4 ELISA: High sensitivity but prone to false positives; useful for screening.

• SRA (Serotonin Release Assay): The gold standard test for HIT; confirms actual platelet-activating antibodies.

ELSO and The ECMO Book recommend using both the 4T Score and functional assays to improve diagnostic accuracy.

Case Study: HIT in ECMO

Patient: 62-year-old male on VA ECMO for cardiogenic shock
Day 5: Platelets drop from 210k to 95k
Findings: New leg swelling; ultrasound confirms DVT
4T Score: 7/8 (High probability)
Labs: Positive PF4 ELISA; HIT confirmed by SRA
Management: Heparin discontinued; initiated bivalirudin
Outcome: Platelet count rebounded; no new thrombosis

Why Bivalirudin?

Bivalirudin is a direct thrombin inhibitor preferred in ECMO patients with HIT. Compared to heparin:

Bivalirudin’s stable pharmacokinetics and non-dependence on antithrombin make it ideal for ECMO, especially in unstable patients or when HIT is confirmed or suspected.

Monitoring Frequency by Anticoagulant

Takeaway for ECMO Specialists

If your patient’s platelets drop by >50% on Day 5–10 of ECMO—and you see thrombus in the circuit or a failing oxygenator—don’t write it off. Calculate the 4T score, confirm with PF4 ELISA and SRA, and change your anticoagulant early if HIT is likely.

Bivalirudin is often the best alternative, but it must be paired with aPTT monitoring—and frequently reassessed during instability. Remember:

• Heparin → Anti-Xa (or aPTT)

• Bivalirudin / Argatroban → aPTT

Match the drug to the test. Monitor wisely.

AI plays a significant role in how I research, understand, and communicate complex ECMO topics. From analyzing source materials to organizing ideas and generating podcast outlines, AI helps me stay curious and keep learning—so I can keep sharing.

Check out my websites:

• lifesupport.training for ECMO and other professionals

• ecmo.life for patients and loved ones

• Occasional podcasts are on YouTube

• Latest real time ECMO News on my ECMO143 UpToDate X Channel

Disclaimer

This article is for educational purposes only and reflects my understanding and interpretation of available guidelines, literature, and bedside learning. It does not constitute medical advice or represent institutional protocols. Always consult your ECMO team and local policies when making clinical decisions.

References

1. Extracorporeal Life Support Organization (ELSO). Extracorporeal Life Support: The ELSO Red Book. 6th ed. Ann Arbor, MI; 2023.

2. ELSO. ECMO Specialist Training Manual. 4th ed. Ann Arbor, MI; 2022.

3. DellaVolpe J. The ECMO Book. San Antonio, TX: The Institute for Extracorporeal Life Support; 2024.

4. Zhao Y, et al. Bivalirudin Anticoagulation in ECMO: Monitoring and Management. Crit Care Med. 2021.

5. Nguyen TP, et al. Heparin Monitoring in ECMO: aPTT vs. Anti-Xa. J Cardiothorac Vasc Anesth. 2021.

6. Renou A, et al. HIT Risk Stratification Using Modified 4T in ECMO. Intensive Care Med. 2020.

7. Frontiers in Pharmacology. Bivalirudin Anticoagulation Guidelines. 2023.

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What stood out to you in this article? I’d love to hear your take. Join the ECMO 143 learning journey: real-world ECMO education with AI-powered insight, bedside clarity, and no fluff.

Each weekday, I post a short ECMO Vitamin, a quick insight, question, or reminder to sharpen our practice. On Saturdays, I wrap them up into this weekly ECMO Multi-Vitamin recap, even though it's late Saturday night today. If you missed one during the week, here’s your catch-up dose. At the bottom of this article is a YouTube link for you to listen to a podcast of last week's topics.

👇 Here’s what we explored this week:

🟩 Monday, May 12 — How Do You Manage Circuit Pressures in the Proned Patient?

Post Link: Read it on LinkedIn Summary: Prone positioning can challenge ECMO flows by increasing abdominal pressure and impacting drainage. I shared what I’ve seen at the bedside—and how to stay ahead of access pressure issues before they become a bigger problem.

🟦 Tuesday, May 13 — What Do You Do When Platelets Are 30 but You Still Need Anticoagulation?

Post Link: Read it on LinkedIn Summary: Anticoagulation in the setting of thrombocytopenia feels like a trap. I talked about bivalirudin, bleeding risk, and the importance of team-based decision-making when the margins are razor-thin.

🟨 Wednesday, May 14 — How Do You Wean VV ECMO in a Patient with ARDS and Pulmonary Hypertension?

Post Link: Read it on LinkedIn Summary: When pulmonary hypertension complicates ARDS recovery, weaning becomes a high-wire act. I reflected on echo, ventilator settings, and signs of true lung improvement before stepping down support.

🟧 Thursday, May 15 — What’s Your Strategy for Fluid Balance in VA ECMO with AKI?

Post Link: Read it on LinkedIn Summary: VA ECMO plus AKI is a volume management headache. Do you chase urine, wait on CRRT, or preemptively diurese? I asked what others are doing when the kidneys aren’t helping, but the circuit still demands balance.

🟥 Friday, May 16 — How Do You Support Families During Prolonged ECMO?

Post Link: Read it on LinkedIn Summary: We zoom in on numbers and settings—but what about the emotional load families carry? This post explored small, meaningful ways to support loved ones facing weeks (or months) of bedside uncertainty.

🎧 Deep Dive Podcast — Available Now

Each Saturday, I record a 10-minute audio recap and reflection, assisted by NotebookLM and AI voice synthesis. In this episode, we break down:

• Managing prone pressures in VV ECMO

• Bivalirudin when platelets are critically low

• The tricky art of ECMO weaning with pulmonary hypertension

• Balancing fluid in VA ECMO + AKI

• Emotional burnout in families—and what we can do

🎙️ Listen to the Multi-Vitamin podcast on YouTube

🙌 Subscribe. Share. Think Aloud.

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Key Points

• Right radial ABGs may not reflect coronary oxygenation in peripheral VA ECMO.

• Hypoxic native LV ejection can perfuse the coronaries, even when ECMO support looks adequate.

• This may contribute to recurrent VT/VF or ectopy that doesn't respond to shocks or medications.

• Devices like Impella and low ventilator FiO₂ settings may unintentionally worsen the problem.

• Adjusting FiO₂ or using early V-VA ECMO could improve coronary oxygenation without surgical escalation.

Introduction

This is a working hypothesis I’ve been thinking through as I try to better understand what we see during peripheral VA ECMO. I’m still early in my ECMO learning and always trying to make sense of how physiology plays out in real patients.

