A patient arrives in the ED with severe dyspnoea. Bibasal crackles. B-lines on lung ultrasound. A raised NT-proBNP. Perhaps some peripheral oedema.

The reflex is familiar:

“This is acute heart failure. Give IV Lasix.”

But the 2026 ESC Guidelines for the management of heart failure encourage a more nuanced approach. The question is not simply:

“Does this patient have heart failure?”

Nor even:

“How much furosemide should I give?”

The better questions are:

What is the clinical phenotype?
Where is the congestion?
Is the patient perfused?
Is this true volume overload or predominantly fluid redistribution?
And, after treatment, how will I know that decongestion is actually occurring?

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For every physicians, this may be one of the most useful ways to translate the 2026 ESC update into bedside practice.

1. First, the terminology has changed

The 2026 ESC Guidelines have eliminated the previous HFmrEF category.

The new classification is:

• HFrEF: LVEF <50% with symptoms and/or signs of HF

• HFpEF: LVEF ≥50% with symptoms/signs of HF plus objective evidence of structural and/or functional abnormalities consistent with LV diastolic dysfunction or raised LV filling pressures, supported by elevated natriuretic peptides.

The guideline has also replaced the term “acute heart failure” with “decompensated heart failure (DHF)”.

For the acute care physician, however, the more important change is conceptual:

DHF is not one phenotype, and therefore it should not have one reflex treatment.

2. Start with phenotype, not the prescription pad

The 2026 ESC framework separates patients into clinically important phenotypes:

• Cardiogenic shock

• Acute pulmonary oedema

• Decompensated left-sided HF

• Decompensated right-sided HF

And these phenotypes can overlap.

Figure 1. Diagnosing decompensated heart failure. Source: 2026 ESC Guidelines for the management of heart failure.

The guideline also provides non-age-adjusted natriuretic peptide rule-out thresholds for DHF:

• NT-proBNP <300 pg/mL

• BNP <100 pg/mL

• MR-proANP <120 pg/mL

Age-related NT-proBNP thresholds can then support a likely diagnosis in older patients.But once DHF is suspected, the next question is:

What phenotype am I treating?

3. Congestion and perfusion: the two questions that matter

The guideline provides a useful separation between left-sided congestion, right-sided congestion and hypoperfusion.

Left-sided congestion

Think:

• Dyspnoea

• Orthopnoea

• Cough

• Tachypnoea

• Rales

• S3

• Pleural effusion

• Elevated natriuretic peptides

Right-sided congestion

Think:

• Peripheral oedema

• Abdominal distension

• Hepatomegaly

• Raised JVP

• Hepatojugular reflux

• Pleural effusion

Hypoperfusion

Think:

• Cold/sweaty extremities

• Pale skin

• Dizziness

• Confusion

• Oliguria

• Narrow pulse pressure

• Elevated lactate

• AKI

• Hepatic injury.

So at the bedside, I would simplify it to:

WET or DRY?
WARM or COLD?
LEFT, RIGHT or BOTH?

That is more useful than simply labelling the patient “acute HF.”

4. Not every “wet” patient needs aggressive Lasix

This is perhaps the most important message for acute care physicians.

Figure 2. Initial management of decompensated heart failure. Source: 2026 ESC Guidelines for the management of heart failure.

The hypertensive pulmonary oedema patient is the classic example

Consider:

BP 200/110 mmHg
Severe respiratory distress
Diffuse B-lines
Orthopnoea

It is tempting to interpret this as:

“Massive fluid overload → massive dose of furosemide.”

But the guideline specifically highlights that acute pulmonary oedema can occur predominantly because of fluid redistribution into the pulmonary circulation, rather than massive total-body volume overload.

These patients usually do not need high doses of diuretics and may instead require vasodilator therapy. The guideline allows IV vasodilators to be considered as initial therapy in DHF when SBP >110 mmHg, particularly to improve symptoms and reduce congestion.

So:

Pulmonary congestion ≠ automatically massive volume overload.

And:

B-lines ≠ a prescription for high-dose Lasix.

The clinical context matters.

5. Right-sided failure is another phenotype where “Lasix first” deserves caution

Decompensated isolated right-sided HF is characterized by elevated right-sided pressures, systemic congestion and, in advanced disease, hypoperfusion.

The guideline specifically highlights the importance of RV function, ventricular interdependence and the effects on kidney and liver function. Pulmonary embolism and RV infarction may also need to be excluded as acute causes. So a patient with:

Raised JVP + oedema + hepatomegaly + hypotension

is not simply a “fluid overloaded patient.”

The question becomes:

Is this a congested patient who needs decongestion, or a preload-dependent/hypoperfused patient whose haemodynamics need stabilization first?

That distinction is critical.

6. If the patient IS congested, then decongestion becomes the goal

For the genuinely congested patient, IV loop diuretics remain the cornerstone of treatment.

—> For a diuretic-naïve patient:

40 mg IV furosemide or equivalent

—> For a patient already receiving oral loop diuretics:

approximately twice the usual daily oral loop-diuretic dose IV can be considered.

But here’s where the approach becomes much more interesting.

The dose is not the endpoint. The response is.

7. Don’t just give Lasix. Test the response.

Historically, the question after giving furosemide was often:

“Did the patient pee?”

The 2026 ESC approach is more objective.

At approximately 2 hours:

Spot urinary sodium ≥70 mEq/L

OR

During the first 6 hours:

Urine output ≥100 mL/hour

These are the guideline’s markers of a satisfactory early diuretic response.

This gives us a very useful bedside concept:

Don’t ask only how much diuretic you gave.
Ask how much sodium and water the patient actually removed.

The PUSH-AHF and ENACT-HF studies showed that uNa-guided strategies can increase natriuresis/diuresis, although importantly, no trial has yet demonstrated a mortality or recurrent-HF-hospitalization benefit from uNa-guided therapy itself.

So uNa should be viewed as a response-monitoring tool, not a magic prognostic marker.

8. What if the patient doesn’t respond?

This is where the guideline becomes particularly practical.

Figure 15. Management of decongestion. Source: 2026 ESC Guidelines for the management of heart failure.

If congestion persists, progressively escalate pharmacological decongestion and consider sequential nephron blockade. In refractory cases despite maximal pharmacological therapy, ultrafiltration may be considered.

9. Sequential nephron blockade: don’t just keep pushing the loop

The guideline incorporates acetazolamide and thiazide-type therapy into the strategy for inadequate diuretic response. In ADVOR, adding IV acetazolamide 500 mg daily to loop diuretics increased successful decongestion, defined as absence of signs of volume overload within three days.

Hydrochlorothiazide increased weight loss and 24-hour diuresis in CLOROTIC, but was associated with more worsening kidney function and hypokalaemia and did not improve patient-reported dyspnoea. Neither trial demonstrated benefit on hard clinical endpoints.

This is an important distinction:

More diuresis is not automatically better medicine.

The objective remains:

Effective, safe decongestion. Not maximum urine output at any cost.

10. The creatinine trap

One of the commonest reasons we stop effective decongestion is:

“Creatinine has gone up.”

But the ESC guideline specifically cautions against interpreting kidney function in isolation. Small, transient rises in serum creatinine during diuresis are not associated with poor outcomes when adequate decongestion is achieved.

Therefore:

Creatinine ↑ + congestion improving + perfusion adequate

does not automatically mean: STOP DIURESIS.

Compare that with:

Creatinine ↑ + persistent congestion + hypotension/hypoperfusion + poor diuretic response

Now we have a completely different problem. The kidney number needs to be interpreted alongside:

Congestion + perfusion + BP + urine output + natriuresis + trajectory.

11. How congested is the patient?

This is where the concept of a congestion score becomes useful.

The ESC clinical congestion score considers:

• Dyspnoea

• Orthopnoea

• Fatigue

• Rales

• Oedema

• JVP distension

A score of 0 represents absence of clinical congestion, while 1–2 represents mild congestion.

The key is not necessarily the number itself.

It is the trend.

On arrival, After treatment, Before discharge:

Is congestion actually gone?

That is much more meaningful than:

“He made 2.5 litres of urine.”

12. Decongestion is multimodal

Figure 4. Tools used for assessment of decongestion during the pre-discharge phase. Source: 2026 ESC Guidelines for the management of heart failure.

This is an excellent figure for acute care physicians because it brings together several domains.

Clinical

• Congestion score

• Weight loss

• NYHA class

Laboratory

• BNP

• NT-proBNP

Imaging

• Chest X-ray / congestion score index

• LV filling pressure parameters

• IVC

• Lung ultrasound

The guideline recommends assessment of residual congestion before discharge using clinical, laboratory and imaging techniques.

But there is an important caveat:

These tools are optional, because randomized trial evidence demonstrating improved outcomes from their use is lacking.

So POCUS is not a replacement for examination . It is another piece of the puzzle.

13. The POCUS question should change

Instead of simply asking:

“Does this patient have B-lines?”

ask:

“Where is the congestion, and is it resolving?”

Lung ultrasound

Are there B-lines?
Are they diffuse?
Are they changing with treatment?

Heart

What does LV/RV function look like?

Venous system

Is there evidence supporting systemic venous congestion?

Pleura

Is there an effusion?

And then integrate this with:

JVP + oedema + respiratory examination + urine output + uNa + renal function + BP + perfusion.

The guideline itself includes LUS and other imaging modalities as components of decongestion assessment rather than prescribing one imaging measurement as definitive.

14. “Dry” is not the same as “better”

One of the most important messages in the 2026 guideline is residual congestion.

A patient can:

• breathe better,

• have less oedema,

• produce several litres of urine,

and still be congested. Residual congestion is associated with poor outcomes and increased risk of rehospitalization. Therefore, the guideline recommends careful evaluation before discharge to exclude persistent congestion.

This changes our discharge question.

Not:

“Does the patient feel better?”

But:

“Have we achieved adequate decongestion?”

15. Decongestion is only one phase of the hospitalization

Figure 5. Phases and goals for in-hospital management of decompensated heart failure. Source: 2026 ESC Guidelines for the management of heart failure.

The ESC framework divides inpatient management into three broad phases:

Phase 1 — Initial management

• Treat life-threatening conditions

• Identify and treat precipitating factors

• Stabilize haemodynamics

• Initiate treatment of decompensation

Phase 2 — Stabilization

• Consolidate haemodynamic stability

• Attempt full decongestion

• Initiate/optimize foundational medical therapy

• Identify and manage comorbidities

Phase 3 — Pre-discharge and early post-discharge

• Exclude persistent congestion

• Optimize FMT

• Determine need for additional/interventional therapies

• Plan long-term management.

This is an important departure from the old mental model:

“Treat the acute episode and then deal with chronic HF later.”

16. Start disease-modifying therapy during the hospitalization

The guideline emphasizes that decongestion and foundational medical therapy should proceed in parallel once the patient is stabilized. MRAs, SGLT2 inhibitors and ARNIs can be initiated during the stabilization phase, and the traditional sequential approach to FMT is considered time-consuming; simultaneous implementation is preferred when feasible, with more conservative approaches for selected high-risk patients.

In-hospital initiation of an SGLT2 inhibitor after initial stabilization is recommended to improve quality of life/congestion symptoms and reduce HF hospitalization. And importantly, if a patient was already receiving foundational therapy, discontinuation is not recommended unless there are clear signs of hypoperfusion or another specific clinical indication.

17. The patient with shock is a different conversation

A congested patient who is also hypoperfused cannot simply be treated using the same algorithm as an uncomplicated “warm and wet” patient. The guideline emphasizes that cardiogenic shock is defined by critical end-organ hypoperfusion, and there is no single blood-pressure threshold that defines it. Hypoperfusion can occur even with normal blood pressure.

Look for:

Cold extremities
Confusion
Oliguria
Narrow pulse pressure
Lactate elevation
AKI/hepatic injury

The guideline uses the SCAI shock stages from:

A — At risk
B — Beginning/pre-shock
C — Classic shock
D — Deteriorating
E — Extremis.

And when cardiogenic shock with potential need for temporary mechanical circulatory support is suspected, consultation with a Shock Team is recommended.

18. The bedside algorithm I want to remember

If I had to reduce the 2026 ESC approach to one ED mental model:

The bigger mindset shift

Lasix is a tool. Decongestion is the goal. Phenotyping determines the strategy. And on the frontline, that distinction matters.

Must Read : ESC 2026 Heart Failure Guidelines

This is Part 3.

