The Patient in Front of You

It’s 2 AM.

A 72-year-old woman arrives in your Emergency Department with new-onset atrial fibrillation. Her CHA₂DS₂-VASc score is 4.

A few bays away, a 55-year-old man is diagnosed with a segmental pulmonary embolism.

Meanwhile, the oncology service calls regarding a patient with metastatic colon cancer and recurrent DVT despite anticoagulation.

Three patients. Three thrombotic problems. One recurring question:

Which anticoagulant should we choose ?

Not long ago, the answer was usually warfarin.

Today, Direct Oral Anticoagulants (DOACs) have fundamentally changed how we prevent and treat thromboembolic disease. The recently released 2026 ACC Scientific Statement represents perhaps the most comprehensive modern review of DOAC use across atrial fibrillation, venous thromboembolism, cancer-associated thrombosis, stroke prevention, and special populations (Kumbhani et al., 2026).

But while DOACs have become standard therapy, their optimal use remains surprisingly misunderstood. This article explores what has changed, what hasn’t, and how acute care physicians should approach anticoagulation in 2026.

Why DOACs Changed Everything

For decades, warfarin dominated anticoagulation. It worked, but it came with significant challenges:

• Narrow therapeutic window

• Frequent INR monitoring

• Numerous food interactions

• Multiple drug interactions

• High variability between patients

DOACs were developed to overcome these limitations and now account for nearly 80% of oral anticoagulant prescriptions in many regions (Kumbhani et al., 2026).

The currently available DOACs include:

Factor Xa inhibitors

• Apixaban

• Rivaroxaban

• Edoxaban

Direct thrombin inhibitor

• Dabigatran

(Kumbhani et al., 2026)

Unlike warfarin, these agents provide predictable pharmacokinetics, fixed dosing, and generally do not require routine laboratory monitoring (Kumbhani et al., 2026).

The result?

A simpler, safer, and often more effective approach to anticoagulation.

The Most Important Update: Think Risk, Not Scores

One of the subtle but important shifts highlighted in the ACC statement is that anticoagulation decisions should increasingly be based on absolute thromboembolic risk rather than rigid dependence on CHA₂DS₂-VASc alone (Kumbhani et al., 2026).

Historically, clinicians memorized:

• CHA₂DS₂-VASc ≥2 → anti-coagulate

• CHA₂DS₂-VASc <2 → don’t

Reality is more nuanced. Patients with similar scores may have markedly different actual stroke risks depending on AF burden, cardiac substrate, renal function, and co-morbidities.

The modern approach emphasizes:

• Shared decision-making

• Individualized risk assessment

• Consideration of additional modifiers beyond traditional scoring systems

(Kumbhani et al., 2026).

Atrial Fibrillation: DOACs Are the New Default

For most patients with atrial fibrillation requiring anticoagulation, DOACs are now unequivocally preferred over warfarin (Kumbhani et al., 2026).

The reasons are straightforward:

• Similar or better stroke prevention

• Less intracranial hemorrhage

• Easier use

• No INR monitoring

The ACC Scientific Statement strongly supports DOACs as first-line therapy for non-valvular AF.

But There Are Two Major Exceptions

1. Mechanical Heart Valves

Despite years of hope, DOACs remain unsuitable. The RE-ALIGN trial demonstrated excess thromboembolic events and bleeding with dabigatran compared with warfarin in mechanical valve patients (Eikelboom et al., 2013).

More recently, the PROACT Xa trial showed higher rates of valve thrombosis and thromboembolic events with apixaban compared with warfarin (Kumbhani et al., 2026).

For mechanical valves:

Warfarin remains king.

2. Rheumatic Mitral Stenosis

The INVICTUS trial demonstrated superior outcomes with vitamin K antagonists compared with rivaroxaban among patients with rheumatic heart disease and AF (Connolly et al., 2022; Kumbhani et al., 2026).

This remains another domain where warfarin continues to outperform DOACs.

Acute VTE: The Era of DOAC Dominance

The management of DVT and PE has changed dramatically. Multiple pivotal trials and meta-analyses have demonstrated that DOACs achieve similar efficacy with less major bleeding than warfarin (Kumbhani et al., 2026).

Today:

DOACs are first-line treatment for most patients with acute VTE.

(Kumbhani et al., 2026)

Is Apixaban Becoming the Preferred DOAC?

If one theme repeatedly emerges throughout contemporary literature, it is the growing prominence of apixaban.

The 2026 ACC statement notes that recent evidence suggests an apixaban-based strategy may be associated with lower bleeding compared with rivaroxaban during VTE treatment (Kumbhani et al., 2026).

The COBRRA trial further strengthened this observation, showing lower bleeding rates with apixaban in acute VTE management (Kumbhani et al., 2026).

Additionally, the ACC consensus highlights apixaban as the preferred option in:

• Frailty

• Advanced age

• Prior bleeding

• Chronic kidney disease

(Kumbhani et al., 2026).

This does not mean rivaroxaban is obsolete. It means that when uncertainty exists, apixaban increasingly appears to offer the best balance between efficacy and safety.

The Most Common Mistake: Stopping Too Early

Many clinicians continue to think of anticoagulation as a 3–6 month treatment. For many patients, this is no longer true.

The ACC statement emphasizes extended anticoagulation for:

• Unprovoked VTE

• Recurrent VTE

• Persistent risk factors

• High recurrence risk profiles

(Kumbhani et al., 2026).

In these patients:

The question is not whether treatment lasts beyond six months.

The question is whether treatment should ever stop.

Cancer-Associated Thrombosis: One of the Biggest Changes in Modern Medicine

Perhaps no area has evolved faster than cancer-associated thrombosis (CAT). For years, LMWH was the unquestioned standard.

That paradigm has shifted. A 2022 meta-analysis by Frère et al. demonstrated significantly lower recurrent VTE rates with DOACs compared with LMWH, without differences in mortality.

Similarly, Schrag et al. (2023) reported recurrent VTE rates of 6.1% versus 8.8% in favor of DOACs during a randomized trial involving cancer patients.

The strongest contemporary evidence supports:

• Apixaban

• Edoxaban

• Rivaroxaban

for selected cancer patients (Masini et al., 2023; Fujisaki et al., 2024).

But Not Every Cancer Patient Is the Same

Bleeding risk remains highly tumor-specific. The literature consistently identifies:

• Gastrointestinal cancers

• Gastroesophageal tumors

• Some genitourinary malignancies

as populations where bleeding risk may outweigh benefits (O’Connell et al., 2020; Sabatino et al., 2020; Masini et al., 2023).

This is where individualized medicine still matters.

Chronic Kidney Disease: A Persistent Challenge

Anticoagulation in advanced CKD remains difficult. Evidence remains limited, particularly in dialysis populations.

The ACC statement concludes:

• Apixaban may be considered in dialysis patients

• Dabigatran should generally be avoided

(Kumbhani et al., 2026).

For acute care physicians, this often translates into one practical rule:

If severe renal dysfunction is present, pause before reflexively prescribing a DOAC.

Obesity: Time to Retire an Old Myth

Many clinicians remain hesitant to prescribe DOACs in severe obesity. Current evidence no longer strongly supports this concern.

The ACC statement specifically endorses:

• Apixaban

• Rivaroxaban

for patients with BMI ≥40 kg/m² (Kumbhani et al., 2026). The assumption that obesity automatically requires warfarin is increasingly outdated.

What If Your Hospital Doesn’t Have Reversal Agents?

This question frequently arises in low- and middle-income settings. Can DOACs still be used if idarucizumab or andexanet alfa are unavailable?

The literature suggests yes.

Reviews by Weitz (2017), Chaudhary et al. (2019), and Grottke et al. (2024) conclude that most DOAC-associated bleeding can be managed through supportive care, temporary drug interruption, and standard resuscitative measures.

Specific antidotes are primarily reserved for:

• Life-threatening bleeding

• Catastrophic hemorrhage

• Emergency surgery

(Gómez-Outes et al., 2023; Grottke et al., 2024).

When antidotes are unavailable, PCCs remain a reasonable rescue strategy despite lower-quality evidence (Pozzi et al., 2024; Tran et al., 2025).

The practical message:

DOACs do not require onsite antidotes to be prescribed safely.

However, hospitals should maintain protocols for catastrophic bleeding management.

The Future: Beyond AF and DVT

The 2026 ACC Scientific Statement hints at the future direction of anticoagulation.

Emerging areas include:

• Device-detected subclinical AF

• Atrial myopathy

• Post-ablation anticoagulation

• Left atrial appendage closure strategies

• Expanded cancer-associated thrombosis pathways

(Kumbhani et al., 2026).

Many of tomorrow’s anticoagulation decisions may depend less on rhythm and more on underlying atrial disease biology.

Pulse Check

A decade ago, anticoagulation was largely a warfarin-versus-not-warfarin discussion.

In 2026, the conversation has evolved.

DOACs have become the default anticoagulants for most patients with atrial fibrillation and venous thromboembolism. Yet success lies not in prescribing them blindly, but in selecting the right drug, at the right dose, for the right patient.

The emergency physician’s challenge is no longer:

“Should I anticoagulate?”

It is:

“Which anticoagulant offers this patient the greatest net clinical benefit?”

Increasingly, the answer is a DOAC.

And more often than not, it may be apixaban.

References

• Kumbhani DJ, et al. 2026 ACC Scientific Statement on Direct Oral Anticoagulants.

• Frère C, et al. 2022.

• Schrag D, et al. JAMA. 2023.

• Fujisaki T, et al. JACC CardioOncology. 2024.

• Grottke O, et al. Eur J Anaesthesiol. 2024.

• Tran HA, et al. Internal Medicine Journal. 2025.

• Weitz JI. Semin Respir Crit Care Med. 2017.

• Chaudhary R, et al. J Thromb Thrombolysis. 2019.

• Masini M, et al. Curr Oncol Rep. 2023.

• O’Connell C, et al. The Oncologist. 2020.

• Sabatino J, et al. JACC CardioOncology. 2020.

A Case We Have All Seen

A 58-year-old man collapses in a shopping mall. Bystander CPR is initiated. EMS arrives within 6 minutes.

• Initial rhythm: Ventricular fibrillation (VF)

• Shock #1 → VF persists

• Shock #2 → VF persists

• Epinephrine administered

• Shock #3 → VF persists

The monitor continues to display coarse VF. The question now is no longer:

“Should we shock again?”

The question is:

“Should we shock differently?”

For decades, resuscitation algorithms largely focused on repeating the same intervention: deliver another shock through the same pad position using the same vector. Recent evidence suggests that in refractory VF, changing how we defibrillate may be more important than simply shocking again.

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The Problem: Refractory Ventricular Fibrillation

Traditionally, refractory VF has been defined as VF persisting after three consecutive defibrillation attempts. Although only a minority of cardiac arrest patients develop refractory VF, they account for a disproportionate share of cardiac arrest mortality.

The challenge is straightforward:

• Every additional minute spent in VF worsens myocardial ischemia.

• Prolonged VF reduces the likelihood of ROSC.

• Neurologic outcomes deteriorate as low-flow time increases.

The goal therefore becomes:

Terminate VF as early as possible.

Why Standard Defibrillation May Fail

Several mechanisms may contribute to shock failure:

1. Inadequate Current Delivery

Not all delivered energy reaches the myocardium.

Current must pass through:

• Chest wall

• Lung tissue

• Thoracic structures

before reaching the heart.

Higher trans-thoracic impedance means lower effective myocardial current.

2. Suboptimal Shock Vector

Standard anterior-lateral pad placement delivers current along a single pathway.

Some regions of myocardium may receive inadequate current density.

If enough critical myocardium is not depolarized simultaneously, VF may continue.

3. Progressive Electrical Remodeling

The longer VF persists:

• ATP stores deplete

• Cellular acidosis develops

• Myocardial excitability changes

The heart becomes progressively harder to defibrillate.

This is why time in VF matters.

The Evolution of Alternative Defibrillation Strategies

Several strategies have emerged:

Escalating Shock Energy

Increasing delivered joules.

Vector Change (VC)

Changing pad position from:

Anterior-Lateral → Anterior-Posterior

Double Sequential External Defibrillation (DSED)

Using two sets of pads and two defibrillators. Among these, DSED has generated the greatest interest.

What Exactly Is DSED?

Double Sequential External Defibrillation (DSED) uses:

First Defibrillator

Anterior-Lateral pads

Second Defibrillator

Anterior-Posterior pads

Two shocks are delivered in rapid succession after three failed standard shocks. The goal is to expose the myocardium to multiple shock vectors and potentially greater current delivery.

Why Might DSED Work?

Several physiologic explanations have been proposed.

1. Multiple Shock Vectors

Different vectors may recruit myocardial regions not adequately exposed by standard defibrillation.

More myocardium depolarized simultaneously increases the probability of VF termination.

2. Higher Current Delivery

Investigators observed:

• Lower transthoracic impedance with anterior-posterior pads

• Greater estimated myocardial current delivery

Current—not energy—is the primary determinant of successful defibrillation.

3. Reduced Total Time in VF

Alternative defibrillation strategies appear to terminate VF earlier.

The shorter the duration of VF:

• The lower the low-flow state

• The greater the chance of neurologically intact survival

This may be the most important mechanism of all.

The Landmark Trial: DOSE-VF

Everything changed in 2022. The DOSE-VF Trial compared:

Standard Defibrillation

versus

Vector Change Defibrillation

versus

Double Sequential External Defibrillation

in patients who remained in VF after three standard shocks.

What Did DOSE-VF Show?

Compared with standard defibrillation:

DSED Improved

✅ VF termination

✅ ROSC

✅ Survival to hospital discharge

✅ Neurologically intact survival

DSED demonstrated superiority across every clinically meaningful outcome.

Vector Change Also Helped

Compared with standard defibrillation:

• Better VF termination

• Better survival to discharge

However, DSED remained the only strategy associated with improved neurologically intact survival.

The Most Important Clinical Message

The DOSE-VF investigators found that:

The greatest benefit occurred immediately after introducing DSED or vector-change shocks.

This suggests that refractory VF may not need more of the same therapy. It may need a different therapy.

DSED vs Vector Change: Which Should We Use?

This remains controversial.

The trial was not powered to directly compare DSED and vector change.

However:

• Point estimates favored DSED.

• Neurologically intact survival favored DSED.

• Rearrest rates were lower with DSED.

Current expert opinion:

Two Defibrillators Available?

Use DSED.

Only One Defibrillator Available?

Use Vector Change Defibrillation.

What About Defibrillator Damage?

Perhaps the most common concern.

Fortunately, available evidence is reassuring.

A survey involving over 1,100 DSED cases found:

Defibrillator Damage Rate

~0.4%

Importantly:
No damage was reported when using the sequential technique employed in DOSE-VF. Most reported cases occurred with simultaneous shock delivery or non-standard pad positioning.

Simultaneous vs Sequential Shocks

Interestingly, newer analyses suggest:

Very short intervals between shocks may terminate VF more effectively than longer delays. Some data suggest that nearly simultaneous shocks may produce the highest VF termination rates.

However:
Current guideline-supported practice remains the sequential technique used in DOSE-VF until additional evidence emerges.

The 2023 ILCOR Recommendation

Following DOSE-VF, ILCOR updated its guidance:

DSED or vector-change defibrillation may be considered in adults with VF/pVT persisting after three consecutive shocks.

If DSED is used:

• Follow a protocol similar to DOSE-VF

• A single operator should activate both defibrillators sequentially

Where Does ECMO Fit?

For many refractory VF patients, the discussion eventually becomes:

DSED or ECPR?

The answer is likely:

DSED first.

ECMO second.

DSED is:

• Fast

• Widely available

• Low cost

• Immediately deployable

ECMO requires:

• Specialized teams

• Transport logistics

• Significant resources

A reasonable strategy is:

Attempt advanced defibrillation first, then escalate to ECPR if ROSC is not achieved.

What Does the Future Look Like?

Several ongoing trials are now investigating:

Earlier DSED

Instead of waiting for three failed shocks.

Researchers are asking:

• Should DSED be used after the first failed shock?

• Should DSED be the initial strategy?

• Can AI identify patients likely to develop shock-refractory VF?

These studies may fundamentally reshape future cardiac arrest algorithms.

Practical Takeaways for Acute Care Physicians

1. Refractory VF is a Defibrillation Problem

Think beyond drugs.

The intervention most likely to change outcomes remains successful defibrillation.

2. After Three Failed Shocks, Change Your Strategy

Consider:

• Vector Change Defibrillation

• DSED

rather than simply repeating standard shocks.

3. If Two Defibrillators Are Available, Learn DSED

The strongest evidence currently favors DSED for refractory VF.

4. Time in VF Matters

Every minute spent in VF reduces survival.

Earlier VF termination may be the key mechanism behind improved outcomes.

5. The Defibrillation Landscape Is Changing

The future of cardiac arrest may not depend on more medications.

It may depend on delivering the right shock, through the right vector, at the right time.

Closing Thoughts

For decades, defibrillation was viewed as a binary intervention:

Shock or don’t shock.

The emerging evidence from DOSE-VF challenges that mindset. The next evolution in resuscitation may not come from a new drug or a new device. It may come from recognizing that when VF refuses to die, how we shock matters just as much as when we shock.

Read more here - Original Review Article

It’s 2:17 a.m.

A 58-year-old man arrives clutching his chest. The ECG leaves little room for doubt, an anterior STEMI. While the cath lab is being activated, the nurse turns to you.

“Doctor, which anti-platelet should I load?”

Before you’ve answered, another patient rolls in. A 72-year-old woman with a minor ischemic stroke, well within 4.5 hours of symptom onset.

Should she receive aspirin alone? Or dual anti-platelet therapy? or nothing at all?

As you’re reviewing her CT, the surgical registrar calls.

“We’ve got a patient with a perforated bowel. He’s on aspirin and ticagrelor after a stent placed three months ago. Can we stop them?”

Three patients. Three anti-platelet decisions. Three completely different answers.

Yet every one of them starts with the same question.

Why is this patient need an anti-platelet?

Not which drug. Not how long they’ve been taking it. But why?

‘If this article helped simplify a difficult bedside decision, consider sharing it with your ED or acute care team, leave your thoughts in the comments, and subscribe to Life on the Frontline for more practical, evidence-based guides from the world of emergency and acute care.’

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Because modern anti-platelet therapy is no longer about memorizing drugs. It’s about understanding the balance between thrombosis and bleeding, and recognizing that this balance changes with time (Kumbhani et al., 2026).

In the ED, we are often the first physicians to influence that balance. We decide what gets loaded, what gets withheld, what should continue before surgery, and what should never be stopped. This article isn’t a cardiology review.

It’s a practical guide to the anti-platelet decisions emergency and acute care physicians make every shift.

A Mental Model Before We Begin

Whenever you encounter a patient on anti-platelets, pause and ask three questions.

1. Why was it started?

• Acute coronary syndrome?

• PCI?

• Stroke?

• Peripheral arterial disease?

• Primary prevention?

2. How recent was the event?

Hours? Days? Weeks? Years?

A patient one week after PCI is very different from one who had a stent placed five years ago.

3. What is the biggest threat today?

Bleeding? Or thrombosis?

Everything else follows from these three questions.

Decision 1

Which Anti-platelet Should I Load in the Emergency Department?

This is probably the most common and one of the most important antiplatelet decisions we make.

The answer depends entirely on where the patient is going next.

• Primary PCI?

• Fibrinolysis?

• Early invasive NSTEMI?

• Conservative management?

Each pathway has a different strategy.

Scenario 1: STEMI Going for Primary PCI

Imagine you’re in the resuscitation bay. The ECG shows a large anterior STEMI. The cath lab has accepted the patient. Your priority is simple:

Achieve rapid and potent platelet inhibition before coronary instrumentation.

The current standard is:

• Chewed aspirin 162–325 mg

• Plus a P2Y12 inhibitor

For most patients undergoing primary PCI, ticagrelor or prasugrel are preferred over clopidogrel because they produce faster, more potent, and more predictable platelet inhibition, reducing ischemic events and stent thrombosis (Wallentin et al., 2009; Wiviott et al., 2007; Kumbhani et al., 2026).

Which P2Y12 Inhibitor Should I Choose?

Ticagrelor

Ticagrelor has become the default choice in many emergency departments. Why?

• Rapid onset

• No metabolic activation required

• Potent platelet inhibition

• Reversible receptor binding

The PLATO trial demonstrated lower cardiovascular mortality compared with clopidogrel without increasing overall major bleeding, making it an attractive first-line agent in ACS (Wallentin et al., 2009).

Prasugrel

Prasugrel is equally potent and in PCI-treated patients may even outperform ticagrelor in selected populations (Schüpke et al., 2019).

However, remember its major limitations. Avoid prasugrel in patients with:

• Previous stroke or TIA

• Age ≥75 years (unless benefits clearly outweigh risks)

• Weight <60 kg

Unlike ticagrelor, many operators prefer administering prasugrel after coronary anatomy has been defined, particularly if there is a realistic possibility the patient will require CABG.

Clopidogrel

Clopidogrel still has an important place. It remains reasonable when:

• Ticagrelor or prasugrel are unavailable

• Bleeding risk is high

• Cost is a major issue

• Potent P2Y12 inhibitors are contraindicated

Think of clopidogrel not as an “inferior” drug—but as the right drug for selected patients.

Frontline Pearl

PCI favors potent platelet inhibition. If the patient is heading to the cath lab, think ticagrelor or prasugrel first.

Scenario 2: STEMI Receiving Thrombolysis

Now imagine a different hospital. No PCI capability. Transfer will take four hours. The patient is receiving tenecteplase. Should you still load Ticagrelor or Prasugrel?

No.

This is one of the most common misconceptions among junior doctors. The evidence supporting fibrinolysis was built around clopidogrel, not the newer P2Y12 inhibitors.

Recommended Strategy

Why Not Ticagrelor?

Could ticagrelor work? Possibly.

Should it replace clopidogrel routinely with thrombolysis? Not yet.