One question that keeps coming up for me is this:

Could the heart be perfusing itself with hypoxic blood, even when the right radial ABG looks perfectly fine?

This article walks through that idea and considers whether differential hypoxemia, something we already recognize in peripheral VA ECMO, might be playing a bigger role in arrhythmias than we typically assume, especially when native LV output is still present.

Understanding the Potential Problem: Peripheral VA ECMO Dynamics

Right radial arterial blood gases are frequently used as a surrogate for upper body oxygenation and are often assumed to reflect coronary perfusion. However, anatomically, that assumption may not hold.

The coronary arteries branch directly off the aortic root, just two to three centimeters above the aortic valve. The brachiocephalic artery, which supplies the right radial artery, originates farther up in the aortic arch, approximately four to five centimeters from the valve.

In peripheral VA ECMO (e.g., femoral-femoral cannulation), oxygenated blood from the ECMO circuit flows retrograde up the aorta, while the patient’s native heart ejects blood antegrade. If pulmonary function is significantly impaired, this native ejection may consist of hypoxic blood.

These two flow streams meet at a constantly moving “mixing point” in the aorta. The location of this point fluctuates based on the strength of native cardiac output and ECMO flow rates. This anatomical difference is well understood, but its clinical implication, especially in relation to coronary perfusion, is often underappreciated.

The Danger Zone Hypothesis: Mixing Above the Coronaries

This hypothesis centers on a particular scenario: If the patient’s native cardiac output, even if weak, ejects hypoxic blood that reaches as far as the coronary arteries, but not as far as the brachiocephalic artery, then the following may occur:

• The potentially deceptive right radial ABG: If the mixing point lies distal to the brachiocephalic takeoff, the right radial artery may receive fully oxygenated ECMO blood, and an ABG from that site could appear reassuring.

• The hidden threat: If mixing occurs between the coronary ostia and the brachiocephalic artery, the myocardium may be perfused with hypoxic blood from the native circulation, while the right radial ABG falsely suggests adequate systemic oxygenation.

In this scenario, recurrent ectopy, VT, or VF may not simply reflect electrical irritability but rather may represent the heart’s physiologic response to ischemia.

Connecting the Hypothesis to Arrhythmias and Ectopy

Myocardial tissue is highly sensitive to oxygen deprivation. If the coronary arteries are intermittently or persistently perfused with hypoxic blood:

• Myocardial ischemia develops.

• Electrical instability follows, increasing the risk of ventricular arrhythmias (VT/VF) or frequent ectopy (e.g., PVCs).

The hypothesis suggests that when clinicians observe refractory arrhythmias or worsening ectopy, especially when paired with labile or inconsistent right radial oxygenation, they should consider whether unseen coronary hypoxia may be driving the instability.

Treating the Rhythm, Missing the Cause

This leads to a familiar and frustrating clinical picture: A defibrillator at the bedside, the crash cart parked just outside the room, and the patient cycling in and out of VT/VF despite sedation and escalating antiarrhythmic therapy. Lidocaine, amiodarone, magnesium, and even ganglion blocks are attempted, yet the arrhythmias persist.

If the myocardium is ischemic due to hypoxic native LV ejection, these arrhythmias may stem directly from coronary under-oxygenation. In that case, focusing solely on electrical suppression may fail to resolve the underlying problem. Without addressing the oxygen content of blood perfusing the coronaries, arrhythmias may continue regardless of drug therapy or shocks.

When Support Strategies Worsen Coronary Hypoxia

Mechanical support devices such as Impella are often used during peripheral VA ECMO to reduce left ventricular distention and support forward flow. While beneficial for pressure unloading, these devices do not address the oxygen content of blood entering the left ventricle.

In fact, Impella may deliver hypoxic blood from the LV directly into the proximal aorta, where the coronary arteries arise. If the lungs are underperforming and ventilator FiO₂ is low, this native blood may remain desaturated, and coronary perfusion could be compromised despite good right radial oxygenation.

Potential Solutions

Central Cannulation

Escalating to central ECMO can effectively resolve this issue by ensuring antegrade delivery of oxygenated blood to the coronary arteries. However, this is an invasive step, typically reserved for patients in severe decline, and not always feasible in a timely manner.

Early V-VA ECMO Configuration

Rather than increasing ECMO flow, which can worsen LV distention, or waiting until central cannulation becomes necessary, V-VA ECMO may offer an intermediate solution. In this configuration, a portion of oxygenated blood from the arterial limb is returned to the venous drainage limb, enhancing the oxygen content of blood passing through the lungs and ultimately into the LV.

Benefits of this approach may include:

• Improved venous oxygenation, even in low-functioning lungs

• More oxygenated blood entering the left atrium and ventricle

• Reduced hypoxia in native LV ejection

• Better coronary perfusion, potentially breaking the ischemia-arrhythmia cycle

Reconsidering Ventilator Management and the Broader Risk of Coronary Hypoxia

In peripheral VA ECMO, ventilators are often set to “rest settings,” low respiratory rate, low tidal volume, and low FiO₂, based on the assumption that the ECMO circuit provides adequate systemic oxygenation. These settings help minimize ventilator-induced lung injury and reduce pulmonary oxygen toxicity, especially when arterial PaO₂ levels (such as in the right radial) are already elevated due to the ECMO flow.

However, when any native pulmonary blood flow persists, as is often the case, even modestly hypoxic blood may pass through the lungs, enter the left atrium and ventricle, and be ejected by the native heart. If this ejected blood is under-oxygenated and reaches the coronary arteries, it may contribute to myocardial ischemia, even if global oxygen delivery seems sufficient and the right radial ABG appears reassuring.

Increasing ventilator FiO₂, even if it does not significantly affect the right radial PaO₂, may still improve the oxygen content of this small but critical volume of blood. That improvement could meaningfully impact coronary perfusion, particularly in patients showing new ectopy or ventricular arrhythmias.

Importantly, this issue is not limited to patients with severely diseased lungs. Even when pulmonary function is relatively preserved, ventilator FiO₂ may be kept low to avoid oxygen-related lung injury. Yet in the presence of even minor ventilation-perfusion mismatch, this can result in desaturated pulmonary venous blood. That blood, if ejected by the LV, may perfuse the coronaries with insufficient oxygen, despite an apparently normal or even hyperoxic right radial ABG.

This expands the relevance of the hypothesis beyond classic ARDS physiology and highlights the importance of asking not just “what does the ABG say?” but:
“What is the myocardium actually receiving?”

