But here’s the uncomfortable truth:

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

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

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

It is only the beginning.

The Post-Intubation Bundle

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

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

2. Are the ventilator settings appropriate?

3. Have I reassessed gas exchange and ventilation?

4. Is the patient comfortable?

5. Have I prevented the next physiologic disaster?

Let’s walk through each.

Step 1: Confirm the Tube — Then Confirm It Again

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

Continuous waveform capnography

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

Waveform capnography is king.

Additional confirmation

After waveform capnography:

• Bilateral chest rise

• Equal breath sounds

• Absence of gastric sounds

• Improvement in oxygenation

• Appropriate ventilator waveforms

Chest X-ray

Once the patient is stabilized:

• Confirm tube depth

• Evaluate for right mainstem intubation

• Look for pneumothorax

• Assess evolving pulmonary pathology

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

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

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

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

Start with the diagnosis

The ventilator settings for:

• Severe asthma

• ARDS

• Septic shock

• Traumatic brain injury

• Diabetic ketoacidosis

are not the same.

Yet many patients receive identical settings.

A practical starting strategy

For most adults:

Mode

• Volume Assist-Control

Tidal Volume

• 6–8 mL/kg predicted body weight

Respiratory Rate

• 16–22 breaths/min

PEEP

• 5 cmH₂O initially

• Higher if hypoxemic

FiO₂

• Start at 100%

• Rapidly titrate down

Avoid oxygen toxicity

After stabilization:

Target:

• SpO₂ 92–96% in most patients

• Avoid prolonged unnecessary FiO₂ 100%

Disease-specific reminders

ARDS

• Low tidal volume ventilation

• 6 mL/kg predicted body weight

• Higher PEEP strategy

Severe Asthma

• Low respiratory rate

• Long expiratory time

• Accept permissive hypercapnia

Traumatic Brain Injury

• Avoid hypoxia

• Avoid severe hypercapnia

• Target normocapnia

Metabolic Acidosis (DKA, Salicylates)

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

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

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

Obtain an ABG

Usually within:
15–30 minutes after intubation

Then ask:

Is oxygenation adequate?

If PaO₂ is excessive: Reduce FiO₂.

If inadequate: Increase PEEP before endlessly increasing oxygen concentration.

Is ventilation adequate?

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

• Increase respiratory rate

• Adjust tidal volume when appropriate

If PaCO₂ is too low:

Reduce minute ventilation.

Repeat when needed

Every ventilator change should trigger reassessment.

The ABG closes the loop between physiology and intervention.

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

Perhaps the most important post-intubation principle:
Sedation should begin immediately after intubation.
(Will release a post soon on this - Post Intubation Sedation)

Many patients receive:

• Induction agent

• Paralytic

and then nothing.

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

Analgesia First

Pain should be treated before sedation whenever possible.

A common strategy:

Fentanyl, Morphine

Then Sedation

Common options:

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

Target a Sedation Goal

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

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

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

A practical target

Most newly intubated ED patients:

• RASS -2 to -3 initially

Then lighten as physiology allows.

Step 5: Anticipate the Post-Intubation Crash

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

Why?
Positive pressure ventilation changes physiology.

Watch for:

Hypotension

Causes:

• Reduced venous return

• Sedatives

• Occult hypovolemia

Management:

• Fluids when appropriate

• Vasopressors early

• Reassess shock state

Auto-PEEP

Particularly in:

• Asthma

• COPD

Look for:

• Rising airway pressures

• Hypotension

• Ventilator dyssynchrony

Pneumothorax

Especially after:

• Trauma

• Difficult ventilation

• High airway pressures

Ventilator Dyssynchrony

A fighting patient is not always “agitated.”

Sometimes they are:

• In pain

• Undersedated

• Air hungry

• Incorrectly ventilated

Treat the cause.

Not just the monitor.

The Tube Is Not the Finish Line

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

It isn’t, It’s a transition.

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

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

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Why Every Exacerbation Matters More Than You Think ?

A patient arrives breathless.

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

For many clinicians, this is another COPD exacerbation.

For GOLD 2026, it is something more important.

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

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

1. COPD Exacerbations Have a Clearer Definition

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

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

It isn’t.

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

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

2. Not Every Breathless COPD Patient Has a COPD Exacerbation

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

Among the most important are:

• Pneumonia

• Pulmonary embolism

• Acute heart failure

• Pneumothorax

• Cardiac ischemia

• Arrhythmias

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

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

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

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

3. GOLD Has Moved Beyond Admission-Based Severity

Traditionally, exacerbation severity was inferred from healthcare utilization.

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

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

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

Severity should be determined by:

• Work of breathing

• Respiratory rate

• Oxygenation

• Hypercapnia

• Accessory muscle use

• Mental status

• Hemodynamic stress

• Response to initial treatment

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

Physiology matters more than location.

4. Early Treatment Remains the Cornerstone

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

Bronchodilators

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

Corticosteroids

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

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

Antibiotics

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

• Increased sputum purulence

• Increased sputum volume

• Increased dyspnea

Five-day treatment courses are generally sufficient.

Methylxanthines

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

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

5. Respiratory Failure Should Be Recognized Before Exhaustion Occurs

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

GOLD continues to strongly support:

• Controlled oxygen therapy

• High-flow oxygen systems when appropriate

• Non-invasive ventilation (NIV)

The evidence remains compelling.

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

The critical challenge is timing. Patients rarely deteriorate suddenly.

Most show warning signs hours beforehand:

• Increasing respiratory rate

• Rising carbon dioxide levels

• Progressive fatigue

• Reduced air movement

• Altered mental status

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

6. The Real Work Begins After Stabilization

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

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

Before transition of care, clinicians should consider:

• Is maintenance therapy optimized?

• Has inhaler technique been assessed?

• Are there adherence barriers?

• Were modifiable triggers identified?

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

• Is appropriate follow-up arranged?

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

What Changed the Most?

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

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

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References

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

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

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

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

By-
Dr Arihant Jain, MD | lifeonthefrontline.com
Instagram: @humans.of.em
X | Linkedin | ORCID
————————

A patient arrives in septic shock. Blood pressure is 72/40 mmHg. The lactate is climbing. Capillary refill is prolonged. The patient needs vasopressors.

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

The assumption is simple:

Central line first. Vasopressors second.

But modern evidence increasingly challenges this approach.

The Cost of Waiting

Shock is fundamentally a disease of inadequate tissue perfusion.

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

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

In other words:

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

Where Did the Fear Come From?

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

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

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

What Does the Modern Evidence Show?

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

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

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

• Extravasation: 1.43%

• Thrombosis: 1.47%

• Infection: 0.72%

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

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

Central Lines Are Not Risk-Free

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

• Pneumothorax

• Hemothorax

• Arterial puncture

• Arterial cannulation

• Major bleeding

• Venous thrombosis

• Catheter-associated bloodstream infections (CLABSI)

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

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

The comparison therefore is not:

Risk versus no risk

It is:

Peripheral risks versus central-line risks.

Does Peripheral Administration Affect Mortality?

The answer appears to be no.

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

Across these studies:

• Mortality was similar

• Clinical effectiveness was similar

• Organ support requirements were similar

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

Another Unexpected Benefit: Fewer Central Lines

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

This translates into:

• Fewer invasive procedures

• Lower CLABSI risk

• Reduced procedural complications

• Lower healthcare costs

Location Matters: Where Should We Place the IV?

Not all peripheral lines are created equal.

Avoid

❌ Hand veins

❌ Wrist veins

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

Use Caution

⚠️ Antecubital fossa

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

Preferred Sites

✅ Mid-forearm veins

✅ Basilic vein

✅ Cephalic vein

✅ External jugular vein

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

Monitoring Is More Important Than the Catheter

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

It is vigilance. Evidence-based recommendations emphasize:

• Dedicated vasopressor line

• Frequent site inspection

• Documentation of catheter location

• Verification of patency

• Assessment at the start of every nursing shift

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

How Long Can Peripheral Vasopressors Be Used?

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

Traditionally many institutions restricted peripheral vasopressors to 24 hours.

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

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

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

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

How Much Vasopressor Can Be Given Peripherally?

There is currently no universally accepted upper dose limit.

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

Norepinephrine

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

Phenylephrine

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

Epinephrine

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

Vasopressin

Up to 0.08 units/min

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

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

What If Extravasation Occurs?

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

The severity ranges from:

Grade 1

Minor swelling or leakage

Grade 2

Localized tissue injury

Grade 3–4

Progressive ischemia, tissue compromise, or necrosis

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

Immediate Management of Extravasation

Step 1

Stop the infusion immediately.

Step 2

Leave the catheter in place.

Step 3

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

Step 4

Outline and photograph the affected area.

Step 5

Document the event thoroughly.

Step 6

Administer antidotes when indicated.

For catecholamine vasopressors:

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

For vasopressin extravasation:

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

Step 7

Monitor progression closely.

Grade 3–4 injuries warrant early surgical consultation.

The goal is simple:

Document. Learn. Improve. Prevent recurrence.

Where Do We Go From Here?

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

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

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References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

“Why are you giving him this yellow fluid?”

“He has a blood disease.”

“He needs blood.”

“No one is listening to me.”

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

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

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

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

This grandmother had become everything for that child.

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

Whenever her grandson became weak, he needed blood.

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

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

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

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

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

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

They are human.

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

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

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

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

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

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

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

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

Pulse Checks and Reflection

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

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

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

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

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

And then suddenly—

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

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

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

It is called CPR-Induced Consciousness (CPRIC).

What Exactly Is CPR-Induced Consciousness?

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

Patients may demonstrate:

• Eye opening

• Purposeful limb movement

• Following commands

• Speech or vocalization

• Agitation or resistance to CPR

• Emotional expression or pain response

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

In other words:

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

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

How Common Is It?

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

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

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

Even more striking:

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

The phenomenon is no longer rare enough to ignore.

Why Does It Happen?

The physiology behind CPRIC challenges traditional assumptions about cardiac arrest.

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

• circulation absent

• consciousness impossible

But modern resuscitation science paints a far more nuanced picture.

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

The AWARE-II Study

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

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

CPRIC May Actually Signal Better Survival

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

Multiple studies have shown associations between CPRIC and:

• higher ROSC rates

• better survival to discharge

• witnessed arrests

• shockable rhythms

• early CPR initiation

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

This makes intuitive sense.

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

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

The Psychological Reality Nobody Talks About

For providers, CPRIC can be profoundly unsettling.

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

Some providers report:

• hesitation to continue compressions

• emotional distress

• confusion about stopping CPR

• intrusive recollections after the event

• insomnia or mood changes afterward

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

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

The ethical discomfort is enormous.

But perhaps the more important question is:

What does the patient experience?

Research suggests some survivors retain memories during resuscitation.

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

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

This forces us to confront a difficult possibility:

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

The Sedation Dilemma

And this is where resuscitation medicine enters ethically uncharted territory.

Should conscious patients during CPR receive sedation?

Current practice varies wildly.

Reported approaches include:

• ketamine

• fentanyl

• midazolam

• physical restraint

• combinations of the above

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

But there is a major problem:

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

So clinicians face competing priorities:

• relieve suffering

• preserve cerebral perfusion

• avoid interrupting CPR

• maintain team safety

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

CPRIC Is Forcing a Redefinition of Death

Historically, consciousness and pulse were inseparable.

CPRIC breaks that framework.

A patient can:

• have no pulse

• meet criteria for cardiac arrest

• yet still demonstrate awareness

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

Perhaps cardiac arrest is not a singular event.

Perhaps it is a process.

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

What Needs to Happen Next?

The literature is clear on one thing:

We are only at the beginning of understanding CPRIC.

Future priorities must include:

• standardized definitions

• international reporting systems

• sedation algorithms

• EEG and perfusion studies

• survivor psychological follow-up

• provider debriefing frameworks

• ethical guidance for conscious resuscitation

Because CPRIC is no longer an isolated curiosity.

It is now a legitimate frontier in resuscitation science.