The strongest evidence for pharmaco-invasive STEMI still supports aspirin plus clopidogrel after fibrinolysis, and contemporary guidelines continue to recommend this approach (Kumbhani et al., 2026).

Scenario 3: NSTE-ACS

Very High Risk or High Risk NSTE- ACS , continue same approach as of STEMI requiring PCI.
but for others,
This is where things become less straightforward. For years, many of us loaded clopidogrel as soon as we diagnosed NSTEMI. That practice has changed.

Modern evidence suggests routine pretreatment before coronary anatomy is known offers little benefit and may complicate patients who ultimately require CABG (Kumbhani et al., 2026).

My Practical Approach

If early angiography (<24 hours) is planned:

• Give aspirin.

• Discuss P2Y12 timing with cardiology.

• In many patients, defer loading until coronary anatomy is defined.

If angiography will be delayed or the patient is managed conservatively:
Loading with ticagrelor or clopidogrel when appropriate is reasonable.

Common ED Pitfalls

❌ Giving prasugrel to a patient with previous stroke.

❌ Loading ticagrelor in a patient receiving thrombolysis because “it’s newer.”

❌ Automatically loading every NSTEMI before discussing the invasive strategy.

❌ Forgetting that patients over 75 years receiving fibrinolysis do not receive a clopidogrel loading dose.

Decision 2

Does Every ACS Patient Still Need 12 Months of Dual Anti-platelet Therapy?

For years, the answer was simple. Every patient with ACS received 12 months of dual antiplatelet therapy (DAPT)—usually aspirin plus a P2Y12 inhibitor.

It was easy to remember. It was also easy to teach. But like many “rules” in medicine, it turned out to be only partly true. Over the past decade, improvements in stent technology, PCI techniques, and the availability of more potent anti-platelet agents have fundamentally changed the conversation. Today’s question is no longer:

“Should every patient receive 12 months of DAPT?”

Instead, we ask:

“How long does this particular patient need protection from thrombosis before the risk of bleeding becomes the greater threat?”

That shift—from fixed-duration therapy to individualized therapy—is perhaps the biggest conceptual change in modern anti-platelet management (Kumbhani et al., 2026).

The first month after an ACS is a dangerous time. Platelets are highly activated. The stent is still endothelializing. The culprit plaque remains biologically unstable.

This is precisely when dual antiplatelet therapy (DAPT) provides its greatest benefit. But as weeks turn into months, something interesting happens—the risk of stent thrombosis falls rapidly, while the cumulative risk of bleeding continues to rise.

That’s why modern antiplatelet therapy is no longer about one duration for everyone. It is about matching the duration of DAPT to the patient’s evolving balance between ischemic and bleeding risk (Kumbhani et al., 2026).

The New Way to Think About DAPT

Instead of asking:

“Should I stop DAPT at 12 months?”

Ask:

“Has the patient’s bleeding risk now become greater than their ischemic risk?”

If the answer is yes, shortening DAPT may be safer. If the answer is no, prolonged therapy may still provide benefit.

When Can We Shorten DAPT?

Several contemporary trials have shown that selected patients can safely transition to P2Y12 inhibitor monotherapy after 1–3 months of DAPT, reducing bleeding without a significant increase in ischemic events (Mehran et al., 2019; Valgimigli et al., 2021).

Who should you think about?

• Older adults

• Previous GI bleeding

• Chronic kidney disease

• Frailty

• Need for future surgery

• Concurrent anticoagulation

De-escalation: Less Can Be More

Imagine your patient returns three months after PCI. No recurrent ischemia. Now they develop upper GI bleeding.

Do they still need potent DAPT? Maybe not.

In carefully selected patients, switching from ticagrelor or prasugrel to clopidogrel, or stopping aspirin and continuing a P2Y12 inhibitor alone, can substantially reduce bleeding while maintaining acceptable ischemic protection (Kumbhani et al., 2026).

Decision 3

The Patient Has an Acute Ischemic Stroke. Should I Give Aspirin, Dual Antiplatelet Therapy, or Neither?

A 69-year-old man presents 90 minutes after sudden right arm weakness and aphasia. His CT brain shows no hemorrhage.

Before you think about aspirin or clopidogrel, ask yourself one question:

Is this patient a candidate for reperfusion therapy?

This is arguably the most important antiplatelet decision in acute stroke care. Giving anti-platelets too early in a patient proceeding for intravenous thrombolysis or mechanical thrombectomy can increase bleeding risk without improving outcomes.

Step 1: Is the Patient Eligible for Reperfusion?

Intravenous thrombolysis

Eligible?
Do NOT administer aspirin or any P2Y12 inhibitor before thrombolysis.

Following alteplase or tenecteplase, all antiplatelet and anticoagulant therapy should be withheld for the first 24 hours.

A repeat CT (or MRI) demonstrating no intracranial hemorrhage is required before initiating antiplatelet therapy (Powers et al., 2019; European Stroke Organisation, 2023).

Mechanical thrombectomy

Patients proceeding directly for thrombectomy without thrombolysis similarly should not receive routine antiplatelet loading before reperfusion, unless there is another specific indication (such as emergent intracranial stenting).

Once post-procedure imaging excludes hemorrhage, antiplatelet therapy can be started according to the underlying stroke mechanism and procedural findings.

(Kumbhani et al., 2026)

Minor Stroke: Aspirin Alone or Dual Antiplatelet Therapy?

A 69-year-old man presents with sudden right arm weakness that resolved within 20 minutes. His CT brain is normal. He has a National Institutes of Health Stroke Scale (NIHSS) score of 1.

Should he receive aspirin? Or dual antiplatelet therapy? The answer depends on stroke severity.

Minor Stroke and High-Risk TIA

Three landmark trials—CHANCE, POINT, and THALES—changed our practice. For patients with:

• Minor ischemic stroke (NIHSS ≤3)

• High-risk TIA (ABCD² ≥4)

Early initiation of DAPT reduces recurrent stroke, particularly during the first three weeks (Wang et al., 2013; Johnston et al., 2018).

Why Only 21 Days?

Because recurrent stroke risk is highest immediately after the event. After three weeks, the incremental benefit of DAPT diminishes, while bleeding risk continues to increase. Unlike ACS, where DAPT is measured in months, stroke DAPT is measured in weeks. (Kumbhani et al., 2026)

Decision 4

The Surgeon Wants to Stop the Anti-platelets

Few phone calls create more anxiety than this one.

“Doctor, can we stop the aspirin before surgery?”

The answer isn’t simply yes or no. It depends on why the patient is taking it. A patient taking aspirin for primary prevention is very different from one who underwent PCI six weeks ago.

Elective Surgery After PCI

Whenever possible:

• Delay surgery at least 6 months after PCI for chronic coronary disease.

• Delay surgery 12 months after PCI for ACS.

(Kumbhani et al., 2026)

Emergency Surgery

Sometimes surgery simply cannot wait.

Options include:

• Proceeding despite antiplatelet therapy when delay would be more dangerous.

• Platelet transfusion in selected life-threatening bleeding scenarios.

• Bridging with intravenous cangrelor in carefully selected recent PCI patients.

(Kumbhani et al., 2026)

Decision 5

The Patient Is Already Taking a DOAC

An 80-year-old patient with atrial fibrillation undergoes PCI.

Should you prescribe:

Aspirin + Clopidogrel + Apixaban?

That used to be standard practice. Today, prolonged triple therapy has largely disappeared.

Modern Strategy

For most patients:

• Short course of triple therapy (1–4 weeks)

• Then discontinue aspirin

• Continue DOAC + clopidogrel

This strategy substantially reduces bleeding while preserving ischemic protection (Kumbhani et al., 2026).

Final Thoughts

Antiplatelet therapy has become far more nuanced than it was a decade ago. Yet the bedside approach remains surprisingly simple. Understand why the therapy was started. Recognize how the patient’s risk changes with time. And remember that the best antiplatelet strategy is rarely the most aggressive one—it is the one that strikes the right balance between preventing thrombosis and avoiding harm.

As emergency and acute care physicians, we are often the first to make that decision. It may be as simple as choosing the correct loading dose in a STEMI, or as difficult as deciding whether to stop DAPT before emergency surgery. Either way, our decisions shape what happens long after the patient leaves the Emergency Department.

References

1. Kumbhani DJ, Gibson CM, Kinlay S, et al. Antiplatelet Therapy in the Management of Atherosclerotic Cardiovascular Disease: 2026 ACC Scientific Statement. J Am Coll Cardiol. 2026.

2. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009.

3. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in ACS undergoing PCI. N Engl J Med. 2007.

4. Schüpke S, Neumann FJ, Menichelli M, et al. Ticagrelor or prasugrel in patients with acute coronary syndromes. N Engl J Med. 2019.

5. Mehran R, Baber U, Sharma SK, et al. Ticagrelor with or without aspirin after PCI (TWILIGHT). N Engl J Med. 2019.

6. Valgimigli M, Frigoli E, Heg D, et al. Dual antiplatelet therapy after PCI in high bleeding risk patients (MASTER DAPT). N Engl J Med. 2021.

7. Wang Y, Wang Y, Zhao X, et al. Clopidogrel with aspirin in acute minor stroke or TIA (CHANCE). N Engl J Med. 2013.

8. Johnston SC, Easton JD, Farrant M, et al. Clopidogrel and aspirin in acute ischemic stroke and high-risk TIA (POINT). N Engl J Med. 2018.

Let’s start from where we left in Part -1.

Step Three:

Is There Evidence of Ischemia?

An elevated troponin is a laboratory finding. Ischemia is a clinical diagnosis. And this distinction changes everything.

The Fourth Universal Definition of Myocardial Infarction requires

Acute myocardial injury plus evidence of acute myocardial ischemia to establish the diagnosis of myocardial infarction (Thygesen et al., 2018).

That evidence for myocardial ischemia may include:

• Symptoms suggestive of myocardial ischemia.

• New ischemic ECG changes.

• Development of pathological Q waves.

• Imaging evidence of new regional wall motion abnormalities.

• Identification of a coronary thrombus by angiography or autopsy (Thygesen et al., 2018).

Without ischemia, there is no myocardial infarction. There is only myocardial injury.

The Forgotten Truth

For years, clinicians learned a dangerous shortcut:

Elevated troponin = NSTEMI.

High-sensitivity assays have exposed the flaws in that thinking.

As Rokos, Mattu, and Jaffe emphasize, a substantial proportion of elevated troponin values encountered in contemporary practice arise from conditions entirely unrelated to acute coronary syndromes (Rokos, Mattu, & Jaffe, 2025).

The biomarker is extraordinarily sensitive. It is not extraordinarily specific. The physician must provide the specificity.

The Troponin Matrix

A more useful framework is to think in four quadrants:

This simple matrix explains why two patients with identical troponin values may require entirely different management strategies. The number alone never tells the whole story.

Type 1 Myocardial Infarction:

The Classical Paradigm

Type 1 MI remains the condition most clinicians immediately think of when they encounter elevated troponin levels.

It results from:

• Plaque rupture.

• Plaque erosion.

• Coronary thrombosis.

• Acute atherothrombotic occlusion (Thygesen et al., 2018).

The pathophysiology is straightforward: A disrupted plaque causes coronary obstruction, leading to myocardial ischemia, necrosis, and biomarker release.

This is the disease for which our traditional ACS therapies were designed:

• Dual antiplatelet therapy.

• Anticoagulation.

• Early angiography.

• Revascularization.

The challenge is that not every elevated troponin belongs in this category.

Type 2 MI:

The Most Misunderstood Diagnosis in Acute Care

Perhaps no concept creates more confusion than Type 2 myocardial infarction.

The Fourth UDMI defines Type 2 MI as:

Acute myocardial injury with evidence of ischemia resulting from an imbalance between myocardial oxygen supply and demand, unrelated to acute coronary thrombosis (Thygesen et al., 2018).

Examples include:

• Severe anemia.

• Sustained tachy-arrhythmias.

• Hypertensive emergencies.

• Profound hypotension.

• Coronary vasospasm.

• Severe hypoxemia.

Importantly:

Type 2 MI still requires ischemia. That sentence deserves repetition.

Type 2 MI still requires ischemia.

A septic patient with elevated troponin but no ischemic symptoms, ECG changes, or imaging evidence does not automatically have Type 2 MI.

They may simply have acute non-ischemic myocardial injury. This distinction matters because inappropriate labeling influences:

• Cardiology referrals.

• Antiplatelet prescriptions.

• Long-term diagnoses.

• Insurance coding.

• Patient expectations.

Sometimes, the most accurate diagnosis is also the simplest:

Acute myocardial injury secondary to sepsis.

No infarction. No thrombosis. No unnecessary complexity.

The Trop-Zone Concept:

Thinking Beyond Positive and Negative

One of the most elegant recent approaches to high-sensitivity troponin interpretation comes from Rokos, Mattu, and Jaffe (2025). Rather than forcing clinicians through increasingly complex algorithms, they propose thinking in terms of Troponin Zones.

This framework aligns naturally with bedside decision-making.

Zone 1:

The Whisper Zone

Very low values. Typically near the limit of quantification. The myocardium is quiet. For many assays, extremely low troponin levels carry an exceptionally high negative predictive value for acute MI (Rokos, Mattu, & Jaffe, 2025).

But caution remains essential:

Early presenters may still evolve. Clinical context always supersedes a single number.

Zone 2:

The Thinking Zone

Values around the 99th percentile. This is where emergency medicine earns its salary.

The diagnosis depends upon:

• Serial measurements.

• Delta changes.

• Symptoms.

• ECG findings.

• Risk factors.

• Alternative explanations.

Here, the question shifts from:

“Is the troponin elevated?”

to:

“Why is it elevated?”

Zone 3:

The Alarm Zone

Substantially elevated values. The probability of infarction rises. But certainty remains elusive. Massive troponin elevations may occur in:

• Fulminant myocarditis.

• Takotsubo syndrome.

• Massive pulmonary embolism.

• Septic shock.

• Electrical storms.

• Type 1 MI.

Magnitude informs probability. It does not establish diagnosis. The heart only has a limited vocabulary. Troponin is one of its distress signals. It does not tell us why it is suffering.

The Delta:

The Most Important Number You Never Memorized

High-sensitivity assays changed our relationship with time. The absolute troponin value matters. The trend often matters more.

As Januzzi and colleagues noted, one of the greatest advantages of high-sensitivity assays is their ability to detect very small changes over short intervals (Januzzi et al., 2019).

The second troponin frequently provides information that the first cannot. Think of it this way:

The first troponin is a photograph.

The delta is a movie.

Movies tell better stories. A stable troponin suggests chronic injury. A dynamic change suggests an acute process. What remains is determining whether that process is ischemic.

The Five Questions Every Troponin Demands

This is perhaps the most useful bedside framework.

Question 1:

Is the troponin above the 99th percentile?

If no:

No myocardial injury currently.
Do follow up troponin still if high clinical suspicion.

If yes:

Proceed.

Question 2:

Is there a rise or fall?

If yes:
Acute myocardial injury.

If no:
Chronic myocardial injury.

Question 3:

Is there evidence of ischemia?

Look for:

• Symptoms.

• ECG changes.

• Imaging findings.

• Angiographic evidence.

No ischemia?
Stop calling it MI.

If clinical evidence of Ischemia is present.
Repeat Trop, if initially below 99th centile,
monitor patients, repeat ECGs, keep cardiologist in loop.

Question 4:

If ischemia exists, why?

Type 1 to 5 MI.

Question 5:

What disease process explains the injury, if no evidence of myocardial ischemia?

Sepsis?
Pulmonary embolism?
Heart failure?
Myocarditis?
Arrhythmia?
Renal disease?

The troponin tells us that myocardium has suffered. It is our responsibility to determine why.

Three Patients, Three Diagnoses

Case One:

The Septic Patient

A 72-year-old woman with septic shock. Troponin rises from 24 ng/L to 68 ng/L. No chest pain. No ischemic ECG changes. Bedside echo shows global hyperdynamic function.

Diagnosis?

Acute non-ischemic myocardial injury secondary to sepsis.

Not NSTEMI. Not Type 2 MI. The injury is real. The ischemia is absent.

Case Two:

The Tachyarrhythmia Patient

A 58-year-old man presents with atrial fibrillation at 180 beats per minute. Chest discomfort occurs during the episode. Troponin rises from 18 ng/L to 95 ng/L. Diffuse ST depressions resolve after rate control.

Diagnosis?

Type 2 myocardial infarction due to oxygen supply-demand mismatch.

Acute injury. Evidence of ischemia. No plaque rupture.

Case Three:

The Dialysis Patient

A chronic hemodialysis patient presents with pneumonia.

Troponin is 140 ng/L.

Repeat value six hours later remains 142 ng/L. NO symptoms suggestive of ACS. No ischemic ECG changes.

Diagnosis? Chronic myocardial injury.

The elevated number is background information. The stability is the key.

The New Philosophy of Troponin

The era of:

Positive versus negative

is over.

The era of:

Injury versus infarction

has begun.

High-sensitivity assays did not simply improve diagnostics. They forced us to rethink the biology of myocardial damage itself.

They taught us that:

• Injury can be acute or chronic.

• Acute injury can be ischemic or non-ischemic.

• Infarction is only one subset of myocardial injury.

The biomarker became more precise. Our thinking must become equally precise.

Final Reflections

The next time someone tells you:

“The troponin is positive i.e. above 99th percentile URL.”

Pause.

Ask five questions.

Is there injury? Is it acute? Is it ischemic? If ischemic, is it Type 1 or Type 2?

And what underlying disease process explains it? Because the elevated troponin is rarely the diagnosis. It is the heart asking for context. And modern acute care begins by listening carefully to that question.

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References

Januzzi JL Jr, Mahler SA, Christenson RH, et al. Recommendations for institutions transitioning to high-sensitivity troponin testing. Journal of the American College of Cardiology. 2019;73(9):1059-1077.

Rokos IC, Mattu A, Jaffe AS. High-sensitivity troponin zones: An alternative approach to clinical decisions. The Journal of Emergency Medicine. 2025.

Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Circulation. 2018;138:e618-e651.

Troponin: 86 ng/L.

The resident looks up and says:
“Sir, the troponin is positive.”

Other than the obvious STEMI or High Risk OMI patient.
Do you get confused how to intrepret this trop results?

Positive for what?

Acute coronary syndrome?
Myocardial infarction (MI)?
Sepsis-induced myocardial injury?
Chronic kidney disease?
Tachyarrhythmia?
Heart failure?

For decades, we treated troponin as a binary test: positive or negative, infarction or no infarction. High-sensitivity assays have shattered that illusion.

Modern troponin testing has taught us an uncomfortable but essential truth:

Troponin does not diagnose myocardial infarction. Troponin detects myocardial injury.

Everything else requires clinical thinking.

One thing to remember, if there is any evidence of Ischemia (Will be defined later ) or Obvious ST - T changes suggestive of Ischemic Injury, you escalate to ACS protocol, irrespective of initial trop report, but if it doesn’t fit there, then what to do?

The Great Troponin Misconception

Perhaps the most important contribution of the Fourth Universal Definition of Myocardial Infarction (UDMI) was not a new classification system, but a new vocabulary.

It separated three concepts that clinicians often use interchangeably:

• Myocardial injury

• Myocardial ischemia

• Myocardial infarction

They are not synonymous.

According to the Fourth UDMI, myocardial injury exists whenever cardiac troponin exceeds the 99th percentile upper reference limit (URL) . Myocardial infarction, however, requires much more than an elevated biomarker. It requires evidence that the injury occurred because of ischemia. (Thygesen et al., 2018)

This distinction fundamentally changed cardiovascular medicine.

As Jaffe and colleagues noted, high-sensitivity assays have unmasked the reality that many patients experience myocardial injury in the absence of acute ischemic heart disease (Januzzi et al., 2019).

The challenge for acute care physicians is therefore not simply to recognize an elevated troponin. The challenge is to determine what kind of myocardial injury we are looking at.

The Troponin Triangle: A New Mental Model

Instead of asking:

“Does this patient have an MI?”

We should ask three sequential questions:

Only one pathway leads to myocardial infarction:

Acute myocardial injury + evidence of ischemia = MI

Everything else remains myocardial injury.

This framework appears deceptively simple, but it immediately clarifies many common diagnostic errors. The patient with septic shock and a rising troponin may have acute myocardial injury.

The patient with CKD and stable troponin elevation may have chronic myocardial injury.

Neither automatically has myocardial infarction. The troponin merely begins the investigation.

Step One:

Is There Myocardial Injury?

The definition is straightforward.

Any cardiac troponin value above the assay-specific 99th percentile URL constitutes myocardial injury (Thygesen et al., 2018).

This 99th percentile URL - is defined for a population and particular assay for both men and women, separately and is specific to the kit.

Not myocardial infarction. Not acute coronary syndrome.

Simply myocardial injury.

High-sensitivity assays now identify extremely small amounts of cardio-myocyte damage that previous generations of tests could never detect (Januzzi et al., 2019).

This increased analytical sensitivity is both a blessing and a burden. It improves early detection of true infarction. But it also reveals how frequently the myocardium suffers injury from non-coronary diseases. The heart, it turns out, is remarkably vulnerable to systemic illness.

The Heart as an Innocent Bystander

Acute care physicians encounter elevated troponin values in almost every critical illness imaginable:

• Sepsis

• Pulmonary embolism

• Stroke

• Renal failure

• Tachyarrhythmias

• Hypertensive emergencies

• Acute heart failure

• Severe anemia

• Carbon monoxide poisoning

• Burns

• Major trauma

• Myocarditis

These conditions injure myocardium. They do not necessarily infarct it. Understanding this distinction is the foundation of modern troponin interpretation.

Step Two:

Is the Injury Acute or Chronic?

This is perhaps the single most under appreciated question in acute care medicine.

However, if the patient has obvious ECG evidence of STEMI or OMI, you can effectively move directly to Step 3 and look for evidence of myocardial ischemia. In such patients, the diagnosis is driven primarily by the clinical presentation and ECG findings, with troponin serving as supportive evidence rather than the deciding factor.