Conclusion

This remains a physiologic hypothesis I have been thinking about: Early V-VA ECMO configurations, along with thoughtful ventilator management (especially FiO₂ adjustments), might improve coronary oxygenation in select patients on peripheral VA ECMO. In cases of recurrent arrhythmias, we may need to ask whether the myocardium is being perfused with hypoxic blood, even when conventional markers like the right radial ABG appear normal.

I am still relatively new to ECMO and learning every day. It is possible that what feels like a major realization to me may already be well understood by others. But sometimes, as the saying goes, "Actual learning requires that you do those things." (Frank Herbert)

Clinicians managing refractory arrhythmias in pVA ECMO may benefit from widening their diagnostic lens and considering interventions that specifically improve myocardial oxygen delivery, rather than relying solely on rhythm suppression.

Note

This article is for educational purposes and is not a substitute for professional medical advice. Always consult qualified healthcare professionals for patient care and clinical decisions.

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My ECMO Projects and Tools

I’ve built the following platforms to support both clinical professionals and families navigating ECMO:

• lifesupport.training – My primary platform for full-length ECMO articles, future ELSO exam preparation, and certification support (ACLS/PALS/BLS/ATLS)

• ecmo.life – A simplified ECMO explainer site for patients and families

AI Tools I created and actively use the following custom GPTs to support my research and writing process:

• AI ECMO Expert – A physiologic reasoning assistant trained to analyze ECMO-specific documents

• Micro Definitions (MD-GPT) – A terminology tool to clarify clinical terms in real time

Thanks to OpenEvidence, GPT-4o, Perplexity, Gemini Advanced 2.5 Pro, Claude 3.7, Grammarly, Leonardo AI, DALL·E 3, Microsoft Designer, and others.

Image Credit

Visual Anatomy 3D – Human, by GraphicVizion. Used with permission.

References

• Extracorporeal Life Support Organization (ELSO). ELSO Red Book: Guidelines for Cardiopulmonary Extracorporeal Life Support Organization. 5th ed. ELSO, 2017.

• Lorusso R, Shekar K, MacLaren G, Schmidt M, Pellegrino V, Fraser JF, eds. ECMO Specialist Training Manual. 1st ed. Extracorporeal Life Support Organization; 2018.

In 2009, David Richards became critically ill with swine flu. His ARDS diagnosis led to an ECMO transfer to Glenfield Hospital, and his survival helped catalyze the creation of England’s adult ECMO network. I recently published David’s story—raw, moving, and generous in detail—on ecmo.life, our patient and family education site.

However, for healthcare providers, it also offers clinical and human takeaways.

🔍 6 Reflections for ECMO Teams:

1. Early delays matter. David had three GP calls before hospitalization. ECMO saves lives—but early recognition of severe respiratory deterioration is just as critical.

2. The power of mobile ECMO teams. His transfer to Glenfield was only possible thanks to a bed opening and a retrieval team equipped to initiate ECMO pre-transfer.

3. ICU diaries aren't soft—they're survival tools. David credits his ICU diary with helping him sort hallucinations from reality and recover emotionally.

4. Delirium is more than confusion. Vivid hallucinations and paranoia were David’s reality for weeks. Recognizing and supporting this is essential.

5. Rehab starts in the ICU. His care team began rehab within 48 hours of waking. Even ankle rotations and sitting up were milestones.

6. Discharge isn't the end—it’s a new phase. PTSD, medical retirement, financial strain, and chronic symptoms followed David home. Survivorship care is part of ECMO care.

Read David’s full story here: 🔗 ecmo.life – David’s Long Battle

Let me know what stood out to you—or what your ICU is doing to support ECMO survivors long-term.

🔑Key Points

• RIDDLER Syndrome refers to a CO₂ mismatch during peripheral V-A ECMO—when CO₂-rich ECMO blood perfuses the brainstem, causing tachypnea even though ABGs may look “normal.”

• The right radial ABG can mislead you—showing low PaCO₂ while the brainstem is actually seeing high CO₂ from the ECMO circuit.

• This syndrome underscores the importance of post-oxygenator ABGs and considering regional aspects of gas delivery, rather than focusing solely on systemic approaches.

I’m a novice ECMO specialist. I didn’t come into this job with all the answers—but I came with curiosity and a willingness to learn. I’ve been fortunate enough to land in a workplace full of smart, experienced people who have been generous with their time and guidance.

I use AI to help me read, research, and write about what I’m learning. This article is another step in that journey. I don’t write these posts as an expert—just as someone trying to understand ECMO better, one concept at a time.

This week, I came across a new syndrome described in Circulation, which helped me think differently about the role of CO₂ in V-A ECMO patients…

We’re used to hearing about Differential Oxygenation (a.k.a. North-South syndrome) in V-A ECMO—when the upper body receives poorly oxygenated native cardiac output, and the lower body is perfused by well-oxygenated ECMO blood. However, a new article in Circulation introduces a novel angle that caught my attention: RIDDLER Syndrome, also known as East-West Syndrome. Here is a breakdown of the Circulation article.

Why call it RIDDLER Syndrome?

The title of the article is a masterpiece of academic maximalism:
“Relatively Increased CO₂ Delivered to the Brain From the Descending Aorta Leading to an Elevated Respiratory Rate Causing Differential Hypocapnia (RIDDLER or East-West Syndrome): New Pitfalls in Awake Peripheral V-A ECMO.”

I looked everywhere trying to figure out what RIDDLER stood for—scanned the article top to bottom, hunted through references, chased blog posts, Reddit threads, anything. Nothing. Just endless recycling of the same title. No explanation. No acronym breakdown. No decoder ring.

After a long night of overcaffeinated searching… it hit me.
The RIDDLE was literally the title.

No, seriously. It’s just the first letters of the words.

R — Relatively
I — Increased
D — Delivered
D — Descending
L — Leading
E — Elevated
R — Respiratory

That’s it. That’s the whole thing.

Someone, somewhere, looked at that word avalanche and decided—correctly—that it spelled RIDDLER, and then just walked away like it was the most normal thing in the world. And honestly? I respect it.

It's ridiculous.
It's genius.
It's ridiculously genius.

And now I’ll never forget it.
The RIDDLE… has been solved.

Why RIDDLER Syndrome Matters

In awake, spontaneously breathing patients on peripheral V-A ECMO, we can inadvertently create a CO₂ imbalance across the brain—one hemisphere receiving decarboxylated blood from the lungs, the other hypercapnic blood from the circuit. This can trick us into making the wrong adjustments.