If you haven’t read Part 1 and Part 2, stop here and read them first.

Part 1 built the foundation:
Troponin → Myocardial Injury ≠ Myocardial Infarction

Part 2 took it further:
Troponin Matrix → Trop-Zones → Delta → Five questions

This post assumes you already have that framework.

Because the Fifth Universal Definition of Myocardial Infarction (2026) doesn’t make us throw that framework away.

It makes us update it.

Start here:
→ Part 1: Troponin Is Not an MI Test
→ Part 2: Troponin Is Not an MI Test

Then come back here.

Let’s see what changed in 2026.
If you have read Part 1 and Part 2 of this series, you already know the central message:

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

We built the Troponin Triangle.

We moved from:

“Is the troponin positive?”

to:

“Is there myocardial injury → Is it acute → Is there evidence of ischemia → If yes, what is the mechanism?”

We discussed the Troponin Matrix, Type 1 versus Type 2 MI, the Trop-Zones, and why the delta is often more informative than the first troponin.

All of that came from the framework of the Fourth Universal Definition of Myocardial Infarction (2018). Now, the Fifth Universal Definition of Myocardial Infarction (2026) has arrived.

And importantly, it does not throw away the mental model. It makes it more sophisticated.

The fundamental question remains:

Is this myocardial injury or myocardial infarction?

But the Fifth UDMI gives us better tools for answering the questions that come after the troponin comes back.

What actually changed?

There are several important updates. But for the acute-care physician, I think three deserve particular attention:

1. The delta is no longer just “rise or fall”

2. Imaging becomes much more important in determining what the injury actually represents

3. The classification of MI has been reorganized around clinical setting and pathophysiology

Let’s unpack these.

1. The Delta Is Not a Number

In Part 2, we called the delta:

“The most important number you never memorized.”

The Fifth UDMI adds an important qualification:

There is no single absolute or relative troponin change that works for every patient, every assay, and every clinical situation.

Why?

Because the meaning of a delta depends on three things.

Factor 1: Time from symptom onset

Troponin does not behave like a light switch. It follows a biological curve. Early after an ischemic event, the absolute change may be small. Several hours later, the rise can become much more pronounced. Around the peak, the change may become relatively small again. And during the later phase, the troponin begins to fall.

The Fifth UDMI therefore emphasizes that the same delta can mean very different things depending on when the patient presents.

Think about two patients:

Patient A

Chest pain started 45 minutes ago.

Troponin:
10 → 14 ng/L

Patient B

Chest pain started 10 hours ago.

Troponin:
10 → 14 ng/L

Same delta.

Very different biological stories.

This is why:

Delta without a timeline is incomplete information.

Factor 2: Time between samples

The second troponin is not simply “another troponin.” It is a measurement taken at a particular point in time.

A 1-hour delta and a 6-hour delta are not interchangeable.

The longer the interval, the greater the opportunity for a biological rise or fall to occur. This is one reason accelerated diagnostic pathways use fixed sampling intervals, such as 0/1-hour or 0/2-hour strategies. But even here, the Fifth UDMI emphasizes that the thresholds and deltas are assay-specific.

So:

A delta without knowing the interval between samples is also incomplete information.

Factor 3: The baseline troponin

This one is particularly important.

Suppose the troponin is:

8 → 18 ng/L

A 10 ng/L rise. That absolute change may be quite meaningful when the baseline is low.

Now consider:

800 → 810 ng/L

Same absolute change. But the biological interpretation is very different.

The Fifth UDMI highlights that the relationship between absolute and relative change depends on the baseline concentration.

When troponin is around or below the 99th percentile, absolute changes can be particularly useful. When baseline troponin is already substantially elevated, relative change may be easier to interpret.

And importantly:

Absolute delta thresholds cannot simply be transferred from one assay to another.

They are assay-specific. So the new mental model becomes:

Don’t ask:

“What is the delta?”

Ask:

“What is the delta, over what interval, from what baseline, and at what point in the patient’s illness?”

The New Delta Triangle

I would therefore modify our Part 2 framework.

Previously:

TROPONIN → DELTA → ACUTE INJURY

Now:

DELTA =

Time from symptom onset

+

Time between samples

+

Baseline troponin

Only then does the number start to make biological sense.

2. Imaging Moves Further Into the Story

This may be the most important conceptual change for me. And there is an important caveat:

Imaging is not new to the Universal Definition.

The Fourth UDMI already included imaging as evidence of ischemia and myocardial infarction. So the Fifth UDMI does not suddenly “introduce imaging.”

Instead, it expands and organizes the role of multimodality coronary and cardiac imaging in determining the mechanism and consequences of myocardial injury.

And this is where things become particularly interesting for emergency and acute-care medicine. Because sometimes:

The troponin tells you that myocardium is injured.

But it cannot tell you:

What happened to the myocardium?

And it certainly cannot always tell you:

What happened to the coronary artery?

That is where imaging comes in.

Think of the modalities as answering different questions

Troponin

Is the myocardium injured?

ECG

Is there evidence of electrical ischemia?

Echocardiography

Is there a new functional consequence?

But then we have:

CMR

What happened to the myocardium?

CCTA

What does the coronary anatomy and plaque look like?

IVUS/OCT

What actually happened inside the coronary artery?

This is a very different way of thinking about imaging.

CMR: What happened to the myocardium?

Cardiac MRI is particularly powerful because it can characterize myocardial tissue.

It can demonstrate:

• myocardial infarction

• edema

• inflammation

• microvascular obstruction

• intramyocardial haemorrhage

• patterns of myocardial injury

using multimodality tissue-characterization sequences. This becomes particularly important when the diagnosis is not obvious from the initial presentation.

A patient has:

Chest pain + troponin elevation + non-obstructive coronaries.

What now? The answer is not:

“Angiogram is normal, so nothing happened.”

The myocardium may have infarcted. Or the patient may have myocarditis. Or Takotsubo syndrome. Or another cardiomyopathy.

This is where CMR can help establish the final diagnosis. The Fifth UDMI specifically emphasizes its role in situations such as MINOCA and unrecognized myocardial infarction.

CCTA: What do the coronaries look like?

CT coronary angiography provides another piece of the puzzle.

It can evaluate:

• coronary anatomy

• obstructive CAD

• plaque characteristics

• graft patency

and newer CT techniques are expanding its ability to characterize myocardial viability and alternative diagnoses. But this does not mean:

“Every patient with a raised troponin needs a CCTA.”

Absolutely not. The Fifth UDMI still recognizes that its role depends on clinical context and pre-test probability.

The important change is conceptual:

Coronary anatomy can become part of the diagnostic explanation for myocardial injury.

IVUS/OCT: What actually happened to the plaque?

This is perhaps the most fascinating part.

Sometimes angiography tells us:

“There is no major obstruction.”

But that does not necessarily mean:

“There is no coronary pathology.”

Intravascular imaging with IVUS or OCT can reveal pathology that angiography may miss, including:

• plaque rupture

• plaque erosion

• mural thrombus

• spontaneous coronary artery dissection

• stent-related pathology

• other subtle coronary abnormalities.

And this is especially relevant to MINOCA.

Because:

MINOCA is not necessarily the final diagnosis.

It can be a working diagnosis that tells us:

“The patient appears to have had an MI, but we have not yet established why.”

Further investigation may involve intravascular imaging, functional coronary testing and CMR to identify the underlying mechanism.

The New Imaging Mental Model

This is how I would now think about it:

TROPONIN

↓

MYOCARDIAL INJURY

↓

IS IT ISCHEMIC?

↓

If yes:

WHAT HAPPENED TO THE CORONARY?
→ Angiography
→ IVUS/OCT
→ Functional testing

WHAT HAPPENED TO THE MYOCARDIUM?
→ CMR
→ Echo
→ Other appropriate imaging

WHAT IS THE UNDERLYING MECHANISM?

That is a much richer diagnostic pathway than:

Troponin positive → NSTEMI

3. MINOCA: “Nothing Significant on Angiography” Is Not the End

This is where the imaging emphasis becomes clinically relevant.

Imagine:

Chest pain

Dynamic troponin rise

Ischemic ECG changes

Angiography: no obstructive coronary lesion

The old instinct might be:

“The angiogram is normal.”

The better question is:

“Why did this patient have an infarction?”

Possibilities include plaque disruption, coronary spasm, microvascular dysfunction, SCAD and other mechanisms.

The Fifth UDMI therefore reinforces MINOCA as a working diagnosis requiring further investigation, rather than simply a final label.

And that is exactly where multimodality imaging becomes clinically useful.

4. The Type 1–5 World Has Been Reorganized

There is another major change.

For years, we have taught:

Type 1 MI
Type 2 MI
Type 3 MI
Type 4 MI
Type 5 MI

The Fifth UDMI replaces this numerical classification with three broader clinical settings:

Primary MI

Secondary MI

Procedure-related MI

This is not simply a change in vocabulary. It is an attempt to align the classification more closely with the clinical setting and underlying pathophysiology. The underlying concepts have not disappeared. The point is to make the classification more clinically intuitive.

5. What About the 99th Percentile?

Here is another important nuance.

The Fifth UDMI continues to define acute myocardial injury using a rise and/or fall in cardiac troponin with at least one value above the assay’s sex-specific 99th percentile URL.

But don’t read this as:

“Sex-specific 99th percentile is a completely new 2026 concept.”

It isn’t. The Fourth UDMI had already recommended sex-specific 99th-percentile values for hs-cTn assays.

What the Fifth UDMI does is further emphasize and operationalize this issue, recognizing the potential for under-recognition of myocardial injury when a single threshold is applied across sexes. And another important distinction:

The 99th percentile defines myocardial injury.

It is not automatically the same thing as a rule-in threshold for MI. Accelerated diagnostic pathways may use assay-specific thresholds and deltas that are different from the 99th percentile.

So What Should We Change at the Bedside?

Let’s go back to the five questions from Part 2.

They still work. But the Fifth UDMI makes them better.

Question 1

Is there myocardial injury?

Look at the assay-specific 99th percentile.

Question 2

Is it acute or chronic?

Look at the pattern over time.

Question 3

Is there evidence of ischemia?

Symptoms.
ECG.
Imaging.
Coronary findings.

Question 4

If ischemic, what is the mechanism?

Primary?
Secondary?
Procedure-related?

Question 5

If the mechanism is unclear, what additional information do I need?

And this is where the Fifth UDMI pushes us further.

Maybe the answer is:

Repeat troponin.

Maybe:

Repeat ECG.

Maybe:

Echo.

But sometimes:

CMR.

CCTA.

IVUS/OCT.

Functional coronary assessment.

The Updated Troponin Mental Model

So perhaps our original framework needs one more layer.

The old shortcut:

TROPONIN → MI

was wrong.

Our Part 1 model:

TROPONIN

↓

INJURY

↓

ACUTE OR CHRONIC

↓

ISCHEMIC OR NON-ISCHEMIC

↓

MI

was much better.

The 2026 model:

TROPONIN

↓

MYOCARDIAL INJURY

↓

ACUTE OR CHRONIC

↓

INTERPRET THE DELTA

Time from onset
Sampling interval
Baseline concentration

↓

IS THERE ISCHAEMIA?

↓

USE CLINICAL + ECG + IMAGING EVIDENCE

↓

IS IT INFARCTION?

↓

WHAT IS THE MECHANISM?

↓

PRIMARY / SECONDARY / PROCEDURE-RELATED

And when the answer remains unclear:

↓

IMAGE THE CORONARY. IMAGE THE MYOCARDIUM.

The Take-Home Message

The Fifth Universal Definition does not overturn the central lesson of our previous two posts. It reinforces it. Troponin still detects myocardial injury. It does not tell you whether that injury is an infarction. But the 2026 update makes us more precise about two things.

First:

The delta is not a magic number.

Its interpretation depends on:

when the injury occurred + when you sampled + where the troponin started.

Second:

The diagnosis does not necessarily end with the troponin—or even the angiogram.

Modern MI diagnosis increasingly asks:

What happened to the myocardium?

and

What happened to the coronary artery?

Sometimes the answer comes from the ECG.

Sometimes from echocardiography.

Sometimes from angiography.

But increasingly, the answer may require:

CMR.

CCTA.

IVUS/OCT.

Functional coronary testing.

And perhaps that is the most important evolution from our original mental model.

One Last Time

The next time someone tells you:

“The troponin is positive.”

Don’t ask:

“Is this an NSTEMI?”

Ask:

Is there myocardial injury?