Final Thoughts

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

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

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

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

And perhaps the most important question is no longer:

“Can consciousness occur during CPR?”

But rather:

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

In Summary:
What CPR-Induced Consciousness Really Means

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

What Positive Things Does CPRIC Indicate?

Current evidence suggests CPRIC is often associated with:

• High-quality CPR

• Better cerebral perfusion during compressions

• Early recognition and treatment of arrest

• Witnessed cardiac arrest

• Shockable rhythms

• Higher likelihood of ROSC and survival

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

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

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

What Negative Consequences Can It Lead To?

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

For the Patient

• Potential pain and distress during compressions

• Awareness of invasive procedures

• Psychological trauma

• Possible PTSD, depression, or recalled traumatic experiences

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

For the Resuscitation Team

• Hesitation to continue CPR

• Increased interruptions in compressions

• Emotional distress among providers

• Ethical uncertainty regarding sedation and restraint

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

For Systems of Care

• Lack of protocols

• Inconsistent sedation practices

• No universally accepted international guidelines

• Poor documentation and underreporting

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

So What Is the Way Forward?

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

1. Recognize and confirm CPRIC Early

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

Stopping compressions repeatedly for pulse checks may worsen outcomes.

2. Prioritize Uninterrupted High-Quality CPR

The primary objective remains:

• effective compressions

• defibrillation when indicated

• reversible cause management

CPRIC should not distract from core resuscitation priorities.

3. Develop Structured Sedation Protocols

Sedation may become necessary when:

• CPR is interrupted

• defibrillation becomes unsafe

• patient agitation compromises resuscitation

But future protocols must balance:

• patient comfort

• cerebral perfusion

• hemodynamic effects

• provider safety

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

4. Introduce Team Debriefing and Psychological Support

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

Formal debriefing should become part of post-resuscitation care.

5. Expand Research Aggressively

The next decade of resuscitation science should focus on:

• EEG-guided CPR research

• cerebral perfusion monitoring

• sedation trials during CPR

• long-term neuropsychological outcomes

• ethical frameworks for conscious cardiac arrest

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

6. Avoid Premature Termination of Resuscitation

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

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

• CPRIC is present,

• high-quality CPR is ongoing,

• and the patient remains within an active resuscitation pathway.

A practical approach may be to:

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

• reassess rhythm, physiology, and reversible causes systematically,

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

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

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

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References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

“She had finally won.”

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

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

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

No metabolically active lesion.

Her PET-CT showed remission.

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

The scan date was given three days later.

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

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

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

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

The venous blood gas returned:

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

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

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

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

Most textbooks make the next step sound straightforward.

“Give thrombolysis.”

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

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

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

The conversation.

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

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

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

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

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

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

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

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

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

This is why Emergency Medicine exists.

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

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

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

That someone is the Emergency Physician.

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

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

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

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

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

Our first instinct is always the same:

Stabilize.
Resuscitate.
Buy time for life.

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

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

“Thank you, doctor.”

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

Not glamour.
Not heroism.
Not dramatic television scenes.

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

Because salvageable patients do not always reach ideal systems.

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

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

This is where Emergency Medicine comes in.

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

Sometimes, before death.

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

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

A – Air & oxygenation

B – Blood pressure & hemodynamics

C – Contingency plans

D – Decision & drug modulation

E – Execution & rescue

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

Would love to hear thoughts and feedback from the group.

Link to original paper

It was 2:30 AM in the Emergency Department.

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

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

The procedure went smoothly.

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

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

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

“Doctor… there’s a pneumothorax.”

Suddenly, the room shifted.

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

But this wasn’t that kind of pneumothorax.

This was pneumothorax ex vacuo.

The Diagnostic Trap in the ED

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

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

• Comfortable

• Hemodynamically stable

• Improved dyspnea

• No worsening hypoxia

• No respiratory distress

The physiology and the radiology were telling different stories.

That mismatch matters.

What Actually Happened?

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

The real problem is an unexpandable lung.

Usually this happens because of:

• Malignant pleural disease

• Trapped lung from chronic inflammation

• Endobronchial obstruction

• Visceral pleural restriction

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

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

So What Should We Actually Do?

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

The ideal management depends on one simple principle:

Treat the patient, not the radiograph.

If the patient is:

• Hemodynamically stable

• Maintaining oxygenation

• Clinically improving after thoracentesis

• Without signs of tension physiology

…then the best treatment is often:

Observation.

Not another procedure.

Not reflex chest tube insertion.

Not panic.

Why Observation Is Usually Better

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

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

• Persistent air leak

• Procedural pain

• Infection risk

• Repeated interventions

• Prolonged hospitalization

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

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

Then What Is the Treatment?

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

Depending on the etiology, management may involve:

1. Treating Endobronchial Obstruction

If due to a central airway lesion:

• Bronchoscopy

• Tumor debulking

• Stenting

• Oncology-directed therapy

may allow lung re-expansion.

2. Managing Malignant Trapped Lung

In malignant disease:

• Indwelling pleural catheter

• Symptom-guided drainage

• Palliative management

are often more appropriate than repeated thoracenteses.

3. Surgical Decortication

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

• VATS decortication

• Surgical pleural peel removal

may restore lung expansion.

But this is rarely an ED decision.

4. Supportive Care

Most ED patients only need:

• Observation

• Oxygen if required

• Monitoring

• Repeat imaging only if clinically indicated

• Specialty follow-up

And often, reassurance.

When Should We Worry?

Observation is appropriate only if the patient remains clinically stable.

Red flags that should prompt reconsideration include:

• Worsening respiratory distress

• Hemodynamic instability

• Progressive hypoxia

• Rapid enlargement on imaging

• Features suggestive of true procedural lung injury

Because not every post-thoracentesis pneumothorax is ex vacuo.

Clinical context matters.

The Ultrasound Era

Traditionally, any pneumothorax after thoracentesis was considered procedural injury.

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

Not all post-procedure pneumothoraces are created equal.

And that distinction changes management entirely.

Pulse Checks and Reflections

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

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

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

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

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

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

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

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

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

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

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

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

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

Not:
“You’re wrong.”

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

That is not disrespect.
That is safe medicine.

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

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

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

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

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

It is to the patient.

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References

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

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

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

Recently, I watched Michael.

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

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

Can mean completely different things to two different people.

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

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

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

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

And maybe outside medicine too, we forget this often.

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

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

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

- Dr Arihant Jain, MD

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

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

And the dangerous part is this:

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

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

Heat Illness Is a Spectrum

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

The spectrum includes:

• Heat rash

• Heat edema

• Heat cramps

• Heat syncope

• Heat exhaustion

• Heat stroke

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

The Physiology: Why the Body Fails

The human body normally dissipates heat through:

• Evaporation

• Radiation

• Convection

• Conduction

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

Once environmental temperature approaches body temperature:

• Sweat evaporation becomes inadequate

• Peripheral vasodilation worsens hypotension

• Cardiac output becomes strained

• Splanchnic perfusion decreases

• Cellular proteins begin to denature

• Cytokine-mediated inflammation escalates

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

This is not simply “fever.”

It is:

• Cellular injury

• Endothelial dysfunction

• Coagulopathy

• Organ ischemia

• Metabolic collapse

The Most Important Clinical Distinction

Heat Exhaustion vs Heat Stroke

This distinction matters enormously.

Heat Exhaustion

Patients may present with:

• Weakness

• Heavy sweating

• Nausea

• Tachycardia

• Dizziness

• Syncope

• Muscle cramps

Core temperature is usually:

• <40°C

Mental status remains largely preserved.

Thermoregulation still functions (Wexler, 2002).

Heat Stroke

Heat stroke is defined by:

• Core temperature ≥40°C (104* F)

• CNS dysfunction

(CorePendium, 2025).

Central nervous system dysfunction is the hallmark.

This may include:

• Irritability

• Ataxia

• Delirium

• Confusion

• Seizures

• Coma

Once CNS dysfunction appears in the setting of hyperthermia:

Assume heat stroke until proven otherwise.

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

Exertional vs Classic Heat Stroke: Same Endpoint, Different Patient

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

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

Exertional Heat Stroke (EHS)

EHS typically occurs in:

• Athletes

• Military recruits

• Outdoor laborers

• Young healthy individuals performing intense physical activity

The mechanism is:

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

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

Clinically, EHS patients often:

• Continue sweating

• Develop profound rhabdomyolysis

• Have severe metabolic acidosis

• Show higher rates of acute kidney injury

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

This is why sports medicine and military protocols emphasize:

“Cool first, transport second.”

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

Classic / Non-exertional Heat Stroke (CHS)

Classic heat stroke typically affects:

• Elderly individuals

• Infants and young children

• Patients with chronic illness

• Socially isolated individuals

• Patients during prolonged heat waves

The trigger is usually:

Passive environmental heat exposure combined with impaired thermoregulation.

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

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

• Altered mental status

• Hot dry skin

• Cardiovascular collapse

• Delayed recognition

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

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

• Sepsis

• Stroke

• Toxicologic emergencies

• Delirium

• CNS infection

This diagnostic delay contributes significantly to poor outcomes.

The Patients We Commonly Miss

Heat stroke is not limited to athletes.

Classic heat stroke often affects:

• Elderly patients

• Socially isolated individuals

• Psychiatric patients

• Patients without access to cooling

• Individuals on anticholinergics, neuroleptics, or sympathomimetics

(CorePendium, 2025).

Exertional heat stroke affects:

• Athletes

• Military personnel

• Outdoor workers

• Laborers using heavy protective equipment

Importantly:

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

The ED Approach: Think Fast, Cool Faster

1. Airway & Breathing

Airway management follows standard indications.

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

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

If intubation is required:

• Rocuronium is preferred

• Benzodiazepines are useful for seizure control and sedation

2. Circulation

These patients are profoundly volume depleted.

Start with:

• 1–2 L isotonic crystalloids

• Frequent reassessment

(CorePendium, 2025).

But remember:
Not all hypotension is dehydration alone.

Peripheral vasodilation, systemic inflammation, and myocardial injury all contribute to shock physiology.

Myocardial injury occurs in up to 21% of patients and may precipitate arrhythmias or cardiac arrest (CorePendium, 2025).

Cooling Is the Definitive Treatment

Not antibiotics.
Not vasopressors.
Not antipyretics.

Cooling.

Rapid cooling is the single most important intervention in heat stroke (Barletta et al., 2025).

And critically:

Cooling should begin immediately — even before the full workup is complete.

(CorePendium, 2025).

Cold Water Immersion: The Gold Standard

Among all cooling modalities:

Cold water immersion remains the fastest and most effective.

Preferred water temperature:

• 1–17°C

Evidence consistently demonstrates:

• Faster core temperature reduction

• Better neurologic outcomes

• Lower mortality

This is especially true in exertional heat stroke (Douma et al., 2020; Pryor et al., 2015).

Modern ED adaptations include:

• Ice-water body bags

• Portable immersion setups

• Athletic event cooling stations

The old concern regarding shivering and peripheral vasoconstriction should not delay immersion therapy. Benefits far outweigh risks (CorePendium, 2025).

If Immersion Is Not Possible

Evaporative cooling remains an effective alternative.

Technique:

1. Remove clothing

2. Spray tepid water

3. Apply high-flow fans

(CorePendium, 2025).

Additional adjuncts:

• Ice sheets

• Rotating ice towels

• Whole-body ice packs

• Cooling blankets

• Cold IV fluids

But cold IV fluids alone are insufficient (Smith, 2005).

A Common Pitfall: Waiting for “True” Hyperthermia

One of the most dangerous delays occurs when clinicians wait for temperatures above 40°C before initiating cooling.

In altered hyperthermic patients, cooling should not be delayed even if the measured temperature is below 40°C.

Why?

Because:

• Temperatures continue rising

• Prehospital cooling may transiently reduce readings

• Delay worsens organ injury

Clinical suspicion matters more than exact numbers.

What Should NOT Be Used

Antipyretics:

• Paracetamol

• NSAIDs

have no role.