The Setup: How RIDDLER Happens

Here’s the six-step cascade:

1. Tachypnea develops (pain, exertion, sepsis, etc.), which increases native lung CO₂ clearance.

2. Right arm ABG shows a low PaCO₂ and high pH—looks like we’re over-sweeping.

3. Clinicians reduce ECMO sweep, expecting less CO₂ clearance.

4. But retrograde ECMO blood becomes more hypercapnic, perfusing the left brain via the left carotid artery.

5. Brainstem chemoreceptors detect rising CO₂ → further increase in respiratory drive → worsening tachypnea.

6. We respond to the wrong signal—the low PaCO₂ in the right radial artery—and drop the sweep even more.

You can see where this is going. It’s a vicious cycle, where right arm blood gases falsely reassure us, while the left hemisphere (and respiratory centers) are drowning in CO₂.

This isn’t just a theoretical issue—it led to reintubation in a patient with myocarditis on ECPELLA (ECMO+Impella) support.

Differential Oxygenation vs. RIDDLER: Know the Difference

How to Avoid the Trap

1. Don’t rely solely on the right radial ABG—it’s giving you only half the story.

2. Check post-oxygenator CO₂ to verify circuit decarboxylation.

3. Consider left radial or central venous gas sampling for a more complete picture.

4. Watch for inappropriate tachypnea that doesn’t respond to sedation or pain control.

5. Don’t reflexively reduce sweep gas just because of low PaCO₂ in the right arm—context is key.

Break the Cycle

• Match sweep to blood flow (e.g., 1:1 ratio) once stable.

• Aim for physiologic post-oxygenator pH and CO₂ targets.

• Treat underlying causes of tachypnea: pain, anxiety, sepsis.

• Consider gentle re-sedation, noninvasive support, or even reintubation in severe cases.

Final Thought

RIDDLER Syndrome is differential decarboxylation, requiring a shift in our thinking—especially in awake, peripheral V-A ECMO patients.

Don’t be fooled by the right radial blood gas.

I’ll admit—I hadn’t thought of CO₂ delivery as a regional issue until a previous article, Case Study: Refractory Metabolic Alkalosis, by guest editors Dr. Felipe de Andrade Arnaud and Dr. Jeffrey M. Scott. While pCO2 is the issue in both cases, the increased pCO2 in the case study was leading to increased refractory HCO3. We’re learning that gas exchange on ECMO isn’t just about oxygen anymore. It's about context, anatomy, and staying humble enough to say: “What’s going on here?”

📝 Note: This article is for educational purposes only and is not a substitute for professional medical advice. Always consult with qualified healthcare professionals for clinical decisions and patient care.

🚀 Join the ECMO 143 Learning Journey

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🧠 Acknowledgments

I created this article using a mix of AI-assisted research and curiosity-driven study. I’ve built two custom GPTs to help me dig deeper:
• AI ECMO Expert
• Micro Definitions (MD-GPT)

Special thanks to:
OpenEvidence · GPT-4o/o1 · Claude 3.5 · Perplexity · Gemini 2.5 · Storm (Stanford) · Grammarly · Leonardo AI · DALL·E3 · Microsoft Designer · Adobe Express

📖 Reference

Jung, C., Wengenmayer, T., & Duerschmied, D. (2025). Relatively Increased CO₂ Delivered to the Brain From the Descending Aorta Leading to an Elevated Respiratory Rate Causing Differential Hypocapnia. Circulation, 151(4), 289–291.
👉 https://doi.org/10.1161/CIRCULATIONAHA.124.071524

If you’ve ever tried to explain ECMO to a patient’s loved one at the bedside—while alarms are going off, the team is rounding, or a consult is calling—you know how tough it can be. The language of ECMO and intensive care is packed with technical terms that can overwhelm even the most attentive family member.

That’s why I created a new resource on my companion site: 👉 ECMO and ICU Terms: A Glossary for Patients & Families

It’s part of ECMO 143: A Patient & Family Guide, where I’m building clear, compassionate, and practical tools to support the people who matter most—our patients and their loved ones.

💌 Bonus: If you subscribe at ecmo.life, I’ll send you a PDF copy of the glossary to print or share with anyone who might benefit from it.

💡 Why a Glossary?

As a newer ECMO specialist, I remember constantly looking up terms early on. If it was hard for me—with a clinical background—how much harder must it be for families to hear these words for the first time in the middle of a crisis?

Whether it’s “VA vs. VV,” “oxygenator failure,” or “anticoagulation monitoring,” this glossary breaks down over 150 terms in plain language—without dumbing anything down.

📱 How You Can Use It

• At the bedside: Share the link with families when they’re overwhelmed by acronyms.

• During family meetings: Use it to create a shared vocabulary.

• As part of discharge planning: Give it to survivors transitioning out of the ICU who want to understand what they went through.

The glossary is still growing, but I’ll cap it at around 200 terms to keep it clean and readable. I'd love to hear from you if you have suggestions or terms I missed.

🙏 Thanks for being part of the ECMO 143 learning journey. Jon

📬 Subscribe to ecmo.life to get the full glossary PDF and stay updated on new patient- and family-focused resources.

I am excited to introduce ecmo.life "ECMO 143: A Patient & Family Guide," a new resource dedicated to demystifying Extracorporeal Membrane Oxygenation (ECMO) for patients and their families. This initiative stems from my ongoing journey as an ECMO specialist and my desire to bridge the gap between complex medical procedures and patient understanding.​

Why "ECMO 143: A Patient & Family Guide"?

While my original newsletter, ECMO 143: Learning as I Go, focuses on simplifying ECMO concepts for myself, fellow novices, and other curious medical professionals, I’ve come to see the need for something different—something for patients and families. Facing ECMO can be overwhelming, especially in the middle of a crisis. That’s why I’ve just launched a companion site, ECMO 143: A Patient & Family Guide, at ecmo.life. It’s still a work in progress, but the goal is simple: to offer clear, compassionate, and easy-to-understand information that helps patients and their loved ones feel a little more grounded during a very uncertain time.

What to Expect

The website offers a variety of resources, including:​

• Educational Articles: Simplified explanations of ECMO procedures, benefits, and potential risks.​

• Patient Stories: Real-life experiences to offer hope and insights.​

• FAQs: Answers to common questions to alleviate concerns.​

• Glossary: Definitions of medical terms related to ECMO.​

Join the Journey

I invite you to explore the site, share it with patients and families who might benefit from it, and provide feedback to help us improve continually.​

Thank you for your ongoing support.