Is it acute?

Does the delta make biological sense given the timing, sampling interval and baseline?

Is there evidence of ischemia?

If there is ischemia, what is the mechanism?

And if the answer is still unclear—what does the coronary artery and the myocardium actually look like?

Because:

Troponin tells you that the myocardium is speaking.

The Fifth UDMI reminds us that we still have to listen to the whole story.

References

1. Fifth Universal Definition of Myocardial Infarction. ESC/ACC/AHA/WHF, 2026.

2. Jain A. Troponin Is Not an MI Test: Part 1 — A New Mental Model for Acute Care Physicians. Life on the Frontline. July 1, 2026. Read Part 1

3. Jain A. Troponin Is Not an MI Test: Part 2 — A New Mental Model for Acute Care Physicians. Life on the Frontline. July 4, 2026. Read Part 2

Summarised By -
Dr Arihant Jain, MD | lifeonthefrontline.com
Instagram: @humans.of.em
X | Linkedin | ORCID
—————————————————————
It Started Like Every Other Night Shift

It was 2:17 a.m.

The emergency call from triage was brief.

“Sixty-eight-year-old male. Severe breathlessness. Oxygen saturation 84%.”

Within minutes, he was wheeled into the resuscitation bay. He looked frightened.

His respiratory rate was nearly 40 breaths per minute. Every breath was laboured. The accessory muscles in his neck were contracting with each inspiration, and despite receiving oxygen through a non-rebreather mask at 15 litres per minute, his oxygen saturation refused to climb beyond 86%.

The chest radiograph showed bilateral infiltrates. The arterial blood gas confirmed severe hypoxaemia. There was no significant hypercapnia.

The respiratory therapist looked at me.

“Should we start High-Flow Nasal Cannula?”

Across the room another physician asked,

“What about non-invasive ventilation?”

Meanwhile, someone quietly prepared the intubation drugs.

Three experienced clinicians.
Three different answers.
One patient.

Ten years ago, all three decisions could probably have been justified.

Today, the conversation is different—not because we have better machines, but because we have better evidence.

The recently published 2026 American Thoracic Society (ATS) Clinical Practice Guideline on Non-Invasive Respiratory Support for Adult Patients with Acute Respiratory Failure brings together nearly two decades of research to answer one simple question:

Which respiratory support should we choose, and more importantly, why?

Interestingly, the guideline is not organised around devices like HFNC, NIV or CPAP. Instead, it focuses on clinical syndromes—acute hypoxaemic respiratory failure, acute hypercapnic respiratory failure, pre-intubation support and post-extubation care. That shift may seem subtle, but it fundamentally changes how we think about respiratory support.

Stop Choosing Devices.
Start Understanding Physiology.

One of the biggest lessons from this guideline is that respiratory failure is not a single disease. Our patient with pneumonia is hypoxaemic because oxygen cannot effectively cross injured alveoli into the bloodstream.

A patient with COPD, on the other hand, often fails because they cannot ventilate adequately. Carbon dioxide accumulates, respiratory muscles fatigue and the work of breathing becomes unsustainable.

Both patients may look equally distressed. Both may have similar oxygen saturations. Yet they need completely different treatments. The question therefore is no longer,

“Which machine should I use?”

Instead, it becomes,

“What physiological problem am I trying to solve?”

That single question explains almost every recommendation in the ATS guideline.

How Are Guidelines Actually Made?

Most of us skip straight to the recommendations.

Strong recommendation.
Conditional recommendation.
Use.
Don’t use.
Move on.

But recommendations don’t appear overnight.

The ATS panel reviewed the available evidence using systematic reviews, network meta-analyses and the GRADE Evidence-to-Decision framework. Rather than asking whether a single trial was “positive” or “negative,” they looked at the totality of evidence, considering benefits, harms, certainty of evidence, patient values, feasibility and resource implications before making each recommendation.

This explains something many clinicians find confusing.

A strong recommendation does not necessarily mean there is overwhelming evidence for mortality benefit.

Instead, it means the panel is confident that, for most patients, the overall benefits outweigh the harms.

That distinction becomes very important as we return to our patient.

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The Story of High-Flow Nasal Cannula

Twenty years ago, patients like ours had very few options. They usually received conventional oxygen therapy until one of two things happened. Either they improved or they deteriorated enough to require intubation.

Conventional oxygen therapy has obvious limitations. Patients with severe respiratory distress often generate inspiratory flow rates much higher than the oxygen delivered through a face mask. As a result, room air becomes entrained, reducing the effective oxygen concentration reaching the lungs.

Clinicians therefore began looking for better alternatives.

High-flow nasal cannula (HFNC) appeared promising because it could deliver heated, humidified oxygen at much higher flow rates while maintaining a more consistent inspired oxygen concentration. Physiological studies also suggested that HFNC reduced anatomical dead space, generated a small amount of positive airway pressure and decreased the work of breathing.

The physiology made sense.

But physiology alone is never enough.

Clinical trials had to prove that these benefits translated into better patient outcomes.

The Trial That Changed the Conversation

A major turning point came with the FLORALI trial by Frat and colleagues (2015).

The investigators compared HFNC with conventional oxygen therapy and non-invasive ventilation in patients with acute hypoxaemic respiratory failure.

Although the primary outcome did not show a statistically significant reduction in intubation across the entire study population, HFNC demonstrated encouraging results, particularly among patients with more severe hypoxaemia. Mortality also appeared lower in some groups.

Perhaps more importantly, patients tolerated HFNC remarkably well. Suddenly, clinicians began asking a new question. Could HFNC become the first-line treatment for hypoxaemic respiratory failure?

FLORALI did not answer that question completely. But it changed the direction of research for the next decade.

Then Came COVID-19

The COVID-19 pandemic accelerated respiratory research more than anyone could have imagined. Hospitals across the world faced thousands of patients with severe viral pneumonia. Researchers rapidly compared HFNC, CPAP and non-invasive ventilation in randomised clinical trials.

Studies such as HENIVOT (Grieco et al., 2021) and RECOVERY-RS (Perkins et al., 2022) added valuable evidence, although they did not always reach identical conclusions. Some trials suggested benefits with CPAP. Others supported HFNC.

Some remained inconclusive.

Instead of providing one clear answer, the growing evidence highlighted an important reality:

No single trial should determine clinical practice.

This is exactly why the ATS panel performed a comprehensive evidence synthesis rather than relying on individual studies.

So Why Does ATS Recommend HFNC?

This is perhaps the most important question.

After reviewing 39 randomised controlled trials, the ATS panel concluded that HFNC should be preferred over conventional oxygen therapy for adults with de novo acute hypoxaemic respiratory failure, issuing a strong recommendation.

At first glance, that may seem surprising. The evidence for reducing mortality is not definitive. So why such a strong recommendation?

Because mortality is not the only outcome that matters.

Across multiple studies, HFNC consistently reduced the need for invasive mechanical ventilation, improved patient comfort and was generally well tolerated. Patients could communicate, eat, drink and clear secretions more easily than those receiving tightly fitting masks.

Importantly, HFNC also carried relatively few serious adverse effects.

When the ATS panel weighed all these outcomes together, the balance clearly favoured HFNC. This is an important reminder that evidence-based medicine is about more than a single p-value.

Why Not Simply Use NIV?

Many clinicians naturally ask another question. If non-invasive ventilation provides positive pressure, shouldn’t it work even better?

The answer is more nuanced.

NIV certainly has physiological advantages. It can reduce the work of breathing and improve gas exchange. However, it also comes with important drawbacks.

Tight-fitting masks are often uncomfortable.

Air leaks are common.

Pressure injuries may develop.

Patients frequently struggle to tolerate prolonged treatment.

Perhaps the greatest concern is delayed recognition of treatment failure. Continuing NIV in a patient who is steadily worsening may postpone intubation, potentially worsening outcomes. The ATS panel also discussed concerns that excessive spontaneous tidal volumes during NIV could contribute to further lung injury in some patients.

For these reasons, the guideline makes only a conditional recommendation for NIV in de novo hypoxaemic respiratory failure, while strongly recommending HFNC as the preferred initial strategy.

Back to Our Patient

The high-flow nasal cannula is connected.

Warm, humidified oxygen begins flowing.

Within minutes, his breathing slows.

His oxygen saturation climbs into the low 90s.

He is still critically ill.

But he is more comfortable.

More importantly, we have bought ourselves time to reassess, investigate and decide whether he truly needs intubation.

That is perhaps the biggest lesson from this part of the ATS guideline.

HFNC is not simply a better oxygen mask. It is a form of respiratory support that allows us to treat hypoxaemic respiratory failure while reducing the need for invasive ventilation in many patients. But as we leave this patient and walk toward the next bed, we encounter a completely different problem.

A woman with severe COPD.

She is not hypoxaemic because her lungs cannot absorb oxygen. She is hypercapnic because her lungs cannot eliminate carbon dioxide.

The same device that helped our first patient may not be the best choice for her.

Because in acute care, the right treatment is determined not by the machine, but by the physiology.

A Different Patient. A Different Problem.

As we finished stabilising our patient with severe pneumonia, another call came from the acute care unit. A 72-year-old woman with severe chronic obstructive pulmonary disease (COPD) had become progressively drowsy over the past few hours.

Unlike the previous patient, she was not gasping for breath.

She looked tired.

Every breath was shallow.

Her respiratory rate was only 24 breaths per minute, but her accessory muscles had clearly been working for hours.

The arterial blood gas told the real story.

pH: 7.22

PaCO₂: 78 mmHg

PaO₂: 64 mmHg

This wasn’t simply hypoxaemia.

This was ventilatory failure.

The resident, fresh from treating the previous patient, asked confidently,

“Should we start High-Flow Nasal Cannula?”

The consultant smiled.

“Different physiology, Different treatment.”

That single sentence probably summarises the entire ATS guideline better than any recommendation table.

When Carbon Dioxide Is the Problem

The patient with pneumonia struggled because oxygen couldn’t cross injured alveoli. The patient with COPD struggles because she cannot remove carbon dioxide. Years of airway obstruction have increased airway resistance, caused dynamic hyperinflation and placed enormous demands on already fatigued respiratory muscles.

Each breath requires tremendous effort. Eventually those muscles tire. Ventilation falls. Carbon dioxide rises. Acidosis develops. Unlike hypoxaemic respiratory failure, simply increasing oxygen does not solve the problem.

The patient needs assistance with ventilation, not just oxygenation.

That distinction explains why the ATS guideline makes very different recommendations for acute hypercapnic respiratory failure.

The Trial That Changed Everything

If there is one landmark trial that transformed acute respiratory care, it is the study by Brochard et al. (1995). Before this study, many patients with severe COPD exacerbations progressed directly to invasive mechanical ventilation.

Brochard and colleagues demonstrated that non-invasive ventilation (NIV) significantly reduced the need for intubation and improved clinical outcomes in carefully selected patients. For the first time, clinicians realised they could support ventilation without placing an endotracheal tube.

Several years later, Plant et al. (2000) showed that NIV could also be successfully delivered outside the intensive care unit, making this therapy available to far more patients. Together, these studies changed clinical practice worldwide.

Unlike many newer respiratory interventions, the evidence supporting NIV in COPD has remained remarkably consistent over time.

Does High-Flow Change the Story?

Over the past decade, enthusiasm for HFNC naturally extended to patients with COPD. After all, HFNC improves comfort, reduces anatomical dead space and decreases the work of breathing.

Could it replace NIV?

Several recent randomised trials explored this possibility. Some suggested that HFNC produced similar improvements in carefully selected patients with mild hypercapnia. Others showed better patient comfort and tolerance. These findings generated considerable excitement.

But the ATS panel looked beyond individual studies.

They examined the entire body of evidence. Most of these trials enrolled patients with relatively mild respiratory acidosis. Many allowed patients to cross over from HFNC to NIV when deterioration occurred. Very few included patients with severe hypercapnic respiratory failure. As a result, the evidence remained less certain than it initially appeared.

Why NIV Still Comes First

After reviewing 43 randomised controlled trials, the ATS panel concluded that NIV remains the preferred initial treatment for adults with acute hypercapnic respiratory failure, issuing a strong recommendation.

The reasoning is straightforward. NIV does something HFNC cannot reliably achieve. It actively assists ventilation. Inspiratory pressure support unloads fatigued respiratory muscles. Minute ventilation improves. Carbon dioxide falls. Acidosis begins to correct.