Dantrolene also lacks evidence of benefit (Barletta et al., 2025).

Heat stroke is not a hypothalamic set-point problem like infectious fever.

Using antipyretics may actually worsen hepatic and renal injury (Glazer, 2005).

The Organ Damage We Must Anticipate

Heat stroke is a multiorgan disease.

Clinicians should actively monitor for:

• Rhabdomyolysis

• Hyperkalemia

• Acute kidney injury

• Liver injury

• DIC

• ARDS

• Cardiac dysrhythmias

CK >5,000 U/L suggests significant muscle injury.
CK >16,000 U/L correlates with higher renal failure risk (CorePendium, 2025).

AST >1000 is associated with mortality (CorePendium, 2025).

Importantly:
Coagulopathy often worsens over 24–72 hours, meaning initially stable patients can deteriorate later (Savioli et al., 2022).

Disposition: Do Not Underestimate Heat Stroke

Most minor heat illnesses can safely be discharged after observation and symptom improvement.

But:

All heat stroke patients require admission.

Usually ICU admission.

(CorePendium, 2025).

Why?
Because end-organ injury may evolve hours after initial stabilization.

Prevention: The Most Effective Treatment

Heat illness is largely preventable.

Final Thoughts

Heat-related emergencies are increasing worldwide.

For clinicians, the priorities are remarkably simple:

1. Recognize early

2. Measure core temperature

3. Cool aggressively

4. Anticipate organ failure

5. Monitor beyond apparent recovery

Because in heat stroke:

Time to cooling determines outcome.

And often:

Cooling itself is the lifesaving intervention.

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References

• Adapted from CorePendium chapter on Heat Related Emergencies by Cindy Bitter and team.

• Barletta J et al. (2024). Management of Heat-Related Illness and Injury in the ICU. Critical Care Medicine.

• Barletta J et al. (2025). SCCM Guidelines for the Treatment of Heat Stroke. Critical Care Medicine.

• Bein T. (2023). Pathophysiology and management of heat illness.

• Douma M et al. (2020). Cooling techniques for heat stroke. Resuscitation.

• Gauer R & Meyers B. (2019). Heat-Related Illnesses. American Family Physician.

• Glazer J. (2005). Management of heatstroke and heat exhaustion.

• Pryor R et al. (2015). Exertional Heat Illness. Prehospital and Disaster Medicine.

• Roberts W et al. (2021). ACSM Consensus on Exertional Heat Illness. Current Sports Medicine Reports.

• Savioli G et al. (2022). Heat-Related Illness in Emergency and Critical Care. Biomedicines.

• Smith J. (2005). Cooling methods used in exertional heat illness.

• Sorensen C & Hess J. (2022). Treatment and Prevention of Heat-Related Illness. NEJM.

Dr Arihant Jain, MD | lifeonthefrontline.com
Instagram: @humans.of.em
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PART 1 — Understanding Diuretic Resistance

The problem

Loop diuretics are the cornerstone of decongestion—yet:

• 20–30% of patients fail to respond adequately

• Associated with longer hospital stay, ICU need, and mortality

What is Diuretic Resistance?

Failure to achieve negative sodium and fluid balance despite adequate dosing

• Often misdiagnosed

• Many cases are actually a result of:

  • Under-dosing

  • Poor drug delivery

  • Wrong physiology

PART 2 — Mechanisms of Diuretic Resistance

(This is the key to everything that follows)

Diuretic resistance is multifactorial, driven by 3 major pathways:

1️⃣ Pharmacokinetic Failure (Drug never reaches kidney)

• Gut edema → ↓ oral absorption

• Low cardiac output → ↓ renal perfusion

• High CVP → renal congestion

• Hypoalbuminemia → altered drug delivery

👉 Result: insufficient drug at site of action

2️⃣ Tubular Adaptation (“Nephron fights back”)

• Chronic loop use → distal nephron hypertrophy

• ↑ Na-Cl cotransporter (NCC)

• ↑ ENaC activity

👉 Result: distal sodium reabsorption overrides loop effect

3️⃣ Neurohormonal Activation (“Body wants sodium”)

• RAAS activation

• Sympathetic activation

• Vasopressin

👉 Creates a state of “basal sodium avidity”
👉 Kidney is primed to retain sodium despite diuretics

The Forgotten Player — Chloride

• Hypochloremia → activates WNK kinases

• ↑ Sodium reabsorption

• ↓ Diuretic response

👉 Diuretics worsen chloride depletion → vicious cycle

Diuretic resistance is NOT just “need more dose”
It’s a mismatch between drug, kidney, and physiology

Read further about pathophysiology behind Diuretic Resistance here

PART 3 — How to Monitor Diuretic Therapy in ED

(Where most clinicians go wrong)

❌ What NOT to rely on:

• Weight

• Fluid balance charts

• “Urine looks good”

👉 These do NOT reflect sodium removal

✅ What actually matters:

1. Urinary Sodium (U. Na+) — THE GOLD STANDARD

⏱ Check 1–2 hours after IV diuretic

• >70 mmol/L → Adequate response

• <50–70 mmol/L → Resistance

👉 This predicts response before clinical deterioration

2. Urine Output

• Target: >100–150 mL/hour (first 6 hours)

3. Bedside Ultrasound

• Lung B-lines → pulmonary congestion

• VExUS → systemic venous congestion

Dynamic Monitoring with all 3 adjuncts.

Assess → Adjust → Reassess every 2–6 hours

Not next morning. Not after ward transfer.

PART 4 — The Shift: Phenotype-Based Diuretic Therapy

Same drug. Same dose. Different patients → different failures.

👉 That’s because different mechanisms dominate in different phenotypes

PHENOTYPE 1 — RIGHT HEART FAILURE

“Venous congestion is the problem”

🔬 Mechanism

• ↑ CVP → renal congestion

• ↓ renal perfusion gradient

• ↓ drug delivery

Strategy

• Aggressive decongestion (even if borderline BP)

• Higher loop doses

• Early combination therapy

If low output:

• Add inotropes (dobutamine/milrinone)

• Use norepinephrine if hypotensive

👉 Decongestion improves renal function

PHENOTYPE 2 — ADVANCED CKD

“Delivery + tubular resistance”

Mechanism

• ↓ tubular secretion

• Chronic sodium retention

• Distal nephron adaptation

Strategy

• Use higher loop doses (expected)

• Prefer IV route

Early add-ons:

• Acetazolamide → if metabolic alkalosis

• Thiazide → if chronic loop use

👉 Sequential nephron blockade is essential

Critical points:

• Correct chloride

• Accept mild creatinine rise

PHENOTYPE 3 — OBESITY

“Hidden congestion + neurohormonal activation”

Mechanism

• Adipose tissue → RAAS + SNS activation

• ↑ plasma volume

• ↑ intra-abdominal pressure → ↓ renal perfusion

Strategy

• Assume underestimated congestion

• Use higher doses early

• Early combination therapy

Add:

• SGLT2 inhibitors (if appropriate)

Clinical pearl

BNP & exam are unreliable → rely on physiology

PHENOTYPE 4 — ELDERLY / FRAIL

“Balance between diuresis and harm”

Mechanism

• Altered pharmacokinetics

• ↓ renal reserve

• High vulnerability

Strategy

• Gradual decongestion

• Close monitoring

Use:

• Urine output

• UNa

• Ultrasound

Goal:

👉 Not aggressive fluid removal
👉 Stable euvolemia + preserved function

Putting It All Together (ED Algorithm)

Based on :-

1. Aletras G, Bachlitzanaki M, Stratinaki M, Foukarakis E, Petrakis I, Pantazis Y, Hamilos M and Stylianou K (2026) Diuretic resistance in cardiorenal syndrome: mechanisms, monitoring and phenotype-tailored management. Front. Cardiovasc. Med. 12:1731305. doi: 10.3389/fcvm.2025.1731305
   
   

FINAL TAKEAWAY

Diuretic resistance is not about the drug.
It is about which physiological barrier is dominant.

When you:

• Monitor early

• Identify mechanism

• Treat phenotype

👉 Diuretics start working again.

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The problem with “normal vitals”

A 58-year-old man walks into the ED with chest pain.
Blood pressure? Normal. Oxygen saturation? Normal.

Another patient arrives with unilateral weakness — airway intact, breathing fine.

If we rely only on physiology…
both might wait.

And that’s exactly where triage fails.

Triage is not just numbers

Traditional triage systems often lean heavily on physiology.

But patients don’t present as numbers.

They present as:

• Complaints

• Patterns

• First impressions

• Time-sensitive risks

👉 The dangerous truth:
Some of the sickest patients look deceptively stable early (Rauniyar et al., 2025 )

The ATP backbone — necessary, but not sufficient

The AIIMS Triage Protocol (ATP) gives us:

• A simple Red–Yellow–Green system

• A physiology-first approach

• A validated framework in Indian EDs (Singh et al., 2022 )

And it works.

But not completely.

Because:

• Early ACS may have normal vitals

• Stroke may not trigger physiologic alarms

• GI bleed or poisoning may evolve silently

👉 Physiology detects instability — not always risk.

What actually improves triage?

A better model emerges when we stop thinking in silos.

Triage should integrate four simultaneous lenses:

1. Visual impression

“Does this patient look sick?”

Before monitors. Before scores.

• Gasping

• Seizing

• Pale, diaphoretic

• “Something is off”

👉 A simple clinical assessment can outperform structured triage in predicting mortality (Iversen et al., 2019 )

2. Physiology (ATP)

Still the backbone.

• Airway compromise

• Hypoxia

• Shock

• Low GCS

👉 ATP remains a validated triage framework in LMIC settings (Sahu et al., 2020 )

3. Time-critical diagnoses

Some conditions are dangerous not because of current vitals…
…but because delay kills.

• Stroke

• Acute coronary syndrome

• Major trauma

• Sepsis

• GI bleed

• Poisoning

👉 These are triage diagnoses, not final diagnoses.

But this concept goes beyond traditional medical emergencies.

In many systems, certain conditions are prioritized because early intervention is time-dependent, even when vitals are normal:

• Sexual assault survivors (urgent forensic + medical care)

• Needle-stick injuries in healthcare workers (time-sensitive prophylaxis)

• Testicular or ovarian torsion (time-dependent organ salvage)

👉 These patients may look stable.
👉 Their vitals may be normal.

But delay here is harmful.

Not all Red patients are unstable.
Some are simply time-critical.

4. High-risk chief complaints

Patients arrive with complaints — not diagnoses.

Evidence shows chief complaints independently predict mortality, even after adjusting for vitals (Rice et al., 2020 )

Local AIIMS data further refines this:

• Shortness of breath

• Altered mental status

• Hematemesis

• Fall from height

• Unilateral weakness

• Chest pain

👉 Combining ATP + high-risk complaints
significantly improves predictive accuracy (Rauniyar et al., 2025 )

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Dr Arihant Jain, MD
lifeonthefrontline.com
Instagram: @humans.of.em
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The integrated triage algorithm

This is the shift:

From single-axis triage → multi-layered triage

⚠️ The most dangerous patient in the ED

Is not the one who is crashing.

It is the one who:

• Looks stable

• Has “normal vitals”

• Is quietly evolving

🤖 Where does AI fit in?

AI is promising — but not ready to replace clinicians.

It may help:

• Predict deterioration

• Identify hidden risk patterns

• Support triage decisions

But current systems face challenges of validation, interpretability, and implementation (Petrella, 2024 )

👉 Triage remains clinician-led.

AI in Emergency Department Triage: What the Research Shows

Artificial intelligence is increasingly being explored to improve triage accuracy, detect deterioration early, and reduce ED burden.