Step 2 becomes particularly valuable in the far more common and often challenging patients who do not fit the classic STEMI or OMI picture.

The septic patient with an elevated troponin. The patient with atrial fibrillation and rapid ventricular response. The individual with renal dysfunction, pulmonary embolism, or acute heart failure.In these scenarios, the critical question is:

Is this myocardial injury acute, or has it been present chronically?

The Fourth UDMI defines:

Acute myocardial injury as a rise and/or fall in troponin values.

In contrast:

Chronic myocardial injury refers to persistently elevated but relatively stable troponin concentrations over time (Thygesen et al., 2018).

The number itself matters less than its trajectory.

What Defines Acute Myocardial Injury?

The Fourth Universal Definition states:

Myocardial injury is acute if there is a rise and/or fall in cTn values. (Thygesen et al., 2018)

But it intentionally does not specify a universal numeric cutoff for what constitutes a significant rise or fall. Why?

Because analytical variation differs between assays, and biological variation differs between patients.

Both Rise and Fall Matter

Importantly, both directions are equally significant.

A patient whose troponin changes from:

• 10 → 30 ng/L has acute myocardial injury.

• 300 → 180 ng/L also has acute myocardial injury.

The second patient may simply be presenting later in the course of disease, when troponin concentrations are already declining. The myocardium does not care about the direction of the curve.

What matters is that the curve is moving.

A dynamic pattern—whether upward or downward—suggests an active or recently active process, whereas relatively stable values point toward chronic myocardial injury.

Clinical Pearl

Troponin movement matters more than troponin direction.

A patient whose troponin falls from 500 to 300 ng/L may be just as acute as one whose troponin rises from 50 to 250 ng/L. The difference often reflects where the patient sits on the timeline of injury rather than a difference in severity.

Absolute Change vs Percentage Change

This is where modern practice has evolved.

The Current Recommendation

Use ABSOLUTE changes for low or mildly elevated troponin values. Use PERCENTAGE changes only when baseline troponin is substantially elevated.

This is strongly emphasized in modern hs-cTn literature.

Rokos, Mattu, and Jaffe write:

Near the 99th percentile, absolute deltas are statistically superior to relative changes. (Rokos et al., 2025)

Why Absolute Changes Are Better Near the 99th Percentile

Example:

Patient A

Troponin:
10 → 20 ng/L

Absolute change:
+10 ng/L

Relative change:
100%

Clearly significant.

Patient B

Troponin:
500 → 510 ng/L

Absolute change:
+10 ng/L

Relative change:
2%

Probably not clinically meaningful.

Patient C

Troponin:
10 → 12 ng/L

Absolute change:
+2 ng/L

Relative change:
20%

Probably just biological variation. So percentages become misleading at lower concentrations.

This is why:

Modern hs-cTn algorithms prioritize absolute deltas rather than percentage changes.

Practical Rule from the JACC Expert Panel

The JACC Scientific Panel recommends:

If the initial value is near the 99th percentile:

Use absolute change (ng/L).

If the baseline troponin is already substantially elevated (for example, CKD, chronic HF):

A relative change of >20% is often used to suggest superimposed acute injury. This is not perfect science. It is pragmatic bedside medicine.

The famous 20% Rule:

When Should We Use It?

The “20% rule” should be applied carefully.

Appropriate situations:

• CKD with chronically elevated troponin.

• Chronic heart failure.

• Known structural heart disease.

• Patients with stable baseline elevations.

Example:

Baseline:
120 ng/L

Repeat:
150 ng/L

Change:
25%

This suggests possible acute-on-chronic injury.

When NOT to use 20%

Do not use percentage changes when:

• Values are close to the 99th percentile.

• Troponins are in single digits or low double digits.

• Using accelerated 0/1-hour or 0/2-hour algorithms.

Absolute values perform better in these situations.

How Much Absolute Change Is Significant?

Unfortunately:

There is no universal number.

It depends entirely on the assay.

Examples from common hs-cTn pathways: (Rokos et al., 2025)

Your hospital must always know:

• Which assay is being used.

• The assay-specific 99th percentile.

• The validated delta thresholds.

There is no “one-size-fits-all” number.

After How Much Time Should We Look for Change?

This is another major shift in the hs-cTn era.
Depends upon the baseline tropI performed for such cases, and the population dynamics where it is validated.

Classical approach

0 hours and 3 hours. ( well validated, can be used in almost all populations)

Modern hs-cTn approach

0–1 hour protocols

Preferred in Europe. Very small absolute changes become meaningful.

0–2 hour protocols

Widely adopted in North America.

Excellent balance between sensitivity and practicality.

3-hour protocols (Only thing useful for INDIA, since others are not validated)

Still useful:

• Late presenters.

• Resource-limited settings.

• When clinical suspicion remains high despite initial testing.

The Most Important Part

Every myocardial infarction causes myocardial injury. But not every myocardial injury is myocardial infarction.

The distinction sounds semantic.

In reality, it changes everything:

• Documentation.

• Coding.

• Prognosis.

• Treatment.

• Antiplatelet use.

• Anticoagulation decisions.

• Coronary angiography.

• Patient counselling.

Most importantly, it changes how we think.

Coming in Part Two

Once we establish that myocardial injury exists—and determine whether it is acute or chronic—the next question becomes unavoidable:

Is the injury ischemic?

And only then can we discuss:

• Type 1 versus Type 2 myocardial infarction.

• The modern Trop-Zone approach.

• Why the delta often matters more than the absolute number.

• The five questions every troponin demands.

• A practical bedside algorithm for emergency physicians.

Because in modern acute care:

The elevated troponin is rarely the diagnosis.

It is merely the beginning of the story.

References

Januzzi JL Jr, Mahler SA, Christenson RH, et al. Recommendations for institutions transitioning to high-sensitivity troponin testing. Journal of the American College of Cardiology. 2019;73(9):1059-1077.

Rokos IC, Mattu A, Jaffe AS. High-sensitivity troponin zones: An alternative approach to clinical decisions. The Journal of Emergency Medicine. 2025.

Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Circulation. 2018;138:e618-e651.

The emergency department had no beds left. Three ambulances were waiting outside. The ICU was full. A 42-year-old man with a large left MCA infarct had been thrombolysed and undergone thrombectomy two hours earlier.

He remained aphasic. Dense right hemiplegia. NIHSS 22. The family looked at us and asked the question we hear far too often—and far too early:

“Doctor, will he ever recover?”

In many overcrowded emergency departments, that question quietly transforms into another:

“Should we continue aggressive care?”

The uncomfortable truth is that we often neuro-prognosticate acute ischemic stroke far earlier than the science allows.

The newly published 2026 Neuro-critical Care Society Guidelines for Neuro-prognostication in Critically Ill Adults with Acute Ischemic Stroke challenge many of our traditional assumptions—and force us to reconsider how, and more importantly when, we counsel families (Mainali et al., 2026).

Why Should Acute Care Physicians Care About This?

It is tempting to think that these recommendations belong exclusively to stroke units, neuro-ICUs, or comprehensive stroke centres. After all, many patients are no longer in the emergency department 8, 12, or 72 hours after symptom onset.

But acute care medicine rarely follows ideal timelines.

Patients arrive directly from home after delayed recognition of symptoms. Others are transferred from smaller referral centres after thrombolysis, failed thrombectomy attempts, or progressive neurological deterioration. Some return days later with aspiration, cerebral edema, seizures, or worsening neurological deficits. For many of us, the first meaningful conversation about prognosis therefore happens not at 60 minutes, but at 12 hours, 24 hours, or even 72 hours after the index event, when no department is willing to take up the patient for admission.

That is precisely why these guidelines matter to every acute care physician, for such cases.

The admission NIHSS, infarct size, age, or hemorrhagic transformation do not suddenly become reliable predictors simply because more time has elapsed. The principles remain unchanged: consider the complete clinical picture, eliminate confounders, obtain appropriate imaging, and allow neurological evolution to declare itself before making definitive judgments (Mainali et al., 2026).

Whether a patient reaches your doors directly from home or after traversing multiple layers of the healthcare system, the responsibility is the same:

We must not allow geography, referral pathways, or overcrowding to shorten the timeline that the injured brain requires for recovery.

And while many patients leave our emergency departments within hours, others arrive at our doors 12, 24, or 72 hours later—from home, from smaller hospitals, or after deterioration—forcing us to answer the same difficult question: "What happens next?"

The Guideline’s Most Important Message:

Avoid Premature Neuro-prognostication

The guideline makes an unequivocal recommendation:

Avoid premature neuro-prognostication in critically ill patients with acute ischemic stroke, including severe stroke. The appropriate observation period should consider anticipated neurological evolution, confounders, and completion of diagnostic imaging (Mainali et al., 2026).

This is not a weak suggestion. It is a strong good-practice recommendation. The rationale is simple but profound. Most deaths after severe ischemic stroke occur following decisions to withhold or withdraw life-sustaining treatment, and these decisions are heavily influenced by clinician prognostication (Mainali et al., 2026).

An inaccurate early prediction can therefore become a self-fulfilling prophecy. The patient who might have walked out of the hospital six months later never gets the opportunity.

The Danger of the Self-Fulfilling Prophecy

The guideline repeatedly warns about the self-fulfilling prophecy in stroke care: when early pessimistic predictions lead to treatment limitations, and those limitations themselves determine the final outcome (Mainali et al., 2026). Most early deaths after severe ischemic stroke occur following decisions to withhold or withdraw life-sustaining treatment rather than from the primary neurological injury alone.

The message is uncomfortable but important:

The greatest risk in neuro-prognostication is not uncertainty. It is false certainty.

What We Commonly Use in the ED—And Why the Guidelines Say “Not Alone”

Perhaps the most surprising aspect of the document is how many traditional predictors failed to meet criteria for reliable neuro-prognostication.

The following should not be used alone to predict poor long-term outcome:

• Age

• Admission NIHSS

• Hyperglycemia

• Infarct size

• Hemorrhagic transformation

• Previous stroke history

• Cerebral collateral status

• Established prediction scores including ASTRAL, DRAGON, iScore, and THRIVE (Mainali et al., 2026)

In other words:

The things we often quote to families in the first few hours after presentation are precisely the things the guideline warns us against using in isolation.

Things We Should Stop Saying in the First 24 Hours

❌ “The NIHSS is 22. Recovery is unlikely.”

❌ “The infarct is too large.”

❌ “He’s too old to do well.”

❌ “There was hemorrhagic transformation, so the outcome will be poor.”

❌ “The DRAGON score predicts a bad outcome.”

What We Should Say Instead

✅ “We need to watch the neurological trajectory over the next few days before making confident predictions.”

✅ “The complete clinical picture, repeat imaging, and response to treatment matter more than any single variable.”

Even Large Infarcts Deserve Time

Large core infarcts frequently trigger therapeutic nihilism. Yet contemporary thrombectomy trials tell a more nuanced story. The guideline notes that among patients with large infarct cores receiving endovascular therapy, approximately 41% regained independent ambulation and 23% achieved functional independence—despite imaging appearances that many clinicians would traditionally associate with futility (Mainali et al., 2026).

The message is clear:

A large infarct is not synonymous with a predetermined poor outcome.

The guideline specifically notes that modern thrombectomy trials have challenged decades of therapeutic nihilism. Even among patients with large core infarcts, recovery to independent ambulation—and occasionally functional independence—is possible. Clinical trial outcomes should therefore be viewed as best-case estimates, but they remind us that imaging alone cannot determine destiny (Mainali et al., 2026).

The One Predictor That Actually Matters Early

Among all individual predictors reviewed, only one emerged as a moderately reliable predictor of good functional outcome:

Early Neurological Improvement (ENI)

Defined as:

• An improvement of ≥8 NIHSS points within 24 hours, or

• Recovery to an NIHSS of 0–1 at 24 hours (Mainali et al., 2026).

Patients demonstrating ENI had a 61–84% likelihood of returning to functional independence at three months (Mainali et al., 2026). Importantly, the absence of ENI should not be interpreted as futility.

The guideline explicitly states that delayed neurological recovery remains common, and more than one in five patients without early improvement after successful thrombectomy still achieved functional independence at three months (Mainali et al., 2026).

But Absence of Improvement Is Not Failure

The guideline is equally clear about what doesn’t matter:

Failure to improve in the first 24 hours does not preclude meaningful recovery.

More than one in five patients who did not demonstrate early neurological improvement after successful thrombectomy still achieved functional independence by three months (Mainali et al., 2026).

For acute care clinicians, that distinction matters enormously. The absence of hope is not evidence of hopelessness.

Recovery Is a Timeline, Not a Moment

Emergency physicians work in minutes. Neurological recovery unfolds across months.

The guideline recommends counseling families that patients with severe ischemic stroke may continue to experience meaningful functional gains for up to six months—and sometimes even longer (Mainali et al., 2026).

That reality changes the way we frame uncertainty. The person lying in front of us on Day 1 is not the person they may become on Month 6. And perhaps our greatest responsibility is to ensure they have the opportunity to reach that point.

The Conversation We Should Be Having Instead

Rather than saying:

“The stroke is massive. Recovery is unlikely.”

Perhaps we should say:

“It is still too early to know. The next 24–72 hours, repeat imaging, and neurological evolution will provide a clearer picture. Many patients continue improving for weeks and months.”

The guideline repeatedly emphasizes:

• Prognostication should consider the complete clinical picture.

• Confounders must be excluded before neurological assessment.

• Pre-stroke functional status matters.

• Discussions should focus on long-term outcomes rather than day-to-day fluctuations.

• Recovery after severe ischemic stroke can continue for six months or longer (Mainali et al., 2026).

These are not merely academic recommendations.

They are safeguards against therapeutic nihilism.

What Early Signs Actually Encourage Recovery?

The guideline highlights several domain-specific markers that should give clinicians cautious optimism:

🖐️ Finger extension and shoulder abduction within 48 hours often predict meaningful hand function at six months.

🚶 The ability to maintain sitting balance and demonstrate any leg contraction within 72 hours strongly predicts later ambulation.

🗣️ Aphasia recovery continues for weeks and months, sometimes beyond six months.

👁️ Visual neglect and field deficits frequently improve long after hospital discharge.

Neurological recovery is rarely binary.

It is incremental, uneven, and often far slower than our emergency department timelines allow.

What I Am Taking Back to the ED

Five Rules from the 2026 Guidelines

1. Never prognosticate from admission NIHSS alone.

2. Large infarcts deserve time.

3. Avoid discussions of futility before neurological evolution declares itself.

4. Early improvement is encouraging—but its absence is not failure.

5. Recovery after severe stroke is measured in months, not days.

Back to Our Patient

The man from the 3 a.m. shift remained hemiplegic on day one. By day three, he could lift his leg. By week two, he spoke single words. Three months later, he walked into clinic with a stick. Not independent. Not perfect.

But unquestionably a life worth living. And a reminder that overcrowding, bed shortages, and system pressures must never compress the timeline of human neurological recovery.

The 2026 guidelines ask us to replace prognostic certainty with intellectual humility.

In severe acute ischemic stroke, early findings should inform observation—not determine destiny. The most accurate prognosis is often the one delivered after allowing the brain sufficient time to declare its trajectory.

Reference

Mainali S, Fontaine GV, Rajajee V, et al. Guidelines for Neuroprognostication in Critically Ill Adults with Acute Ischemic Stroke. Neurocritical Care. 2026;44:745–769.

A 50-year-old man walked into our Emergency Department after a high-speed road traffic collision. He was the driver. A solo rider. No eyewitnesses. No accompanying family. No medical records. He had sustained blunt trauma. His blood pressure was low. His eFAST was positive in abdomen and lung. The diagnosis seemed obvious.

Hemorrhagic shock. We moved quickly.

A pneumothorax was identified and an intercostal drain was inserted. The lungs appeared relatively clear on the initial ultrasound examination. The FAST examination demonstrated free intra-peritoneal fluid.

Blood products were requested immediately. As they should have been. A hypotensive trauma patient with a positive FAST should be presumed to be bleeding until proven otherwise (Bloom & Gibbons, 2019; Savoia et al., 2023). The first 2 units of blood started running. Then things became interesting.

Something Didn’t Fit

Instead of improving, the patient’s oxygen saturation began to worsen. The chest tube was functioning. The pneumothorax had been addressed. The repeat examination revealed no obvious procedural complication. Yet the patient was becoming increasingly hypoxic. A repeat lung ultrasound was performed. This time, symmetrical and diffuse bilateral B-lines had appeared.

Pulmonary edema.

After approximately one litre of blood. That wasn’t what we expected. This was supposed to be hemorrhagic shock. So why was he behaving like a patient with acute heart failure?

Looking Beyond The eFAST

A focused cardiac ultrasound was performed. The answer appeared within seconds. The left ventricle was severely impaired. Estimated left ventricular ejection fraction: approximately 20%. (later confirmed that he had underlying DCMP when family arrived with old records)

Suddenly the entire physiology made sense. The patient was indeed bleeding. The eFAST was not wrong. The shock was real. The blood was necessary. But he was also carrying severe underlying cardiac dysfunction that nobody knew about.

No previous records existed. No previous echocardiogram was available. No family member was present to provide a history. He arrived not only with traumatic injuries, but also with a failing heart. The blood products were treating one problem while simultaneously exposing another.

The Reality Of Trauma Care In LMICs

Cases like this are not rare. Many trauma patients in low- and middle-income countries arrive with years of undiagnosed or poorly managed cardiovascular disease.

Hypertension.
Ischemic heart disease.
Dilated cardiomyopathy.
Valvular pathology.
Heart failure.

Often untreated. Often undocumented. Often unknown even to the patient. Yet our trauma algorithms generally assume that hypotension in trauma equals hemorrhagic shock until proven otherwise.

Most of the time, that assumption is correct. But not always. And when it is incomplete, our resuscitation strategy may become incomplete as well.

eFAST Is One Of The Greatest Success Stories In Trauma

Before discussing alternatives, it is important to acknowledge what eFAST does exceptionally well. The extended Focused Assessment with Sonography in Trauma (eFAST) remains one of the most validated point-of-care ultrasound examinations in emergency medicine and trauma care (Netherton et al., 2019; Bella et al., 2025).

It rapidly identifies:

• Hemoperitoneum

• Hemopericardium

• Pneumothorax

• Hemothorax

These are diagnoses that directly influence immediate management decisions.

A systematic review and meta-analysis involving 75 studies and over 24,000 trauma patients demonstrated high specificity for identifying traumatic pathology, making eFAST an excellent rule-in tool in hemodynamically unstable trauma patients (Netherton et al., 2019).

For the question:

“Is traumatic bleeding or thoracic injury contributing to this patient’s shock?”

eFAST is extraordinarily effective. This is why it remains embedded within trauma protocols and ATLS-based assessment pathways worldwide (Bloom & Gibbons, 2019; Savoia et al., 2023).

Nothing in this article argues otherwise.

But eFAST Answers A Trauma Question

Not A Physiology Question. This distinction is important. eFAST tells us where blood may be accumulating. It tells us whether there is free fluid. It tells us whether there is a pneumothorax. It tells us whether there is a pericardial effusion.

What it does not tell us is:

• How well the heart is pumping.

• Whether the patient has severe cardiomyopathy.

• Whether the right ventricle is failing.

• Whether the patient can tolerate aggressive volume administration.

In other words:

eFAST identifies injuries. It does not fully characterize shock physiology. And these are not always the same thing.

Enter RUSH

The Rapid Ultrasound in Shock and Hypotension (RUSH) examination was designed to evaluate undifferentiated shock by assessing what ultrasound educators often call:

The Pump

• Cardiac contractility

• Pericardial effusion

• Right ventricular function

The Tank

• Volume status

• Inferior vena cava characteristics

• Pulmonary edema

The Pipes

• Aorta

• Major venous structures

(Estoos et al., 2019; Talayeh et al., 2018)

Unlike eFAST, which asks:

“Where is the bleeding?”

RUSH asks:

“Why is this patient in shock?”

The difference may seem subtle. At the bedside, it can be profound.

Does The Evidence Support Replacing eFAST?

No. And this is where we must be careful.

The current literature does not support replacing eFAST with RUSH in hypotensive trauma patients. There are no high-quality comparative studies demonstrating that routine RUSH examination improves mortality, accelerates definitive interventions, or provides superior outcomes compared with eFAST alone in trauma populations (Stickles et al., 2019; Talayeh et al., 2018).

In fact, trauma-specific evidence remains substantially stronger for eFAST (Netherton et al., 2019; Bella et al., 2025).

A prospective study of 100 unstable polytrauma patients reported a sensitivity of 94.2% and diagnostic accuracy of 95.2% for RUSH when compared with CT findings and final diagnoses (Elbaih et al., 2018).

These findings are encouraging. But they do not establish superiority over eFAST.

At present, the evidence suggests that RUSH broadens the differential diagnosis of shock rather than replacing established trauma ultrasound pathways (Elbaih et al., 2018; Berger et al., 2024).

Maybe We Are Asking The Wrong Question

The debate should not be:

eFAST versus RUSH.

Perhaps the more useful question is:

Should selected hypotensive trauma patients receive a rapid RUSH-style extension immediately after eFAST?

Particularly when:

• The physiology appears disproportionate to the injuries.

• The patient is older with unknown medical history.

• Shock persists despite apparently appropriate resuscitation.

• Respiratory status worsens unexpectedly.

• There is concern regarding cardiac reserve.

• The response to blood products is not what we anticipated.

In these situations, a 30-second cardiac and lung ultrasound examination may provide information that fundamentally alters our understanding of the patient. Not necessarily the diagnosis. But certainly the physiology.

Returning To Our Patient

Would identifying an ejection fraction of 20% before transfusion have stopped us from giving blood?

Absolutely not. The patient was hypotensive. The patient was FAST positive. The patient was bleeding. Blood products were indicated.

But would it have changed how we administered those blood products?