HFNC certainly has physiological benefits, but the available evidence does not yet demonstrate that it consistently replaces NIV in patients with clinically significant ventilatory failure.

That is why the ATS guideline takes a cautious approach.

HFNC may be considered in selected patients with mild respiratory acidosis, particularly when NIV is poorly tolerated, provided clinicians monitor the patient closely and are prepared to escalate treatment rapidly if deterioration occurs.

Once again, the recommendation reflects physiology.

Patients who cannot ventilate generally require ventilatory assistance.

Another Critical Moment: PreIntubation

Our first patient with pneumonia initially improved on HFNC. Six hours later, everything changed. His oxygen requirement continued to increase. He became increasingly confused. His respiratory muscles finally began to fail.

Now there was no debate.

He needed intubation. A new question emerged.

How should we oxygenate him before laryngoscopy?

For years, clinicians relied on conventional bag-mask ventilation. More recently, HFNC and NIV have both been proposed as superior preoxygenation strategies.

Randomised studies have shown benefits with both approaches in different clinical settings.

After reviewing the available evidence, the ATS guideline concludes that either HFNC or NIV is preferable to conventional oxygen therapy before intubation in acute hypoxemic respiratory failure, while recognising that current evidence is insufficient to recommend one clearly over the other.

Perhaps the most important message is that preoxygenation should not be an afterthought.

A patient with severe respiratory failure has very little physiological reserve.

Optimising oxygenation before induction may reduce life-threatening desaturation during airway management.

The Journey Doesn’t End After Extubation

Several days later, our patient improved. The infection resolved. Vasopressors were discontinued. He successfully completed a spontaneous breathing trial. Now another important decision awaited.

Should he receive conventional oxygen after extubation?

HFNC?

Or NIV?

Extubation is often viewed as the finish line. In reality, it is another high-risk transition. Some patients develop respiratory failure shortly after extubation and require re-intubation, an event associated with increased morbidity and mortality.

The ATS guideline therefore addresses respiratory support after extubation separately.

Rather than recommending the same strategy for every patient, the panel emphasises individual risk assessment.

Patients at higher risk of extubation failure may benefit from NIV, whereas HFNC represents an effective alternative in many others. Both strategies are favoured over conventional oxygen in appropriate clinical settings.

Once again, the message is remarkably consistent. Choose the therapy that matches the patient’s physiology and clinical risk.

What Makes This Guideline Different?

Every guideline tells us what to do. Good guidelines explain why. This ATS guideline succeeds because it avoids oversimplifying respiratory support. It does not claim that HFNC is universally superior. It does not suggest NIV is obsolete. Instead, it reminds us that every device has strengths, limitations and an appropriate clinical context.

Perhaps more importantly, it demonstrates how recommendations should be developed. The panel did not rely on a single influential study.

Instead, they systematically reviewed the available evidence, evaluated its certainty, balanced benefits against harms and considered patient values, feasibility and resource implications before issuing recommendations. For clinicians, this approach is just as valuable as the recommendations themselves.

Five Lessons I’ll Take Back to the Bedside

After reading the guideline, five practical lessons stand out.

1. Treat physiology before devices.

The question is never “HFNC or NIV?”

It is “What type of respiratory failure does this patient have?”

2. High-flow nasal cannula is no longer just an oxygen device.

It is a form of respiratory support that has become the preferred first-line therapy for many patients with de novo acute hypoxaemic respiratory failure.

3. NIV remains the cornerstone of acute hypercapnic respiratory failure.

Despite exciting research on HFNC, patients with significant ventilatory failure still benefit most from ventilatory assistance.

4. Strong recommendations are not based on mortality alone.

Comfort, avoidance of intubation, adverse events and patient preferences all matter.

5. Reassessment is more important than the initial device.

No form of respiratory support is successful if clinicians fail to recognise deterioration and escalate treatment when necessary.

Pulse Check

When I first started training, respiratory support often felt like choosing between machines. Today, I realise it is really about understanding physiology. The patient with pneumonia and the patient with COPD may arrive breathless, frightened and hypoxic. They may even occupy neighbouring beds. But their lungs are failing for completely different reasons.

The 2026 ATS guideline reminds us that evidence-based medicine is not about finding one device that works for everyone.

It is about recognising the physiological problem in front of us and choosing the therapy most likely to solve it. Technology will continue to evolve. New interfaces will emerge. Future trials may modify today’s recommendations.

But one principle is unlikely to change:

The best respiratory support is not the newest machine. It is the one that best matches the patient’s physiology, is supported by the strongest available evidence and is accompanied by continuous bedside reassessment.

That is the real lesson from twenty years of research—and perhaps the most important lesson for every acute care clinician.

Suggested Reading -
Goel A, Rochwerg B, Nava S, et al. Noninvasive respiratory support for adult patients with acute respiratory failure: An official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2026;214(4):e30-e58. doi:10.1164/rccm.202607-1135ST

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.

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

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

You are stabilising a 34‑year‑old STEMI at 3 a.m. or admitting a 45‑year‑old with necrotising pancreatitis and triglycerides of 1400 mg/dL.

In those moments, dyslipidemia can feel like someone else’s follow‑up problem. The 2026 ACC/AHA Dyslipidemia Guideline is a polite but firm reminder that it is your problem too.

This guideline replaces the 2018 “blood cholesterol” document and expands the focus to LDL‑C, triglycerides, and lipoprotein(a), with an explicit goal: reduce lifelong exposure to atherogenic lipoproteins and prevent recurrent events. For acute care physicians, this means aligning in‑hospital decisions with long‑term targets rather than leaving lipids to vague outpatient plans.

Big picture: what actually changed?

Three shifts matter in acute care:

• From “current LDL” to “lifetime exposure”
  The guideline emphasizes early lifestyle and pharmacologic treatment in youth and young adults, especially those with familial hypercholesterolemia (FH) or LDL‑C ≥160 mg/dL with strong family history of premature ASCVD. The rationale is simple: event risk in the ED often reflects decades of cumulative LDL burden.​

• From Pooled Cohort Equations to PREVENT
  For adults 30–79 years with LDL‑C 70–189 mg/dL and no clinical or subclinical ASCVD, the PREVENT‑ASCVD equations replace the Pooled Cohort Equations for 10‑ and 30‑year risk estimation. Categories are:​

  • Low: <3%

  • Borderline: 3–<5%

  • Intermediate: 5–<10%

  • High: ≥10% 10‑year risk.​
    As an acute physician, you may not open a calculator mid‑resus, but you should know that risk tools have changed and now explicitly incorporate 30‑year risk for 30–59‑year‑olds.​

• From “start a statin” to “hit a target”
  LDL‑C and non‑HDL‑C goals are back. Secondary prevention and high‑risk groups now have targets like LDL‑C <70 mg/dL for all ASCVD and <55 mg/dL for very‑high‑risk or heavy CAC. Your discharge prescriptions should be written with these numbers in mind.

In the ED and ICU: what should you actually do?

1. Treat every ACS as a lipid intervention opportunity

For any patient with clinical ASCVD (ACS, prior MI, stroke, PAD):

• Start or escalate to high‑intensity statin (e.g., atorvastatin 40–80 mg, rosuvastatin 20–40 mg) during the index admission unless contraindicated.​

• The goal in “standard‑risk” ASCVD is:

  • ≥50% reduction in LDL‑C, and

  • LDL‑C <70 mg/dL with non‑HDL‑C <100 mg/dL (Class I).​

For very high‑risk ASCVD (e.g., multiple events, multivessel coronary disease, diabetes plus ASCVD):

• The recommended goal is:

  • LDL‑C <55 mg/dL and non‑HDL‑C <85 mg/dL.​

• If your patient is already on a high‑intensity statin and clearly above these targets, document the need to add ezetimibe and/or a PCSK9 monoclonal antibody as soon as feasible (Class IIa).​

Your role: make sure high‑intensity statin is started, contraindications are documented, and the discharge summary explicitly states the LDL‑C target and the need to escalate if it is not met.

2. Recognise severe hypercholesterolemia and FH in young MI

In a 30‑ or 40‑year‑old with MI:

• If LDL‑C is ≥190 mg/dL, this is severe hypercholesterolemia and often FH.​

• The guideline recommends:

  • High‑intensity statin as a baseline.

  • For those without ASCVD, additional non‑statins (ezetimibe, PCSK9 mAb, bempedoic acid) to reach LDL‑C <100 mg/dL and non‑HDL‑C <130 mg/dL are Class I.​

  • If there is clinical ASCVD or confirmed HeFH/high CAC, targets tighten to LDL‑C <70 or <55 mg/dL depending on risk, with combination therapy recommended.​

Your role: identify these patients early, flag possible FH, and ensure the team plans family screening and multi‑drug therapy rather than “MI at 35, statin alone”.

3. Manage hypertriglyceridemia to prevent pancreatitis and later events

For patients presenting with severe hypertriglyceridemia, especially with pancreatitis:

• TG ≥1000 mg/dL:

  • Very low‑fat diet, restricted refined carbohydrates, complete elimination of alcohol and added sugars, plus referral to a registered dietitian nutritionist are Class I recommendations to lower TG and prevent pancreatitis.​

  • In familial chylomicronemia syndrome with TG ≥1000 mg/dL, olezarsen (apoC3 inhibitor) is recommended as adjunct to diet to reduce pancreatitis risk (Class I).​

• TG 500–999 mg/dL:

  • Similar aggressive lifestyle measures plus pharmacologic TG‑lowering (fibrates or omega‑3 ethyl esters), tailored to clinical context.​

Once the acute phase is controlled, statins remain the backbone of long‑term ASCVD risk reduction in these patients.​

Your role: in pancreatitis and severe hyperTG, act decisively in the first 24–48 hours on diet, secondary causes, and TG‑lowering therapy, and then ensure a plan to start/intensify statins is documented for follow‑up.

4. Use admissions to trigger Lp(a) and future risk workup

The guideline recommends measuring lipoprotein(a) once in all adults for ASCVD risk assessment (Class I).​

For emergency/hospital physicians, practical opportunities include:

• Young or “unexpected” MI or stroke.

• Patients with premature ASCVD in multiple family members.

• Recurrent events despite “acceptable” LDL‑C.

Elevated Lp(a) (≥125 nmol/L or ≥50 mg/dL) is a risk‑enhancing factor associated with ~1.4‑fold higher ASCVD risk; ≥250 nmol/L or ≥100 mg/dL roughly doubles risk. In those with ASCVD and elevated Lp(a), adding a PCSK9 mAb with proven CV benefit when LDL‑C goals are not met is recommended (Class I).​

Your role: in high‑yield cases (young MI, stroke, heavy family history), order Lp(a) during admission and hand off its interpretation to cardiology or lipid clinic with a note that elevated levels warrant more intensive LDL‑C lowering.

Risk tools and imaging: what do you need to know?

PREVENT equations (C‑P‑R model)

You may not be the one running risk calculators in the ED, but you will see PREVENT‑derived risk printed in discharge summaries. For adults 30–79 with LDL‑C 70–189 mg/dL and no ASCVD or subclinical disease, PREVENT‑ASCVD equations are now the preferred tool (Class I).​

The guideline recommends a C‑P‑R framework:​

• Calculate PREVENT 10‑year (and 30‑year if 30–59 years).

• Personalise with risk enhancers (e.g., Lp(a), ApoB, adverse pregnancy history, CKM syndrome, inflammatory disease).

• Reclassify with Coronary Artery Calcification (CAC) if decisions remain uncertain in intermediate or select borderline risk patients.

For acute care physicians, the key is recognising that borderline risk is no longer “ignore” territory; it’s a zone where risk enhancers and CAC can tip you toward statins.

CAC and incidental findings

Coronary artery calcium is now a major decision tool:

• In intermediate‑risk and selected borderline‑risk adults with no ASCVD, if you’re unsure about LLT, CAC should be used (Class I).​

• CAC thresholds tie directly to LDL‑C goals:

  • CAC 100–299 or ≥75th percentile: recommend LLT to LDL‑C <70 and non‑HDL‑C <100.​

  • CAC 300–999: treat to at least LDL‑C <70, and it is reasonable to intensify toward <55 and non‑HDL‑C <85 (I/IIa).​

  • CAC ≥1000: treat like very‑high‑risk ASCVD with LDL‑C <55 and non‑HDL‑C <85 (Class I).​

Importantly, incidental CAC on non-cardiac CT (e.g., HRCT chest, CT aorta, CTKUB) “should be considered” in LLT decisions (Class I).​

Your role: when you see “moderate‑severe coronary calcification” in a CT report on an ED or ward patient, don’t ignore it. Document that this is subclinical ASCVD and that aggressive LLT and risk factor modification are indicated.