📈 Performance and accuracy

Multiple studies show machine learning models outperform traditional triage systems:

• AUROC ~0.82–0.92 vs 0.69–0.80 for standard tools (Raita et al., 2019; Goto et al., 2019; Kang et al., 2020; Yun et al., 2021; Grant et al., 2024)

• Improved admission prediction and risk stratification (Hong et al., 2018; Lee et al., 2021)

Advanced models using NLP + multimodal data further enhance prediction and early deterioration detection (Porto, 2024; Choi et al., 2024; Chai et al., 2024)

👉 AI can reduce mis-triage and improve efficiency, though real-world impact remains limited (Abdalhalim et al., 2025; Yi et al., 2024; Kim et al., 2025; Boonstra & Laven, 2022)

🤖 LLMs and chatbot triage

• GPT-4 shows high agreement with emergency specialists in controlled settings (Paslı et al., 2024)

• But general chatbots show dangerous under-triage rates and are unsafe independently (Halwani et al., 2025; Tortum & Kaşali, 2024)

⚠️ Limitations and risks

• Bias, calibration issues, lack of external validation

• Over- and under-triage risks

• Workflow integration challenges

• Explainability concerns

👉 AI is best viewed as decision support, not replacement (Petrella, 2024 ; Porto, 2024; Yi et al., 2024)

Human + AI = the future

AI can:

• Improve accuracy

• Reduce workload

• Support decisions

But triage remains fundamentally clinical, contextual, and human-driven

The takeaway

Use ATP as the backbone.
Upgrade using visual concern, time-critical diagnoses, and high-risk complaints.

Because triage is not a label.

It is a dynamic clinical decision.

Final thought

The question is not:

“What are the vitals?”

The real question is:

“Who should never be allowed to wait?”

References (AMA Style)

1. Rice B, Leanza J, Mowafi H, et al. Defining high-risk emergency chief complaints: data-driven triage for low- and middle-income countries. Acad Emerg Med. 2020;27:1291–1301.

2. Petrella RJ. The AI future of emergency medicine. Ann Emerg Med. 2024;84:139–153.

3. Sahu AK, Bhoi S, Aggarwal P, et al. AIIMS triage protocol (ATP) of a busy ED. J Emerg Trauma Shock. 2020.

4. Rauniyar N, Sahu AK, Gopinath B, et al. Association of presenting complaint at triage with 72-h mortality and ICU admission. J Emerg Trauma Shock. 2025;18:62–68.

5. Singh SK, Sahu AK, Kumar A, et al. Prospective validation of a novel triage system developed in a middle-income country—AIIMS triage protocol. J Emerg Trauma Shock. 2022;15:124–127.

6. Iversen AKS, Kristensen M, Østervig RM, et al. A simple clinical assessment is superior to systematic triage in prediction of mortality in the emergency department. Emerg Med J. 2019;36:66–71.

7. Raita Y, Goto T, Faridi MK, Brown DFM, Camargo CA Jr, Hasegawa K. Emergency department triage prediction of clinical outcomes using machine learning models. Crit Care. 2019;23:64.

8. Goto T, Camargo CA Jr, Faridi MK, Freishtat RJ, Hasegawa K. Machine learning–based prediction of clinical outcomes for children during emergency department triage. JAMA Netw Open. 2019;2(1):e186937.

9. Kang DY, Cho KJ, Kwon O, et al. Artificial intelligence algorithm to predict the need for critical care in prehospital emergency medical services. Scand J Trauma Resusc Emerg Med. 2020;28:17.

10. Yun H, Choi J, Park J. Prediction of critical care outcomes for adult patients presenting to the emergency department using initial triage information: an XGBoost algorithm analysis. JMIR Med Inform. 2021;9(6):e30770.

11. Grant L, Diagne M, Aroutiunian R, et al. Machine learning outperforms the Canadian Triage and Acuity Scale (CTAS) in predicting need for early critical care. Can J Emerg Med. 2024;27:43-52.

12. Hong WS, Haimovich AD, Taylor RA. Predicting hospital admission at emergency department triage using machine learning. PLoS One. 2018;13(7):e0201016.

13. Lee JH, Hsieh CC, Lin CC, Lin YK, Kao CC. Prediction of hospitalization using artificial intelligence for urgent patients in the emergency department. Sci Rep. 2021;11:98961.

14. Porto B. Improving triage performance in emergency departments using machine learning and natural language processing: a systematic review. BMC Emerg Med. 2024;24:113.

15. Choi A, Lee K, Hyun H, et al. A novel deep learning algorithm for real-time prediction of clinical deterioration in the emergency department for a multimodal clinical decision support system. Sci Rep. 2024;14:80268.

16. Chai C, Peng S, Zhang R, Li C, Zhao Y. Advancing emergency department triage prediction with machine learning to optimize triage for abdominal pain surgery patients. Surg Innov. 2024;31:583-597.

17. Abdalhalim A, Ahmed S, Ezzelarab A, et al. Clinical impact of artificial intelligence-based triage systems in emergency departments: a systematic review. Cureus. 2025;17:e85667.

18. Yi N, Baik D, Baek G. The effects of applying artificial intelligence to triage in the emergency department: a systematic review of prospective studies. J Nurs Scholarsh. 2024;57:105-118.

19. Kim S, Nam S, Lee J. Artificial intelligence in emergency department triage: a scoping review on workload reduction and patient safety enhancement. J Korean Biol Nurs Sci. 2025;25:45.

20. Boonstra A, Laven M. Influence of artificial intelligence on the work design of emergency department clinicians: a systematic literature review. BMC Health Serv Res. 2022;22:807.

21. Paslı S, Sahin A, Beşer M, et al. Assessing the precision of artificial intelligence in emergency department triage decisions: insights from a study with ChatGPT. Am J Emerg Med. 2024;78:170-175.

22. Halwani M, Merdad G, Almasre M, et al. Predicting triage of pediatric patients in the emergency department using machine learning approach. Int J Emerg Med. 2025;18:61.

23. Tortum F, Kaşali K. Exploring the potential of artificial intelligence models for triage in the emergency department. Postgrad Med. 2024;136:841-846.

24. Nasser L, McLeod SL, Hall J. Evaluating the reliability of a remote acuity prediction tool in a Canadian academic emergency department. Ann Emerg Med. 2024.

25. Petrica A, Marza A, Bârsac C, et al. Artificial intelligence in emergency department triage: perspective of human professionals. Front Digit Health. 2026;5:1693060.

26. Piliuk K, Tomforde S. Artificial intelligence in emergency medicine: a systematic literature review. Int J Med Inform. 2023;180:105274.

A 58-year-old patient with a tracheostomy, in ED, is on:

• High-flow oxygen via T-piece

• Flow: 15 L/min

Over the next 12 hours, you notice:

• Increasingly thick secretions

• Frequent suctioning

• Rising airway pressures

• Intermittent desaturation

👉 The setup seems “adequate” — oxygen is being delivered.
👉 But is something fundamentally wrong?

❗ The Hidden Problem

Yes — this patient is receiving high-flow dry gas.

• The upper airway has been bypassed (tracheostomy)

• The natural system for:

  • Heating

  • Humidification
    is completely lost

And now:

• You are delivering high flow + dry oxygen directly into the trachea

👉 This is not just suboptimal — it is physiologically harmful

Why This Happens (Link to Physiology)

Under normal conditions:

• Inspired air reaches 37°C, 100% RH, ~44 mg/L AH at the Isothermic Saturation Boundary (ISB)

• Located ~5 cm below the carina (Al Ashry & Modrykamien, 2014)

But in this patient:

• No nasal conditioning

• No pharyngeal humidification

• No heat exchange

➡️ ISB shifts distally
➡️ Lower airway forced to compensate (which it cannot adequately do)

Consequences You Are Seeing

• Thick, inspissated secretions

• Mucociliary dysfunction

• Increased airway resistance

• Risk of tube blockage

• Atelectasis

(Re et al., 2024; Al Ashry & Modrykamien, 2014)

The Core Question

👉 Are you delivering oxygen… or are you delivering injury?

Transition to Concept

This scenario highlights a fundamental truth:

Oxygen therapy is not just about FiO₂ — it is about gas conditioning

To understand this, we need to revisit:

• Absolute vs Relative Humidity

• Temperature–humidity relationship

• The Isothermic Saturation Boundary

…and how these principles dictate device selection across oxygen therapy, NIV, and ventilation

1. Fundamental Physiology

Absolute vs Relative Humidity

Absolute humidity (AH) is the mass of water vapor present in a given volume of gas (mg H₂O/L) and represents the true water delivered to the airway.

Relative humidity (RH) is the ratio of actual water content to the maximum possible at that temperature, expressed as a percentage.

A key physiological principle:

• ↑ Temperature → ↑ water-carrying capacity → ↓ RH

• ↓ Temperature → ↑ RH → → condensation beyond saturation

This explains condensation (“rainout”) in ventilator circuits, where cooling of saturated gas leads to water deposition (Re et al., 2024).

Isothermic Saturation Boundary (ISB)

The ISB is the point where inspired gas reaches:

• 37°C

• 100% RH

• ~44 mg/L AH (BTPS)

Normally located ~5 cm below the carina (Al Ashry & Modrykamien, 2014).

Clinical Relevance of ISB Shift

Bypassing upper airway (ETT, tracheostomy, high flows) → ISB shifts distally → lower airway exposed to dry gas →

• Mucociliary dysfunction

• Thick secretions

• Increased airway resistance

• Atelectasis

2. Translating Physiology → Targets

3. Device Selection Across Respiratory Support

A. Low-Flow Oxygen

• Usually no humidification needed

• Add if prolonged or >4–5 L/min

🔧 Bubble humidifier

• Gas bubbled through water (low efficiency)

• Limited AH delivery

(Concept illustrated in humidifier types, Al Ashry & Modrykamien, 2014)

B. High-Flow Nasal Oxygen (HFNC)

• High flows overwhelm native humidification

🔧 Heated active humidifier (passover type)

• Heated circuit prevents cooling

Based on Figure 1 concept (heated humidifier + condensation):

• Gas leaves fully saturated

• Cooling → condensation → reduced effective delivery

(Al Ashry & Modrykamien, 2014)

C. Non-Invasive Ventilation (NIV)

Target:

• ~28°C

• ~10 mg/L AH

(Re et al., 2024)

🔧 Device:

• Prefer active humidifier

💡 Rationale:

• Dry pressurized gas + high flow → overwhelms natural airway conditioning

D. Invasive Mechanical Ventilation

Mandatory humidification
Target:

• 37°C

• 44 mg/L AH
  (Re et al., 2024)

Device Options

1. Active Humidifiers

• Passover (most common) - learn modern concepts at Re et al., 2024

• Bubble / counterflow variants

✔ High humidity delivery
✔ Ideal for thick secretions

⚠️ Issues:

• Condensation

• Circuit maintenance

(Figure 3: humidifier types, Al Ashry & Modrykamien, 2014)

💧 2. Passive Humidifiers

(HME – Heat & Moisture Exchangers)

Placed between Y-piece and patient

(Figure 5: HME function, Al Ashry & Modrykamien, 2014)

Types of Passive Humidifiers

A. Hydrophobic HME

Structure:

• Water-repellent membrane

• Low thermal conductivity

Mechanism:

• Condenses exhaled moisture on surface

• Returns it during inspiration

Performance:

• Lower humidity delivery (~22–28 mg/L)

Limitations:

• Less efficient heat transfer

• Greater risk of airway narrowing and secretion retention

👉 Clinically:

• Less preferred in ICU practice

B. Hygroscopic HME

Structure:

• Contains hygroscopic salts (e.g., calcium chloride, lithium chloride)

Mechanism:

• Chemical attraction of water molecules

• Stores more moisture than hydrophobic HMEs

Performance:

• Higher AH (~28–36 mg/L)

• Better approximation of physiological humidity

(Re et al., 2024; Al Ashry & Modrykamien, 2014)

C. Combined Hygroscopic + Hydrophobic (Modern HMEs)

• Combine:

  • Hygroscopic element (moisture retention)

  • Hydrophobic filter (barrier + structure)

✔ Best balance:

• Improved humidification

• Infection control

D. HME with Filter (HMEF)

• Adds bacterial/viral filtration

• Types:

  • Pleated (mechanical) → better filtration, ↑ resistance

  • Electrostatic → lower resistance

Practical Comparison

🚫 Avoid HME in:

• Thick secretions

• ARDS (low tidal volume)

• High minute ventilation

• Hypothermia

(Al Ashry & Modrykamien, 2014)

E. Tracheostomy

• Complete bypass of upper airway

🔧 Use:

• Heated humidifier OR

• Heated trach collar OR

• Tracheostomy HME

Essential to prevent:

• Crusting

• Tube blockage

4. Clinical Pitfalls

• Dry circuit ≠ adequate humidification

• Condensation ≠ incorrect setup

• Ignoring environment (temperature, flow) affects performance

(Al Ashry & Modrykamien, 2014)

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Dr Arihant Jain, MD
lifeonthefrontline.com
Instagram: @humans.of.em
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Final Framework

1. Airway bypassed? → Full humidification

2. High flow? → Active humidifier

Closing Insight

👉 Humidity is a physiological variable—not an accessory setting

It directly impacts:

• Gas exchange

• Airway resistance

• Secretion clearance

• Patient outcomes

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References

• Al Ashry HS, Modrykamien AM. Humidification during mechanical ventilation in the adult patient. 2014.