Probably.

Would it have changed our monitoring strategy?

Almost certainly.

Would it have made pulmonary edema less surprising?

Definitely.

Would it have prompted earlier consideration of Surgical interventions, vasopressors, invasive monitoring, or damage-control resuscitation strategies tailored to limited cardiac reserve?

Possibly.

And perhaps that alone is enough reason to look beyond the abdomen.

The Frontline Takeaway

eFAST remains the cornerstone of ultrasound assessment in hypotensive trauma. The evidence supports it. The guidelines support it. The outcomes support it. But trauma patients are more than their injuries.

Especially in resource-limited settings, they often arrive carrying years of undocumented disease alongside their traumatic pathology.

A positive FAST explains where blood may be accumulating. It does not explain how the patient will respond to our resuscitation. The next evolution in trauma ultrasound may not be replacing eFAST with RUSH. It may simply be remembering to look at the heart before assuming that every shocked trauma patient needs the same resuscitation strategy. Sometimes the most important finding is not the free fluid. Sometimes it is the ventricle struggling silently beside it.

Pulse Checks and Reflections

1. Guidelines Are Frameworks, Not Replacements for Clinical Judgment

Trauma guidelines exist to standardize care, reduce variability, and ensure that life-threatening injuries are identified and treated rapidly. They provide an essential framework, particularly in high-acuity situations where decisions must be made quickly.

However, no guideline can account for every patient, every physiology, or every clinical context. As clinicians gain experience, the challenge is not knowing when to follow guidelines, but recognizing when a patient’s physiology requires us to look beyond the algorithm while still respecting its principles.

In this case, the guideline-directed approach was appropriate. The experience simply reinforced the importance of continuously reassessing whether the patient’s response matches our expectations.

2. Looking Beyond eFAST Is Not Necessarily Departing From Trauma Principles

This reflection is not an argument against eFAST, nor is it a proposal to replace established trauma protocols.

Rather, it highlights the potential value of extending the ultrasound examination to include a rapid assessment of cardiac function and volume status in selected hypotensive trauma patients.

A RUSH-style examination incorporates the core components of eFAST while adding information about the heart and the patient’s overall shock physiology. The goal is not to change the diagnosis of hemorrhagic shock, but to better understand how a patient may tolerate ongoing fluid or blood product administration.

In some cases, identifying limited cardiac reserve early may allow clinicians to anticipate complications, tailor resuscitation strategies, and expedite definitive hemorrhage control when appropriate.

3. Trauma Patients Do Not Always Present With Trauma Alone

In many low- and middle-income countries, patients frequently arrive without prior medical records, medication lists, or accessible health information.

Significant comorbidities often remain undiagnosed or poorly documented. Conditions such as heart failure, ischemic heart disease, chronic kidney disease, and valvular pathology may coexist with traumatic injuries and influence the patient’s response to resuscitation.

While trauma may be the reason for presentation, underlying physiology often determines how that patient responds to treatment.

This case served as a reminder that understanding the patient sometimes requires looking beyond the injury itself.

4. A Personal Change in Practice

This case has not changed my belief in the value of eFAST or the principles of trauma resuscitation.

What it has changed is my threshold for performing a brief cardiac assessment in hypotensive trauma patients, particularly when the patient’s age, physiology, or response to treatment raises questions. Not because every patient requires it. Not because guidelines are inadequate. But because occasionally, a 30-second look at the heart may reveal information that helps us better understand the physiology in front of us. And sometimes, that additional piece of information can make all the difference.

"Trauma may explain why the patient is here. Physiology often explains how they will respond to what we do next."

References

1. Bella F, Bonfichi A, Esposito C, et al. Extended Focused Assessment with Sonography for Trauma in the Emergency Department: A Comprehensive Review. J Clin Med. 2025;14.

2. Berger M, Hussain J, Anshien M. RUSH to the Diagnosis: Identifying Occult Pathology in Hypotensive Patients. Clin Pract Cases Emerg Med. 2024;8:379-380.

3. Bloom BM, Gibbons R. Focused Assessment with Sonography for Trauma (FAST). 2019.

4. Elbaih A, Housseini A, Khalifa M. Accuracy and outcome of rapid ultrasound in shock and hypotension (RUSH) in Egyptian polytrauma patients. Chin J Traumatol. 2018;21:156-162.

5. Estoos E, Nakitende D, Bhimji S, Cole J. Diagnostic Ultrasound Use in Undifferentiated Hypotension. 2019.

6. Netherton S, Milenkovic V, Taylor MR, Davis P. Diagnostic accuracy of eFAST in the trauma patient: a systematic review and meta-analysis. CJEM. 2019.

7. Savoia P, Jayanthi SK, Chammas M. Focused Assessment with Sonography for Trauma (FAST). J Med Ultrasound. 2023;31:101-106.

8. Stickles S, Carpenter C, Gekle R, et al. The diagnostic accuracy of a point-of-care ultrasound protocol for shock etiology: A systematic review and meta-analysis. CJEM. 2019.

9. Talayeh R, et al. Early Protocolized Bedside Ultrasound in Shock: Renal Function Improvements and Other Lessons Learned. Int J Crit Care Emerg Med. 2018.

One of the most preventable harms in emergency and critical care occurs after successful intubation—not during it. A patient receives induction with etomidate, ketamine, or propofol. A paralytic is administered. The airway is secured. The team celebrates a successful intubation.

But then the sedative wears off. The paralysis does not. For the next 30–60 minutes, the patient may be awake, aware, unable to move, unable to communicate, and unable to breathe independently.

Few experiences in medicine are more terrifying. Post-intubation sedation is not an optional intervention. It is the continuation of the intubation procedure itself.

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The Goal Is Not Deep Sedation

Before discussing drugs, we must define the target.

Modern acute care has shifted away from routine deep sedation. Multiple studies have demonstrated that excessive sedation is associated with longer mechanical ventilation, increased delirium, prolonged ICU stays, and worse long-term outcomes.

For most mechanically ventilated patients, the target should be:

RASS -2 to 0

• 0 = Alert and calm

• -1 = Drowsy

• -2 = Light sedation

Patients should be comfortable, cooperative when appropriate, and free from pain—not chemically comatose.

Deep sedation (RASS -4 to -5) should be reserved for specific indications:

• Severe ARDS requiring ventilator synchrony

• Neuromuscular blockade

• Refractory intracranial hypertension

• Status epilepticus

• Severe agitation threatening patient safety

The question is not “How deeply sedated can I make my patient?”, The question is “What is the lightest level of sedation that safely achieves my goals?”

This seemingly small shift in philosophy has transformed modern ICU practice.

You Can’t Target What You Don’t Measure

Post-intubation sedation, like shock resuscitation, must be goal-directed. (Baumgartner K, 2026)

Yet studies show sedation assessment in mechanically ventilated ED patients remains inconsistent, with documentation rates varying dramatically between institutions (Steel et al., 2021; Fuller et al., 2019).

Every intubated patient should have two explicit targets:

• Pain target: Critical Care Pain Observation Tool (CPOT) if possible

• Sedation target: Richmond Agitation-Sedation Scale (RASS), must

These assessments should be repeated regularly and tied to nursing-driven titration protocols. Because sedation is not a drug order. Consider it as a treatment target.

For most patients:

• CPOT: As low as possible

• RASS: -2 to 0

Without structured assessment, clinicians frequently default to over-sedation—a practice consistently associated with more delirium, longer ventilation, longer ICU stays, and higher mortality (Shehabi et al., 2012; Tanaka et al., 2014; Shehabi et al., 2018). What gets measured gets managed.

Sedation Begins the Moment the Tube Goes In

The most dangerous misconception after rapid sequence intubation is assuming that induction agents provide ongoing sedation. They do not. Typical durations are remarkably short:

This creates a potentially devastating mismatch. The patient may regain awareness long before they regain movement. Every clinician who performs RSI should develop a habit:

Before the intubation begins, know what your post-intubation sedation plan will be.

Not afterward. Not when the chest X-ray returns. Not when the nurse reminds you. Before.

Awareness With Paralysis: The Complication We Don’t Measure Enough

Awareness during neuromuscular blockade is not rare. Prospective emergency department studies demonstrate unacceptably high rates of recall among mechanically ventilated patients (Pappal et al., 2021; Driver et al., 2023).

Risk factors include:

• Rocuronium use

• Delayed sedation initiation

• Lack of sedation monitoring

• Deeply sedated appearance masking inadequate analgesia

Patients who are paralyzed cannot demonstrate distress. Silence is not comfort.

The most effective prevention strategy is simple: Plan post-intubation sedation before intubation.

Build Sedation Into Your Airway Checklist

One of the simplest ways to prevent awareness with paralysis is to stop treating post-intubation sedation as an afterthought. Before administering induction drugs, ask:

“What is our sedation plan after the tube goes in?”

The answer should include:

• Target RASS

• Initial analgesic

• Initial sedative

• Vasopressor strategy if needed

• Planned reassessment interval

Ideally, post-intubation medications should be prepared before laryngoscopy begins. (Baumgartner K, 2026). Multiple quality-improvement initiatives have shown that incorporating sedation into peri-intubation checklists reduces delays in analgesia and sedation initiation (Irwin et al., 2022; Ayers et al., 2024).

The patient should never wait for a chest radiograph, ICU bed assignment, or medication order reconciliation before receiving analgesia and sedation. Airway management does not end at endotracheal tube confirmation. It ends when the patient is comfortable.

The Rise—and Nuance—of Analgosedation

(Baumgartner K, 2026)

For decades, sedation-focused strategies dominated critical care. Patients received sedatives first, with analgesia added later if needed. Modern practice has shifted toward an analgesia-first philosophy.

Why?

Because many mechanically ventilated patients are not agitated because they need more sedation. They are agitated because they are in pain.

Pain increases:

• Tachycardia

• Hypertension

• Ventilator dyssynchrony

• Oxygen consumption

• Agitation

• Sedative requirements

Treating pain first often reduces the amount of sedative required. This approach is known as analgosedation.

However, post-intubation analgesia and sedation are linked—but distinct—interventions. (Baumgartner K, 2026)

Not every patient benefits from opioid escalation, and pain assessment can be challenging in critically ill, non-communicative patients. Current guidelines have softened earlier recommendations for strict analgesia-first approaches, emphasizing individualized care based on patient physiology and validated assessment tools (Devlin et al., 2018).

The practical message remains unchanged:

Do not mistake pain for a need for more sedation.

And do not mistake analgesia for sedation. Fentanyl may make patients more comfortable. It does not reliably make them unaware.

Fentanyl: The Most Misunderstood Drug in Post-Intubation Care

One concept deserves particular emphasis. Fentanyl is an analgesic. It is not primarily a sedative. This distinction is frequently misunderstood in emergency departments.

Mechanism

Fentanyl is a potent μ-opioid receptor agonist.

Its primary effects are:

• Analgesia

• Blunting of sympathetic responses

• Reduction of pain-related agitation

At high doses, fentanyl can certainly contribute to sedation. However, sedation is not its principal therapeutic role.

Typical Dosing

Loading dose
25–100 mcg IV

Continuous infusion
25–200 mcg/hour

or approximately

0.5–3 mcg/kg/hour

Advantages

• Rapid onset

• Reliable analgesia

• Familiarity

• Minimal histamine release

Limitations

• Respiratory depression

• Chest wall rigidity with rapid high-dose administration

• Drug accumulation during prolonged infusions

The practical takeaway is straightforward:
If your patient is receiving fentanyl alone, they may have excellent analgesia while remaining inadequately sedated.

Pain control and sedation are not synonymous.

Midazolam: The Old Workhorse

Midazolam remains one of the most commonly used sedatives worldwide.

Mechanism

Midazolam enhances GABA-A receptor activity, producing:

• Sedation

• Anxiolysis

• Amnesia

• Anticonvulsant effects

Typical Dosing

Loading
2–5 mg IV

Infusion
1–10 mg/hour

(approximately 0.02–0.1 mg/kg/hour)

When Midazolam Still Shines

Despite its declining popularity, midazolam remains valuable in:

• Hemodynamically unstable patients

• Status epilepticus

• Alcohol withdrawal

• Situations requiring profound amnesia

• Deep sedation requirements

The Problem

The major issue with benzodiazepines is not inadequate sedation. It is excessive sedation.

Accumulation, particularly during prolonged infusions, contributes to:

• Delayed awakening

• Prolonged ventilation

• Increased delirium

• Longer ICU stays

Meta-analyses comparing midazolam with propofol and dexmedetomidine consistently demonstrate slower extubation and higher delirium rates with benzodiazepine-based strategies (Garcia et al., 2021; Chen & Ho, 2025).

Intermittent bolus doses of midazolam for breakthrough agitation are unlikely to carry the same risks as prolonged continuous infusions. The adverse outcome data are driven primarily by infusion-based benzodiazepine strategies.

For this reason, contemporary guidelines generally favor non-benzodiazepine sedatives whenever feasible.

Dexmedetomidine: Cooperative Sedation

If benzodiazepines represent traditional ICU sedation, dexmedetomidine represents the modern philosophy.

Mechanism

Dexmedetomidine is a selective alpha-2 adrenergic agonist. Unlike GABAergic sedatives, it produces a unique form of sedation. Patients often appear asleep but awaken easily and interact appropriately when stimulated.

Typical Dosing

Loading dose
Often omitted in critically ill patients due to hemodynamic effects.
Infusion
0.2–1.5 mcg/kg/hour

Advantages

• Reduced delirium

• Easier neurological assessment

• Preserved respiratory drive

• Improved patient interaction

• Shorter time to extubation compared with benzodiazepines

Large meta-analyses demonstrate lower delirium rates and modest reductions in ventilation duration compared with traditional sedatives (Wen et al., 2023; Walsh et al., 2025).

Dexmedetomidine has a delayed onset. Without a loading dose, peak sedative effect may take 30–60 minutes. When rapid sedation is required, dexmedetomidine should be bridged with a faster-acting agent such as propofol.

Limitations

The trade-off is predictable:

• Bradycardia

• Hypotension

As with every sedative in critical care, benefits must be balanced against physiology.

Ketamine: More Than an Induction Agent

Most emergency physicians are comfortable using ketamine for induction.

Fewer use it as part of a post-intubation strategy.

Mechanism

Ketamine acts primarily through NMDA receptor antagonism.

Unlike most sedatives, it provides:

• Analgesia

• Sedation

• Relative preservation of airway reflexes

• Sympathomimetic effects

Typical Dosing

Loading
0.25–1 mg/kg

Infusion
0.1–2 mg/kg/hour

Where Ketamine Excels

Ketamine is particularly attractive in:

• Severe bronchospasm

• Opioid-tolerant patients

• Hemodynamic instability

• Patients requiring opioid-sparing strategies

Ketamine may be particularly useful in severe bronchospasm, polytrauma with difficult-to-control pain, refractory status epilepticus, or when propofol intolerance limits sedation options.

Recent reviews suggest ketamine’s greatest strength is as an adjunctive agent that reduces overall sedative and opioid requirements rather than as routine monotherapy (Hendrikse et al., 2023; Amer et al., 2024).

What About Propofol?

No discussion of post-intubation sedation would be complete without propofol. In many ICUs, propofol remains the default sedative.

Why?

Because it is:

• Rapidly titratable

• Predictable

• Short acting

• Associated with faster awakening and extubation

Typical dosing ranges from:

5–80 mcg/kg/min

Its major limitations are equally familiar:

• Hypotension

• Bradycardia

• Hypertriglyceridemia

• Propofol infusion syndrome (rare)

Compared with midazolam, propofol consistently shortens ventilation duration and accelerates extubation in mechanically ventilated patients (Garcia et al., 2021).

Propofol should be dosed using ideal body weight rather than actual body weight, particularly in obesity, to reduce the risk of hypotension. (Baumgartner K, 2026)

Rather than abandoning propofol when hypotension develops, clinicians should first consider reducing the infusion rate and initiating vasopressor support. Given its short duration of action, persistent hypotension despite dose reduction should prompt evaluation for alternative causes. (Baumgartner K, 2026)

For many patients, a combination of:

Fentanyl + Propofol

remains an excellent starting strategy.

This article focuses on emergency department management during the immediate post-intubation period. Sedation strategies should always be individualized based on patient physiology, institutional protocols, and evolving ICU goals.

Choosing the Right Sedative

There is no universally superior sedative.

The best agent depends on the physiology in front of you. The goal is not to find the perfect drug. The goal is to match the drug to the patient.

The Bottom Line

The airway is not secured when the tube passes the cords.

The airway is secured when the patient is:

• Adequately analgesed

• Adequately sedated

• Appropriately monitored

• Maintained within a defined sedation target

Post-intubation sedation is not an afterthought.

It is not an ICU issue.

It is not something to “sort out later.”

It is a core component of airway management.

Because a patient who is awake, frightened, and paralyzed behind an endotracheal tube has not received complete care.

They have received an incomplete intubation.

References

1. Baumgartner K, Fuller BM. Postintubation sedation and analgesia in the emergency department: the basics and beyond. Emergency Medicine Clinics of North America. 2026. doi:10.1016/j.emc.2026.02.004.

2. Devlin JW, Skrobik Y, Gélinas C, et al. Clinical practice guidelines for the prevention and management of pain, agitation/sedation, delirium, immobility, and sleep disruption in adult patients in the ICU. Critical Care Medicine. 2018;46(9):e825-e873. doi:10.1097/CCM.0000000000003299

3. Pandharipande PP, Girard TD, Jackson JC, et al. Long-term cognitive impairment after critical illness. New England Journal of Medicine. 2013;369(14):1306-1316. doi:10.1056/NEJMoa1301372

4. Shehabi Y, Bellomo R, Reade MC, et al. Early intensive care sedation predicts long-term mortality in ventilated critically ill patients. American Journal of Respiratory and Critical Care Medicine. 2012;186(8):724-731. doi:10.1164/rccm.201203-0522OC

5. Tanaka LMS, Azevedo LCP, Park M, et al. Early sedation and clinical outcomes of mechanically ventilated patients: a prospective multicenter cohort study. Critical Care. 2014;18(4):R156. doi:10.1186/cc13941

6. Shehabi Y, Bellomo R, Kadiman S, et al. Sedation intensity in the first 48 hours of mechanical ventilation and 180-day mortality: a multinational prospective longitudinal cohort study. Critical Care Medicine. 2018;46(6):850-859. doi:10.1097/CCM.0000000000003071

7. Boncyk C, Rolfsen M, Richards D, et al. Management of pain and sedation in the intensive care unit. BMJ. 2024;387:e079789. doi:10.1136/bmj-2024-079789

8. Garcia R, Salluh J, Andrade TR, et al. A systematic review and meta-analysis of propofol versus midazolam sedation in adult intensive care patients. Journal of Critical Care. 2021;64:91-99. doi:10.1016/j.jcrc.2021.04.001

9. Chen Y, Ho MH. Comparative risks and clinical outcomes of midazolam versus other intravenous sedatives in critically ill mechanically ventilated patients: a systematic review and meta-analysis of randomized trials. Intensive & Critical Care Nursing. 2025;103945. doi:10.1016/j.iccn.2025.103945

10. Wen J, Ding X, Liu C, et al. A comparison of dexmedetomidine and midazolam for sedation in patients with mechanical ventilation in ICU: a systematic review and meta-analysis. PLOS One. 2023;18:e0294292. doi:10.1371/journal.pone.0294292

11. Walsh TS, Parker RA, Aitken LM, et al. Dexmedetomidine- or clonidine-based sedation compared with propofol in critically ill patients: the A2B randomized clinical trial. JAMA. 2025. doi:10.1001/jama.2025.7200

12. Lewis K, Alshamsi F, Carayannopoulos K, et al. Dexmedetomidine versus other sedatives in critically ill mechanically ventilated adults: a systematic review and meta-analysis of randomized trials. Intensive Care Medicine. 2022;48:811-840. doi:10.1007/s00134-022-06712-2

13. Kawazoe Y, Miyamoto K, Morimoto T, et al. Effect of dexmedetomidine on mortality and ventilator-free days in patients requiring mechanical ventilation with sepsis: a randomized clinical trial. JAMA. 2017;317(13):1321-1328. doi:10.1001/jama.2017.2088

14. Hendrikse C, Ngah V, Kallon I, et al. Ketamine as adjunctive or monotherapy for post-intubation sedation in patients with trauma on mechanical ventilation: a rapid review. African Journal of Emergency Medicine. 2023;13:313-321. doi:10.1016/j.afjem.2023.10.002

15. Amer M, Møller MH, Alshahrani M, et al. Ketamine analgosedation for mechanically ventilated critically ill adults: a rapid practice guideline from the Saudi Critical Care Society and the Scandinavian Society of Anesthesiology and Intensive Care Medicine. Anesthesia & Analgesia. 2024. doi:10.1213/ANE.0000000000007173

16. Matchett G, Gasanova I, Riccio CA, et al. Continuous infusion ketamine for adjunctive analgosedation in mechanically ventilated, critically ill patients. Pharmacotherapy. 2019;39(3):288-296. doi:10.1002/phar.2223

17. Pappal RD, Roberts BW, Mohr NM, et al. The ED-AWARENESS study: a prospective observational cohort study of awareness with paralysis in mechanically ventilated patients admitted from the emergency department. Annals of Emergency Medicine. 2021;77(5):532-544. doi:10.1016/j.annemergmed.2020.09.026

18. Driver BE, Prekker ME, Wagner E, et al. Recall of awareness during paralysis among emergency department patients undergoing tracheal intubation. Chest. 2023;163(2):313-323. doi:10.1016/j.chest.2022.09.035

19. Fuller BM, Roberts BW, Mohr NM, et al. The ED-SED study: a multicenter, prospective cohort study of practice patterns and clinical outcomes associated with emergency department sedation for mechanically ventilated patients. Critical Care Medicine. 2019;47(11):1539-1548. doi:10.1097/CCM.0000000000003956

20. Fuller BM, Roberts BW, Mohr NM, et al. The feasibility of implementing targeted sedation in mechanically ventilated emergency department patients: the ED-SED pilot trial. Critical Care Medicine. 2022;50(8):1224-1235. doi:10.1097/CCM.0000000000005559

21. Steel TL, Lokhandwala S, Caldwell ES, et al. Variability in sedation assessment among intubated patients in the emergency department. Academic Emergency Medicine. 2021;28(10):1173-1176. doi:10.1111/acem.14329

22. Ely EW, Truman B, Shintani A, et al. Monitoring sedation status over time in ICU patients: reliability and validity of the Richmond Agitation-Sedation Scale. JAMA. 2003;289(22):2983-2991. doi:10.1001/jama.289.22.2983

23. Gélinas C, Fillion L, Puntillo KA, et al. Validation of the Critical-Care Pain Observation Tool in adult patients. American Journal of Critical Care. 2006;15(4):420-427.