Triglycerides, diet, and the RDN: practical bedside moves

The lifestyle section may seem “clinic‑heavy”, but there are ED/ward implications:

• For TG ≥1000 mg/dL, involving an RDN is Class I; for TG 150–999 mg/dL with CKM features it is reasonable (IIa).​

• Core diet messages for acute care:

  • Eliminate alcohol in severe hyperTG and pancreatitis.

  • Restrict total fat in TG ≥1000 mg/dL, and reduce added sugars and refined carbs across hyperTG strata.​

  • Encourage modest weight loss (5–10%) and progressive physical activity once stable.​

You may not design the whole diet plan, but putting “RDN referral” and “alcohol elimination” into your initial orders is now guideline‑aligned.

New drugs: what you need to recognise by name

You will increasingly see these agents in medication histories and discharge plans:

• PCSK9 mAbs (evolocumab, alirocumab)

  • Indicated for severe hypercholesterolemia and very‑high‑risk ASCVD not at LDL‑C goals despite maximally tolerated statin ± ezetimibe (Class I/IIa).​

• Bempedoic acid

  • Oral agent recommended or reasonable in severe hypercholesterolemia and ASCVD when LDL‑C remains above goal on statin ± ezetimibe or in statin‑intolerant cases (Class I/IIa).​

• Inclisiran

  • Twice‑yearly siRNA, reasonable in severe hypercholesterolemia or very‑high‑risk ASCVD when PCSK9 mAbs are not tolerated or available, or when less frequent dosing is preferred (IIa; outcomes pending).​

• Olezarsen

  • ApoC3 inhibitor recommended in familial chylomicronemia with TG ≥1000 mg/dL to reduce TG and pancreatitis (Class I).​

Your role is not to initiate these from the ED in most settings, but to recognise their indications, avoid harmful drug interactions, and avoid inadvertently stopping them on admission unless absolutely necessary.

Where this guideline is strong, and where you should be cautious

Strengths for acute care:

• Clear Class I mandates for high‑intensity statin use in all appropriate ASCVD admissions.​

• Explicit LDL‑C and non‑HDL‑C targets that make discharge planning goal‑oriented.​

• Structured handling of severe hyperTG and pancreatitis risk, including diet and new therapies.​

• Integration of Lp(a), ApoB, and CAC to explain “why did this young patient infarct?”​

Cautions from the ED/ICU perspective:

• Complexity: PREVENT, risk enhancers, ApoB, Lp(a), CAC, and multiple LDL targets are too much to carry in memory; local protocols and order sets will be crucial.​

• US‑centric risk: PREVENT is not calibrated for South Asians and may underestimate risk; for Indian patients, have a lower threshold to treat.​

• Resource constraints: routine Lp(a), ApoB, CAC and advanced drugs may not be widely available; you may need to adapt the principles (aggressive statin, early identification of FH) to what is feasible in your context.​

At first glance, the 2026 Surviving Sepsis Campaign guidelines look familiar.
Same bundles. Same urgency. Same resuscitation priorities.

But look closer.

This is not a routine revision.
It’s a philosophical shift — from protocol-driven sepsis care to context-aware, system-level, precision acute care.

And if you work in the emergency department or ICU, this changes how you think — not just what you do.

Follow us on Instagram: @humans.of.em

What Changed (and Why It Matters)

1. Sepsis is now a system problem, not just a bedside problem

2026:

• Performance improvement programs + quality improvement (QI)
  → Strong recommendation, moderate certainty of evidence

• Introduction of:

  • “Code sepsis” / sepsis huddle
    → Conditional recommendation, low certainty

2021:

• Performance programs recommended
  → Strong, moderate-quality evidence (screening)

What changed?

QI is no longer administrative — it’s therapeutic.

Acute care takeaway:

You’re not just treating septic shock anymore.
You’re part of a hospital-wide intervention system.

2. Antibiotics: The death of the “1-hour rule for everyone”

2021:

• Antibiotics within 1 hour for all sepsis
  → Strong recommendation (low/very low evidence)

2026:

• Septic shock / high suspicion → immediate antibiotics

• Possible sepsis (no shock) → investigate, give within 3 hours

• Low likelihood → defer antibiotics

👉 Evidence:

• Strong (shock)

• Weak / very low (non-shock)

Why this matters:

A major pivot toward antimicrobial stewardship

Acute care reality:

You now need to balance:

• Delay = harm

• Overuse = harm

That’s a harder — and more honest — guideline.

👉 Dosing strategy finally gets attention

Prolonged infusion of beta-lactams over bolus dosing
→ Weak recommendation, moderate-quality evidence

Why this matters

• Aligns with PK/PD principles

• Improves time above MIC, especially in:

  • Septic shock

  • Altered pharmacokinetics

Practical takeaway

• Start thinking beyond “which antibiotic”

• Move toward:
  👉 How you give it matters as much as what you give

Antibiotics don’t just start early — they must stop early

👉 Daily assessment for de-escalation based on culture and susceptibility
→ Weak recommendation, very low-quality evidence

👉 Avoid prolonged broad-spectrum therapy once pathogen is identified

Why this matters

This is a major philosophical shift:

• Earlier guidelines focused on early administration

• 2026 emphasizes early de-escalation

Acute care takeaway

• Antibiotics are not a one-time decision

• They are a dynamic therapy

👉 Start broad (when needed)
👉 Narrow early (when possible)

3. Screening: Less faith in qSOFA, more in broader tools

2021:

• Against using qSOFA alone
  → Strong recommendation, moderate-quality evidence

2026 reinforces and clarifies:

👉 Use NEWS, NEWS2, MEWS, or SIRS over qSOFA as a single screening tool
→ Strong recommendation, moderate certainty of evidence

Also adds:

• Prehospital screening
  → Conditional, very low evidence

Why this matters

qSOFA was attractive because it was simple.
But simplicity came at the cost of sensitivity.

👉 The 2026 guideline firmly moves away from qSOFA as a standalone tool.

Acute care takeaway

• Stop relying on qSOFA alone

• Use early warning scores + clinical judgment

• Screening is not a number — it’s a system + process

4. Fluids: The quiet downgrade

2021:

• 30 ml/kg fluids
  → Weak recommendation, low-quality evidence (downgraded)

2026 direction:

• Reinforces individualized resuscitation

• Moves away from rigid fluid mandates

Takeaway:

The guideline no longer believes in “one-size-fits-all fluids”

5. Lactate, CRT, and monitoring: still here, still weak

• Lactate-guided resuscitation
  → Weak, low-quality evidence

• Capillary refill time
  → Weak evidence

Translation:

We use them.
We trust them.
But the evidence is still not strong.

6. Adjuncts: Less enthusiasm, more skepticism

Strong:

• No starch → Strong, high-quality evidence

• Norepinephrine first-line → strong

Weak / against:

• Vitamin C → Weak against

• Hemoperfusion → Weak against

Pattern:

Most adjuncts either:

• Don’t work

• Or don’t have good evidence

7. Ventilation: One of the few stable areas

• Low tidal volume → Strong, high-quality evidence

• Proning → Strong, moderate-quality evidence

• HFNC over NIV → Weak, low-quality evidence

Insight:

Respiratory care remains one of the most evidence-consistent domains

8. New emphasis: survivorship and transitions of care

2026 expands into:

• Goals of care discussions

• Post-sepsis syndrome

• Transitions of care

Mostly:
👉 Best practice / weak evidence

Shift:

Sepsis is no longer an ICU event.
It is a longitudinal disease process

If you remember only few things from 2026:

• Think before antibiotics (unless shock)

• How you give antibiotics (infusion strategy) matters

• De-escalate early — stewardship is core care

• Fluids are individualized, and type matters

What This Means: A Critical Appraisal

a). The uncomfortable truth: Evidence is still weak

Across domains:

• Antibiotics (non-shock) → very low certainty

• Fluids → low certainty

• CRT/lactate → low certainty

• Code sepsis → low certainty

👉 Despite decades of research, high-certainty evidence is limited

b). The “GRADE paradox”

The guideline uses structured GRADE methodology:

• “We recommend” → strong

• “We suggest” → conditional

But:

👉 Strong recommendations sometimes sit on low-quality evidence (especially earlier guidelines)
👉 Many new recommendations remain conditional

💡 Implication:

This is transparent science — but still uncertain medicine

c). From protocols → clinical judgment

Old era:

• Bundles

• Timelines

• Protocol compliance

2026:

• Diagnostic probability

• Stewardship

• Context-aware decisions

This is the real shift:

The guideline now expects thinking, not just following

d). The antibiotic pivot is the most practice-changing update

Before:

• Everyone gets antibiotics early

Now:

• Timing depends on:

  • Severity

  • Probability of infection

Clinical reality:

You are now balancing:

• Sepsis mortality vs antimicrobial harm

This is harder — but more accurate.

e). Real-world applicability (especially LMIC settings)

The guideline acknowledges:

• Resource variability

• Need for adaptable systems

💡 Interpretation:

• “Code sepsis” may help more in chaotic, resource-limited systems

• Protocols alone don’t fix outcomes without infrastructure

f). The deeper truth: Sepsis remains poorly understood

Even in 2026:

• Few high-certainty interventions

• Many weak recommendations

• Heavy reliance on physiology and pragmatism

👉 Sepsis is still a syndrome, not a single disease

The 2026 Surviving Sepsis Guidelines don’t give you more answers.
They give you better questions.

And in the resuscitation bay at 3 AM —
that might be exactly what we needed.

Source -

SSC 2026 guidelines update

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The 2026 ACG Clinical Guideline reframes HE as a systems disease, not just a biochemical one. When combined with ACC 2022 ICU care principles, it demands a shift in how we triage, investigate, and treat these patients.

1. HE Is Not “Just Ammonia”

The Three Villages + Five Axes Framework

The guideline introduces a conceptual model that should anchor bedside thinking:

“Three Villages of HE”

• Village 1 – Pathogenesis (gut–brain axis, inflammation, ammonia, sarcopenia)

• Village 2 – Impact (patients, caregivers, healthcare systems)

• Village 3 – Multidisciplinary care (ED, hepatology, ICU, rehab, social systems)

HE is now classified across five axes:

1. Type (A/B/C)

2. Severity (West Haven)

3. Time course

4. Precipitated vs non-precipitated

5. Social infrastructure (NEW)

👉 Game changer:
You must now ask:

“Can this patient actually survive outside the hospital?”

• Covert HE → Overt HE → Recurrent admissions → Cognitive decline

• ED clinicians often see patients too late in this curve

2. Covert/Minimal HE (CHE/MHE): The Missed Diagnosis in ED

Who should trigger suspicion?

• Hypoalbuminemia

• Decompensated cirrhosis

• Portal hypertension/shunts

• Falls, traffic violations, navigation issues

• Subtle cognitive complaints

👉 Key ED pearl:
Isolated asterixis ≠ OHE

How to test (NOT ammonia)

• Single-test strategy (ACG recommendation)

• Practical tools:

  • Stroop / EncephalApp

  • Animal Naming Test

  • Critical Flicker Frequency

❌ Do NOT use ammonia to diagnose CHE

Treatment: “Theragnostic trial”

• Lactulose (4–8 week trial)

• Reassess cognition + function

Useful in ED follow-up planning and liaison clinics

3. “Is This Really HE?” — The Cognitive Differential

“Cirrhosis + Cognitive Complaint Pathway”

More than 50% of suspected HE ≠ HE

Common mimics:

• Dementia / MCI

• Depression / PTSD

• Obstructive sleep apnea

• Substance use

• Metabolic/endocrine disorders

👉 ED shift:
Stop reflex lactulose escalation → start structured differential evaluation

4. Overt HE in ED & ICU

Triage: Who Needs Admission?