• Re R, Lassola S, De Rosa S, Bellani G. Humidification during invasive and non-invasive ventilation: A starting tool kit for correct setting. 2024.

The Problem We Don’t Talk About Enough

In resuscitation, we rely on TTE (POCUS)—until it fails.

And it does fail:

• Obesity

• Mechanical ventilation

• Ongoing CPR

• Chest trauma / emphysema

• Dressings, drains, defibrillator pads

At the exact moment when physiology is collapsing, our window disappears.

This is where Resuscitative TEE emerges—not as an adjunct, but as a shift in how we see critically ill patients.

What Is Resuscitative TEE?

Resuscitative TEE is:

A focused, goal-directed, point-of-care transesophageal echocardiographic exam used during cardiac arrest, shock, and critical illness to guide real-time management (Teran et al., 2025).

It evolved from:

• Rescue TEE (Shillcutt et al., 2012)

• Critical care TEE (Mayo et al., 2015)

But today, it represents a distinct resuscitation tool.

Why TEE? — The Physiological Edge

TEE works where TTE fails because:

• Esophagus = direct acoustic window to heart

• No lung or chest wall interference

• Continuous imaging during CPR

👉 Especially valuable when TTE windows are limited (Teran et al., 2025; Torre & Pirri, 2025; Prager et al., 2022).

This allows:

• Continuous monitoring

• Superior image quality

• Additional diagnostic planes

• Procedural visualization

Where TEE Changes Practice

1. Cardiac Arrest — From Blind CPR to Visual Resuscitation

TEE enables:

• Identification of reversible causes:

  • Tamponade

  • Massive PE

  • Aortic dissection

  • Severe hypovolemia (Teran et al., 2020; Edmiston et al., 2024)

• Differentiation of:

  • True PEA vs pseudo-PEA

  • Fine VF missed on monitor (Jung et al., 2020; Parker et al., 2018)

• Optimization of CPR:

  • Avoid LVOT compression (Hwang et al., 2009; Cha et al., 2013)

  • Improve compression location

• Reduction in CPR interruptions (Fair et al., 2019)

👉 TEE identifies the cause of arrest in ~25–35% of cases (Prager et al., 2022; Edmiston et al., 2024).

2. Undifferentiated Shock

TEE excels when TTE is inadequate in ICU patients.

It allows:

• LV/RV function assessment

• Obstructive pathology detection

• Volume responsiveness (SVC collapsibility) (Vieillard-Baron et al., 2004)

• Continuous reassessment

👉 Leads to change in diagnosis in ~52–78% and management in ~32–89% of cases.(Prager et al., 2022; Kegel & Chenkin, 2023; Teran et al., 2024).

3. Hemodynamic Monitoring — The Hidden Superpower

TEE enables continuous bedside monitoring, unlike TTE:

• Stroke volume / cardiac output

• Ventricular function trends

• Response to fluids/inotropes

👉 Validated as a monitoring tool in critical care (Vignon, 2017; Porter et al., 2015)

👉 Particularly useful in:

• Sepsis

• Cardiogenic shock

• Mixed shock states

4. Trauma & Acute Care

TEE provides simultaneous diagnosis + resuscitation:

• Blunt aortic injury detection (Osman et al., 2020)

• LVOT obstruction in trauma physiology (Prager et al., 2024)

👉 Critical when CT is not feasible.

5. Procedural Guidance — From Blind to Visual

TEE enhances:

• ECMO cannulation (Fair et al., 2016; Banfi et al., 2016)

• Transvenous pacing (Lerner et al., 2020)

• PA catheter placement (Cronin et al., 2017)

👉 Reduces complications and improves accuracy.

6. Special Situations

• Prone ARDS → TEE remains feasible (Mekontso Dessap et al., 2011)

• COVID / severe hypoxemia → identifies shunts (Teran et al., 2020)

• TELUS → posterior lung imaging (Cavayas et al., 2016)

Real-World Impact (What the Data Shows)

• Diagnostic change: 52–78%

• Management change: 32–89%

• Interpretable images: >98–99% success

• Complications: rare to negligible

(Wray et al., 2021; Arntfield et al., 2018; Reardon et al., 2021; Teran et al., 2024)

👉 This is not just imaging—this is decision-altering technology.

Critical Appraisal — The Balanced View

Advantages

1. Continuous Imaging During CPR

No interruptions → better perfusion

2. High Diagnostic Yield

Especially when TTE fails

3. Real-Time Decision Support

Immediate therapeutic impact

4. Procedural Precision

Safer ECMO, pacing, catheter placement

5. Broad Applicability

ED + ICU + OR integration

Pitfalls

1. Operator Dependence

Requires structured training

2. Misinterpretation Risk

Incorrect findings → wrong interventions

3. Lack of Standardized Protocols

Still evolving (Tseng et al., 2025)

4. Cognitive Load

Can overwhelm inexperienced teams

Disadvantages

1. Invasive Modality

Potential complications:

• Esophageal injury

• Oropharyngeal trauma

Though rare (~0.01–0.08%) (Kallmeyer et al., 2001; Ramalingam et al., 2020)

👉 Large ICU series show no major complications (Prager et al., 2022).

2. Training Gap

• Requires TTE foundation

• Simulation-based learning

• Supervised exams (~30 studies) (Charron et al., 2013)

3. Resource Barriers

• Probe cost

• Maintenance

• Credentialing

👉 Major implementation barriers (Teran et al., 2023; McGuire et al., 2022)

4. Limited High-Level Evidence

• Strong observational data

• Limited RCTs

👉 Field still evolving.

TEE vs TTE — Not a Competition

FeatureTTE (POCUS) Resuscitative TEEInvasivenessNon-invasiveSemi-invasiveImage qualityVariableConsistently highCPR compatibilityLimitedContinuousMonitoringIntermittentContinuousAccessibilityHighLimited

👉 TEE is a complement, not replacement.

Where the Field Is Heading (2025–2026)

Recent literature shows:

• Rapid growth in adoption and research (Tseng et al., 2025)

• Expansion beyond arrest → full-spectrum critical care

• Increasing ED uptake (~20% programs in NA) (Teran et al., 2023)

• Emergence of registries and multicenter data (Teran et al., 2024)

👉 We are witnessing the mainstreaming of resuscitative TEE.

Take-Home Points

• Resuscitative TEE is a high-impact tool in acute care

• Most useful in:

  • Cardiac arrest

  • Undifferentiated shock

  • Procedural guidance

• Provides continuous, real-time hemodynamic insight

• Improves:

  • Diagnosis

  • Decision-making

  • Procedural safety

But:

• Requires training

• Needs resources

• Still evolving in evidence

Final Thought

The next leap in resuscitation is not faster hands—but better vision.

TEE gives us that vision.

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References

1. Teran F, Diederich T, Owyang CG, et al. Resuscitative transesophageal echocardiography in critical care. J Intensive Care Med. 2025;40(11):1133-1142.

2. Via G, Hussain A, Wells M, et al. International evidence-based recommendations for focused cardiac ultrasound. J Am Soc Echocardiogr. 2014;27(7):683.e1-683.e33.

3. Shillcutt SK, Markin NW, Montzingo CR, Brakke TR. Use of rapid “rescue” perioperative echocardiography. J Cardiothorac Vasc Anesth. 2012;26(3):362-370.

4. Mayo PH, Narasimhan M, Koenig S. Critical care transesophageal echocardiography. Chest. 2015;148(5):1323-1332.

5. Teran F. Resuscitative cardiopulmonary ultrasound and transesophageal echocardiography in the ED. Emerg Med Clin North Am. 2019;37(3):409-430.

6. Arntfield R, Lau V, Landry Y, et al. Impact of critical care TEE in ICU patients. J Intensive Care Med. 2018;35(9):896-902.

7. Arntfield R, Pace J, Hewak M, Thompson D. Focused TEE by emergency physicians. J Emerg Med. 2016;50(2):286-294.

8. Teran F, Dean AJ, Centeno C, et al. TEE in out-of-hospital cardiac arrest. Resuscitation. 2019;137:140-147.

9. Teran F, Burns KM, Narasimhan M, et al. Critical care TEE during COVID-19. J Am Soc Echocardiogr. 2020;33(8):1040-1047.

10. Teran F, Owyang C, Wray T, et al. Development of a multicenter registry for resuscitative TEE. Ann Emerg Med. 2024.

11. Teran F, West FM, Jelic T, et al. Resuscitative TEE in EDs: cross-sectional survey. Am J Emerg Med. 2023;76:164-172.

12. Prager R, Bowdridge J, Pratte M, et al. Indications, clinical impact, and complications of critical care TEE. J Intensive Care Med. 2022;38(3):245-272.

13. Wray T, Johnson M, Cluff S, et al. TEE by intensivists and emergency physicians: 5-year experience. J Intensive Care Med. 2021;37(7):917-924.

14. Reardon R, Chinn E, Plummer D, et al. Feasibility and safety of TEE in emergency medicine. Acad Emerg Med. 2021;29(3):334-343.

15. Kegel F, Chenkin J. Resuscitative TEE in the ED: case series. Scand J Trauma Resusc Emerg Med. 2023;31:XX.

16. Edmiston T, Sangalli F, Soliman-Aboumarie H, et al. TEE in cardiac arrest. Resuscitation. 2024;XX:110372.

17. Bora V, Pulijal S. Transesophageal echocardiography in critical care. Curr Pulmonol Rep. 2024;13:152-172.

18. Torre D, Pirri C. Point-of-care TEE in emergency and intensive care. Biomedicines. 2025;13:XXXX.

19. Tseng B, Yang C, Sun J, et al. Trends in TEE research in emergency medicine. West J Emerg Med. 2025;26:469-477.

20. McGuire D, Johnson S, Mielke N, Bahl A. TEE in the ED: implementation and QA. JACEP Open. 2022;3:e12758.

21. Parker BK, Salerno A, Euerle BD. TEE during cardiac arrest: literature review. J Ultrasound Med. 2018;38:1421-1430.

22. Vieillard-Baron A, Slama M, Mayo P, et al. SVC collapsibility and volume status. Intensive Care Med. 2004;30:2283-2289.

23. Vieillard-Baron A, Millington SJ, Sanfilippo F, et al. A decade of progress in critical care echocardiography. Intensive Care Med. 2019;45:770-788.

24. Vignon P. Hemodynamic assessment using echocardiography Doppler. Curr Opin Crit Care. 2005;11:227-234.

25. Porter TR, Shillcutt SK, Adams MS, et al. Echocardiography for therapeutic monitoring. J Am Soc Echocardiogr. 2015;28:40-56.