24. Irwin WW, Berg KT, Ruttan T K, et al. Initiative to improve postintubation sedation in a pediatric emergency department. Journal for Healthcare Quality. 2022;44(1):31-39. doi:10.1097/JHQ.0000000000000304

25. Ayers C, Johnson DP, Noffsinger L, et al. Reducing time to postintubation sedation in a pediatric emergency department. Pediatrics. 2024;153(4):e2023062665. doi:10.1542/peds.2023-062665

This article synthesizes current evidence and recommendations from the 2018 SCCM PADIS Guidelines, recent emergency medicine literature, and the review by Baumgartner and Fuller (2026), “Postintubation Sedation and Analgesia in the Emergency Department: The Basics and Beyond.” It is intended for educational purposes and should complement—not replace—local protocols and clinical judgment.

But here’s the uncomfortable truth:

Your patient is still critically ill.
In fact, the first 15–30 minutes after intubation may be among the most dangerous periods in the entire resuscitation.
Over the last decade, emergency medicine has dramatically improved its focus on pre-intubation optimization. We talk about delayed sequence intubation, hemodynamic resuscitation, apneic oxygenation, ketamine versus etomidate, and peri-intubation hypotension.

Yet I continue to see a recurring problem:
Once the tube passes the cords, many clinicians mentally declare victory.

The patient is “airway secured,” and attention shifts elsewhere. But intubation is not the endpoint of resuscitation.

It is only the beginning.

The Post-Intubation Bundle

Whenever I intubate a patient, I immediately ask myself five questions:

1. Is the tube really where I think it is?

2. Are the ventilator settings appropriate?

3. Have I reassessed gas exchange and ventilation?

4. Is the patient comfortable?

5. Have I prevented the next physiologic disaster?

Let’s walk through each.

Step 1: Confirm the Tube — Then Confirm It Again

Successful laryngoscopy does not equal successful intubation. The gold standard for immediate confirmation remains:

Continuous waveform capnography

A persistent waveform with exhaled CO₂ confirms tracheal placement. Not colorimetric devices. Not chest rise. Not misting in the tube. Not auscultation alone.

Waveform capnography is king.

Additional confirmation

After waveform capnography:

• Bilateral chest rise

• Equal breath sounds

• Absence of gastric sounds

• Improvement in oxygenation

• Appropriate ventilator waveforms

Chest X-ray

Once the patient is stabilized:

• Confirm tube depth

• Evaluate for right mainstem intubation

• Look for pneumothorax

• Assess evolving pulmonary pathology

A useful target:
Tube tip approximately 3–5 cm above the carina

Remember:
The first confirmation is physiologic. The second confirmation is radiographic.
Both matter.

Step 2: Don’t Let the Ventilator Ventilate by Default

One of the most common errors after intubation is accepting whatever settings were initially entered. The ventilator should be prescribed like any other critical medication.

Start with the diagnosis

The ventilator settings for:

• Severe asthma

• ARDS

• Septic shock

• Traumatic brain injury

• Diabetic ketoacidosis

are not the same. Yet many patients receive identical settings.

A practical starting strategy

For most adults:

Mode

• Volume Assist-Control

Tidal Volume

• 6–8 mL/kg predicted body weight

Respiratory Rate

• 16–22 breaths/min

PEEP

• 5 cmH₂O initially

• Higher if hypoxemic

FiO₂

• Start at 100%

• Rapidly titrate down

Avoid oxygen toxicity

After stabilization:

Target:

• SpO₂ 92–96% in most patients

• Avoid prolonged unnecessary FiO₂ 100%

Disease-specific reminders

ARDS

• Low tidal volume ventilation

• 6 mL/kg predicted body weight

• Higher PEEP strategy

Severe Asthma

• Low respiratory rate

• Long expiratory time

• Avoid Auto-PEEP

Traumatic Brain Injury

• Avoid hypoxia

• Avoid severe hypercapnia

• Target normocapnia

Metabolic Acidosis (DKA, Salicylates)

The ventilator must match or approximate the patient’s pre-intubation minute ventilation. Failure to do so can rapidly worsen acidosis and precipitate arrest.

Step 3: The ABG is Not a Trophy. It’s Feedback.

Many clinicians order an ABG after intubation. Far fewer actually use it to change management. The purpose of an ABG is not documentation. The purpose is ventilator adjustment.

Obtain an ABG

Usually within:
15–30 minutes after intubation

Then ask:

Is oxygenation adequate?

If PaO₂ is excessive: Reduce FiO₂.

If inadequate: Increase PEEP before endlessly increasing oxygen concentration.

Is ventilation adequate?

If PaCO₂ is high: (see here )
Increase minute ventilation:

• Increase respiratory rate

• Adjust tidal volume when appropriate

If PaCO₂ is too low:

Reduce minute ventilation.

Repeat when needed

Every ventilator change should trigger reassessment.

The ABG closes the loop between physiology and intervention.

Step 4: The Paralytic Has Worn Off. The Patient Is Awake.

Perhaps the most important post-intubation principle:
Sedation should begin immediately after intubation.
(Read more in detail from here)

Many patients receive:

• Induction agent

• Paralytic

and then nothing.

Ten minutes later they are awake, frightened, unable to speak, and fighting the ventilator. This is one of the most distressing experiences a critically ill patient can endure.

Analgesia First

Pain should be treated before sedation whenever possible.

A common strategy:

Fentanyl, Morphine

Then Sedation

Common options:

Propofol, Ketamine, Dexmed, Midazolam (new post will be released on individual drugs)

Target a Sedation Goal

Sedation should never be:
“Run propofol at 40.”

Sedation should be:
“Target RASS -2 to 0.”

The 2018 SCCM PADIS guidelines support protocolized sedation with defined targets and favor maintaining lighter levels of sedation whenever clinically feasible.

A practical target

Most newly intubated ED patients:

• RASS -2 to -3 initially

Then lighten as physiology allows.

Step 5: Anticipate the Post-Intubation Crash

The patient who looked stable before intubation may suddenly become unstable afterward.

Why?
Positive pressure ventilation changes physiology.

Watch for:

Hypotension

Causes:

• Reduced venous return

• Sedatives

• Occult hypovolemia

Management:

• Fluids when appropriate

• Vasopressors early

• Reassess shock state

Auto-PEEP

Particularly in:

• Asthma

• COPD

Look for:

• Rising airway pressures

• Hypotension

• Ventilator dyssynchrony

Pneumothorax

Especially after:

• Trauma

• Difficult ventilation

• High airway pressures

Ventilator Dyssynchrony

A fighting patient is not always “agitated.”

Sometimes they are:

• In pain

• Undersedated

• Air hungry

• Incorrectly ventilated

Treat the cause.

Not just the monitor.

The Tube Is Not the Finish Line

One of the most dangerous myths in emergency medicine is that intubation is a procedure.

It isn’t, It’s a transition.

The patient has moved from spontaneous physiology to physician-controlled physiology.
For the next 30 minutes, every breath, every milliliter of ventilation, every molecule of oxygen, every sedative dose, and every hemodynamic consequence is now your responsibility.

The airway may be secured. But the resuscitation is far from over.

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Why Every Exacerbation Matters More Than You Think ?

A patient arrives breathless.

They have increased cough, more sputum than usual, and worsening exercise tolerance over the last week. The oxygen saturation is 86%, respiratory rate is 32, and they are using every accessory muscle available.

For many clinicians, this is another COPD exacerbation.

For GOLD 2026, it is something more important.

An exacerbation is no longer viewed as a temporary flare-up that resolves with nebulizers, steroids, and a discharge summary. Instead, GOLD increasingly frames exacerbations as trajectory-changing events—episodes associated with accelerated lung function decline, increased risk of future hospitalization, reduced quality of life, and increased mortality.

For acute care physicians, this shift in thinking may be the most important update in the entire document. The goal is no longer simply treating today’s breathlessness. The goal is preventing tomorrow’s deterioration.

1. COPD Exacerbations Have a Clearer Definition

The 2026 GOLD update defines an exacerbation as an acute worsening of respiratory symptoms occurring over several days and up to 14 days, typically characterized by increased dyspnea and/or cough and sputum production, often accompanied by tachypnea or tachycardia.

At first glance, this seems like a minor wording change.

It isn’t.

The revised definition emphasizes the clinical syndrome itself rather than the treatment that follows. An exacerbation is not defined by whether a patient receives steroids, antibiotics, or hospitalization. It is defined by a recognizable pattern of symptom deterioration associated with increased airway and systemic inflammation.

For clinicians working in emergency departments, acute medical units, respiratory wards, and intensive care settings, this provides a more practical framework for diagnosis and management.

2. Not Every Breathless COPD Patient Has a COPD Exacerbation

One of the most important reminders in GOLD 2026 is that several conditions can mimic or worsen an exacerbation.

Among the most important are:

• Pneumonia

• Pulmonary embolism

• Acute heart failure

• Pneumothorax

• Cardiac ischemia

• Arrhythmias

Many patients admitted with presumed COPD exacerbation ultimately have a competing or coexisting diagnosis driving their deterioration.

The challenge for acute care physicians is not merely recognizing COPD. It is identifying what else may be happening simultaneously or what could have triggered this episode.

When a patient fails to respond as expected, reassessment should occur early rather than assuming treatment failure.

A “COPD exacerbation” diagnosis should never end clinical reasoning.

3. GOLD Has Moved Beyond Admission-Based Severity

Traditionally, exacerbation severity was inferred from healthcare utilization.

If a patient was admitted, the exacerbation was severe. If they were discharged, it was moderate.

This approach was convenient for research but often unhelpful at the bedside.

GOLD 2026 aligns severity assessment more closely with the Rome Proposal, emphasizing physiological assessment rather than disposition decisions.

Severity should be determined by:

• Work of breathing

• Respiratory rate

• Oxygenation

• Hypercapnia

• Accessory muscle use

• Mental status

• Hemodynamic stress

• Response to initial treatment

This reflects how acute care clinicians already think. A patient becoming progressively fatigued and hypercapnic is severe regardless of where they ultimately receive care.

Physiology matters more than location.

4. Early Treatment Remains the Cornerstone

Although the philosophy has evolved, the fundamentals of treatment remain remarkably consistent.

Bronchodilators

Short-acting beta-agonists remain first-line therapy. Short-acting anticholinergics may be added when additional bronchodilation is required.

Corticosteroids

Systemic corticosteroids improve lung function, shorten recovery time, reduce treatment failure, and decrease hospital length of stay. Current recommendations continue to support short courses of approximately five days.

Longer courses generally provide little additional benefit while increasing adverse effects.

Antibiotics

Antibiotics should be reserved for patients with evidence suggesting bacterial infection, particularly:

• Increased sputum purulence

• Increased sputum volume

• Increased dyspnea

Five-day treatment courses are generally sufficient.

Methylxanthines

Despite their historical role, methylxanthines remain discouraged because the risk of adverse effects outweighs clinical benefit.

Sometimes the most important update is recognizing what has not changed.

5. Respiratory Failure Should Be Recognized Before Exhaustion Occurs

One of the recurring themes throughout modern COPD care is earlier intervention. This is particularly true for acute hypercapnic respiratory failure.

GOLD continues to strongly support:

• Controlled oxygen therapy

• High-flow oxygen systems when appropriate

• Non-invasive ventilation (NIV)

The evidence remains compelling.

Early NIV improves gas exchange, reduces work of breathing, decreases intubation rates, shortens hospitalization, and improves survival.

The critical challenge is timing. Patients rarely deteriorate suddenly.

Most show warning signs hours beforehand:

• Increasing respiratory rate

• Rising carbon dioxide levels

• Progressive fatigue

• Reduced air movement

• Altered mental status

The best outcomes occur when NIV is initiated before exhaustion develops. Waiting for collapse is rarely a successful strategy.

6. The Real Work Begins After Stabilization

Perhaps the most underappreciated message in GOLD 2026 is that recovery extends far beyond the acute episode. Recovery from an exacerbation often requires four to six weeks. Many patients never fully return to their previous baseline.

Every acute care encounter therefore represents an opportunity to reduce future risk.

Before transition of care, clinicians should consider:

• Is maintenance therapy optimized?

• Has inhaler technique been assessed?

• Are there adherence barriers?

• Were modifiable triggers identified?

• Does the patient have elevated eosinophils that may support ICS-containing therapy?

• Is appropriate follow-up arranged?

Acute care is not separate from chronic disease management. It is often the moment that determines the next year of a patient’s disease course.

What Changed the Most?

The most important change in GOLD 2026 is not a new medication. It is a new perspective. COPD exacerbations are increasingly viewed as biologically significant events that alter long-term outcomes. Each exacerbation increases the risk of future exacerbations. Each hospitalization increases future vulnerability. Each episode of respiratory failure carries consequences that persist long after discharge.

For acute care physicians, that means every exacerbation deserves urgency, careful evaluation, and a prevention-focused mindset. Because the objective is no longer simply getting patients through today’s crisis. The objective is changing what happens next.

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References

1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of COPD. 2026 Report.

2. Celli BR, Fabbri LM, Aaron SD, et al. An Updated Definition and Severity Classification of COPD Exacerbations: The Rome Proposal. Am J Respir Crit Care Med. 2021;204(11):1251-1258.

3. Wedzicha JA, Seemungal TAR. COPD Exacerbations: Defining Their Cause and Prevention. Lancet. 2007;370:786-796.

4. Agustí A, Vogelmeier CF, Criner GJ, et al. Global Initiative for Chronic Obstructive Lung Disease 2026 Report.

By-
Dr Arihant Jain, MD | lifeonthefrontline.com
Instagram: @humans.of.em
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A patient arrives in septic shock. Blood pressure is 72/40 mmHg. The lactate is climbing. Capillary refill is prolonged. The patient needs vasopressors.

Yet in many emergency departments and ICUs, treatment pauses while clinicians prepare for central venous access.

The assumption is simple:

Central line first. Vasopressors second.

But modern evidence increasingly challenges this approach.

The Cost of Waiting

Shock is fundamentally a disease of inadequate tissue perfusion.

Every minute of persistent hypotension contributes to worsening organ dysfunction, cellular hypoxia, and increased mortality.

Perhaps one of the most compelling reasons to reconsider routine delays for central line placement comes from studies examining the timing of vasopressor initiation. In septic shock, mortality increases by approximately 2–3% for every hour delay in vasopressor administration after shock recognition (Bai et al., 2014; Beck et al., 2014).

In other words:

The patient is not waiting for a central line. Their organs are not waiting either.

Where Did the Fear Come From?

Historically, vasopressors were considered unsafe for peripheral administration because of concerns regarding extravasation, tissue necrosis, and limb ischemia.

Many of these concerns arose from older reports involving distal intravenous sites, prolonged infusions, small-caliber catheters, and limited monitoring (Loubani & Green, 2015).

Over time, anecdote became dogma. However, contemporary evidence paints a very different picture.

What Does the Modern Evidence Show?

A systematic review by Tian et al. (2019) evaluated 1,382 patients receiving peripheral vasopressors and found an extravasation rate of just 3.4%, with no reported tissue necrosis or limb ischemia.

A larger meta-analysis by Owen et al. (2021) involving more than 16,000 patients reported an overall adverse event rate of only 1.8% in adults, with most complications consisting of mild extravasation, erythema, or phlebitis.

More recently, Wu et al. (2025) analyzed 6,852 patients and reported:

• Extravasation: 1.43%

• Thrombosis: 1.47%

• Infection: 0.72%

Across modern cohorts and systematic reviews, the overall complication rate of peripheral vasopressors generally ranges between 2.5–5%, with the overwhelming majority of events being minor and managed conservatively (Tran et al., 2020; Zichichi et al., 2024; Petros et al., 2025).

Most importantly, contemporary prospective studies have reported virtually no requirement for surgical intervention following peripheral vasopressor extravasation (Petros et al., 2025; Asher et al., 2023).

Central Lines Are Not Risk-Free

When discussing peripheral vasopressors, clinicians often focus on what could go wrong. But central venous catheters carry their own complications:

• Pneumothorax

• Hemothorax

• Arterial puncture

• Arterial cannulation

• Major bleeding

• Venous thrombosis

• Catheter-associated bloodstream infections (CLABSI)

Serious central-line complications occur in approximately 3% of insertions and remain an important source of patient morbidity (Chen et al., 2025).

In the CLOVERS secondary analysis, peripheral vasopressor complications occurred in only 0.6% of patients, compared with 3.7% central-line complications (Munroe et al., 2025).

The comparison therefore is not:

Risk versus no risk

It is:

Peripheral risks versus central-line risks.

Does Peripheral Administration Affect Mortality?

The answer appears to be no.

Multiple contemporary studies have demonstrated comparable outcomes between peripheral and central vasopressor initiation (Delaney et al., 2020; Asher et al., 2023; Munroe et al., 2023; Munroe et al., 2025; Shyu et al., 2025).

Across these studies:

• Mortality was similar

• Clinical effectiveness was similar

• Organ support requirements were similar

No convincing evidence suggests that initiating vasopressors through a peripheral IV worsens outcomes.

Another Unexpected Benefit: Fewer Central Lines

One of the most consistent findings across modern studies is that many patients never require a central venous catheter at all. Institutions implementing peripheral vasopressor protocols have demonstrated that approximately 30–60% of patients started on peripheral vasopressors avoid central-line placement altogether (Marti et al., 2022; Dansereau et al., 2024; Shyu et al., 2025).

This translates into:

• Fewer invasive procedures

• Lower CLABSI risk

• Reduced procedural complications

• Lower healthcare costs

Location Matters: Where Should We Place the IV?

Not all peripheral lines are created equal.

Avoid

❌ Hand veins

❌ Wrist veins

These smaller distal veins are associated with higher risks of infiltration and tissue injury.

Use Caution

⚠️ Antecubital fossa

Although commonly used during resuscitation, frequent elbow movement can lead to catheter dislodgement, delayed recognition of infiltration, and increased extravasation risk.

Preferred Sites

✅ Mid-forearm veins

✅ Basilic vein

✅ Cephalic vein

✅ External jugular vein

The ideal site is a large-caliber vein with reliable blood flow and minimal catheter movement.

Monitoring Is More Important Than the Catheter

The safest peripheral vasopressor protocol is not a specific gauge or brand of catheter.

It is vigilance. Evidence-based recommendations emphasize:

• Dedicated vasopressor line

• Frequent site inspection

• Documentation of catheter location

• Verification of patency

• Assessment at the start of every nursing shift

Structured monitoring protocols consistently demonstrate lower complication rates than non-protocolized care (Tran et al., 2020; Chen et al., 2025).

How Long Can Peripheral Vasopressors Be Used?

(Inspired by Dr Eddy’s lecture in ResusX’ 26)
Follow & Subscribe - Dr Eddy - for top notch similar content !

Traditionally many institutions restricted peripheral vasopressors to 24 hours.

However, contemporary evidence suggests this limit may be unnecessarily conservative.

Most studies report average infusion durations between 12 and 24 hours (Tian et al., 2019; Owen et al., 2021).

More recent protocolized programs have demonstrated safe administration for up to 48 hours, and occasionally longer, when strict monitoring protocols are followed (Marti et al., 2022; Zichichi et al., 2024; Petros et al., 2025).

The risk appears to rise substantially only with prolonged administration extending over several days.

How Much Vasopressor Can Be Given Peripherally?

There is currently no universally accepted upper dose limit.

However, contemporary literature reports successful peripheral administration at doses approaching:

Norepinephrine

Up to approximately 0.7 mcg/kg/min
(≈48 mcg/min in a 70-kg adult)

Phenylephrine

Up to approximately 3.5 mcg/kg/min
(≈200 mcg/min)

Epinephrine

Up to approximately 0.3 mcg/kg/min
(≈13 mcg/min)

Vasopressin

Up to 0.08 units/min

These represent reported doses from observational studies and institutional protocols rather than universally validated safety thresholds (Marti et al., 2022; Chen et al., 2025; Zichichi et al., 2024).

Many institutions also mitigate risk by administering vasopressors at lower concentrations when peripheral access is used.

What If Extravasation Occurs?

Extravasation remains uncommon, but every clinician administering peripheral vasopressors should know how to respond.

The severity ranges from:

Grade 1

Minor swelling or leakage

Grade 2

Localized tissue injury

Grade 3–4

Progressive ischemia, tissue compromise, or necrosis

Fortunately, severe injuries remain exceptionally rare (Tran et al., 2020; Owen et al., 2021).

Immediate Management of Extravasation

Step 1

Stop the infusion immediately.

Step 2

Leave the catheter in place.

Step 3

Attempt aspiration through the existing catheter to remove as much infiltrated drug as possible.

Step 4

Outline and photograph the affected area.

Step 5

Document the event thoroughly.

Step 6

Administer antidotes when indicated.

For catecholamine vasopressors:

Phentolamine remains the preferred antidote and should be infiltrated locally using sterile technique and a small-gauge needle.

For vasopressin extravasation:

No specific antidote currently exists. Topical nitroglycerin paste may be considered.

Step 7

Monitor progression closely.

Grade 3–4 injuries warrant early surgical consultation.