Thank you! Jon

As a novice ECMO specialist, I often find myself with various terms used to describe ECMO circuit components. Different centers, teams, and even individual providers may use different language for the same part of the ECMO circuit. To ensure clear communication and avoid confusion, it's helpful to recognize the most commonly used terms while also being aware of less common alternative names.

ECMO Drainage vs. Return: What's the Difference?

The ECMO circuit consists of two primary functions: drainage and return:

• Drainage: Deoxygenated blood is withdrawn from the patient into the ECMO circuit, usually via a venous cannula.

• Return: Oxygenated blood is delivered back to the patient, either through a vein (VV-ECMO) or an artery (VA-ECMO).

Many different names exist for these functions, so I compiled a chart to clarify the most commonly used terminology alongside less common alternatives.

Why Does This Matter?

Clear communication is critical in ECMO management. If different team members use different terminology, this can lead to misunderstandings during patient handoff, troubleshooting, and emergencies.

• The most commonly used terms align with ELSO guidelines and ECMO specialist training manuals.

• The less common terms may still be used in certain ECMO centers, among perfusionists, or in specialized discussions.

If you work in an ECMO center where alternative terms are used, it's worth clarifying and ensuring everyone on the team understands the same terminology.

Whether new to ECMO or a seasoned specialist, understanding and using standardized terms improves communication, reduces errors, and enhances patient safety. If different team members use varied terminology, it can lead to misunderstandings during handoff, troubleshooting, and emergencies.

Have you encountered variations in ECMO terminology during a shift? Do you use any of the less common terms in your practice? Could you share your experiences in the comments? Standardizing our language strengthens team communication and patient care.

Other Links:

https://bit.ly/ecmo143-newsletter

https://bit.ly/ecmo143-youtube

https://bit.ly/ecmo143-company

https://bit.ly/ecmo143-fbpage

Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.7 Sonnet/Opus, Perplexity, Gemini 2.0 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

Note: This article is intended for educational purposes only. It should not be used as a substitute for professional medical advice or guidance. Always consult with qualified healthcare professionals for clinical decisions and patient care.

Guest Editor: Dr. David Jergenson, DPT, a physical therapist at Mayo Clinic in Rochester, MN

In ECMO care, we focus heavily on hemodynamics and oxygenation, but recovery extends beyond the circuit. Early mobilization is key in reducing delirium, shortening hospital stays, and restoring independence, yet it comes with unique challenges.

This week’s guest editor, Dr. David Jergenson, DPT, a physical therapist at Mayo Clinic in Rochester, MN, shares his insights on safely mobilizing ECMO patients. He discusses the barriers, strategies, and interdisciplinary collaboration needed to make movement possible.

Let’s explore how mobilization can transform ECMO recovery:

Like so many in the inpatient population, there are countless benefits to patients on ECMO mobilizing. Not only do patients get stronger, but it also helps reduce delirium, decreasing length of stay and undoubtedly provides hope for the critically ill. As a physical therapist, it’s my job to make it happen.

Patient abilities can vary due to their strength, cognition, hemodynamics, or all of the above, and rates of ICU-acquired weakness in ECMO patients are often higher than those of the general ICU population. Some patients are so debilitated that we focus on sitting balance or performing sit-to-stand exercises for several weeks. If the patient cannot take steps, we sometimes use a ceiling lift or Sara Stedy device to transfer a patient to a chair. Others have the strength to ambulate several hundred feet! Each patient's ECMO journey is unique. Some had complicated cardiac surgery. Others are awaiting heart and/or lung transplants. Regardless of their differences in background and complexity, the goals of returning to independence remain the same.

The Power of Movement in ECMO Recovery

Studies have shown that mobilizing patients on ECMO is overall safe. As with all mobility, risks are always involved, but the benefits far outweigh the low chance of harm. At my facility, we frequently mobilize patients with various cannulation strategies and support (VA, VV, VAV, etc.). There used to be a previous thought that patients who were femorally cannulated needed to be on bedrest; we frequently mobilize these patients and have not had any major adverse events. For these patients, flexing the hip to 90 degrees on the cannulated side while supine helps assess whether ECMO flows change in a seated position.

Interdisciplinary communication is vital for success in mobilizing ECMO patients. There is frequent dialogue regarding line management and patient response to activity between the critical care team, PT, OT, nursing, and the ECMO specialist. The ECMO specialist sometimes increases the FiO2 or sweep to improve patient symptoms or hemodynamics. These changes are documented in our therapy notes for reference in future sessions. We also mobilize patients whose sweep gas is clamped on ECMO, as their activity tolerance can help determine decannulation readiness. The journey for these patients can be very challenging, but the mobility team is undoubtedly integral to recovery.

Sources: Abrams, D., Madahar, P., Eckhardt, C. M., Short, B., Yip, N. H., Parekh, M., Serra, A., Dubois, R. L., Saleem, D., Agerstrand, C., Scala, P., Benvenuto, L., Arcasoy, S. M., Sonett, J. R., Takeda, K., Meier, A., Beck, J., Ryan, P., Fan, E., Hodgson, C. L. (2022). Early Mobilization during Extracorporeal Membrane Oxygenation for Cardiopulmonary Failure in Adults: Factors Associated with Intensity of Treatment. Annals of the American Thoracic Society, 19(1), 90–98. https://doi.org/10.1513/AnnalsATS.202102-151OC

Chatziefstratiou, A. A., Fotos, N. V., Giakoumidakis, K., & Brokalaki, H. (2023). The Early Mobilization of Patients on Extracorporeal Membrane Oxygenation: A Systematic Review. Nursing reports (Pavia, Italy), 13(2), 751–764. https://doi.org/10.3390/nursrep13020066

Chen, X., Lei, X., Xu, X., Zhou, Y., & Huang, M. (2022). Intensive Care Unit-Acquired Weakness in Patients With Extracorporeal Membrane Oxygenation Support: Frequency and Clinical Characteristics. Frontiers in medicine, 9, 792201. https://doi.org/10.3389/fmed.2022.792201

Note: This article is intended for educational purposes only. It should not be used as a substitute for professional medical advice or guidance. Always consult with qualified healthcare professionals for clinical decisions and patient care

I just returned from the SWAAC ELSO Conference in Abu Dhabi, where one roundtable discussion was titled: "Is OI an Outdated Tool?" This conversation challenged one of the longest-standing ECMO initiation markers—Oxygen Index (OI) > 40—and explored whether it still holds up in today’s practice.

As a respiratory therapist, I’ve always recognized that a good blood gas doesn’t always mean a good ventilator strategy. It wasn’t long ago that we routinely ventilated patients with 15 mL/kg tidal volumes and driving pressures that were way too high—and back then, we thought we were doing the right thing! The ABGs looked great, but we now know that we were causing massive ventilator-induced lung injury.