26. Osman A, Fong CP, Wahab SFA, et al. TEE for blunt aortic injury. J Emerg Med. 2020;59(3):418-423.

27. Prager R, Walser E, Balta KY, et al. Resuscitative TEE in trauma. J Crit Care. 2024;79:154426.

28. Fair J, Tonna J, Ockerse P, et al. TEE-guided ECMO cannulation. Am J Emerg Med. 2016;34:1637-1639.

29. Banfi C, Pozzi M, Siegenthaler N, et al. VV-ECMO cannulation techniques. J Thorac Dis. 2016;8(12):3762-3773.

30. Cronin B, Robbins R, Maus T. PA catheter placement using TEE. J Cardiothorac Vasc Anesth. 2017;31:178-183.

31. Lerner RP, Haaland A, Lin J. Transvenous pacing under TEE guidance. Am J Emerg Med. 2020;38:1044.e3-1044.e4.

32. Cavayas YA, Girard M, Desjardins G, Denault AY. Transesophageal lung ultrasonography. Can J Anaesth. 2016;63(11):1266-1276.

33. Mekontso Dessap A, Proost O, Boissier F, et al. TEE in prone ARDS patients. Intensive Care Med. 2011;37:430-434.

34. Hwang SO, Zhao PG, Choi HJ, et al. LVOT compression during CPR. Acad Emerg Med. 2009;16:928-933.

35. Cha KC, Kim YJ, Shin HJ, et al. Optimal compression position in CPR. Emerg Med J. 2013;30:615-619.

36. Fair J, Mallin MP, Adler A, et al. TEE reduces CPR interruptions. Ann Emerg Med. 2019;73:610-616.

37. Jung WJ, Cha KC, Kim YW, et al. Intra-arrest TEE findings and outcomes. Resuscitation. 2020;154:31-37.

38. Kim YW, Jung WJ, Cha KC, et al. Diagnosis of aortic dissection during CPR with TEE. Am J Emerg Med. 2021;39:92-95.

The Venous Excess Ultrasound (VExUS) score is a point-of-care ultrasound (POCUS) method that integrates inferior vena cava (IVC) size with Doppler assessment of hepatic, portal, and intrarenal veins to quantify systemic venous congestion. By capturing the downstream effects of elevated right atrial pressure (RAP), VExUS provides a dynamic and organ-relevant assessment of hemodynamics .

Physiological Basis

Elevation in RAP is transmitted backward through the venous system, producing characteristic Doppler changes:

• Hepatic veins: direct transmission from right atrium

• Portal vein: loss of hepatic buffering

• Intrarenal veins: end-organ venous congestion

This leads to reduced effective organ perfusion pressure (MAP − CVP) and contributes to organ dysfunction such as acute kidney injury and hepatic congestion .

Read more about doppler USG here - Physics of doppler

Ultrasound Presets and Machine Settings

Accurate VExUS assessment requires appropriate preset selection and Doppler optimization.

Preset Selection

• Cardiac, abdominal, or FAST presets may be used

• Cardiac preset allows ECG integration but often requires scale adjustment

• Abdominal/FAST presets provide better color Doppler sensitivity

Key Settings

• Doppler scale:

  • ~40 cm/s (IVC, HV, PV)

  • <20 cm/s (intrarenal veins)

• Sweep speed: 50–66.7 mm/s

• Optimize gain and sample volume

Pitfalls

• High scale → no color signal (false low flow)

• Low scale → aliasing (false turbulence)

Proper machine setup is essential before interpreting any waveform .

Step 1: Inferior Vena Cava (IVC)

How to Obtain the View

• Place probe subxiphoid using liver as window

• Start with short-axis view (marker at 3 o’clock)

• Identify IVC within liver (right side), aorta midline

• Rotate to long axis (marker at 12 o’clock)

• Visualize IVC entering right atrium and hepatic vein junction

Measurement

• 2 cm below RA-IVC junction OR

• 1 cm below hepatic vein junction

• Use B-mode, not M-mode

Short-Axis Importance

The short-axis view avoids the “cylinder effect” of long-axis imaging and provides a true cross-sectional representation. It also allows qualitative assessment of a plethoric, circular IVC, which may better reflect elevated RAP, particularly in Asian populations .

Interpretation

• ≤2 cm → no congestion

• ≥2 cm → proceed to Doppler

Indian/Asian Considerations

The 2 cm cutoff is widely used but may not be universally applicable. Indian studies apply this threshold without revalidation, while Asian data suggest incorporating collapsibility and morphology for better RAP estimation (Bhardwaj et al., 2020; Khan et al., 2025; Gupta et al., 2023; Assavapokee et al., 2024; Klangthamneam et al., 2024).

Pitfalls

• Confusing IVC with aorta

• Cylinder effect (long axis underestimation)

• Collapsed IVC despite high RAP (raised intra-abdominal pressure)

• Dilated IVC in athletes

• Misinterpretation using a single view

Step 2: Hepatic Vein Doppler

How to Obtain the View

Subxiphoid approach:

• Probe below xiphoid, marker at 12 o’clock

• Tilt right to visualize hepatic vein entering IVC

Coronal approach (preferred):

• Place probe along line from xiphoid to midaxillary line

• Marker toward right axilla

• Slide cephalad and tilt downward

Doppler technique:

• Use color Doppler to identify vein

• Place sample volume 1–2 cm from HV-IVC junction

• Avoid junctions

Interpretation

• S > D → normal

• S < D → mild congestion

• S reversal → severe congestion

Pitfalls

• Atrial fibrillation (absent A wave)

• Tricuspid regurgitation (persistent S reversal)

• Cirrhosis (blunted waveform)

• Lack of ECG correlation

Step 3: Portal Vein Doppler

How to Obtain the View

• Use coronal approach similar to hepatic vein

• Slide caudally to visualize liver and kidney

• Fan anteriorly to identify portal vein

• Place Doppler gate in main portal vein (avoid hepatic artery overlap)

Interpretation

• PVPF <30% → normal

• 30–50% → mild

50% → severe

Pitfalls

• Cirrhosis altering baseline

• Respiratory variation mimicking pulsatility

• Hepatic artery contamination

• Incorrect gate placement

Step 4: Intrarenal Vein Doppler

How to Obtain the View

• Coronal approach (xiphoid to posterior axillary line)

• Visualize kidney → zoom parenchyma

• Use color Doppler to identify interlobar vessels

• Place Doppler gate within vein

Interpretation

• Continuous → normal

• Biphasic → mild

• Monophasic (D only) → severe

Pitfalls

• Technically difficult

• Poor visualization in critically ill

• Requires low Doppler scale

• Limited evidence in CKD

VExUS Grading System

VExUS and Fluid Intolerance

VExUS should be understood as a tool for assessing fluid intolerance, rather than volume status alone. Increasing VExUS grades reflect worsening venous congestion and reduced capacity of the circulation to tolerate additional fluid. Studies have shown that higher VExUS scores correlate with adverse outcomes, including acute kidney injury, and can guide de-resuscitation strategies such as diuretics or ultrafiltration (Jury and Shaw, 2021; Chin et al., 2025; Pierre-Grégoire, 2025; Rola et al., 2024; Bhardwaj et al., 2020). Importantly, VExUS does not predict fluid responsiveness but instead answers whether further fluid administration is likely to be harmful .

Clinical Integration

• Not a standalone tool

• Must be integrated with cardiac POCUS and clinical context

• Does not differentiate volume vs pressure overload

Caution in:

• Pulmonary hypertension

• Pericardial effusion

• Severe tricuspid regurgitation

Conceptual Framework

Venous congestion progresses sequentially:

Right atrium → hepatic veins → portal vein → kidney

The presence of abnormalities further downstream reflects increasing severity of systemic congestion.

Conclusion

VExUS provides a structured, physiologically grounded method for bedside assessment of venous congestion. Its strength lies in integrating multiple venous Doppler signals to reflect organ-level hemodynamics. In Indian and Asian populations, interpretation should emphasize morphology and Doppler findings rather than rigid adherence to IVC diameter thresholds. When applied correctly, VExUS offers a powerful tool to guide fluid management and prevent organ injury.

Read more about views and how to get them here - Decoding VExUS article

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References (AMA Style)

1. Assavapokee T, Rola P, Assavapokee N, Koratala A. Decoding VExUS: a practical guide for excelling in point-of-care ultrasound assessment of venous congestion. Ultrasound J. 2024;16.

2. Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J. 2020;12(1):16.

3. Rola P, Haycock K, Spiegel R, et al. VExUS: common misconceptions, clinical use and future directions. Ultrasound J. 2024;16.

4. Pierre-Grégoire G. VExUS score: optimizing its use in perioperative and critical care management. Crit Care. 2025;29.

Clinical Application & Fluid Intolerance

5. Jury D, Shaw A. Utility of bedside ultrasound derived hepatic and renal parenchymal flow patterns to guide management of acute kidney injury. Curr Opin Crit Care. 2021;27:587–592.

6. Chin W, Ngai M, See K. Venous excess ultrasound: a mini-review and practical guide for its application in critically ill patients. World J Crit Care Med. 2025;14.

7. Bhardwaj V, Vikneswaran G, Rola P, et al. Combination of inferior vena cava diameter, hepatic venous flow, and portal vein pulsatility index (VExUS) in predicting AKI in cardiorenal syndrome. Indian J Crit Care Med. 2020;24:783–789.

8. De Santamaría C, Fiestas Z, Crespo-Aznarez S, et al. VExUS protocol along cardiorenal syndrome: an updated review. J Clin Med. 2025;14.

9. Teran S, Mantha A, Siegel G, et al. The role of VExUS in predicting AKI and diuresis in acute decompensated heart failure. Circulation. 2025.

10. Gravina I, Meo A, La Verde A, et al. VExUS score as a method to guide diuretic treatment in CKD patients with congestive nephropathy. Nephrol Dial Transplant. 2024.

AKI, ICU & Outcomes

11. Khan W, Saini V, Goel A, Valiyaparambath A. Evaluating the predictive power of VExUS scoring in critically ill noncardiac patients. Indian J Crit Care Med. 2025;29:236–243.

12. Karki B, Ghimire S, Vaddi B, et al. VExUS: the holy grail or Achilles heel of fluid management? J Nepal Soc Crit Care Med. 2024.

13. Meshram A, Lalitha A, Philip B, Raj J. Utility of VExUS to quantify venous congestion in critically ill children. Indian J Crit Care Med. 2025;29(Suppl).

14. Espinosa-Almanza C, Ruiz-Ávila H, Gomez-Tobar J, Acosta-Gutiérrez E. Relationship between cumulative fluid balance and venous congestion using VExUS. J Ultrasound Med. 2025;44.

15. Utami M, Prawira Y, Djer M, et al. Correlation between fluid balance and VExUS score in critically ill children. BMC Pediatr. 2025;25.

Indian / Regional Context

16. Gupta B, Ahluwalia P, Gupta A, et al. Utility of VExUS score in perioperative and ICU settings: a systematic review. Indian J Anaesth. 2023;67:S218–S226.

Asian Validation & IVC Considerations

17. Klangthamneam S, Meemook K, Petnak T, et al. Correlation between right atrial pressure and VExUS, IVC diameter, and jugular venous pressure. Ultrasound J. 2024;16.

18. Anastasiou V, Peteinidou E, Moysidis D, et al. Multiorgan congestion assessment by VExUS in acute heart failure. J Am Soc Echocardiogr. 2024.

19. Torres-Arrese M, Mata-Martínez A, Luordo-Tedesco D, et al. Usefulness of systemic venous ultrasound protocols in heart failure prognosis. J Clin Med. 2023;12.

20. Wong A, Olusanya O, Watchorn J, et al. Utility of VExUS to track dynamic volume status in hemodialysis. Ultrasound J. 2024;16.

21. Koratala A, Romero-González G, Soliman-Aboumarie H, Kazory A. Unlocking the potential of VExUS in assessing venous congestion. Cardiorenal Med. 2024.

22. Ahn A, Desai K. Fluid status assessment and the role of VExUS. Tech Vasc Interv Radiol. 2025;28:101026.

23. Dinesen C, Vistisen S, Aagaard R, et al. Doppler ultrasound assessment of venous congestion for prediction of fluid responsiveness. J Cardiothorac Vasc Anesth. 2024.