“Admission Decision Flowchart”

Admit if:

• Grade 3–4 HE

• First episode

• Infection, bleed, AKI

• Poor social support

Strong Recommendations That Change Practice

• Lactulose for OHE (strong)

• Secondary prophylaxis after first episode (strong)

• Add rifaximin for recurrence (strong)

• Protein 1.2–1.5 g/kg/day (strong)

• Branched Chain Amino Acid (BCAA) —> if needed (strong)

• Rifaximin pre-TIPS (strong)

🚨 What to STOP Doing

• Routine ammonia testing

• Routine CT brain without focal deficit

👉 A normal ammonia ≠ no HE
👉 HE = clinical diagnosis of exclusion

5. Acute Management: ED + ICU Integration (ACG 2026 + ACC 2022)

Acute HE Treatment Algorithm

First-line (ED + ICU)

Lactulose

• Oral/NG: every 1–2 hrs → 2–3 soft stools

• Enema if needed

⚠️ Avoid overuse → dehydration, hypernatremia

See more about Lactulose in HE, here

PEG (Alternative)

• Faster resolution in trials

• Useful if ileus/bloating

Rifaximin

• Add in recurrent HE

• Consider early in severe ICU cases

ACC 2022 ICU Principles (Add These to Your Workflow)

Airway & Neuroprotection

• Intubate if:

  • GCS ≤ 8

  • Aspiration risk

• Avoid oversedation (benzodiazepines worsen HE)

Hemodynamic & Metabolic Targets

• Maintain MAP ≥ 65 mmHg

• Correct:

  • Hypokalemia

  • Hyponatremia

  • Hypoglycemia

Infection Control

• Low threshold for antibiotics

• Sepsis = major precipitant

ICP & Cerebral Edema (Severe HE / ACLF)

• Head elevation

• Avoid hypercapnia

• Consider hypertonic saline if needed

Nutrition (Critical Update)

• DO NOT restrict protein

• ICU patients may need up to 2 g/kg/day

6. Nonresponse at 48–72 Hours

📌 Insert Figure 9 here – “Nonresponse Algorithm”

If not improving:

1. Reconsider diagnosis

2. Re-look for precipitants

3. Evaluate for:

   • TIPS

   • Large shunts

👉 Do NOT just increase lactulose blindly

7. Preventing Recurrence

“Recurrence Prevention Pathway”

Core Strategy

• Lactulose (target 2–3 stools/day)

• Rifaximin (↓ recurrence 58%)

System-Level Changes

• Use Bristol stool scale

• EMR alerts/order sets

• Patient education tools

Deprescribing (Critical ED Role)

Stop/minimize:

• Benzodiazepines

• Opiates

• Gabapentinoids

• Z-drugs

• PPIs (when inappropriate)

Nutrition & Sarcopenia

• Protein: 1.2–1.5 g/kg/day

• Late-night snack

• Exercise programs

👉 Muscle = ammonia buffer

8. TIPS, Refractory HE & Transplant

TIPS-related HE

• Start rifaximin 14 days before TIPS

• Continue ≥ 6 months

Refractory HE

• Consider:

  • Shunt embolization

  • TIPS revision

Transplant Implications

• HE underestimates MELD risk

• Consider transplant even at low MELD

👉 Early referral if:

• Recurrent HE

• Grade III–IV

• Persistent cognitive decline

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Share

References

1. Bajaj JS, Jakab SS, Jesudian AB, et al. ACG Clinical Guideline: Hepatic Encephalopathy. Am J Gastroenterol. 2026;121:588-618. doi:10.14309/ajg.0000000000003899

2. Vilstrup H, Amodio P, Bajaj J, et al. Hepatic Encephalopathy in Chronic Liver Disease: 2022 Practice Guidance. Hepatology. 2022;76(3):1027-1040. doi:10.1002/hep.32477
   
   

Sepsis management in emergency and acute care does not fail because we lack guidelines.
It fails when we mistake protocol compliance for physiologic care.

Across emergency departments, wards, and ICUs, the modern understanding of sepsis is evolving. The shift is subtle but profound:

From rigid bundles → to individualized, physiology-guided resuscitation.

For acute care clinicians, this is not an academic nuance. It is the difference between fluid overload and organ recovery. Between delayed vasopressors and preserved perfusion. Between antibiotics alone and definitive source control.

Let’s break this down pragmatically.

1️⃣ Sepsis Is a Time-Critical Emergency — Like STEMI or Stroke

We would never wait for ST elevation to “fully declare itself” before activating a cath lab.
We should not wait for hypotension before activating a sepsis response.

Early recognition hinges on identifying:

• Suspected infection plus

• Evidence of organ dysfunction

Not just shock.

Red flags at the front door:

• Altered mentation

• Tachypnea

• Rising oxygen requirement

• Oliguria

• Cool or mottled extremities

• Elevated lactate despite preserved BP

The dangerous patient is often the one with “normal blood pressure.”

This is cryptic shock — where hypoperfusion precedes hypotension.

Acute care clinicians must integrate early warning scores with clinical gestalt. No scoring system replaces bedside judgment.

2️⃣ The First Hours Matter — But Not All Fluids Are Beneficial

The traditional 30 mL/kg reflex has simplified thinking — but oversimplification carries harm.

Excess fluid leads to:

• Pulmonary edema

• Delayed extubation

• Worsened renal outcomes

• Increased mortality in some subgroups

The emerging model is dynamic:

Small bolus (250–500 mL) → reassess → repeat if responsive

Use physiology to guide you:

• Passive leg raise

• Stroke volume change

• Bedside echo (LV function)

• Capillary refill

• Urine output

• Lactate trend (not single value)

Sepsis resuscitation should be a loop:

Resuscitate → Reassess → Redirect.

Not a one-time fluid event.

Particularly in elderly patients or those with heart failure, CKD, or cirrhosis, restraint is not undertreatment — it is precision.

3️⃣ Earlier Vasopressors Prevent Fluid Creep

Waiting to “finish fluids” before starting vasopressors is increasingly indefensible.

When hypotension persists after limited fluid resuscitation:

• Start norepinephrine early.

• Peripheral initiation via a well-functioning IV is acceptable.

• Target MAP ≈ 65 mmHg, individualized to perfusion markers.

Earlier vasopressors:

• Restore perfusion sooner

• Limit excess fluid accumulation

• Shorten time to hemodynamic stability

Septic shock is distributive at its core. Fluids alone cannot correct vasoplegia.

4️⃣ Antibiotics Are Urgent — But Source Control Is Definitive

Timely antibiotics save lives — especially in septic shock.
Early intravenous antibiotics remain the only intervention consistently associated with reduced mortality in sepsis — particularly in septic shock.

In patients with septic shock or life-threatening instability, antibiotics should be administered within 1 hour of recognition, after obtaining appropriate cultures if this does not cause delay.

In patients without shock, where diagnostic uncertainty exists, a short period of focused evaluation is reasonable. Current guidance supports administration within 3 hours if concern for infection persists, with closer monitoring throughout. The mortality signal for delay is strongest in shock; in stable patients, modest delays to improve diagnostic precision are unlikely to worsen outcomes.

Empirical therapy should reflect local resistance patterns and individual risk factors for drug-resistant organisms. Once microbiology data become available, prompt de-escalation to narrow-spectrum therapy is essential to limit antimicrobial resistance and toxicity.

Shorter courses (generally 5–7 days) are adequate for most infections unless there is deep-seated or complicated disease. Importantly, antibiotics are not definitive therapy when source control is required.

Modern sepsis care demands both urgency and stewardship —
1 hour for the unstable, 3 hours with thoughtful precision for the uncertain.

But antibiotics are not the endpoint. They are the bridge.

Definitive therapy often requires :- Source Control

• Drainage

• Debridement

• Decompression

• Device removal

Obstructed urosepsis.
Perforated viscus.
Necrotizing soft tissue infection.
Infected lines.

The emergency department must initiate source control conversations immediately — not defer them.

Time-to-source-control may matter as much as time-to-antibiotics.

5️⃣ Point-of-Care Ultrasound Is Now Foundational

Sepsis is hemodynamically heterogeneous.

Some patients are:

• Pure vasoplegia

• Septic cardiomyopathy

• Mixed shock

• Fluid responsive

• Fluid intolerant

Without ultrasound, we are often guessing.

POCUS allows rapid differentiation:

• LV systolic function

• RV strain

• IVC variability

• B-lines (early pulmonary edema)

• Pericardial effusion

• Intra-abdominal source clues

Modern sepsis care in acute settings is incomplete without bedside echocardiographic assessment.

6️⃣ Organ Support Begins in the ED — Not in the ICU

Many decisive interventions occur before ICU transfer:

• High-flow nasal oxygen

• Noninvasive ventilation

• Early intubation with hemodynamic preparation

• Lung-protective ventilation

• Vasopressor titration

• Renal function surveillance

Disposition is not administrative. It is physiological triage.

Patients on vasopressors, escalating oxygen support, rising lactate, or evolving multi-organ dysfunction require ICU-level care — early.

Clear handovers must include:

• Fluids administered

• Current vasopressor dose

• Lactate trajectory

• POCUS findings

• Source control plan

7️⃣ Stewardship and Individualization Matter

Sepsis pathways must balance urgency with precision.

Over-resuscitation harms.
Indiscriminate broad-spectrum antibiotics drive resistance.
Delayed de-escalation perpetuates ICU burden.

Clinical decisions must incorporate:

• Age

• Co-morbidities

• Functional baseline

• Patient preferences

• Resource realities

Early goals-of-care discussions are not therapeutic defeat — they are ethical medicine.

The Shift We Must Embrace

The evolution in sepsis management is not about abandoning bundles.
It is about maturing beyond them.

Sepsis is not a protocol problem.

It is a physiology problem.

And physiology demands continuous reassessment.

Reference -

Singer M, Angus DC, Annane D, et al. Sepsis. Lancet. Published online February 26, 2026. doi:10.1016/S0140-6736(25)02422-5

1. SGLT-2 Inhibitors as Foundational Therapy

What has changed

SGLT-2 inhibitors are now recommended first-line (with metformin) across:

• No comorbidity

• Heart failure

• ASCVD

• CKD (down to eGFR 20)

• Early-onset T2DM

• Obesity

Acute Care Relevance

1.1 Expect near-universal exposure

A large proportion of T2DM patients presenting to ED will be on:

• Empagliflozin

• Dapagliflozin

This includes patients with:

• Advanced CKD (eGFR 20–30, combined with DPP-4 inhibitor)

  type-2-diabetes-in-adults-manag…

• Heart failure with preserved or reduced EF

• ASCVD on triple therapy

1.2 Increased Risk of Eu-glycaemic DKA

The guideline explicitly:

• Requires DKA risk assessment before starting SGLT-2

• Advises suspension during ketogenic diets and intercurrent illness

EM/ICU Translation

Lower threshold to:

• Check blood ketones in:

  • Sepsis

  • Major surgery

  • AKI

  • Reduced oral intake

  • Steroid therapy

• Diagnose DKA despite glucose <250 mg/dL

• Stop SGLT-2 immediately on admission if:

  • Shock

  • Hypoxia

  • AKI

  • Severe infection

  • Peri-operative state

Clinical shift: Hyperglycaemia is no longer required to suspect DKA.

2. Sick-Day Rules Become Mandatory Documentation

The updated guideline mandates explicit sick-day plans including temporary cessation of:

• Metformin

• SGLT-2 inhibitors

Acute Care Implication

In ED/ICU you are now:

• Justified in holding these agents in:

  • Dehydration

  • Hypotension

  • Sepsis

  • Contrast exposure

• Expected to document:

  • When to restart

  • Under what renal/hemodynamic parameters

Metformin: Stop in hypoxia, shock, significant AKI (lactic acidosis risk).
SGLT-2: Stop early in any catabolic or volume-depleted state.