The goal is simple:

Document. Learn. Improve. Prevent recurrence.

Where Do We Go From Here?

Despite rapidly accumulating evidence, an important limitation remains. Nearly all available literature consists of observational studies, cohort studies, systematic reviews, and meta-analyses. Large definitive randomized controlled trials are still lacking. A pilot randomized trial evaluating peripheral versus central vasopressor strategies is currently underway (NCT06920173) and may provide important answers regarding safety and efficacy.

Until then, the available evidence strongly supports development of institutional protocols that allow protocolized peripheral vasopressor administration during the early phases of shock resuscitation.

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References

1. Bai X, Yu W, Ji W, et al. Early versus delayed administration of norepinephrine in patients with septic shock. Crit Care. 2014;18(5):532. doi:10.1186/s13054-014-0532-y

2. Beck V, Chateau D, Bryson GL, et al. Timing of vasopressor initiation and mortality in septic shock: a cohort study. Crit Care. 2014;18(3):R97. doi:10.1186/cc13868

3. Tian DH, Smyth C, Keijzers G, et al. Safety of peripheral administration of vasopressor medications: a systematic review. Emerg Med Australas. 2020;32(2):220-227. doi:10.1111/1742-6723.13406

4. Owen VS, Rosgen BK, Cherak SJ, et al. Adverse events associated with administration of vasopressor medications through a peripheral intravenous catheter: a systematic review and meta-analysis. Crit Care. 2021;25(1):146. doi:10.1186/s13054-021-03553-1

5. Tran QK, Mester G, Bzhilyanskaya V, et al. Complication of vasopressor infusion through peripheral venous catheter: a systematic review and meta-analysis. Am J Emerg Med. 2020;38(11):2434-2443. doi:10.1016/j.ajem.2020.09.047

6. Delaney A, Finnis M, Bellomo R, et al. Initiation of vasopressor infusions via peripheral versus central access in patients with early septic shock: a retrospective cohort study. Emerg Med Australas. 2020;32(2):210-219. doi:10.1111/1742-6723.13394

7. Marti K, Hartley C, Sweeney E, Mah J, Pugliese N. Evaluation of the safety of a novel peripheral vasopressor pilot program and the impact on central line placement in medical and surgical intensive care units. Am J Health Syst Pharm. 2022;79(24):2238-2245. doi:10.1093/ajhp/zxac144

8. Asher E, Karameh H, Nassar H, et al. Safety and outcomes of peripherally administered vasopressor infusion in patients admitted with shock to an intensive cardiac care unit: a single-center prospective study. J Clin Med. 2023;12(17):5734. doi:10.3390/jcm12175734

9. Dansereau A, Marti K, Mah J, Pugliese N. Evaluation of the safety and efficacy of peripheral vasopressors to decrease central line placement and associated bloodstream infections. J Infect Prev. 2024;25(4):153-160. doi:10.1177/17571774241245437

10. Zichichi A, Wallace R, Daniell J, et al. Safety of peripherally infused sympathomimetic vasopressors in the intensive care unit and emergency department. Ann Pharmacother. 2024;59(4):397-405. doi:10.1177/10600280241284796

11. Chen G, Shen C, Pan C, et al. Summary of best evidence for safe management of vasopressors through peripheral intravenous catheters. BMC Nurs. 2025;24:35. doi:10.1186/s12912-025-03635-3

12. Munroe E, Co I, Douglas IS, et al. Peripheral vasopressor use in early sepsis-induced hypotension. JAMA Netw Open. 2025;8(7):e2529148. doi:10.1001/jamanetworkopen.2025.29148

13. Petros A, Melkie A, Kotiso K, et al. Peripheral line for vasopressor administration: prospective multicenter observational cohort study for survival and safety. PLoS One. 2025;20:e0333275. doi:10.1371/journal.pone.0333275

14. Wu W, Yang X, Kou L. Extravasation, thrombosis, and infection with vasopressor infusion through peripheral intravenous catheters: a systematic review and meta-analysis. Cardiovasc Diagn Ther. 2025;15(3):847-860. doi:10.21037/cdt-2025-290

15. Shyu D, Ingraham N, Linke C, et al. Overview of peripheral vasopressor usage in an academic health system. Ann Am Thorac Soc. 2025. doi:10.1513/AnnalsATS.202411-1135OC

16. Loubani OM, Green RS. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters. J Crit Care. 2015;30(3):653.e9-653.e17. doi:10.1016/j.jcrc.2015.01.014

17. Brewer JM, Puskarich MA, Jones AE. Can vasopressors safely be administered through peripheral intravenous catheters compared with central venous catheters? Ann Emerg Med. 2015;66(6):629-631. doi:10.1016/j.annemergmed.2015.05.026

He was thin, malnourished, and battling aplastic anemia. His hemoglobin was critically low. His platelet counts were dangerously reduced. Earlier imaging had revealed a small intracranial bleed—a consequence of the severe thrombocytopenia. Fortunately, he was awake, talking, and neurologically intact.

Beside him sat his grandmother. She looked tired. More than tired—angry. At first, it was easy to mistake that anger for hostility. Around midnight, the platelets arrived. Within minutes, voices began rising from the bedside.

“Why are you giving him this yellow fluid?”

“He has a blood disease.”

“He needs blood.”

“No one is listening to me.”

My junior resident and the nursing staff tried to continue the transfusion, but the grandmother resisted. At one point, she removed the transfusion herself. The situation quickly became tense.

From the healthcare team’s perspective, the treatment plan was straightforward.

The child had active bleeding inside his skull. Platelets were urgently needed to reduce the risk of further hemorrhage. Red blood cells would also be transfused, but in carefully calculated doses appropriate for his weight. Giving multiple units rapidly was neither safe nor necessary.

Medically, the plan made perfect sense. But there was a problem. Nobody had explained it to her. To understand what was happening, we need to step away from the monitor and look at the person sitting beside the bed.

This grandmother had become everything for that child.

The burden of a chronic blood disorder had slowly pushed everyone else away. She was the one accompanying him to hospital visits, standing in outpatient queues, arranging previous transfusions, and somehow earning enough to keep life moving. Over time, she had learned one thing:

Whenever her grandson became weak, he needed blood.

That was the pattern she understood. That was the reality she had lived. Now she was being told that the doctors were refusing to give blood and were instead hanging a yellow-colored bag she had never seen before. From her perspective, it looked as though the people caring for her grandson were ignoring the obvious.

Her anger was not opposition. It was fear. It was exhaustion. It was love trying to protect someone when it did not have enough information to understand what was happening. When we sat down and explained the situation, everything changed.

We explained that her grandson was bleeding inside his brain. We explained the role of yellow fluid (platelets). We explained why platelets were more urgent than red blood cells at that moment. We explained why blood transfusions had to be given carefully slowly and safely. Most importantly, we explained the plan.

For the first time that night, she could see what we were seeing. The resistance disappeared. The arguments stopped. She agreed to treatment.

The next morning, she thanked the team. The art of medicine had not changed.

The communication had. As we grow older in this profession, many of us realize that some of the biggest challenges in medicine are not clinical.

They are human.

Families enter emergency departments carrying fear, financial stress, exhaustion, grief, and uncertainty. They are suddenly surrounded by unfamiliar equipment, unfamiliar medications, unfamiliar decisions, and unfamiliar language. When they don’t understand what is happening, that fear often comes out as anger.

Sometimes we label them as difficult. Sometimes we become frustrated. Sometimes, in the exhaustion of a busy shift, we forget that they are trying to make sense of a world that is completely foreign to them.

Communication is often viewed as a soft skill. In reality, it is a clinical skill.

‘Good communication prevents conflict.
Good communication improves adherence to treatment.
Good communication builds trust.
Good communication protects patients, families, and healthcare workers alike.’

In another setting, with a different relative, this encounter could easily have escalated into verbal abuse or even violence. The ingredients were all there: fear, misunderstanding, emotional distress, and a crowded emergency department.

The solution was not a better transfusion. It was a better conversation.

This was not a failure of an individual doctor, nurse, or family member. It was a reminder of a system under pressure, where exhausted clinicians care for more patients than time allows and where explanations are often sacrificed to urgency. Yet those few minutes spent explaining may be among the most important interventions we perform. Because medicine is not only about making the right decision.

It is about helping others understand why that decision is right. Sometimes the difference between conflict and cooperation is not another test, another drug, or another procedure. Sometimes it is simply a chair pulled beside a worried grandmother and a conversation she desperately needed to hear.

Pulse Checks and Reflection

Before we ask why a family member is angry, perhaps we should first ask:

‘What important piece of the story do they not know yet?

A grandmother saw a yellow bag.
We saw platelets.
She saw delay in correct treatment.
We saw protection.
She saw danger.
We saw treatment.
Between what she saw
and what we knew
stood only a conversation.
And sometimes,
the distance between conflict and trust
is no greater than that.’

There are moments in emergency medicine/acute care that stay with you forever.

A patient in cardiac arrest.
No pulse. No measurable circulation.
A resuscitation in full motion.

And then suddenly—

The patient opens their eyes.
They try to push rescuers away.
They grimace in pain.
Some even attempt to speak.

The chest compressions stop for a pulse check earlier than complete cycle… and the movements disappear.

For decades, these moments were dismissed as anecdotal, misunderstood, or simply too uncomfortable to discuss openly. Today, however, a growing body of literature confirms that this phenomenon is real, increasingly recognized, and scientifically fascinating.

It is called CPR-Induced Consciousness (CPRIC).

What Exactly Is CPR-Induced Consciousness?

CPRIC refers to signs of awareness or purposeful neurological activity occurring during ongoing chest compressions, despite the absence of spontaneous circulation.

Patients may demonstrate:

• Eye opening

• Purposeful limb movement

• Following commands

• Speech or vocalization

• Agitation or resistance to CPR

• Emotional expression or pain response

What makes CPRIC unique is that these signs disappear when compressions stop. The “consciousness” exists only because CPR is generating enough cerebral perfusion to transiently sustain cortical activity.

In other words:

High-quality CPR may be creating a temporary bridge between death and consciousness.

(Abboud & Varanasi, 2022; West et al., 2022)

How Common Is It?

The true incidence remains uncertain, partly because many clinicians still hesitate to report or document it.

Current observational data estimate CPRIC occurs in approximately 0.23–0.9% of resuscitations (Doan et al., 2020; West et al., 2022; Brede et al., 2024).

That number may appear small. But in high-volume emergency systems worldwide, it translates to thousands of cases annually.

Even more striking:

Surveys suggest that nearly half of prehospital clinicians have witnessed CPRIC at least once in their careers (Gregory et al., 2021; Carty & Bury, 2022).

The phenomenon is no longer rare enough to ignore.

Why Does It Happen?

The physiology behind CPRIC challenges traditional assumptions about cardiac arrest.

For years, cardiac arrest was viewed as a binary state:

• circulation absent

• consciousness impossible

But modern resuscitation science paints a far more nuanced picture.

High-quality compressions—particularly with early initiation, shockable rhythms, and mechanical CPR devices—can generate sufficient cerebral blood flow to preserve intermittent higher neurological function.
This is supported by one of the most remarkable recent studies in resuscitation science:

The AWARE-II Study

In the multicenter study by Sam Parnia and colleagues (2023), continuous EEG monitoring during CPR demonstrated organized brain activity—including delta, theta, and alpha waves associated with consciousness—occurring up to 35–60 minutes into resuscitation.

This finding fundamentally changes our understanding of the dying brain. The brain during cardiac arrest may not simply “switch off.” Instead, consciousness may persist in fragmented, fluctuating, or covert forms far longer than previously believed.

CPRIC May Actually Signal Better Survival

Paradoxically, CPRIC may represent effective resuscitation rather than failed resuscitation.

Multiple studies have shown associations between CPRIC and:

• higher ROSC rates

• better survival to discharge

• witnessed arrests

• shockable rhythms

• early CPR initiation

(Doan et al., 2020; Zhou & Sun, 2024)

This makes intuitive sense.

If compressions are generating enough cerebral perfusion to produce awareness, they are likely generating better systemic perfusion overall.

CPRIC may therefore be a marker of high-quality CPR physiology.

The Psychological Reality Nobody Talks About

For providers, CPRIC can be profoundly unsettling.

Emergency clinicians are trained to perform CPR on an unconscious patient. CPRIC breaks that expectation completely.

Some providers report:

• hesitation to continue compressions

• emotional distress

• confusion about stopping CPR

• intrusive recollections after the event

• insomnia or mood changes afterward

(Gregory et al., 2021; Brede et al., 2024)

Imagine delivering chest compressions while a patient looks directly at you.

The ethical discomfort is enormous.

But perhaps the more important question is:

What does the patient experience?

Research suggests some survivors retain memories during resuscitation.

In AWARE-II, approximately 39% of interviewed survivors described experiences suggestive of consciousness during CPR, ranging from dream-like perceptions to vivid recollections (Parnia et al., 2023).

Another study by Jaffe et al. (2021) found higher rates of depression and possible PTSD among survivors who recalled awareness during cardiac arrest.

This forces us to confront a difficult possibility:

Some patients may be experiencing pain, fear, awareness, or distress while CPR is ongoing.

The Sedation Dilemma

And this is where resuscitation medicine enters ethically uncharted territory.

Should conscious patients during CPR receive sedation?

Current practice varies wildly.

Reported approaches include:

• ketamine

• fentanyl

• midazolam

• physical restraint

• combinations of the above

(Pourmand et al., 2019; Switalski & Lechleuthner, 2025)

But there is a major problem:

Sedatives can worsen hypotension and impair perfusion during a state where circulation is already critically dependent on compressions.

So clinicians face competing priorities:

• relieve suffering

• preserve cerebral perfusion

• avoid interrupting CPR

• maintain team safety

And currently, there are no universally accepted international guidelines for managing CPRIC (West et al., 2022; Yusty-Prada et al., 2025).

CPRIC Is Forcing a Redefinition of Death

Historically, consciousness and pulse were inseparable.

CPRIC breaks that framework.

A patient can:

• have no pulse

• meet criteria for cardiac arrest

• yet still demonstrate awareness

This blurs the boundary between life and death in ways medicine is only beginning to understand.

Perhaps cardiac arrest is not a singular event.

Perhaps it is a process.

And CPR—when performed effectively—may transiently reverse parts of that process in ways previously thought impossible.

What Needs to Happen Next?

The literature is clear on one thing:

We are only at the beginning of understanding CPRIC.

Future priorities must include:

• standardized definitions

• international reporting systems

• sedation algorithms

• EEG and perfusion studies

• survivor psychological follow-up

• provider debriefing frameworks

• ethical guidance for conscious resuscitation

Because CPRIC is no longer an isolated curiosity.

It is now a legitimate frontier in resuscitation science.

Final Thoughts

Every emergency physician, paramedic, intensivist, and resuscitationist eventually learns that medicine is not always binary.

CPRIC reminds us of that in the most confronting way possible.

The patient with open eyes during CPR is not merely a dramatic anecdote.

They are evidence that modern resuscitation may be preserving fragments of consciousness far beyond what we once believed possible.

And perhaps the most important question is no longer:

“Can consciousness occur during CPR?”

But rather:

“What responsibility do we have once we know that it can?”

In Summary:
What CPR-Induced Consciousness Really Means

CPR-induced consciousness (CPRIC) is more than a resuscitation curiosity. It is likely a physiological marker of effective perfusion during cardiac arrest—and at the same time, a phenomenon with profound ethical, psychological, and clinical consequences.

What Positive Things Does CPRIC Indicate?

Current evidence suggests CPRIC is often associated with:

• High-quality CPR

• Better cerebral perfusion during compressions

• Early recognition and treatment of arrest

• Witnessed cardiac arrest

• Shockable rhythms

• Higher likelihood of ROSC and survival

(Doan et al., 2020; West et al., 2022)

In many ways, CPRIC may represent a “physiological success signal” during resuscitation—evidence that chest compressions are generating meaningful circulation to the brain.

It also challenges older assumptions that consciousness immediately disappears after cardiac arrest, opening new scientific understanding about the dying brain and cerebral resilience.

What Negative Consequences Can It Lead To?

Despite its possible association with better outcomes, CPRIC creates major challenges:

For the Patient

• Potential pain and distress during compressions

• Awareness of invasive procedures

• Psychological trauma

• Possible PTSD, depression, or recalled traumatic experiences

(Jaffe et al., 2021; Parnia et al., 2023)

For the Resuscitation Team

• Hesitation to continue CPR

• Increased interruptions in compressions

• Emotional distress among providers

• Ethical uncertainty regarding sedation and restraint

(Gregory et al., 2021; Brede et al., 2024)

For Systems of Care

• Lack of protocols

• Inconsistent sedation practices

• No universally accepted international guidelines

• Poor documentation and underreporting

(West et al., 2022; Zhou & Sun, 2024)

So What Is the Way Forward?

Until stronger evidence and formal guidelines emerge, the most reasonable approach is likely a balanced, physiology-driven strategy:

1. Recognize and confirm CPRIC Early

Providers should understand that purposeful movements during CPR do not necessarily indicate ROSC. Confirm using POCUS during next pulse check.

Stopping compressions repeatedly for pulse checks may worsen outcomes.

2. Prioritize Uninterrupted High-Quality CPR

The primary objective remains:

• effective compressions

• defibrillation when indicated

• reversible cause management

CPRIC should not distract from core resuscitation priorities.

3. Develop Structured Sedation Protocols

Sedation may become necessary when:

• CPR is interrupted

• defibrillation becomes unsafe

• patient agitation compromises resuscitation

But future protocols must balance:

• patient comfort

• cerebral perfusion

• hemodynamic effects

• provider safety

At present, ketamine is frequently discussed because of relative hemodynamic stability, but evidence remains limited.

4. Introduce Team Debriefing and Psychological Support

CPRIC events can be emotionally difficult for clinicians and survivors alike.

Formal debriefing should become part of post-resuscitation care.

5. Expand Research Aggressively

The next decade of resuscitation science should focus on:

• EEG-guided CPR research

• cerebral perfusion monitoring

• sedation trials during CPR

• long-term neuropsychological outcomes

• ethical frameworks for conscious cardiac arrest

Because CPRIC may ultimately redefine not only how we perform resuscitation—but how we understand consciousness itself.

6. Avoid Premature Termination of Resuscitation

One important implication of CPRIC is that visible neurological activity may coexist with profoundly low-flow states during cardiac arrest.

When point-of-care ultrasound (POCUS) during pulse checks demonstrates cardiac standstill, clinicians should be cautious about prematurely terminating resuscitation if:

• CPRIC is present,

• high-quality CPR is ongoing,

• and the patient remains within an active resuscitation pathway.

A practical approach may be to:

• continue a complete cycle of uninterrupted high-quality CPR before making termination decisions,

• reassess rhythm, physiology, and reversible causes systematically,

• and avoid allowing transient CPRIC-related confusion to alter structured cardiac arrest management.

This is especially relevant because CPRIC itself indirectly indicates that compressions are generating meaningful cerebral perfusion.

At present, there is insufficient evidence to define how CPRIC should influence termination-of-resuscitation decisions, making this an important future research priority.

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References

1. Abboud Y, Varanasi S. Cardiopulmonary resuscitation induced consciousness—A case report from United Arab Emirates. Open J Emerg Med. 2022;10(2). doi:10.4236/ojem.2022.102007

2. Atbi A, Mandhari A, Reesi A. Cardiopulmonary resuscitation induced consciousness: A case report. Oman Med J. 2022;37:e356. doi:10.5001/omj.2021.51

3. Brede J, Skjærseth E, Rehn M. Prehospital anaesthesiologists experience with cardiopulmonary resuscitation-induced consciousness in Norway – A national cross-sectional survey. Resuscitation Plus. 2024;18. doi:10.1016/j.resplu.2024.100591

4. Carty N, Bury G. Prehospital practitioner awareness and experience of CPR-induced consciousness. J Paramed Pract. 2022;14(9):358-364. doi:10.12968/jpar.2022.14.9.358

5. De Sousa Arci M, De Sá L, Oliveira L, et al. Cardiopulmonary resuscitation-induced consciousness (CPRIC): Occurrence and perception of health professionals and firemen. Int J Cardiovasc Sci. 2025. doi:10.36660/ijcs.20240130

6. Doan T, Adams L, Schultz B, et al. Insights into the epidemiology of cardiopulmonary resuscitation-induced consciousness in out-of-hospital cardiac arrest. Emerg Med Australas. 2020;32. doi:10.1111/1742-6723.13505

7. Gregory P, Mays B, Kilner T, Sudron C. An exploration of UK paramedics’ experiences of cardiopulmonary resuscitation-induced consciousness. Br Paramed J. 2021;5(4):9-17. doi:10.29045/14784726.2021.3.5.4.9

8. Hoa N, Cong D, Diep N. Cardiopulmonary resuscitation induced consciousness in asystolic cardiac arrest: A case report from Vinmec Smart City Hospital, Vietnam. Asian J Med Health. 2025. doi:10.9734/ajmah/2025/v23i101306

9. Jaffe I, Shirazi T, Gonzales A, Parnia S. Psychological outcomes and awareness during CPR in cardiac arrest survivors. Chest. 2021. doi:10.1016/j.chest.2021.07.1028

10. Mansour A, Ali L, Abbas Y, et al. An unusual resuscitation experience: The phenomenon of CPR-induced consciousness. Glob J Crit Care Emerg Med. 2025. doi:10.33425/3065-5641.1013

11. Migiel Ł, Darocha T, Hymczak H, et al. CPR-induced consciousness in hypothermic cardiac arrest: Where is the limit of tolerance of the human brain? A case report. Scand J Trauma Resusc Emerg Med. 2025;33. doi:10.1186/s13049-025-01426-y

12. Olaussen A, Shepherd M, Nehme Z, Smith K, Bernard S, Mitra B. Return of consciousness during ongoing cardiopulmonary resuscitation: A systematic review. Resuscitation. 2015;86:44-48. doi:10.1016/j.resuscitation.2014.10.017

13. Parnia S, Shirazi T, Patel J, et al. AWAREness during REsuscitation-II: A multicenter study of consciousness and awareness in cardiac arrest. Resuscitation. 2023. doi:10.2139/ssrn.4246760

14. Pourmand A, Hill B, Yamane D, Kuhl E. Approach to cardiopulmonary resuscitation induced consciousness, an emergency medicine perspective. Am J Emerg Med. 2019;37(4):751-756. doi:10.1016/j.ajem.2019.01.051

15. Switalski J, Lechleuthner A. Cardiopulmonary resuscitation-induced consciousness (CPRIC). Die Anaesthesiologie. 2025;74:765-776. doi:10.1007/s00101-025-01593-8

16. West R, Otto Q, Drennan I, et al. CPR-related cognitive activity, consciousness, awareness and recall, and its management: A scoping review. Resuscitation Plus. 2022;10. doi:10.1016/j.resplu.2022.100241

17. Yusty-Prada J, Portuguez-Jaramillo N, Piñeros-Alvarez J. Cardiopulmonary resuscitation-induced consciousness in an elderly patient: A case report in the prehospital setting. Int J Emerg Med. 2025;18. doi:10.1186/s12245-025-01032-w

18. Zhou X, Sun B. CPR-induced consciousness during ventricular fibrillation: Case report and literature review. Emerg Med Int. 2024;2024. doi:10.1155/2024/2834376

On this Emergency Medicine Day, let me tell you a recent story from a peripheral center where I am currently working — a story that reminded me why I chose this specialty, and why, despite the chaos, exhaustion, uncertainty, and emotional burden, I remain deeply proud of what we do as Emergency Physicians. Because Emergency Medicine is not merely about treating disease.