The patient who looked “tight but stable” an hour ago is now:

• Exhausted

• Silent

• Hypercapneic

And the physiology has shifted.

This is no longer about broncho-dilation.
This is about ventilation, mechanics, and survival.

In severe asthma, the danger is not hypoxia—it is failure to ventilate.

Recognising the Turn: When Compensated Becomes Pre-terminal

Early asthma is loud.
Severe asthma is often quiet.

Red flags of impending respiratory failure:

• Rising or normal PaCO₂

• Exhaustion / reduced respiratory effort

• Altered mentation

• Silent chest

• Bradycardia (late)

A normal PaCO₂ in acute asthma is not reassuring—it is a warning of imminent collapse (Cahill et al., 2025).

What is happening physiologically?

• Airflow obstruction worsens

• Expiratory time becomes insufficient

• Dynamic hyperinflation increases

• Intra-thoracic pressure rises

• Venous return falls

• Cardiac output drops

(Mein & Ferrera, 2025)

‘The patient is not tiring because they are hypoxic—they are tiring because they cannot exhale.’

Adjuncts and Escalation: What Actually Works

Once initial therapy fails, escalation must be targeted—not reflexive.

Ketamine in Acute Asthma:

Rescue Bronchodilator, Not Routine Therapy

Ketamine occupies a unique space in acute asthma—pharmacologically appealing, clinically inconsistent, and often used when options are running out.

Where does Ketamine fit?

Ketamine is best understood as a rescue therapy in refractory status asthmaticus—not as routine ED treatment.

It is typically considered when:

• Severe asthma persists despite maximal inhaled therapy + steroids ± magnesium

• The patient is deteriorating toward intubation

• Or as the induction agent of choice during RSI

(Goyal & Agrawal, 2013; La Via et al., 2022)

Mechanism: Why it makes sense

Ketamine produces broncho-dilation through multiple pathways:

• NMDA receptor antagonism

• Increased endogenous catecholamines → β₂ stimulation

• Reduced vagal tone

• Direct smooth muscle relaxation

(Goyal & Agrawal, 2013; La Via et al., 2022)

It also demonstrates:

• Anti-inflammatory effects

• Reduction in airway hyperresponsiveness (experimental data)

(Xiao et al., 2022)

Dosing (acute care context)

• Induction (RSI):

  • 1–2 mg/kg IV

• Infusion (refractory cases):

  • 0.5–2 mg/kg/hour

(Ueoka et al., 2021; Goyal & Agrawal, 2013)

What does the evidence say?

Despite strong physiological rationale:

• Systematic reviews show no consistent benefit in ED patients

• RCTs demonstrate minimal or no improvement over standard therapy

• Meta-analysis shows non-significant improvement in PEF

(La Via et al., 2022; Alshehri et al., 2022)

In contrast:

• ICU case series in life-threatening status asthmaticus report:

  • Improved pH and PaCO₂

  • Reduced airway pressures

  • Facilitation of ventilator weaning

(Heshmati et al., 2003; Ueoka et al., 2021)

Adverse effects

• Hallucinations / dysphoria

• Increased secretions

• Tachycardia, hypertension

Usually manageable with:

• Sedation

• Anticholinergics

(La Via et al., 2022; Binsaeedu et al., 2023)

Clinical takeaway

Ketamine is not a bronchodilator you reach for early—it is one you reach for when everything else is failing.

Its strongest roles:

• RSI induction in asthmatics

• Adjunct infusion in refractory, intubated patients

Adrenaline (Epinephrine) in Asthma:
Old Drug, New Role

Adrenaline was once the cornerstone of asthma therapy. Today, its role is far more selective.

Mechanism

• β₂ → bronchodilation

• α₁ → reduces airway edema

• β₁ → increases cardiac output

(Baggott et al., 2021; Mclean-Tooke et al., 2003)

Effectiveness vs β₂-agonists

Modern evidence shows:

Adrenaline is not superior to inhaled β₂-agonists.

• Equivalent efficacy

• No reduction in treatment failure

• More cardiovascular side effects

(Baggott et al., 2021)

Current role: Not routine

Adrenaline should not be used routinely in asthma exacerbations.

Selective β₂-agonists (e.g., salbutamol) are:

• Safer

• Equally effective

(Indinnimeo et al., 2018)

When should you use adrenaline?

1. Asthma or Anaphylaxis (critical indication)

Adrenaline is first-line therapy here.

• Treats bronchospasm

• Reduces airway edema

• Prevents cardiovascular collapse

(Cardona et al., 2020; Ring et al., 2018)

2. Severe, refractory asthma (rescue use)

Consider when:

• Inhaled therapy is ineffective or not feasible

• Patient is deteriorating rapidly

Dosing

IM adrenaline:

• 0.3–0.5 mg (1:1000)

• Repeat every 20 minutes (max 3 doses)

SC terbutaline alternative:

• 0.25 mg every 20 minutes (max 0.75 mg)

(McFarlin et al., 2026; Leung, 2021)

Emerging data:

• Recent RCT suggests low-dose SC adrenaline may improve airflow and oxygenation when added to standard therapy

(Gong et al., 2024)

Cautions

• Tachy-arrhythmias

• Hypertension

• Myocardial ischemia (rare but relevant in older patients)

Clinical takeaway

Adrenaline is no longer a first-line bronchodilator—it is a situational drug.

Use it when:

• There is anaphylaxis

• Or severe asthma where inhaled therapy cannot be delivered effectively

Integrated Clinical Insight

Ketamine and adrenaline share a similar theme:

Both are powerful drugs—but neither belongs in routine asthma care.

They are:

• Not first-line

• Not substitutes for proper broncho-dilation

• Not replacements for steroids

They are:

• Bridging therapies in extreme physiology

In asthma, the right drug at the wrong time is as dangerous as the wrong drug.

Magnesium Sulfate: Selective but Effective

Dose:

• 2 g IV over 20–30 minutes

Mechanism:

• Smooth muscle relaxation

• Calcium antagonism

Evidence:

• Improves lung function

• Reduces hospitalisation in severe exacerbations

Magnesium is not a routine drug—it is a severity marker.

Use when:

• Persistent severe obstruction after initial therapy

(Cahill et al., 2025; McFarlin et al., 2026)

Non-Invasive Ventilation (NIV): A Narrow Window

NIV can:

• Reduce work of breathing

• Improve ventilation

• Delay or prevent intubation

But only in the right patient:

• Awake and cooperative

• Hemodynamically stable

• No impending arrest

Typical starting settings:

• IPAP: ~8 cm H₂O

• EPAP: ~3 cm H₂O

(McFarlin et al., 2026)

NIV is a bridge—not a rescue for the crashing patient.

Evidence remains limited; use cautiously (Mein & Ferrera, 2025).

Systemic Beta-Agonists: Rescue Only

Not routine—but lifesaving in specific contexts.

Indications:

• Failure of inhaled therapy

• Inability to effectively inhale

Terbutaline (SC):

• 0.25 mg every 20 minutes (max 0.75 mg)

(McFarlin et al., 2026)

If the drug cannot reach the airway, change the route.

What Not to Do (Evidence-Based De-adoption)

Modern asthma care is defined as much by what we avoid:

• ❌ Aminophylline / theophylline → toxicity without benefit

• ❌ Routine antibiotics → mostly viral triggers

• ❌ Aggressive IV fluids → worsens pulmonary mechanics

• ❌ Mucolytics / chest physiotherapy → no benefit

In asthma, unnecessary treatments are not neutral—they are harmful.

(Mein & Ferrera, 2025; Farkas, 2024)

The Crashing Asthmatic: The Intubation Trap

Intubation in asthma is high-risk.

It can:

• Worsen hyperinflation

• Cause hypotension

• Precipitate cardiac arrest

The goal is not to intubate early—it is to intubate safely, when unavoidable.

When to Intubate

• Altered mental status

• Exhaustion

• Rising CO₂

• Refractory hypoxemia

• Failure of maximal therapy

(Cahill et al., 2025)

Intubation Strategy: Physiology First

Induction:

• Ketamine 1–2 mg/kg IV

Why?

• Bronchodilator

• Preserves hemodynamics

(McFarlin et al., 2026)

Tube:

• Use larger ETT → reduces resistance

Ventilation Strategy: This Determines Survival

The ventilator can save—or kill—the patient.

Core principles:

• Tidal volume: ~6 mL/kg IBW

• Respiratory rate: 8–12/min

• I:E ratio: ≥1:3

• Low or minimal PEEP

Why?

To:

• Maximise expiratory time

• Reduce air trapping

• Prevent barotrauma

(Mein & Ferrera, 2025; McFarlin et al., 2026)

Permissive Hypercapnia

• Accept PaCO₂ 70–100 mmHg

• Maintain pH ≥7.15

Trying to normalise CO₂ in asthma is a common and dangerous mistake.

Post-intubation Collapse: The Critical Pearl

If the patient becomes:

• Hypotensive

• Hypoxic

Think:

Dynamic hyperinflation (auto-PEEP)

Immediate action:

• Disconnect ventilator

• Allow full exhalation

This can rapidly restore hemodynamics (Mein & Ferrera, 2025).

Beyond the ED:

The Next 7 Days Matter More Than the Next 7 Minutes

An exacerbation is a risk marker for future deterioration.

Discharge Essentials

Every patient should leave with:

• Systemic steroids (5–7 days)

• ICS-based controller therapy

• Early follow-up (2–7 days)

(Cahill et al., 2025; GINA, 2025)

🔄 The Big Shift: ICS-Based Reliever Therapy

SABA-only therapy is obsolete.

Preferred strategy (GINA 2025):

• ICS–formoterol as reliever (SMART/MART)

Benefits:

• ↓ exacerbations

• ↓ hospitalisations

• ↓ steroid exposure

(GINA, 2025)

The Most Underrated Intervention: Education

• Correct inhaler technique

• Provide written action plan

• Address triggers and comorbidities

The best way to treat asthma in the ED is to prevent the next visit.

🧠 Final Clinical Synthesis

Acute asthma is a disease of:

• Airflow limitation

• Time-sensitive escalation

• Ventilatory mechanics

Recognise early. Escalate appropriately. Ventilate gently. Discharge intelligently.

Final Take-home

Asthma kills by air trapping—not hypoxia. Treat accordingly.

References (AMA Style)

1. Mein SA, Ferrera MC. Management of asthma and COPD exacerbations in adults in the ICU. Chest Crit Care. 2025;3(1):100107.

2. Cahill KN, Dixon AE, Zachrison KS. Acute exacerbations of asthma in adults: Emergency department and inpatient management. UpToDate. Updated September 2025.

3. Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. 2025 update.

4. McFarlin A, Chan C, Winters M, et al. Asthma in adults. EM:RAP CorePendium. Updated February 2026.

5. Farkas J. Asthma. EMCrit Project. January 2024.

6. Helman A, Sommer L, Mal S. The crashing asthmatic: Recognition and management of life-threatening asthma. Emergency Medicine Cases. April 2024.

7. Morris MJ, Mosenifar Z. Asthma guidelines: Guidelines summary. Medscape. Updated March 2026.

8. Goyal S, Agrawal A. Ketamine in status asthmaticus: A review. Indian J Crit Care Med. 2013;17:154–161.

9. La Via L, Sanfilippo F, Cuttone G, et al. Use of ketamine in patients with refractory severe asthma exacerbations: systematic review. Eur J Clin Pharmacol. 2022;78:1613–1622.

10. Alshehri F, Aloqaily H, Enabi J, Nafisah S. Ketamine for adults with severe asthma exacerbation: systematic review and meta-analysis. J Med Law Public Health. 2022.

11. Ueoka M, Subia G, Hipp C, et al. Ketamine infusion for refractory status asthmaticus: a case series. Chest. 2021.

12. Heshmati F, Zeinali M, Noroozinia H, et al. Use of ketamine in severe status asthmaticus. Iran J Allergy Asthma Immunol. 2003;2:175–180.

13. Binsaeedu A, Prabakar D, Ashkar M, et al. Safety and efficacy of ketamine in acute asthma exacerbation. Cureus. 2023;15.