This same principle applies to OI as an ECMO threshold—it’s one piece of the puzzle, but ventilator settings play a huge role in making that number look better or worse than it really is.

What is the Oxygen Index (OI), and Why is it Used?

OI is a calculated measure of how much ventilatory support is required to maintain oxygenation. It is commonly used in pediatric and neonatal respiratory failure but applies to adults with severe ARDS.

OI Formula:

OI=(MAP×FiO2×100)/PaO

Where:

• MAP = Mean Airway Pressure (cmH₂O) from the ventilator

• FiO₂ = Fraction of Inspired Oxygen (expressed as a decimal)

• PaO₂ = Partial Pressure of Arterial Oxygen (mmHg)

Why Has OI Been Used for ECMO?

During the roundtable, it was mentioned that, historically, OI correlates with worsening oxygenation failure. It has been used to determine when conventional ventilation is failing and Nitric or ECMO should be considered.

• OI < 5 Normal oxygenation

• OI 10-20 Mild lung injury

• OI 20-30 Moderate lung injury

• OI > 30 Severe lung injury (possibly NO)

• OI > 40 for several hours, then Historically,y a strong ECMO trigger

But does OI truly reflect the need for ECMO, or is it just another number that ventilator settings can manipulate?

The Roundtable Discussion: "Is OI an Outdated Tool?"

At the SWAAC ELSO Conference, experts debated whether OI should still be the primary trigger for ECMO initiation or if newer clinical decision-making strategies should take priority. Here are 4 takeaways I got, with some of my thoughts added:

1. A "Great" Blood Gas Doesn't Mean a Safe Ventilator Strategy

As I learned in the early days of being a Respiratory Therapist, a normal PaO₂ and CO₂ don’t mean the patient is okay. If those numbers were achieved with damaging ventilator settings (e.g., high tidal volumes, excessive PEEP, or high driving pressures), the lungs would still be in trouble.

• Since MAP is part of the formula, aggressive ventilator settings (e.g., high PEEP, high inspiratory pressures) can artificially raise OI, making a patient appear sicker than they are.

• Conversely, a lower OI doesn’t always mean stability—a patient may have rising CO₂, worsening lung compliance, or hemodynamic compromise.

2. ECMO Decisions Must Be Based on More Than OI Alone

Instead of using OI alone, many centers now incorporate a broader assessment, including:

• PaO₂/FiO₂ Ratio (P/F Ratio) < 80. A strong indicator of severe hypoxemia

• Ventilator Pressures & Compliance. A Driving Pressure > 15 cmH₂O, Pplat > 30 cmH₂O indicate worsening lung injury

• Rising CO₂ and Respiratory Acidosis, a pH < 7.15 despite max vent settings, suggests hypercapnic failure.

• Signs of Cardiovascular Compromise. A Rising lactate, hypotension, and shock indicate imminent organ failure

3. Timing is Everything—Waiting for OI > 40 Can Be Too Late

Some centers initiate ECMO at OI 30-35 if:

• The trend is worsening despite optimal lung-protective settings.

• There are signs of high ventilator-induced lung injury (VILI)

• Hypercapnic respiratory failure is progressing.

4. What This Means for ECMO Practice

• OI > 40 is still an important warning sign but should not be used in isolation. The best ECMO centers now:

• Follow OI trends instead of a single-value

• Consider ECMO at OI 30-35 if other failure signs are present.

• Look at indicators like P/F ratio, ventilatory pressures, and organ function.

Final Thoughts

The roundtable discussion at SWAAC ELSO reinforced a key principle: ECMO decision-making must evolve beyond rigid OI thresholds. While OI remains valuable, today’s practice should focus on patient trends, overall lung mechanics, and organ function rather than a single number.

Free ECMO & Critical Care Newsletter

This website, lifesupport.training, offers this free newsletter covering ECMO, critical care, and exam prep insights.

I’m also working on premium content, including ELSO exam prep, ACLS/PALS/BLS/ATLS study materials, and ECMO summary sheets.

Sign up now to stay updated and get early access when premium content launches.

Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.5 Sonnet/Opus, Perplexity, Gemini 1.5 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

Join my ECMO learning journey. As a novice, I simplify concepts to enhance my understanding, one article at a time.

I recently watched The Brutalist, a three-hour and 35-minute film produced by A24 that profoundly impacted me. It made me think about perseverance and our sacrifices to reach our goals.

We often hear the saying, "It's about the journey, not the destination." But what if, sometimes, it's actually the other way around? In The Brutalist, a character offers a different perspective: "It's about the destination, not the journey." This idea struck a chord with me, not just personally but also in the world of healthcare.

In the film, Lázló is deeply disappointed when he finally reaches his destination, but that isn’t always true. While reaching a goal may not always meet our expectations, it can be incredibly fulfilling and rewarding.

For new graduates in nursing and medical residents, the journey to proficiency is filled with endless learning, uncertainty, and navigating differing opinions on guidelines and best practices. Doubt can creep in—wondering if you're making the right decisions, interpreting things correctly, or keeping up with the ever-evolving field. The journey itself is often full of frustration and mental exhaustion. But why do we keep going? Because we have our eyes on the destination—helping patients, improving outcomes, and pushing the boundaries of what’s possible in modern medicine.

The truth is that healthcare professionals often endure high-pressure environments, differing viewpoints, and the constant need to adapt. There are moments of doubt and uncertainty, but we persist. Ultimately, it’s not about how hard the journey is—it’s about why we take it in the first place.

The reward is in the destination: the patient who walks out of the hospital after weeks of intensive care. This family gets to hold their loved one again, knowing our efforts contributed to something bigger than ourselves. That’s what makes it all worth it.

So, as we continue in this field, let’s remind ourselves that we don’t have to love the journey all the time. We have to believe in where it’s leading us.

Other Links:

ECMO 143: Learning as I go

Join my ECMO learning journey. As a novice, I simplify concepts to enhance my understanding, one article at a time.

By Jonathan Jung, RRT-NPS

(Future platform for this free Newsletter, plus a main focus of premium content, including ELSO exam prep and ACLS/PALS/BLS/ATLS materials, with ECMO only as one component; sign up now for updates)

https://bit.ly/ecmo143-newsletter

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https://bit.ly/ecmo143-company

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Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research: AI ECMO Expert, ECMO Specialist Handover Practice, and Micro Definitions (MD-GPT). These tools were instrumental in gathering and analyzing information from key sources.