It is about standing beside human beings during the worst hour of their lives, making critical decisions before certainty arrives, and fighting for patients who still have a chance to come back from the edge. This is a story from a peripheral center where I am currently posted. Not a large tertiary-care resuscitation bay. Not a perfectly staffed academic unit. Just one of the many frontline centers in our healthcare system where critically ill patients arrive first — often before systems are ready for them.

“She had finally won.”

For almost a decade, cancer had dictated the rhythm of her life.

Hospital corridors.
Chemotherapy cycles.
Surgical scars.
Follow-up scans.
The quiet anxiety before every report.

Cervical cancer had taken years from her life, but not her fight. And then, fifteen days before I met her, she heard the words every cancer patient waits for:

No metabolically active lesion.

Her PET-CT showed remission.

For her family, it was not merely a report. It was resurrection. But medicine has a cruel way of reminding us that survival is rarely linear. Seven days before arriving to our Emergency Department, she had noticed swelling in her left leg. She visited the outpatient department of our peripheral center, where a lower limb ultrasound was advised.

The scan date was given three days later.

Nobody was wrong.
Nobody was careless.
Just another ordinary delay inside an overburdened healthcare system.

Three days later, she returned. She walked into the ultrasound room alive. While lying down during the scan, she suddenly became breathless. The scan was somehow completed. But now she could barely complete sentences. She was visibly short of breath and rapidly deteriorating. She was rushed into our Emergency Department.

When she arrived, her blood pressure was not recordable.
Her oxygen saturation hovered in the 80s.
Her body had already entered shock.

The monitors were connected. IV lines secured. The first fluid bolus started.

The venous blood gas returned:

pH: 6.7
Lactate: 15
Hco3 = 6
pCo2 = 19

Her body was failing faster than words could describe it. We performed Point-of-Care Ultrasound (POCUS). The right atrium was grossly enlarged, right ventricle ballooned against a struggling septum. McConnell’s sign stared back from the screen.

At that moment, the diagnosis became painfully clear. Massive pulmonary embolism.

A clot had likely traveled silently from the swollen leg she noticed days ago, into the pulmonary circulation, and now her right heart was collapsing under the pressure.

Most textbooks make the next step sound straightforward.

“Give thrombolysis.”

But medicine at the bedside is never written like textbooks. Because now came the real problem. We were functioning in a peripheral center. No unit was willing to admit a post-thrombolysis unstable patient in this centre, before even documenting they were told not to admit the patient. And she was too unstable to survive transfer elsewhere.

There are moments in Emergency Medicine where the physician stands alone between protocol and reality.

This was one of them. Giving thrombolysis carried enormous risk. Not giving it would almost certainly kill her. And then came the hardest part of Emergency Medicine — not the procedures, not the drugs, not the ultrasound.

The conversation.

I had to sit beside her daughter and explain that the mother who had just survived cancer was now standing at the edge of another catastrophe.

I explained the diagnosis.
The risks.
The bleeding possibility.
The uncertainty.
The fact that we did not have the ideal system support around us.
The fact that shifting her in this condition might itself become fatal.

I still remember the silence after that conversation. The daughter’s eyes filled with tears. Fifteen days ago, they celebrated remission. Now they were discussing whether her mother would survive the next few hours. Emergency physicians witness human beings at the exact moment life changes direction.

Not in conference halls.
Not in polished discharge summaries.
But in overcrowded resuscitation bays, where decisions must be made before certainty arrives.

We minimized fluids after identifying the failing right ventricle.
Noradrenaline was started.
Vasopressin followed.
Anticoagulation initiated.
Nebulized nitroglycerin was prepared.

And finally, after informed consent, the thrombolytic infusion began. At that point, another decision had to be made. Should we intubate?

Many critically ill patients eventually require airway support, but in massive pulmonary embolism, induction and positive pressure ventilation can precipitate cardiovascular collapse. She was compensating for her acidosis still — and we decided to maintain a very high threshold for intubation.

So we waited. Watched closely. Adjusted vasopressors. Repeated assessments. Managed physiology minute by minute.

Slowly, she began improving. The blood pressure returned. The oxygenation improved.
The storm inside her pulmonary circulation began to settle. And sitting there afterward, exhausted in that resuscitation room, I kept thinking:

This is why Emergency Medicine exists.

Emergency Medicine is not merely triage.
It is not just “initial management.”
It is not a transit lounge before “real specialties” take over.

Emergency Medicine is the specialty of the first hour, the resucitation, the time.

The hour where diagnosis is uncertain. Where systems are imperfect. Where protocols collide with reality. Where families collapse emotionally. Where physiology deteriorates by the minute. Where someone must integrate ultrasound, resuscitation, communication, pharmacology, risk-benefit analysis, airway judgment, hemodynamics, and ethics — simultaneously.

That someone is the Emergency Physician.

Emergency Medicine also exists for another uncomfortable reality in healthcare. It exists when diseases stop fitting neatly into one specialty. When the patient has shock, respiratory failure, metabolic acidosis, hemodynamic collapse, and an unclear disposition — all at the same time. It exists when multiple systems are failing together, and multiple departments hesitate because the patient belongs partially to everyone, and completely to no one. It exists when nobody wants to take responsibility first. It exists when a patient has nowhere else to go.

When transfer is impossible. When admission is uncertain.
When the patient is denied from everywhere else because they are “too unstable,” “too high-risk,” or “too complicated.”

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That is when the Emergency Department becomes more than a physical space. It becomes the safety net of the healthcare system. And the people holding that net together are Emergency Physicians. Because at the core of Emergency Medicine lies one simple responsibility:

To resuscitate the patient who made it to the hospital in time. To pull them back from the edge of physiological collapse. To bring them out from the doom of illness before the body crosses a point where recovery is no longer possible.

That responsibility exists regardless of whether the diagnosis is clear. Regardless of whether a bed is available. Regardless of whether another department has accepted the patient. Regardless of how chaotic the environment becomes.

Our first instinct is always the same:

Stabilize.
Resuscitate.
Buy time for life.

And the strange thing about Emergency Medicine is that most patients never truly remember us afterward. They move to wards, ICUs. Then discharge summaries.
Then follow-up clinics. Then life slowly returns to normal.

The emergency department becomes just a blurred chapter in their memory. And honestly, that is okay. Because our work was never about recognition. But sometimes, families remember. Sometimes they see the physician running from one crashing patient to another, handling chaos while still trying to reassure a frightened daughter standing beside her critically ill mother. At the end of that shift, after hours of vasopressors, thrombolysis, difficult decisions, and uncertainty, her daughter came to me and simply said:

“Thank you, doctor.”

It was a small moment. But after one of the heaviest shifts, it made my entire day. Because in that moment, someone understood what Emergency Medicine truly is.

Not glamour.
Not heroism.
Not dramatic television scenes.

Just human beings trying to hold life together in its most fragile moments. This is why we exist. Qualified Emergency Physicians are not a luxury for tertiary hospitals.
They are a necessity for every medical college, every emergency room, every frontline center where critically ill patients first arrive.

Because salvageable patients do not always reach ideal systems.

Sometimes they reach peripheral centers.
Sometimes they arrive before specialists.
Sometimes they deteriorate in front of junior doctors with minimal support.
Sometimes the difference between life and death is whether someone in that room understands shock physiology well enough to act before certainty appears.

Emergency Medicine exists for those moments. Not every patient can be saved. But many can be salvaged if the right decisions are made early enough. And that is what Emergency Physicians are trained to do:
make critical decisions inside physically chaotic, emotionally overwhelming, resource-limited environments — while time itself is collapsing around the patient.

This is where Emergency Medicine comes in.

At the frontline.
Before clarity.
Before admission.
Before certainty.

Sometimes, before death.

We propose the concept of the “Unprepared Airway” — reframing many peri-intubation complications not just as anatomical difficulty, but as failures of physiologic and situational preparation.

Along with this, we introduce an ABCDE preparation framework as a cognitive strategy for safer emergency intubation:

A – Air & oxygenation

B – Blood pressure & hemodynamics

C – Contingency plans

D – Decision & drug modulation

E – Execution & rescue

The aim is to shift the question from “Can I intubate?” to “Is this airway truly prepared?”

Would love to hear thoughts and feedback from the group.

Link to original paper

It was 2:30 AM in the Emergency Department.

A middle-aged man with metastatic lung malignancy arrived breathless, exhausted, and unable to complete sentences. His chest radiograph showed a massive right pleural effusion with near-complete white-out of the hemithorax. Bedside ultrasound confirmed a large anechoic effusion with passive lung collapse.

His oxygen saturation improved slightly with non-invasive support, but he remained uncomfortable. The decision was made for therapeutic thoracentesis.

The procedure went smoothly.

Ultrasound-guided.
Single attempt.
No cough.
No obvious complication.

About 1.2 liters of straw-colored fluid was drained. The patient immediately reported relief.

And then came the post-procedure chest X-ray.

“Doctor… there’s a pneumothorax.”

Suddenly, the room shifted.

The reflex in Emergency Medicine is almost automatic:
Pneumothorax = chest tube.

But this wasn’t that kind of pneumothorax.

This was pneumothorax ex vacuo.

The Diagnostic Trap in the ED

One of the hardest things in Emergency Medicine is resisting the urge to treat the image instead of the patient.

The X-ray showed a moderate pneumothorax.
But the patient?

• Comfortable

• Hemodynamically stable

• Improved dyspnea

• No worsening hypoxia

• No respiratory distress

The physiology and the radiology were telling different stories.

That mismatch matters.

What Actually Happened?

In pneumothorax ex vacuo, the issue is not accidental lung puncture.

The real problem is an unexpandable lung.

Usually this happens because of:

• Malignant pleural disease

• Trapped lung from chronic inflammation

• Endobronchial obstruction

• Visceral pleural restriction

The pleural effusion is often not the primary disease — it is a consequence of chronic negative pleural pressure from a collapsed lung. When fluid is removed, the lung fails to re-expand. A transient pressure gradient develops, allowing air to enter the pleural space and “fill the vacuum” (Farkas, 2014; Heidecker et al., 2006).

That air is not under tension.
It is not rapidly progressive.
And most importantly — a chest tube usually does not fix it.

So What Should We Actually Do?

This is where Emergency Medicine becomes less procedural and more physiological.

The ideal management depends on one simple principle:

Treat the patient, not the radiograph.

If the patient is:

• Hemodynamically stable

• Maintaining oxygenation

• Clinically improving after thoracentesis

• Without signs of tension physiology

…then the best treatment is often:

Observation.

Not another procedure.

Not reflex chest tube insertion.

Not panic.

Why Observation Is Usually Better

Pneumothorax ex vacuo is fundamentally different from traumatic or spontaneous pneumothorax.

The lung is unable to expand because of underlying pathology. Draining the pleural space with an intercostal drain does not solve the primary issue. Instead, it may expose the patient to:

• Persistent air leak

• Procedural pain

• Infection risk

• Repeated interventions

• Prolonged hospitalization

Heidecker et al. (2006) and Huggins et al. (2010) demonstrated that these pneumothoraces are usually benign and rarely progress to tension physiology.

In many cases, the pneumothorax remains stable or gradually gets replaced again by pleural fluid over time.

Then What Is the Treatment?

The real treatment is identifying and managing the cause of the trapped or non-expandable lung.

Depending on the etiology, management may involve:

1. Treating Endobronchial Obstruction

If due to a central airway lesion:

• Bronchoscopy

• Tumor debulking

• Stenting

• Oncology-directed therapy

may allow lung re-expansion.

2. Managing Malignant Trapped Lung

In malignant disease:

• Indwelling pleural catheter

• Symptom-guided drainage

• Palliative management

are often more appropriate than repeated thoracenteses.

3. Surgical Decortication

In selected patients with fibrous visceral pleural restriction and good functional reserve:

• VATS decortication

• Surgical pleural peel removal

may restore lung expansion.

But this is rarely an ED decision.

4. Supportive Care

Most ED patients only need:

• Observation

• Oxygen if required

• Monitoring

• Repeat imaging only if clinically indicated

• Specialty follow-up

And often, reassurance.

When Should We Worry?

Observation is appropriate only if the patient remains clinically stable.

Red flags that should prompt reconsideration include:

• Worsening respiratory distress

• Hemodynamic instability

• Progressive hypoxia

• Rapid enlargement on imaging

• Features suggestive of true procedural lung injury

Because not every post-thoracentesis pneumothorax is ex vacuo.

Clinical context matters.

The Ultrasound Era

Traditionally, any pneumothorax after thoracentesis was considered procedural injury.

But with modern ultrasound guidance, true traumatic pneumothorax has become less common. Pneumothorax ex vacuo is now increasingly recognized as a distinct physiological entity rather than a procedural complication (Farkas, 2014).

Not all post-procedure pneumothoraces are created equal.

And that distinction changes management entirely.

Pulse Checks and Reflections

What stayed with me after this case wasn’t just the physiology of pneumothorax ex vacuo — it was the emotional reality of practicing medicine within hierarchy.

Sometimes you stand in a centre of excellence, surrounded by experienced clinicians, yet still feel the tension between evidence and authority.

The patient was stable.
The physiology made sense.
The literature supported observation.

And still, the reflex around the room was:
“Insert a chest tube.”

One difficult truth in medicine is that knowledge and authority do not always evolve at the same pace.

Medicine changes constantly. Protocols evolve. Evidence updates itself. What was once standard teaching may later become outdated practice. That is why no opinion — no matter how senior or widely accepted — should replace clinical reasoning.

That night reminded me that medicine demands humility from everyone, not just juniors.

Because even respected clinicians can occasionally be wrong.
And sometimes the quietest person in the room may notice something important.

Later, when the specialty team agreed with conservative management and discharged the patient, it reinforced an important lesson:

Always return to the patient.
Not the panic.
Not the image.
Not the hierarchy.

In moments of uncertainty, it helps to anchor yourself in physiology and evidence. Revisit the teaching. Cross-check the literature. Discuss with people you trust. Seek another perspective if something does not feel right.

Not to challenge authority for ego —
but to protect patients from unquestioned assumptions.

And when disagreement with a senior becomes necessary, it should be constructive, respectful, and preferably private.

Not:
“You’re wrong.”

But:
“Could this represent something else?”
“Should we reconsider this based on the clinical picture?”
“I read newer evidence suggesting observation may be reasonable here.”

That is not disrespect.
That is safe medicine.

The challenge is learning how to balance humility with independent thinking — respecting experience without surrendering your ability to reason critically.

Because medicine is too complex for blind obedience and too human for absolute certainty.

Acute Medicine eventually teaches you that good clinical practice is not only about knowing when to intervene.

It is also about recognizing when restraint, observation, and thoughtful questioning are the better decisions.

And at the end of the day, your responsibility is not to hierarchy.

It is to the patient.

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References

• Farkas J. Pneumothorax ex vacuo: Post-thoracentesis pneumothorax in the ultrasound era. 2014.

• Heidecker J, Huggins JT, Sahn SA, et al. Pneumothorax ex vacuo. Chest. 2006.

• Huggins JT, Sahn SA, Heidecker J, et al. Characteristics of trapped lung and pneumothorax ex vacuo. Chest. 2010.

Recently, I watched Michael.

What stayed with me wasn’t just the story — it was the reminder of how deeply our childhood experiences shape the way we see the world.

The same sentence.
The same event.
The same silence.

Can mean completely different things to two different people.

Because all of us are interpreting life through memories, fears, insecurities, love, trauma, hope, and experiences we carry from years before.

Working in the Emergency Department and acute care constantly reminds me of this.

Sometimes a patient is not “angry.” They are scared.
Sometimes a relative is not “difficult.” They are exhausted from months of caregiving.
Sometimes chronic illness doesn’t just damage the body — it changes how a person sees themselves, their future, and even their worth.

Acute care medicine teaches you that before treating disease, you first have to understand the human being experiencing it.

And maybe outside medicine too, we forget this often.

We judge reactions without knowing histories.
We hear words without understanding the wounds behind them.

It makes me grateful — for health, for perspective, for the privilege of still having time to live, learn, improve, and connect.

If this resonates with you, I’d love to hear your thoughts or experiences too.
What’s something that shaped the way you perceive life today?

- Dr Arihant Jain, MD

More elderly patients arriving confused during heat waves.
Construction workers collapsing at worksites.
Young athletes becoming encephalopathic after training sessions.
Children arriving lethargic after being left briefly inside vehicles.

Heat-related illness is no longer an uncommon seasonal presentation. It is becoming a daily emergency medicine problem worldwide.

And the dangerous part is this:

Heat stroke is one of the few critical illnesses where definitive treatment begins before the diagnosis is fully confirmed.

If the patient is hot, altered, and crashing:
Cooling is a part of Resuscitation.

Heat Illness Is a Spectrum

Heat-related illness exists on a continuum ranging from minor self-limited conditions to catastrophic multiorgan failure (Gauer & Meyers, 2019).

The spectrum includes:

• Heat rash

• Heat edema

• Heat cramps

• Heat syncope

• Heat exhaustion

• Heat stroke

Most patients initially present somewhere in the middle of this spectrum. Missing progression is what kills.

The Physiology: Why the Body Fails

The human body normally dissipates heat through:

• Evaporation

• Radiation

• Convection

• Conduction

As ambient temperatures and humidity rise, these mechanisms become progressively ineffective (CorePendium, 2025).

Once environmental temperature approaches body temperature:

• Sweat evaporation becomes inadequate

• Peripheral vasodilation worsens hypotension

• Cardiac output becomes strained

• Splanchnic perfusion decreases

• Cellular proteins begin to denature

• Cytokine-mediated inflammation escalates

Heat stroke rapidly evolves into a systemic inflammatory syndrome resembling severe sepsis (Bein, 2023).

This is not simply “fever.”

It is:

• Cellular injury

• Endothelial dysfunction

• Coagulopathy

• Organ ischemia

• Metabolic collapse

The Most Important Clinical Distinction

Heat Exhaustion vs Heat Stroke

This distinction matters enormously.

Heat Exhaustion

Patients may present with:

• Weakness

• Heavy sweating

• Nausea

• Tachycardia

• Dizziness

• Syncope

• Muscle cramps

Core temperature is usually:

• <40°C

Mental status remains largely preserved.

Thermoregulation still functions (Wexler, 2002).

Heat Stroke

Heat stroke is defined by:

• Core temperature ≥40°C (104* F)

• CNS dysfunction

(CorePendium, 2025).

Central nervous system dysfunction is the hallmark.

This may include:

• Irritability

• Ataxia

• Delirium

• Confusion

• Seizures

• Coma

Once CNS dysfunction appears in the setting of hyperthermia:

Assume heat stroke until proven otherwise.

Because waiting delays cooling.
And delayed cooling worsens mortality (Sorensen & Hess, 2022).

Exertional vs Classic Heat Stroke: Same Endpoint, Different Patient

One of the most clinically important distinctions in heat-related illness is understanding the difference between Exertional Heat Stroke (EHS) and Classic/Non-exertional Heat Stroke (CHS/NEHS).

While both share the same final pathway — severe hyperthermia, systemic inflammation, coagulopathy, and multiorgan dysfunction — the triggers, patient populations, and clinical patterns differ significantly (Bouchama et al., 2022; Leon & Bouchama, 2015).

Exertional Heat Stroke (EHS)

EHS typically occurs in:

• Athletes

• Military recruits

• Outdoor laborers

• Young healthy individuals performing intense physical activity

The mechanism is:

Excess endogenous heat production overwhelming the body’s heat dissipation capacity.

Importantly, EHS can occur even in temperate climates when exercise intensity exceeds heat loss capacity (Garcia et al., 2022; Périard et al., 2022).

Clinically, EHS patients often:

• Continue sweating

• Develop profound rhabdomyolysis

• Have severe metabolic acidosis

• Show higher rates of acute kidney injury

Despite appearing critically ill, outcomes are often excellent if cooling is initiated rapidly. Mortality is substantially lower compared with classic heat stroke when evidence-based cooling protocols are followed (Bouchama et al., 2022).

This is why sports medicine and military protocols emphasize:

“Cool first, transport second.”

Cold-water immersion initiated directly in the field dramatically improves neurologic outcomes and survival (Roberts et al., 2023; Belval et al., 2018).