3. Advanced CKD Patients Will Still Be on SGLT-2

The update allows:

• Dapagliflozin or empagliflozin down to eGFR 20

• Combination with DPP-4 inhibitor between eGFR 20–30

EM/ICU Implications

You will encounter:

• Dialysis-adjacent patients still taking SGLT-2

• Lower baseline glucose but ongoing osmotic diuresis risk

Monitor for:

• Volume depletion

• Hypotension

• AKI worsening

• Electrolyte shifts

4. Early Triple Therapy is Now Common

For ASCVD, obesity, and early-onset T2DM:

• Metformin

• SGLT-2 inhibitor

• GLP-1 RA or tirzepatide

ICU Implications

Expect:

• Lower HbA1c but polypharmacy

• Reduced insulin requirements at baseline

• Higher GI side-effect burden

5. GLP-1 Receptor Agonists & Tirzepatide in Acute Care

Recommended strongly for ASCVD and obesity

Acute Care Consequences

5.1 Delayed Gastric Emptying

Implications:

• Increased aspiration risk

• Nausea/vomiting complicating NIV tolerance

• Enteral feeding delays

5.2 Peri-intubation considerations

Consider:

• Full stomach assumption

• RSI preference in unstable patients

6. Glucose Monitoring: Acute Illness and Steroids

The guideline emphasizes:

• Acute intercurrent illness increases hyperglycaemia risk

• Short-term capillary monitoring is appropriate during steroid initiation

EM/ICU Translation

Expect:

• Marked steroid-induced hyperglycaemia

• Rapid escalation of insulin requirements

• Need for structured monitoring post-discharge

Steroid-treated pneumonia/COPD patients will frequently require:

• Basal-bolus insulin

• Escalated capillary monitoring

7. Continuous Glucose Monitors (CGM) Use Will Increase in Hospital

Clear endorsement of:

• isCGM

• rtCGM in insulin-treated T2DM with recurrent/severe hypoglycaemia

Acute Care Implications

You will see:

• CGM sensors in admitted patients

Important:

• Do NOT rely solely on CGM in:

  • Shock

  • Rapid glucose change

  • Vasopressor states

• Capillary testing remains required for accuracy confirmation.

Ensure:

• Backup strips are available

• Device knowledge confirmed at discharge

8. Organ-Protection Bias Over Glycaemia

The guideline states that SGLT-2 and GLP-1 RAs are recommended as much for CV/renal benefit as glycaemia

Critical Care Reframing

When rationalising medications in ICU:

Do not interpret normal HbA1c as overtreatment.

Instead:

• Distinguish glycaemic drugs from organ-protective drugs

• Restart SGLT-2 and GLP-1 early once:

  • Hemodynamically stable

  • Renal function recovered

  • Oral intake adequate

These are now secondary prevention agents.

9. Frailty and Hypotension Risk

For frail adults:

• SGLT-2 only if low risk of volume depletion/hypotension

ED/ICU Implication

In elderly septic patients:

• SGLT-2 may contribute to:

  • Pre-existing volume contraction

  • Orthostatic collapse

  • AKI

High vigilance for polypharmacy-related hypotension.

10. Peri-Operative and Critical Care Protocol Adjustments

Because SGLT-2 use is now foundational:

Every diabetic ICU admission should trigger:

• Medication reconciliation focused on SGLT-2

• Ketone surveillance if acidosis

• Clear peri-operative cessation plan

The era of “metformin only” diabetics is over.

Start/stop decision plan in EM/Acute care

Bedside decision algorithm - for stop/restart of DM drugs in acute care.

For more such updates-
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References-
NICE 2026 update on T2DM

It kills by right ventricular failure.

The role of the emergency physician is not simply to diagnose PE—but to identify which patient will deteriorate, which patient needs reperfusion, and which patient can safely go home.

The 2026 AHA/ACC/ACEP classification (A–E) provides a physiology-based roadmap for treatment escalation, monitoring, and disposition.

This is where classification becomes action.

Step 1: Immediate ED Stabilization

COR 1, LOE B-NR

Initial management priorities in suspected or confirmed PE:

• Oxygenation
• Circulatory support
• RV perfusion preservation
• Prevention of hemodynamic collapse

Key immediate assessments:

• Blood pressure
• Oxygen requirement
• Lactate
• Mental status
• RV function

Patients in Category D or E require immediate resuscitation.

Oxygen and Respiratory Support

COR 1, LOE C-LD

Indicated in hypoxemic patients.

Target:

SpO₂ ≥ 90%-94%

Preferred escalation:

1. Nasal cannula

2. High-flow nasal oxygen

3. Non-invasive ventilation

Avoid unnecessary intubation.

Positive pressure ventilation reduces venous return and worsens RV failure.¹

If intubation unavoidable:

• Use hemodynamically stable induction agents
• Initiate vasopressors first

—> Physiologically difficult airway modification, give RV supporting ionotropes.

Circulatory Support

COR 1, LOE B-NR

Hypotension reflects RV failure and impaired cardiac output.

First-line vasopressor:

Norepinephrine

Benefits:

• Improves coronary perfusion
• Improves RV contractility
• Improves systemic vascular resistance¹

Avoid aggressive fluid boluses.

Excess fluid worsens RV dilation and reduces LV filling.

Step 2: Anticoagulation — The Foundation of Treatment

Anticoagulation prevents clot propagation and allows endogenous fibrinolysis.

COR 1, LOE A

Anticoagulation is recommended in all patients with confirmed PE unless contraindicated.¹

Choice of Anticoagulant

DOACs preferred in stable patients

COR 1, LOE A

Preferred agents:

• Apixaban
• Rivaroxaban

Advantages:

• Lower bleeding risk
• Rapid onset
• No monitoring required
• Suitable for outpatient treatment¹

LMWH preferred when inpatient management required

COR 1, LOE B-R

Preferred in:

• Hospitalized patients
• Cancer-associated thrombosis
• Moderate-risk PE¹

Advantages:

• Predictable anticoagulation
• Lower HIT risk

UFH preferred in unstable patients

COR 1, LOE B-NR

Indications:

• Category C3
• Category D
• Category E
• Planned thrombolysis or thrombectomy¹

Reason:

Rapid reversibility.

Step 3: Reperfusion Therapy

Indicated in RV failure and shock

Reperfusion reduces RV afterload and restores circulation.

Systemic Thrombolysis

COR 1, LOE B-R

Indicated in:

Category E1 — cardiogenic shock
Category E2 — cardiac arrest¹

Reduces mortality and improves hemodynamics.

Consider thrombolysis in Category D

COR 2a, LOE B-NR

Indicated if evidence of:

• Normotensive shock
• Elevated lactate
• Progressive hypoxia
• RV dysfunction¹

These patients are at high risk of deterioration.

Not recommended routinely in Category C

COR 3, LOE B-R

Routine thrombolysis in stable patients increases bleeding risk without mortality benefit.

Alteplase (tPA) Dose for Acute Pulmonary Embolism

Standard dose for high-risk PE (massive PE with shock)

Dose: 100 mg IV over 2 hours

Regimen:

• 100 mg alteplase IV infusion over 120 minutes

• No bolus required (standard regimen)

This is the FDA-approved and guideline-recommended dose.

Alternative accelerated regimen (commonly used in ED / ICU)

Dose: 0.6 mg/kg IV over 15 minutes (max 50 mg)

Used when:

• Rapid hemodynamic collapse

• Need for faster reperfusion

• Peri-arrest or severe shock

Evidence shows similar efficacy with potentially lower bleeding risk.

Alteplase Dose During Cardiac Arrest due to PE

When PE is suspected or confirmed cause of arrest:

Recommended regimen (AHA cardiac arrest guidance)

50 mg IV bolus over 2–5 minutes

Then:

• Continue CPR for at least 15–30 minutes

• If no ROSC, may repeat another 50 mg bolus after 15–30 minutes

Maximum total dose: 100 mg

Most commonly used cardiac arrest protocol in emergency medicine

Option 1 (most widely used):

• Alteplase 50 mg IV push

• Continue CPR 15–30 min

• Repeat 50 mg if needed

Option 2 (alternative):

• Alteplase 100 mg IV bolus over 10 minutes

Used less commonly due to bleeding risk.

Catheter-Directed Therapy

COR 2a, LOE B-NR

Indicated when:

• Thrombolysis contraindicated
• Failed thrombolysis
• Progressive deterioration¹

Advantages:

• Lower bleeding risk
• Targeted therapy

Mechanical Thrombectomy

COR 2a, LOE B-NR

Indications:

• Category D or E
• Contraindication to thrombolysis
• Failed thrombolysis¹

Improves hemodynamics rapidly.

Increasingly used in modern PE management.

ECMO

COR 2a, LOE C-LD

Indicated in refractory shock or cardiac arrest.

Provides circulatory support until reperfusion effective.

Step 4: Treatment and Disposition by A–E Group

This is the most important ED decision.

Category A — Incidental PE

Mortality risk: <1%

Treatment:

Anticoagulation or observation depending on risk factors¹

Disposition:

Discharge with outpatient follow-up

Category B — Symptomatic, Low Risk

Mortality risk: ~1%

Treatment:

DOAC preferred¹

Disposition:

Outpatient management recommended

Criteria:

• Stable vitals
• No hypoxia
• Reliable follow-up¹

Category C1 — Intermediate Risk, No RV Injury

Mortality risk: 3–5%

Treatment:

Anticoagulation¹

Disposition:

Hospital admission, telemetry

Category C2 — RV Injury or Biomarker Elevation

Mortality risk: 5–15%

Treatment:

Anticoagulation

Disposition:

Hospital admission with monitoring¹

Category C3 — RV Injury + Biomarker Elevation

Mortality risk: 15–30%

Treatment:

UFH preferred
Consider reperfusion if deterioration¹

Disposition:

Step-down or ICU

PERT consultation recommended.

Category D — Normotensive Shock

Mortality risk: 20–40%

Treatment:

UFH
Consider thrombolysis or thrombectomy¹

Disposition:

ICU

Immediate specialist consultation required.

Category E — Cardiogenic Shock or Arrest

Mortality risk: >40%

Treatment:

Immediate reperfusion therapy¹

Options:

• Thrombolysis
• Thrombectomy
• ECMO

Disposition:

ICU

Medical emergency.

Step 5: Monitoring

COR 1, LOE B-NR

Monitor for deterioration:

• Blood pressure
• Oxygen requirement
• Heart rate
• Lactate
• Mental status¹

Serial reassessment essential.

Patients may deteriorate rapidly.

Step 6: Complications and Sequelae

Acute complications

Right ventricular failure
Cardiogenic shock
Cardiac arrest

Primary causes of death.

Chronic thromboembolic pulmonary hypertension (CTEPH)

Occurs in 2–4% of patients.¹

Caused by persistent pulmonary vascular obstruction.

Symptoms:

• Progressive dyspnea
• Exercise intolerance

Post-PE syndrome

Occurs in up to 50% of patients.¹

Symptoms:

• Dyspnea
• Reduced exercise tolerance
• Functional impairment

Step 7: Duration of Anticoagulation

COR 1, LOE A

Minimum duration:

3 months¹

Extended anticoagulation recommended if:

• Unprovoked PE
• Persistent risk factors¹

I break down emergency medicine physiology visually and practically.
If you’re an emergency physician, resident, or acute care clinician, you’ll find additional diagrams, algorithms, and case-based insights here:

→ Follow on Instagram: @humans.of.em

This is where most of my visual teaching lives.

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Reference

1. American College of Cardiology/American Heart Association Joint Committee. 2026 AHA/ACC guideline for the diagnosis and management of acute pulmonary embolism. J Am Coll Cardiol. 2026.

Not because it is rare—but because it is unpredictable.

Some patients with PE are discharged safely from the emergency department within hours. Others arrest suddenly despite appearing stable minutes earlier.

The difference is not clot size.

It is physiology of clot against RV.

The 2026 AHA/ACC Pulmonary Embolism guideline replaces the outdated “massive vs submassive vs low-risk” terminology with a dynamic, physiology-based classification system (Groups A–E) that integrates clinical severity scores, biomarkers, RV imaging, hemodynamics, and respiratory status.

This framework begins in the emergency department—at the moment of diagnosis—and directly determines prognosis, monitoring, disposition, and treatment.

This article focuses on definition, classification, evaluation, and diagnosis—from the emergency department.

Definition of Acute Pulmonary Embolism

Acute pulmonary embolism is defined as:

Obstruction of pulmonary arterial circulation by thrombus, resulting in impaired pulmonary perfusion, increased pulmonary vascular resistance, and potential right ventricular (RV) failure.

The clinical consequences depend on the interaction between:

• Clot burden
• Speed of vascular obstruction
• RV reserve
• Cardiopulmonary reserve
• Systemic compensation

The right ventricle—not the clot—is the primary determinant of outcome.

Epidemiology: The ED Reality

Pulmonary embolism presents a paradox in emergency medicine.

It is common—but rarely confirmed.

Key ED statistics:

• Only 4–10% of patients undergoing CTPA for suspected PE actually have PE

• Acceptable diagnostic miss rate: <2% at 3 months

• Age-adjusted D-dimer diagnostic strategy failure rate: 0.3% (95% CI 0.1–1.7%)

• DVT is present in 44–71% of confirmed PE patients

This defines the core emergency medicine challenge:

Identify dangerous PE while safely excluding PE in the majority.

The New AHA/ACC/ACEP Classification (A–E)

The 2026 guideline introduces a five-group classification system reflecting progressive physiological severity.