14. Xiao S, Zhou Y, Wang Q, Yang D. Ketamine attenuates airway inflammation via Nrf2 pathway. Drug Des Devel Ther. 2022;16:4411–4428.

15. Baggott C, Hardy J, Sparks J, et al. Epinephrine versus β₂-agonists in acute asthma: systematic review and meta-analysis. Thorax. 2021;77:563–572.

16. Indinnimeo L, Chiappini E, Del Giudice M, et al. Guideline on management of acute asthma attack in children. Ital J Pediatr. 2018;44.

17. Cardona V, Ansotegui IJ, Ebisawa M, et al. World allergy organization anaphylaxis guidance. World Allergy Organ J. 2020;13.

18. Ring J, Klimek L, Worm M. Adrenaline in acute treatment of anaphylaxis. Dtsch Arztebl Int. 2018;115:528–534.

19. Gong W, Jiang J, Fan H. Low-dose adrenaline in severe asthma. Pharm Bioprocess. 2024;6:106–112.

20. Leung J. Acute asthma exacerbations management. Drugs Context. 2021;10.

Every exacerbation follows a trajectory.
Your role is to alter that course early.
What is reversible can become irreversible.

Patients do well when we:

• Recognise severity early

• Deliver adequate-dose bronchodilation immediately

• Initiate systemic anti-inflammatory therapy without delay

They deteriorate when we:

• Underestimate severity

• Undertreat early bronchospasm

• Focus on oxygenation instead of ventilation

The first hour is not about observation—it is about decisive intervention.

Framing the Acute Attack: Pathophysiology That Drives Decisions

An acute asthma exacerbation represents acute-on-chronic airway inflammation with superimposed broncho-constriction.

Three processes act simultaneously:

• Airway smooth muscle constriction

• Mucosal edema

• Mucus plugging

These lead to:

• Increased airway resistance

• Prolonged expiration

• Dynamic hyperinflation

• Ventilation–perfusion mismatch

• Progressive hypercapnia

This physiological cascade—particularly air trapping and auto-PEEP—is central to deterioration in severe asthma (Mein & Ferrera, 2025).

Asthma is fundamentally a disease of impaired expiration, not inspiration.

Severity Assessment: Why Clinical Impression Fails

Classic signs of severe asthma include:

• Tachypnea ≥30/min

• Tachycardia ≥120/min

• Inability to speak full sentences

• Accessory muscle use

• Diaphoresis

• Pulsus paradoxus

However:

Up to 50% of patients with severe airflow obstruction lack classic signs (Cahill et al., 2025).

This makes objective assessment essential.

Objective assessment

Peak Expiratory Flow (PEF)

• <50% predicted → severe

• <25% or <150 L/min → risk of hypercapnia

PEF is a critical tool for:

• Detecting occult severity

• Monitoring response

• Risk stratification (Cahill et al., 2025)

Oxygenation

• Pulse oximetry for all patients

• SpO₂ <90% → life-threatening exacerbation

Marked hypoxemia should prompt evaluation for complications (Cahill et al., 2025).

⚠️ Critical physiological warning

Even a normal PaCO₂ in acute asthma indicates impending respiratory failure, reflecting reduced alveolar ventilation (Cahill et al., 2025).

The First 5–10 Minutes: High-Stakes Decisions

Early ED management should rapidly determine:

1. Severity

2. Response to initial therapy

3. Need for escalation or ventilatory support

Simultaneously, clinicians must consider alternative or coexisting diagnoses such as pneumothorax, pulmonary embolism, or anaphylaxis (Mein & Ferrera, 2025; Cahill et al., 2025).

💨 Core ED Management: Evidence-Based Therapy

Modern management converges on three interventions:

Oxygen + bronchodilators + systemic corticosteroids

This approach is consistent across GINA, UpToDate, EMCrit, EM Cases, and CorePendium (GINA, 2025; Cahill et al., 2025; Farkas, 2024; McFarlin et al., 2026).

1. Oxygen: Precision, Not Excess

Target:

• SpO₂ 92–95% (most adults)

• ≥95% in pregnancy

• 88–92% in asthma–COPD overlap

Excess oxygen may worsen hypercapnia and V/Q mismatch, particularly in overlap syndromes (McFarlin et al., 2026).

Pulse oximetry may overestimate saturation in certain populations, necessitating clinical correlation (Cahill et al., 2025).

2. Short-Acting Beta₂-Agonists (SABA)

Mechanism:

Broncho-dilation via β₂-receptor stimulation

Dosing:

Nebulised:

• Albuterol 2.5–5 mg every 20 minutes × 3

MDI with spacer:

• 4–8 puffs every 20 minutes × 3

Severe cases:

• Continuous nebulisation 10–15 mg/hour (McFarlin et al., 2026)

Delivery method:

MDI with spacer provides equivalent efficacy to nebulisation with lower aerosolisation risk (Cahill et al., 2025).

Adverse effects:

• Tachycardia

• Tremor

• Hypokalemia

• Lactic acidosis

These effects are expected and should not limit adequate dosing.

Paradigm shift:

SABA-only therapy is associated with worse outcomes and is no longer recommended (GINA, 2025).

3. Anticholinergics (Ipratropium)

Dosing:

• 500 mcg nebulised every 20 minutes × 3 doses

Benefit:

• Improved lung function

• Reduced hospital admission in moderate–severe exacerbations (McFarlin et al., 2026)

Clinical nuance:

Benefit is limited to early management and not required after stabilization.

4. Systemic Corticosteroids

Role:

Reduce airway inflammation and prevent relapse

Indications:

• Moderate–severe exacerbations

• Incomplete response to bronchodilators

Timing:

• Within the first hour (Cahill et al., 2025)

Systemic corticosteroids are one of the few interventions that truly modify the trajectory of an asthma exacerbation when given early. Importantly, evidence consistently shows that oral steroids are as effective as intravenous therapy in most patients, with no meaningful difference in lung function, admission rates, or length of stay—making the oral route the preferred, simpler, and more cost-effective option when feasible.

Among agents, dexamethasone, prednisolone/prednisone, and methylprednisolone offer comparable clinical outcomes; however, dexamethasone stands out for its shorter course, better tolerability, and improved compliance, while prednisolone remains widely used due to familiarity and cost.

In practice, the choice of drug and route matters far less than ensuring early administration of an adequate dose, as timely steroid therapy is what prevents progression from reversible airway inflammation to fixed, refractory disease.

Dosing:

• Prednisone 40–60 mg PO daily for 5–7 days

• Methylprednisolone 60–125 mg IV (McFarlin et al., 2026)

Evidence insights:

• Early steroids reduce hospitalisation and relapse (Cahill et al., 2025)

• High-dose regimens offer no additional benefit and increase adverse effects (Mein & Ferrera, 2025)

Emerging alternative:

Dexamethasone

• 12–16 mg PO/IV once ± repeat dose

Offers:

• Comparable efficacy

• Improved adherence (McFarlin et al., 2026)

🔥 Common Early Pitfalls

• Delayed steroid administration

• Inadequate bronchodilator dosing

• Reliance on auscultation alone

• Failure to use PEF

• Uncontrolled oxygen delivery

• Discharge on SABA-only therapy

Clinical Synthesis

Acute asthma management is about trajectory modification.

Early recognition + aggressive treatment
= prevention of respiratory failure

Part 1 Take-home

The first hour determines the next 24 hours.

📌 Coming in Part 2:

• Refractory asthma

• Magnesium, NIV, rescue therapies

• The crashing asthmatic

• Ventilator strategy

• Discharge & relapse prevention

📚 References (AMA Style)

1. Mein SA, Ferrera MC. Management of asthma and COPD exacerbations in adults in the ICU. Chest Crit Care. 2025;3(1):100107.

2. Cahill KN, Dixon AE, Zachrison KS. Acute exacerbations of asthma in adults: Emergency department and inpatient management. UpToDate. Updated September 2025.

3. Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. 2025 update.

4. McFarlin A, Chan C, Winters M, et al. Asthma in adults. EM:RAP CorePendium. Updated February 2026.

5. Farkas J. Asthma. EMCrit Project. January 2024.

6. Helman A, Sommer L, Mal S. The crashing asthmatic: Recognition and management of life-threatening asthma. Emergency Medicine Cases. April 2024.

7. Morris MJ, Mosenifar Z. Asthma guidelines: Guidelines summary. Medscape. Updated March 2026.

Etomidate is one of the most commonly used induction agents for:

• Rapid Sequence Intubation (RSI)

• Short procedural sedation (e.g., cardioversion)

Its appeal lies in:

• Rapid onset (10–20 sec)

• Short duration (4–10 min)

• Minimal cardiovascular depression

This makes it particularly valuable in critically ill or hypotensive patients, where even small drops in blood pressure can be dangerous.

Dosing essentials

• RSI: 0.3 mg/kg IV (max ~40 mg)

• Unstable / elderly: 0.2 mg/kg

• Procedural sedation: 0.1 mg/kg

Always dose using actual body weight to avoid awareness during paralysis.

Clinical advantages

• Preserves hemodynamic stability better than most induction agents

• Maintains cerebral perfusion pressure → useful in head injury

• Reliable intubating conditions with high first-pass success

• Rapid recovery profile for short procedures

Adrenal suppression: the central controversy

Mechanism

Etomidate inhibits 11β-hydroxylase, impairing cortisol synthesis:

• Leads to reduced endogenous cortisol production

• Effect occurs even after a single dose

Duration:

• Suppression may last 6–72 hours

Biochemical vs clinical significance

• Biochemical suppression:
  Almost universal → low cortisol levels after administration

• Clinical adrenal insufficiency:
  Variable → may present as:

  • Persistent hypotension

  • Increased vasopressor requirement

Key point:
Not all patients with low cortisol develop clinically significant instability.

Adrenal effects in real-world ED practice

In the emergency setting, etomidate-induced adrenal suppression is best understood as a transient physiologic trade-off rather than a definitive clinical harm.

While cortisol levels drop predictably after a single dose, most patients do not manifest overt adrenal crisis.

The effect becomes clinically relevant primarily in septic shock, where endogenous cortisol is crucial for maintaining vascular tone and catecholamine responsiveness.

In such patients, etomidate may contribute to vasopressor dependence or delayed shock reversal, even though a clear increase in mortality has not been consistently demonstrated. In contrast, in undifferentiated shock or cardiogenic instability, the immediate hemodynamic stability provided during intubation often outweighs this transient endocrine effect, making etomidate a reasonable and frequently preferred choice.

What the evidence shows

General ED population

• No consistent increase in mortality after single-dose use

• Benefits in maintaining hemodynamics often outweigh risks

Sepsis and septic shock

• Higher rates of adrenal suppression

• Increased vasopressor requirement seen in several studies

• No clear mortality difference compared with alternatives

Interpretation:

• The signal is physiologic (pressor need) rather than definitively outcome-driven

Other important adverse effects

• Myoclonus (~30%) → limits use in procedural sedation

• No analgesia → must combine with appropriate agents

• Transient apnea/hypoventilation possible

• Injection site pain (~20%)

• Avoid repeat dosing

Etomidate vs Ketamine: bedside decision-making

Outcomes between agents are largely similar—choice depends on physiology and context rather than superiority

Steroids after etomidate?

• Routine steroid use is not recommended

• No clear improvement in outcomes

• Reserve steroids for established refractory septic shock, not prophylaxis

Practical ED approach

Use etomidate when:

• Patient is hemodynamically unstable

• Concern for peri-intubation hypotension

• Need for neuroprotection

Consider alternatives when:

• Septic shock with high vasopressor requirement

• Concern for adrenal insufficiency impact

Take-home message

• Etomidate provides rapid, reliable, hemodynamically stable induction

• It causes predictable, transient adrenal suppression

• Clinical impact is usually limited, but context matters in sepsis

• The decision is not about the drug alone—it’s about the patient in front of you

“Etomidate protects the pressure upfront—just be mindful of the cortisol trade-off.”

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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