Classic / Non-exertional Heat Stroke (CHS)

Classic heat stroke typically affects:

• Elderly individuals

• Infants and young children

• Patients with chronic illness

• Socially isolated individuals

• Patients during prolonged heat waves

The trigger is usually:

Passive environmental heat exposure combined with impaired thermoregulation.

(Bouchama et al., 2022; Bukhari, 2023).

These patients often present later, are physiologically fragile, and may have:

• Altered mental status

• Hot dry skin

• Cardiovascular collapse

• Delayed recognition

Classic heat stroke carries substantially higher mortality, reaching nearly 60% in some reports (Bouchama et al., 2022).

Unlike EHS, where collapse during exercise immediately raises concern, classic heat stroke is frequently mistaken for:

• Sepsis

• Stroke

• Toxicologic emergencies

• Delirium

• CNS infection

This diagnostic delay contributes significantly to poor outcomes.

The Patients We Commonly Miss

Heat stroke is not limited to athletes.

Classic heat stroke often affects:

• Elderly patients

• Socially isolated individuals

• Psychiatric patients

• Patients without access to cooling

• Individuals on anticholinergics, neuroleptics, or sympathomimetics

(CorePendium, 2025).

Exertional heat stroke affects:

• Athletes

• Military personnel

• Outdoor workers

• Laborers using heavy protective equipment

Importantly:

Exertional heat stroke can occur even in temperate climates (Roberts et al., 2021).

The ED Approach: Think Fast, Cool Faster

1. Airway & Breathing

Airway management follows standard indications.

But there is an important nuance:
Some patients improve dramatically after cooling.

CorePendium (2025) notes that temporary oxygenation and ventilatory support may bridge patients while rapid cooling is initiated.

If intubation is required:

• Rocuronium is preferred

• Benzodiazepines are useful for seizure control and sedation

2. Circulation

These patients are profoundly volume depleted.

Start with:

• 1–2 L isotonic crystalloids

• Frequent reassessment

(CorePendium, 2025).

But remember:
Not all hypotension is dehydration alone.

Peripheral vasodilation, systemic inflammation, and myocardial injury all contribute to shock physiology.

Myocardial injury occurs in up to 21% of patients and may precipitate arrhythmias or cardiac arrest (CorePendium, 2025).

Cooling Is the Definitive Treatment

Not antibiotics.
Not vasopressors.
Not antipyretics.

Cooling.

Rapid cooling is the single most important intervention in heat stroke (Barletta et al., 2025).

And critically:

Cooling should begin immediately — even before the full workup is complete.

(CorePendium, 2025).

Cold Water Immersion: The Gold Standard

Among all cooling modalities:

Cold water immersion remains the fastest and most effective.

Preferred water temperature:

• 1–17°C

Evidence consistently demonstrates:

• Faster core temperature reduction

• Better neurologic outcomes

• Lower mortality

This is especially true in exertional heat stroke (Douma et al., 2020; Pryor et al., 2015).

Modern ED adaptations include:

• Ice-water body bags

• Portable immersion setups

• Athletic event cooling stations

The old concern regarding shivering and peripheral vasoconstriction should not delay immersion therapy. Benefits far outweigh risks (CorePendium, 2025).

If Immersion Is Not Possible

Evaporative cooling remains an effective alternative.

Technique:

1. Remove clothing

2. Spray tepid water

3. Apply high-flow fans

(CorePendium, 2025).

Additional adjuncts:

• Ice sheets

• Rotating ice towels

• Whole-body ice packs

• Cooling blankets

• Cold IV fluids

But cold IV fluids alone are insufficient (Smith, 2005).

A Common Pitfall: Waiting for “True” Hyperthermia

One of the most dangerous delays occurs when clinicians wait for temperatures above 40°C before initiating cooling.

In altered hyperthermic patients, cooling should not be delayed even if the measured temperature is below 40°C.

Why?

Because:

• Temperatures continue rising

• Prehospital cooling may transiently reduce readings

• Delay worsens organ injury

Clinical suspicion matters more than exact numbers.

What Should NOT Be Used

Antipyretics:

• Paracetamol

• NSAIDs

have no role.

Dantrolene also lacks evidence of benefit (Barletta et al., 2025).

Heat stroke is not a hypothalamic set-point problem like infectious fever.

Using antipyretics may actually worsen hepatic and renal injury (Glazer, 2005).

The Organ Damage We Must Anticipate

Heat stroke is a multiorgan disease.

Clinicians should actively monitor for:

• Rhabdomyolysis

• Hyperkalemia

• Acute kidney injury

• Liver injury

• DIC

• ARDS

• Cardiac dysrhythmias

CK >5,000 U/L suggests significant muscle injury.
CK >16,000 U/L correlates with higher renal failure risk (CorePendium, 2025).

AST >1000 is associated with mortality (CorePendium, 2025).

Importantly:
Coagulopathy often worsens over 24–72 hours, meaning initially stable patients can deteriorate later (Savioli et al., 2022).

Disposition: Do Not Underestimate Heat Stroke

Most minor heat illnesses can safely be discharged after observation and symptom improvement.

But:

All heat stroke patients require admission.

Usually ICU admission.

(CorePendium, 2025).

Why?
Because end-organ injury may evolve hours after initial stabilization.

Prevention: The Most Effective Treatment

Heat illness is largely preventable.

Final Thoughts

Heat-related emergencies are increasing worldwide.

For clinicians, the priorities are remarkably simple:

1. Recognize early

2. Measure core temperature

3. Cool aggressively

4. Anticipate organ failure

5. Monitor beyond apparent recovery

Because in heat stroke:

Time to cooling determines outcome.

And often:

Cooling itself is the lifesaving intervention.

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References

• Adapted from CorePendium chapter on Heat Related Emergencies by Cindy Bitter and team.

• Barletta J et al. (2024). Management of Heat-Related Illness and Injury in the ICU. Critical Care Medicine.

• Barletta J et al. (2025). SCCM Guidelines for the Treatment of Heat Stroke. Critical Care Medicine.

• Bein T. (2023). Pathophysiology and management of heat illness.

• Douma M et al. (2020). Cooling techniques for heat stroke. Resuscitation.

• Gauer R & Meyers B. (2019). Heat-Related Illnesses. American Family Physician.

• Glazer J. (2005). Management of heatstroke and heat exhaustion.

• Pryor R et al. (2015). Exertional Heat Illness. Prehospital and Disaster Medicine.

• Roberts W et al. (2021). ACSM Consensus on Exertional Heat Illness. Current Sports Medicine Reports.

• Savioli G et al. (2022). Heat-Related Illness in Emergency and Critical Care. Biomedicines.

• Smith J. (2005). Cooling methods used in exertional heat illness.

• Sorensen C & Hess J. (2022). Treatment and Prevention of Heat-Related Illness. NEJM.

Dr Arihant Jain, MD | lifeonthefrontline.com
Instagram: @humans.of.em
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PART 1 — Understanding Diuretic Resistance

The problem

Loop diuretics are the cornerstone of decongestion—yet:

• 20–30% of patients fail to respond adequately

• Associated with longer hospital stay, ICU need, and mortality

What is Diuretic Resistance?

Failure to achieve negative sodium and fluid balance despite adequate dosing

• Often misdiagnosed

• Many cases are actually a result of:

  • Under-dosing

  • Poor drug delivery

  • Wrong physiology

PART 2 — Mechanisms of Diuretic Resistance

(This is the key to everything that follows)

Diuretic resistance is multifactorial, driven by 3 major pathways:

1️⃣ Pharmacokinetic Failure (Drug never reaches kidney)

• Gut edema → ↓ oral absorption

• Low cardiac output → ↓ renal perfusion

• High CVP → renal congestion

• Hypoalbuminemia → altered drug delivery

👉 Result: insufficient drug at site of action

2️⃣ Tubular Adaptation (“Nephron fights back”)

• Chronic loop use → distal nephron hypertrophy

• ↑ Na-Cl cotransporter (NCC)

• ↑ ENaC activity

👉 Result: distal sodium reabsorption overrides loop effect

3️⃣ Neurohormonal Activation (“Body wants sodium”)

• RAAS activation

• Sympathetic activation

• Vasopressin

👉 Creates a state of “basal sodium avidity”
👉 Kidney is primed to retain sodium despite diuretics

The Forgotten Player — Chloride

• Hypochloremia → activates WNK kinases

• ↑ Sodium reabsorption

• ↓ Diuretic response

👉 Diuretics worsen chloride depletion → vicious cycle

Diuretic resistance is NOT just “need more dose”
It’s a mismatch between drug, kidney, and physiology

Read further about pathophysiology behind Diuretic Resistance here

PART 3 — How to Monitor Diuretic Therapy in ED

(Where most clinicians go wrong)

❌ What NOT to rely on:

• Weight

• Fluid balance charts

• “Urine looks good”

👉 These do NOT reflect sodium removal

✅ What actually matters:

1. Urinary Sodium (U. Na+) — THE GOLD STANDARD

⏱ Check 1–2 hours after IV diuretic

• >70 mmol/L → Adequate response

• <50–70 mmol/L → Resistance

👉 This predicts response before clinical deterioration

2. Urine Output

• Target: >100–150 mL/hour (first 6 hours)

3. Bedside Ultrasound

• Lung B-lines → pulmonary congestion

• VExUS → systemic venous congestion

Dynamic Monitoring with all 3 adjuncts.

Assess → Adjust → Reassess every 2–6 hours

Not next morning. Not after ward transfer.

PART 4 — The Shift: Phenotype-Based Diuretic Therapy

Same drug. Same dose. Different patients → different failures.

👉 That’s because different mechanisms dominate in different phenotypes

PHENOTYPE 1 — RIGHT HEART FAILURE

“Venous congestion is the problem”

🔬 Mechanism

• ↑ CVP → renal congestion

• ↓ renal perfusion gradient

• ↓ drug delivery

Strategy

• Aggressive decongestion (even if borderline BP)

• Higher loop doses

• Early combination therapy

If low output:

• Add inotropes (dobutamine/milrinone)

• Use norepinephrine if hypotensive

👉 Decongestion improves renal function

PHENOTYPE 2 — ADVANCED CKD

“Delivery + tubular resistance”

Mechanism

• ↓ tubular secretion

• Chronic sodium retention

• Distal nephron adaptation

Strategy

• Use higher loop doses (expected)

• Prefer IV route

Early add-ons:

• Acetazolamide → if metabolic alkalosis

• Thiazide → if chronic loop use

👉 Sequential nephron blockade is essential

Critical points:

• Correct chloride

• Accept mild creatinine rise

PHENOTYPE 3 — OBESITY

“Hidden congestion + neurohormonal activation”

Mechanism

• Adipose tissue → RAAS + SNS activation

• ↑ plasma volume

• ↑ intra-abdominal pressure → ↓ renal perfusion

Strategy

• Assume underestimated congestion

• Use higher doses early

• Early combination therapy

Add:

• SGLT2 inhibitors (if appropriate)

Clinical pearl

BNP & exam are unreliable → rely on physiology

PHENOTYPE 4 — ELDERLY / FRAIL

“Balance between diuresis and harm”

Mechanism

• Altered pharmacokinetics

• ↓ renal reserve

• High vulnerability

Strategy

• Gradual decongestion

• Close monitoring

Use:

• Urine output

• UNa

• Ultrasound

Goal:

👉 Not aggressive fluid removal
👉 Stable euvolemia + preserved function

Putting It All Together (ED Algorithm)

Based on :-

1. Aletras G, Bachlitzanaki M, Stratinaki M, Foukarakis E, Petrakis I, Pantazis Y, Hamilos M and Stylianou K (2026) Diuretic resistance in cardiorenal syndrome: mechanisms, monitoring and phenotype-tailored management. Front. Cardiovasc. Med. 12:1731305. doi: 10.3389/fcvm.2025.1731305
   
   

FINAL TAKEAWAY

Diuretic resistance is not about the drug.
It is about which physiological barrier is dominant.

When you:

• Monitor early

• Identify mechanism

• Treat phenotype

👉 Diuretics start working again.

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The problem with “normal vitals”

A 58-year-old man walks into the ED with chest pain.
Blood pressure? Normal. Oxygen saturation? Normal.

Another patient arrives with unilateral weakness — airway intact, breathing fine.

If we rely only on physiology…
both might wait.

And that’s exactly where triage fails.

Triage is not just numbers

Traditional triage systems often lean heavily on physiology.

But patients don’t present as numbers.

They present as:

• Complaints

• Patterns

• First impressions

• Time-sensitive risks

👉 The dangerous truth:
Some of the sickest patients look deceptively stable early (Rauniyar et al., 2025 )

The ATP backbone — necessary, but not sufficient

The AIIMS Triage Protocol (ATP) gives us:

• A simple Red–Yellow–Green system

• A physiology-first approach

• A validated framework in Indian EDs (Singh et al., 2022 )

And it works.

But not completely.

Because:

• Early ACS may have normal vitals

• Stroke may not trigger physiologic alarms

• GI bleed or poisoning may evolve silently

👉 Physiology detects instability — not always risk.

What actually improves triage?

A better model emerges when we stop thinking in silos.

Triage should integrate four simultaneous lenses:

1. Visual impression

“Does this patient look sick?”

Before monitors. Before scores.

• Gasping

• Seizing

• Pale, diaphoretic

• “Something is off”

👉 A simple clinical assessment can outperform structured triage in predicting mortality (Iversen et al., 2019 )

2. Physiology (ATP)

Still the backbone.

• Airway compromise

• Hypoxia

• Shock

• Low GCS

👉 ATP remains a validated triage framework in LMIC settings (Sahu et al., 2020 )

3. Time-critical diagnoses

Some conditions are dangerous not because of current vitals…
…but because delay kills.

• Stroke

• Acute coronary syndrome

• Major trauma

• Sepsis

• GI bleed

• Poisoning

👉 These are triage diagnoses, not final diagnoses.

But this concept goes beyond traditional medical emergencies.

In many systems, certain conditions are prioritized because early intervention is time-dependent, even when vitals are normal:

• Sexual assault survivors (urgent forensic + medical care)

• Needle-stick injuries in healthcare workers (time-sensitive prophylaxis)

• Testicular or ovarian torsion (time-dependent organ salvage)

👉 These patients may look stable.
👉 Their vitals may be normal.

But delay here is harmful.

Not all Red patients are unstable.
Some are simply time-critical.

4. High-risk chief complaints

Patients arrive with complaints — not diagnoses.

Evidence shows chief complaints independently predict mortality, even after adjusting for vitals (Rice et al., 2020 )

Local AIIMS data further refines this:

• Shortness of breath

• Altered mental status

• Hematemesis

• Fall from height

• Unilateral weakness

• Chest pain

👉 Combining ATP + high-risk complaints
significantly improves predictive accuracy (Rauniyar et al., 2025 )

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Dr Arihant Jain, MD
lifeonthefrontline.com
Instagram: @humans.of.em
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The integrated triage algorithm

This is the shift:

From single-axis triage → multi-layered triage

⚠️ The most dangerous patient in the ED

Is not the one who is crashing.

It is the one who:

• Looks stable

• Has “normal vitals”

• Is quietly evolving

🤖 Where does AI fit in?

AI is promising — but not ready to replace clinicians.

It may help:

• Predict deterioration

• Identify hidden risk patterns

• Support triage decisions

But current systems face challenges of validation, interpretability, and implementation (Petrella, 2024 )

👉 Triage remains clinician-led.

AI in Emergency Department Triage: What the Research Shows

Artificial intelligence is increasingly being explored to improve triage accuracy, detect deterioration early, and reduce ED burden.

📈 Performance and accuracy

Multiple studies show machine learning models outperform traditional triage systems:

• AUROC ~0.82–0.92 vs 0.69–0.80 for standard tools (Raita et al., 2019; Goto et al., 2019; Kang et al., 2020; Yun et al., 2021; Grant et al., 2024)

• Improved admission prediction and risk stratification (Hong et al., 2018; Lee et al., 2021)

Advanced models using NLP + multimodal data further enhance prediction and early deterioration detection (Porto, 2024; Choi et al., 2024; Chai et al., 2024)

👉 AI can reduce mis-triage and improve efficiency, though real-world impact remains limited (Abdalhalim et al., 2025; Yi et al., 2024; Kim et al., 2025; Boonstra & Laven, 2022)

🤖 LLMs and chatbot triage

• GPT-4 shows high agreement with emergency specialists in controlled settings (Paslı et al., 2024)

• But general chatbots show dangerous under-triage rates and are unsafe independently (Halwani et al., 2025; Tortum & Kaşali, 2024)

⚠️ Limitations and risks

• Bias, calibration issues, lack of external validation

• Over- and under-triage risks

• Workflow integration challenges

• Explainability concerns

👉 AI is best viewed as decision support, not replacement (Petrella, 2024 ; Porto, 2024; Yi et al., 2024)

Human + AI = the future

AI can:

• Improve accuracy

• Reduce workload

• Support decisions

But triage remains fundamentally clinical, contextual, and human-driven

The takeaway

Use ATP as the backbone.
Upgrade using visual concern, time-critical diagnoses, and high-risk complaints.

Because triage is not a label.

It is a dynamic clinical decision.

Final thought

The question is not:

“What are the vitals?”

The real question is:

“Who should never be allowed to wait?”

References (AMA Style)

1. Rice B, Leanza J, Mowafi H, et al. Defining high-risk emergency chief complaints: data-driven triage for low- and middle-income countries. Acad Emerg Med. 2020;27:1291–1301.

2. Petrella RJ. The AI future of emergency medicine. Ann Emerg Med. 2024;84:139–153.

3. Sahu AK, Bhoi S, Aggarwal P, et al. AIIMS triage protocol (ATP) of a busy ED. J Emerg Trauma Shock. 2020.

4. Rauniyar N, Sahu AK, Gopinath B, et al. Association of presenting complaint at triage with 72-h mortality and ICU admission. J Emerg Trauma Shock. 2025;18:62–68.

5. Singh SK, Sahu AK, Kumar A, et al. Prospective validation of a novel triage system developed in a middle-income country—AIIMS triage protocol. J Emerg Trauma Shock. 2022;15:124–127.

6. Iversen AKS, Kristensen M, Østervig RM, et al. A simple clinical assessment is superior to systematic triage in prediction of mortality in the emergency department. Emerg Med J. 2019;36:66–71.

7. Raita Y, Goto T, Faridi MK, Brown DFM, Camargo CA Jr, Hasegawa K. Emergency department triage prediction of clinical outcomes using machine learning models. Crit Care. 2019;23:64.

8. Goto T, Camargo CA Jr, Faridi MK, Freishtat RJ, Hasegawa K. Machine learning–based prediction of clinical outcomes for children during emergency department triage. JAMA Netw Open. 2019;2(1):e186937.

9. Kang DY, Cho KJ, Kwon O, et al. Artificial intelligence algorithm to predict the need for critical care in prehospital emergency medical services. Scand J Trauma Resusc Emerg Med. 2020;28:17.

10. Yun H, Choi J, Park J. Prediction of critical care outcomes for adult patients presenting to the emergency department using initial triage information: an XGBoost algorithm analysis. JMIR Med Inform. 2021;9(6):e30770.

11. Grant L, Diagne M, Aroutiunian R, et al. Machine learning outperforms the Canadian Triage and Acuity Scale (CTAS) in predicting need for early critical care. Can J Emerg Med. 2024;27:43-52.

12. Hong WS, Haimovich AD, Taylor RA. Predicting hospital admission at emergency department triage using machine learning. PLoS One. 2018;13(7):e0201016.

13. Lee JH, Hsieh CC, Lin CC, Lin YK, Kao CC. Prediction of hospitalization using artificial intelligence for urgent patients in the emergency department. Sci Rep. 2021;11:98961.

14. Porto B. Improving triage performance in emergency departments using machine learning and natural language processing: a systematic review. BMC Emerg Med. 2024;24:113.

15. Choi A, Lee K, Hyun H, et al. A novel deep learning algorithm for real-time prediction of clinical deterioration in the emergency department for a multimodal clinical decision support system. Sci Rep. 2024;14:80268.

16. Chai C, Peng S, Zhang R, Li C, Zhao Y. Advancing emergency department triage prediction with machine learning to optimize triage for abdominal pain surgery patients. Surg Innov. 2024;31:583-597.

17. Abdalhalim A, Ahmed S, Ezzelarab A, et al. Clinical impact of artificial intelligence-based triage systems in emergency departments: a systematic review. Cureus. 2025;17:e85667.

18. Yi N, Baik D, Baek G. The effects of applying artificial intelligence to triage in the emergency department: a systematic review of prospective studies. J Nurs Scholarsh. 2024;57:105-118.

19. Kim S, Nam S, Lee J. Artificial intelligence in emergency department triage: a scoping review on workload reduction and patient safety enhancement. J Korean Biol Nurs Sci. 2025;25:45.

20. Boonstra A, Laven M. Influence of artificial intelligence on the work design of emergency department clinicians: a systematic literature review. BMC Health Serv Res. 2022;22:807.

21. Paslı S, Sahin A, Beşer M, et al. Assessing the precision of artificial intelligence in emergency department triage decisions: insights from a study with ChatGPT. Am J Emerg Med. 2024;78:170-175.

22. Halwani M, Merdad G, Almasre M, et al. Predicting triage of pediatric patients in the emergency department using machine learning approach. Int J Emerg Med. 2025;18:61.

23. Tortum F, Kaşali K. Exploring the potential of artificial intelligence models for triage in the emergency department. Postgrad Med. 2024;136:841-846.

24. Nasser L, McLeod SL, Hall J. Evaluating the reliability of a remote acuity prediction tool in a Canadian academic emergency department. Ann Emerg Med. 2024.

25. Petrica A, Marza A, Bârsac C, et al. Artificial intelligence in emergency department triage: perspective of human professionals. Front Digit Health. 2026;5:1693060.

26. Piliuk K, Tomforde S. Artificial intelligence in emergency medicine: a systematic literature review. Int J Med Inform. 2023;180:105274.