Each group directly correlates with mortality risk, disposition, and treatment escalation.

GROUP A: Subclinical (Incidental) PE

Definition:
Pulmonary embolism detected incidentally on imaging, without attributable symptoms.

These patients have no physiological compromise.

Mortality risk: <1%

Subgroups

A1: Subsegmental incidental PE

Features:

• Isolated subsegmental embolus
• No symptoms
• No RV dysfunction
• No hypoxia
• Normal biomarkers

Physiology intact.

Lowest-risk group.

A2: Segmental or proximal incidental PE

Features:

• Larger clot burden
• Still asymptomatic
• Normal hemodynamics
• No RV dysfunction

Anatomical clot present—but physiological compensation intact.

GROUP B: Symptomatic PE, Low Clinical Severity

Definition:
Symptomatic PE with low severity scores:

• PESI Class I–II
• sPESI = 0
• Hestia negative

RV function preserved.

Mortality risk: ~1%

Subgroups

B1: Symptomatic sub-segmental PE

Features:

• Symptoms present
• Minimal clot burden
• Normal RV function
• Normal biomarkers

B2: Symptomatic segmental or proximal PE

Features:

• Larger clot burden
• Symptoms present
• RV function preserved
• Hemodynamically stable

These represent compensated pulmonary embolism physiology.

Many can be safely treated as outpatients.

GROUP C: Symptomatic PE with Elevated Clinical Severity

RV injury present, but no shock

Definition:

Symptomatic PE with elevated clinical severity scores:

• PESI Class III–V
• sPESI ≥1
• Hestia positive
• Bova score ≥4

Represents early RV dysfunction.

Mortality risk increases progressively across subgroups.

Subgroups

C1: Elevated clinical severity score only

Features:

• Elevated PESI/sPESI
• Normal RV function
• Normal troponin
• Normal BNP

Risk driven by co-morbid vulnerability.

Mortality risk: ~3–5%

C2: RV dysfunction OR biomarker elevation

Features:

Either:

• RV dilation on imaging
OR
• Elevated troponin or BNP

Indicates early RV myocardial stress.

Mortality risk: ~5–15%

C3: RV dysfunction AND biomarker elevation

Features:

• RV dilation present
• Elevated troponin
• Elevated BNP

Represents established RV injury.

Blood pressure still preserved due to compensation.

Mortality risk: 15–30%

This is the highest-risk normotensive subgroup.

Equivalent to old ‘Intermediate - High Risk Group’

Respiratory Modifier: “R”

Any subgroup may receive a respiratory modifier (R) if respiratory failure present.

Examples:

C3R
D2R
E1R

Defined by:

• Oxygen requirement ≥6 L/min
• Non-invasive ventilation
• Mechanical ventilation

Pulm Embolism new guidelines

This identifies patients at risk of respiratory collapse independent of hypotension.

GROUP D: Incipient Cardiopulmonary Failure

Shock physiology emerging

Most important group to identify

These patients demonstrate circulatory compromise without persistent hypotension.

Mortality risk: 20–40%

Subgroups

D1: Transient hypotension

Features:

• Temporary hypotension
• Responds to fluids
• No persistent organ hypoperfusion

Represents unstable compensation.

D2: Normotensive shock

Features:

• SBP ≥90 mmHg
• Lactate ≥2 mmol/L
• Evidence of organ hypoperfusion

Shock present despite preserved blood pressure.

Extremely high risk.

GROUP E: Cardiopulmonary Failure

Established shock or cardiac arrest

Highest-risk group.

Mortality risk: >40%

Pulm Embolism new guidelines

Subgroups

E1: Cardiogenic shock

Features:

• Persistent hypotension
• Vasopressor requirement
• RV failure present

E2: Refractory shock or cardiac arrest

Features:

• Persistent shock despite therapy
• Cardiac arrest

Highest mortality subgroup.

Emergency Department Diagnostic Approach (COR and LOE)

The guideline recommends a structured, stepwise approach.

Step 1: Clinical Assessment

COR 1, LOE A

Pulm Embolism new guidelines

Includes:

Symptoms:

• Dyspnea
• Chest pain
• Syncope
• Hemoptysis

Signs:

• Tachycardia
• Hypoxia
• Hypotension
• Signs of DVT

Risk factors:

• Prior VTE
• Surgery
• Immobilization
• Cancer
• Pregnancy

Step 2: Clinical Probability Assessment

COR 1, LOE A

Pulm Embolism new guidelines

Validated tools:

• Wells Score
• Revised Geneva Score
• PERC Rule

These determine need for testing.

Step 3: D-Dimer Testing

COR 2a, LOE B-R

Pulm Embolism new guidelines

Indicated in low or intermediate probability patients.

Age-adjusted D-dimer improves diagnostic efficiency.

Failure rate: 0.3%

Step 4: Imaging with CTPA

COR 1, LOE A

Pulm Embolism new guidelines

CTPA is diagnostic standard.

Advantages:

• High sensitivity and specificity
• Rapid diagnosis
• RV assessment
• Alternative diagnoses identified

Step 5: RV Assessment and Biomarkers

COR 1, LOE B-R

Pulm Embolism new guidelines

Critical prognostic parameters include:

• RV/LV ratio ≥1.0
• Troponin elevation
• BNP elevation
• TAPSE <1.6 cm

These identify RV dysfunction.

Echocardiographic Findings in Acute PE: Sensitivity, Specificity, and Likelihood Ratios

Important guideline principle:
The AHA/ACC guideline emphasizes that echo should NOT be used to rule out PE (COR 3 – No Benefit), but is strongly recommended for risk stratification and identification of RV dysfunction (COR 1, LOE B-NR).

Pulm Embolism new guidelines

Single findings have limited sensitivity.
Multiple findings greatly increase diagnostic probability.

Highest-Value Echo Findings Ranked by Likelihood Ratio

From strongest to weakest diagnostic strength:

1. McConnell sign → LR+ up to 12

2. Septal flattening → LR+ up to 10

3. Multiple RV dysfunction markers → LR+ up to 20

4. TAPSE <1.6 cm → LR+ up to 6

5. RV dilation → LR+ up to 4

Guideline-Specific Key Recommendations on POCUS/Echo (COR and LOE)

POCUS for diagnosis

COR 3 (No Benefit), LOE B-NR

Echo should not be used alone to diagnose or exclude PE.

Reason: poor sensitivity.

Cardiac POCUS for risk stratification

COR 1, LOE B-NR
Echo is recommended to assess RV dysfunction and risk.

Pulm Embolism new guidelines

Multiple parameters improve accuracy

Guideline explicitly states:

Sensitivity and specificity improve significantly when multiple RV dysfunction parameters are present.

Pulm Embolism new guidelines

Emergency Medicine Interpretation Algorithm Using Likelihood Ratios

Pretest probability determines how POCUS (Cardiac) findings affect diagnosis.

Example: Moderate probability patient

Pretest probability: 30%

McConnell sign present
LR+ = 10

Post-test probability → ~80–90%

Strongly supports PE diagnosis and high-risk physiology.

Example: Echo normal

LR− ~0.6

Post-test probability drops modestly.

Cannot exclude PE.

CTPA still required.

Most Important ED Clinical Insight

POCUS is not sensitive enough to exclude PE.

highly valuable for identifying dangerous PE.

identifies physiology—not clot.

answers the question:

Is the right ventricle failing?

Not:

Is there a clot?

Highest-Yield Bedside Rule for Emergency Physicians

Presence of ≥2 of the following strongly supports acute PE with RV strain:

• RV dilation
• McConnell sign
• Septal flattening
• TAPSE <1.6 cm
• Elevated RVSP

Post-test probability becomes very high.

Why Classification Matters in the Emergency Department

This classification determines:

• Who can be discharged
• Who requires admission
• Who requires ICU care
• Who requires reperfusion therapy

This decision begins in the emergency department.

Not after admission.

Critical Emergency Medicine Insight

The most dangerous PE is not the hypotensive patient.

It is the normotensive patient with failing RV physiology.

The new A–E classification allows emergency physicians to identify these patients before collapse occurs.

This is the true purpose of classification.

New Insights: Update on diagnosis of hemo-dynamically unstable patient - unstable to shift to CTPA

In hemodynamically unstable patients where computed tomography pulmonary angiography (CTPA) is unsafe or impossible, multi-organ point-of-care ultrasound (POCUS)—combining focused cardiac, lung, and lower limb venous assessment—can support a working diagnosis of pulmonary embolism and guide urgent reperfusion decisions, although it cannot definitively exclude PE.

Focused cardiac ultrasound primarily evaluates for acute right ventricular (RV) pressure overload, with key findings including RV dilation (RV/LV ratio >1), septal flattening (“D-sign”), reduced TAPSE, tricuspid regurgitation, and McConnell’s sign, which demonstrates high specificity (~98.6%) but low sensitivity (~29%) for acute PE (Fields et al., 2017; Falster et al., 2021; Oh & Park, 2023).

Lung ultrasound may identify peripheral pleural-based wedge-shaped infarcts with sensitivity of approximately 80–81% and specificity of 87%, supporting the diagnosis in the appropriate clinical context (Falster et al., 2021; Du et al., 2024; Mohamed et al., 2023). Compression ultrasound demonstrating proximal deep venous thrombosis is highly specific (96–97%) and, when combined with shock and RV strain, strongly supports PE as the cause of hemodynamic instability (Dwyer et al., 2017; Falster et al., 2021).

Importantly, multiorgan POCUS protocols significantly improve diagnostic performance compared with single-organ assessment, achieving sensitivity up to 90% and specificity ranging from 69–86% in critically ill populations (Girardi et al., 2022; Lieveld et al., 2022; Melo et al., 2025).

In unstable patients with high clinical probability and concordant POCUS findings—particularly RV strain with or without confirmed DVT—current evidence supports initiating anticoagulation or thrombolysis when alternative causes of shock have been reasonably excluded (Falster et al., 2021; Oh & Park, 2023).

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More visual explainers and ED-focused pearls are posted there.

Coming Next: Part 2

Part 2 will cover:

• Anticoagulation selection
• Thrombolysis and thrombectomy indications
• ICU vs ward vs discharge decisions
• Monitoring and escalation
• Complications including CTEPH
• Follow-up strategies

All mapped directly to A–E classification.

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References

1. American College of Cardiology/American Heart Association Joint Committee. 2026 AHA/ACC guideline for the diagnosis and management of acute pulmonary embolism. J Am Coll Cardiol. 2026.

2. Fields JM, Davis J, Girson L, et al. Transthoracic echocardiography for diagnosing pulmonary embolism: a systematic review and meta-analysis. J Am Soc Echocardiogr. 2017;30(7):714-723.e4. doi:10.1016/j.echo.2017.03.004

3. Falster C, Jacobsen N, Coman KE, et al. Diagnostic accuracy of focused deep venous, lung, cardiac and multiorgan ultrasound in suspected pulmonary embolism: a systematic review and meta-analysis. Thorax. 2021;77(7):679-689. doi:10.1136/thoraxjnl-2021-216838

4. Girardi AM, Turra E, Loreto M, et al. Diagnostic accuracy of multiorgan point-of-care ultrasound compared with pulmonary CT angiography in critically ill patients with suspected pulmonary embolism. PLoS One. 2022;17(10):e0276202. doi:10.1371/journal.pone.0276202

5. Mohamed H, Farouk N, Elnaeem E, et al. Sensitivity and specificity of chest ultrasound in the diagnosis of pulmonary embolism in the emergency department. Can J Respir Ther. 2023;59:123-129. doi:10.29390/cjrt-2022-065

6. Dwyer KH, Rempell JS, Stone MB. Diagnosing centrally located pulmonary embolisms in the emergency department using point-of-care ultrasound. Am J Emerg Med. 2017;36(7):1145-1150. doi:10.1016/j.ajem.2017.11.033

7. Melo RB, Gioli-Pereira L, Lourenço I, et al. Diagnostic accuracy of multi-organ point-of-care ultrasound for pulmonary embolism in critically ill patients: a systematic review and meta-analysis. Crit Care. 2025;29:59. doi:10.1186/s13054-025-05359-x

8. Lieveld AWE, Heldeweg MLA, Smit JM, et al. Multi-organ point-of-care ultrasound for detection of pulmonary embolism in critically ill patients. J Crit Care. 2022;69:153992. doi:10.1016/j.jcrc.2022.153992