Special thanks to the AI platforms and tools that facilitated this research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.5 Sonnet/Opus, Perplexity, Gemini 1.5 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

Protamine is a protein derived from fish sperm, specifically the milt—a sperm sac found in fish like salmon. Its strong positive charge allows it to neutralize heparin, an anticoagulant, making it essential for controlling bleeding in medical procedures. Modern pharmaceutical processes ensure its safe and effective clinical use.

Fish Milt in Cuisine

Interestingly, the same substance that forms protamine is also a culinary delicacy. Known as "milt," it is prized for its creamy texture and mild flavor in various cultures:

1. Japan: "Shirako" (白子, “white child”) is served raw, steamed, or grilled in fine dining establishments, often as a seasonal delicacy.

2. Korea: 이리 is commonly used in soups and stews for its rich texture and nutritional value.

3. Russia & Eastern Europe: Smoked milt, often from sturgeon, is a traditional part of seafood platters.

4. Mediterranean Countries: Fried milt or its inclusion in seafood dishes highlights its versatility.

Medicine Meets Cuisine

Protamine’s life-saving capabilities in medical settings and milt’s esteemed role in cuisine demonstrate the incredible adaptability of natural resources. This duality reflects humanity’s ingenuity in harnessing nature for survival and enjoyment.

Quick Facts

• Biochemical Marvel: Protamine’s ability to neutralize heparin is vital for controlling bleeding in critical surgeries.

• Nutritional Value: Milt is rich in proteins, omega-3 fatty acids, and essential nutrients.

• Cultural Impact: Milt is loved across Japan, Korea, and the Mediterranean, and its global presence showcases its significance in culinary traditions.

Closing Thought

Protamine, the unsung hero sourced from fish sperm, is nature’s way of saying, “Why not multitask?” It saves lives in operating rooms while gracing dining tables with fine cuisine, proving that science and tradition can swim in perfect harmony.

For more on how nature inspires medicine, see my article, "What Does an Indian Snake Have to Do with ECMO?"

Note: This article is intended for educational purposes only. It should not be used as a substitute for professional medical advice or guidance. Always consult with qualified healthcare professionals for clinical decisions and patient care.

Join the ECMO 143 Learning Journey:

Enjoy this? Please subscribe to my free Newsletter, ECMO 143: Learning as I Go, to stay updated on my latest insights and experiences.

Other Links:

(Future platform for this free Newsletter, plus a main focus of premium content, including ELSO exam prep and ACLS/PALS/BLS/ATLS materials, with ECMO only as one component; sign up now for updates)

https://bit.ly/ecmo143-newsletter

https://bit.ly/ecmo143-youtube

https://bit.ly/ecmo143-company

https://bit.ly/ecmo143-fbpage

Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research: AI ECMO Expert, ECMO Specialist Handover Practice, and Micro Definitions (MD-GPT). These tools were instrumental in gathering and analyzing information from key sources.

Special thanks to the AI platforms and tools that facilitated this research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.5 Sonnet/Opus, Perplexity, Gemini 1.5 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

Small adjustments in ECMO lead to learning moments. A recent VV ECMO case highlights the balance between ECMO flow, shunt fraction, and sweep gas settings, demonstrating a simple VV ECMO principle.

Case Study

The scenario involves a patient fully dependent on VV ECMO due to non-functional lungs. ECMO flow starts at 4.1 LPM, with the sweep set to 6 LPM and FdO2 at 100%. SpO2 stays in the low 90s and acceptable blood gases. The patient's beta blockers had to be discontinued due to unexpected cardiac side effects. Over several ABGs, the sweep gas needs to be increased due to rising pCO2. Eventually, the sweep is at 8.5 LPM for a pCO2 of 43 and pH of 7.42. The SpO2 is in the mid-80s, while SvO2 remains in the 60s. The patient experiences occasional desaturations with slow recovery. The pulse pressure is fantastic.

A Light-Bulb Moment

During rounds, the ECMO flow is increased from 4.5 LPM to 5.2 LPM to 6 LPM. The impact is immediate and seen in several areas. As expected, the SpO2 increases and stabilizes above 93%, recovery from desaturation quickens, and, to my surprise, the sweep gas requirements significantly decrease from 8.5 LPM to 6.5 LPM for a normocarbic ABG.

After thinking about what had just occurred, a light-bulb comes on!💡Taking the patient off the beta blockers increased the heart rate, increasing the Cardiac Output. The initial ECMO flow was insufficient to supply the new cardiac output flow with blood from the ECMO machine, so the heart was entraining venous blood to make up the difference. The shunt fraction had increased. This, in turn, decreased the total blood saturation and increased the pCO2. Increasing the ECMO flow to match cardiac output allows more ECMO blood and less venous blood to be entrained. By increasing the ecmo flow, the shunt fraction was decreased. The decreased shunt fraction directly reduces the burden on the ECMO sweep gas setting, which can now be lowered. For me, this is the ‘aha’ moment where everything clicks. It highlights how understanding and fine-tuning ECMO parameters leads to better patient outcomes.

Key Principle: ECMO Flow and Shunt Fraction

The principle is straightforward yet profound: The more blood from the ECMO circuit that enters cardiac output, the better the oxygenation and ventilation.

Breaking Down the Concepts

• Shunt Fraction: refers to the percentage of blood bypassing the oxygenator without undergoing gas exchange. A high shunt fraction occurs when ECMO flow is too low relative to cardiac output, meaning a significant portion of blood bypasses the circuit, contributing to poor oxygenation and an increased CO2 burden.

• Optimizing Flow: Increasing ECMO flow raises the proportion of oxygenated blood entering the systemic circulation. This reduces the shunt fraction, improves gas exchange efficiency, stabilizes SpO2, and lowers reliance on high sweep gas flows. However, there are limiting factors to increasing ECMO flow, such as elevated circuit pressures, risks of suckdowns, or concerns about hemolysis. These must be balanced carefully against the need to reduce the shunt fraction and optimize oxygenation.

• Recirculation Risks: When ECMO flow exceeds cardiac output, SvO2 may climb significantly from baseline, indicating recirculation. In such cases, some oxygenated blood re-enters the ECMO circuit rather than contributing to systemic circulation, reducing efficiency.

Lessons Learned in Practice

This case offers several valuable lessons:

1. Optimize Flow: Matching ECMO flow to cardiac output minimizes the shunt fraction, improving oxygenation and CO2 removal.

2. Adjust Sweep Gas: 💡As the shunt fraction decreases, sweep gas demands can be reduced, leading to a more stable and efficient circuit. This is my light-bulb moment—seeing this happen makes everything click.

3. Monitor Recirculation: Watch for signs of excessive ECMO flow, such as rising SvO2, which may indicate increased recirculation.

4. Management: Continuously evaluate and adapt ECMO settings to meet the patient’s needs. This could be due to a change in medication or dosing, the heart or lungs getting sicker or healthier, hemodynamics, volume status, or patient positioning.

Conclusion

The relationship between VV ECMO flow, cardiac output, and shunt fraction provides important insights into patient management. Based on careful observation and understanding, even minor adjustments can significantly improve patient outcomes. This case illustrates the importance of thoughtful, involved ECMO management and is a valuable learning experience for clinicians.

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ECMO 143: Learning as I go

Join my ECMO learning journey. As a novice, I simplify concepts to enhance my understanding, one article at a time.

By Jonathan Jung, RRT-NPS

Note: This article reflects my learning journey in ECMO and is intended for educational purposes only. It should not be used as a substitute for professional medical advice or guidance. Always consult with qualified healthcare professionals for clinical decisions and patient care.

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Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.5 Sonnet/Opus, Perplexity, Gemini 1.5 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

Today, I stumbled across a note I had written almost exactly two years ago—a few months before starting my orientation and learning journey to become an ECMO specialist. The note captured a simple, actionable framework on how to learn anything effectively:

1. Learn Just Enough

2. Implement – Project-Based Learning

3. Iterate – Repeat, Repeat, Repeat

4. Accountability

I can't remember where I got this or who shared it with me, but it was important enough to write down at the time. I will call it the LIIA method (Learn, Implement, Iterate, Accountability). As I thought about it, I realized how much LIIA has shaped my journey in ECMO—even without my conscious awareness.

Applying the Learn, Implement, Iterate, Accountability to my ECMO Journey

1. Learn Just Enough

Goal: Focus on the basics of ECMO before diving into advanced concepts.

Outcome: Gain the confidence to engage in ECMO-related discussions and tasks without being overwhelmed.

How: When I started in ECMO, there was much to learn—from understanding the circuit and physiology to troubleshooting complex scenarios. I tackled it by focusing on the basics first: the core principles of oxygenation, cannulation, and circuit components. Instead of diving into every detail, I picked just enough to apply it practically. This gave me the confidence to engage with the material without feeling paralyzed by the complexity.

2. Implement – Project-Based Learning

Goal: Actively apply your knowledge in real-world scenarios.

Outcome: Develop practical skills by engaging with actual ECMO tasks and challenges

How: The best way to learn ECMO is by doing. During orientation and beyond, I worked on real-world cases and simulations. I created mini-projects, like designing a shift and troubleshooting checklist for myself. I am volunteering, creating educational modules for new orientees, and volunteering on the guideline committee. This will help fill my knowledge gaps. This Newsletter has helped a lot; writing about things I am learning at work forces me to dive deep into different ECMO subjects. Each task had a purpose: to help me apply my learning.

3. Iterate – Repeat, Repeat, Repeat

Goal: Build mastery through continuous practice and refinement.

Outcome: Reinforce your skills, troubleshoot effectively, and deepen my understanding of ECMO management.

How: Mastering ECMO is a journey of continuous learning, where each experience adds to your understanding and ability to provide safe, effective care. It's about doing, reviewing, and refining. Whether responding to emergencies in simulations or managing patients during shifts, every experience added a layer of understanding. I try to get feedback from some of the ECMO Specialists and Physicians I work alongside, using their insights to adjust and improve my approach.

4. Accountability

Goal: Stay motivated, track my growth, and achieve my career objectives.

Outcome: Maintain focus, measure improvement, and consistently work toward advancing my career.

How: Accountability is crucial in staying on track. Most coworkers at my institution are open to questions and don't hold it against you for asking something basic or clarifying something obvious (in other words, a stupid question, LOL). While my LinkedIn newsletter has just reached an exciting milestone of 1,000 subscribers, my Substack audience is smaller, with around 30 subscribers. Both platforms play a key role in keeping me motivated and accountable. I plan to eventually introduce a paid subscription for additional content, such as in-depth articles and guides for ACLS/PALS/BLS/ATLS, and to help others prepare for the ELSO certification exam. I'm focusing on growing these platforms and ensuring the free content remains valuable to my readers. My LinkedIn subscribers have also played a significant role in keeping me accountable, fact-checking me, and letting me know if I've gotten something wrong. Thanks for that! Tracking my progress through a logbook of cases and lessons has helped me see how far I've come and where I need to focus next.

Attending conferences has also been a key part of my learning journey. These events provide valuable opportunities to learn from global experts, network with peers, and stay updated on the latest advancements. While the conferences, flights, and hotels have been expensive, they are an investment in my professional development. So far, I have been to Seattle ELSO, SWAAC ELSO in Kuwait, and a few online one-day events. Next month, I will be attending SWAAC ELSO in Abu Dhabi, and in June, I'll participate in the La Pitié Hospital 5-day course and the ECOS-TCS International Conference. If you're attending any of these events, I hope to see you there!

Looking Back and Moving Forward

When I compare where I started to where I am now, I see how much progress I've made—even through moments of doubt and distraction. LIIA has unconsciously guided me, helping me stay grounded in the learning process, even when things felt overwhelming.

I'm sharing this framework with my LinkedIn newsletter subscribers today, hoping it might resonate with others on their learning journeys—whether in ECMO or elsewhere. It's a reminder to stay the course, even when the road gets tough, and to trust the process of learning, doing, refining, and being held accountable.

As I move forward, I'm recommitting to this approach. ECMO demands constant growth, and I'm ready to embrace the journey with fresh determination. If you've found a similar learning method or have tips that have worked for you, I'd love to hear about them. Let's keep learning together.

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Acknowledgments:

Here is a list of tools and resources that assisted in creating this article and others. I developed three custom GPTs for specialized research: AI ECMO Expert, ECMO Specialist Handover Practice, and Micro Definitions (MD-GPT). These tools were instrumental in gathering and analyzing information from key sources.

Special thanks to the AI platforms and tools that facilitated this research:

• OpenEvidence (Daniel Nadler and Zachary Ziegler, OpenEvidence)

• Storm (Stanford University)

• GPT-4o/o1, Claude 3.5 Sonnet/Opus, Perplexity, Gemini 1.5 Flash

• Grammarly for editorial and proofreading assistance (can't live without it)

• Leonardo AI, DALL-E3 AI Image Generator, Microsoft Designer, and Adobe Express for generating images and visual content

📝 Read the original article here: The Aftermath of ECMO: Beyond Survival

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