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

1. HE Is Not “Just Ammonia”

The Three Villages + Five Axes Framework

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

“Three Villages of HE”

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

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

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

HE is now classified across five axes:

1. Type (A/B/C)

2. Severity (West Haven)

3. Time course

4. Precipitated vs non-precipitated

5. Social infrastructure (NEW)

👉 Game changer:
You must now ask:

“Can this patient actually survive outside the hospital?”

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

• ED clinicians often see patients too late in this curve

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

Who should trigger suspicion?

• Hypoalbuminemia

• Decompensated cirrhosis

• Portal hypertension/shunts

• Falls, traffic violations, navigation issues

• Subtle cognitive complaints

👉 Key ED pearl:
Isolated asterixis ≠ OHE

How to test (NOT ammonia)

• Single-test strategy (ACG recommendation)

• Practical tools:

  • Stroop / EncephalApp

  • Animal Naming Test

  • Critical Flicker Frequency

❌ Do NOT use ammonia to diagnose CHE

Treatment: “Theragnostic trial”

• Lactulose (4–8 week trial)

• Reassess cognition + function

Useful in ED follow-up planning and liaison clinics

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

“Cirrhosis + Cognitive Complaint Pathway”

More than 50% of suspected HE ≠ HE

Common mimics:

• Dementia / MCI

• Depression / PTSD

• Obstructive sleep apnea

• Substance use

• Metabolic/endocrine disorders

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

4. Overt HE in ED & ICU

Triage: Who Needs Admission?

“Admission Decision Flowchart”

Admit if:

• Grade 3–4 HE

• First episode

• Infection, bleed, AKI

• Poor social support

Strong Recommendations That Change Practice

• Lactulose for OHE (strong)

• Secondary prophylaxis after first episode (strong)

• Add rifaximin for recurrence (strong)

• Protein 1.2–1.5 g/kg/day (strong)

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

• Rifaximin pre-TIPS (strong)

🚨 What to STOP Doing

• Routine ammonia testing

• Routine CT brain without focal deficit

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

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

Acute HE Treatment Algorithm

First-line (ED + ICU)

Lactulose

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

• Enema if needed

⚠️ Avoid overuse → dehydration, hypernatremia

See more about Lactulose in HE, here

PEG (Alternative)

• Faster resolution in trials

• Useful if ileus/bloating

Rifaximin

• Add in recurrent HE

• Consider early in severe ICU cases

ACC 2022 ICU Principles (Add These to Your Workflow)

Airway & Neuroprotection

• Intubate if:

  • GCS ≤ 8

  • Aspiration risk

• Avoid oversedation (benzodiazepines worsen HE)

Hemodynamic & Metabolic Targets

• Maintain MAP ≥ 65 mmHg

• Correct:

  • Hypokalemia

  • Hyponatremia

  • Hypoglycemia

Infection Control

• Low threshold for antibiotics

• Sepsis = major precipitant

ICP & Cerebral Edema (Severe HE / ACLF)

• Head elevation

• Avoid hypercapnia

• Consider hypertonic saline if needed

Nutrition (Critical Update)

• DO NOT restrict protein

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

6. Nonresponse at 48–72 Hours

📌 Insert Figure 9 here – “Nonresponse Algorithm”

If not improving:

1. Reconsider diagnosis

2. Re-look for precipitants

3. Evaluate for:

   • TIPS

   • Large shunts

👉 Do NOT just increase lactulose blindly

7. Preventing Recurrence

“Recurrence Prevention Pathway”

Core Strategy

• Lactulose (target 2–3 stools/day)

• Rifaximin (↓ recurrence 58%)

System-Level Changes

• Use Bristol stool scale

• EMR alerts/order sets

• Patient education tools

Deprescribing (Critical ED Role)

Stop/minimize:

• Benzodiazepines

• Opiates

• Gabapentinoids

• Z-drugs

• PPIs (when inappropriate)

Nutrition & Sarcopenia

• Protein: 1.2–1.5 g/kg/day

• Late-night snack

• Exercise programs

👉 Muscle = ammonia buffer

8. TIPS, Refractory HE & Transplant

TIPS-related HE

• Start rifaximin 14 days before TIPS

• Continue ≥ 6 months

Refractory HE

• Consider:

  • Shunt embolization

  • TIPS revision

Transplant Implications

• HE underestimates MELD risk

• Consider transplant even at low MELD

👉 Early referral if:

• Recurrent HE

• Grade III–IV

• Persistent cognitive decline

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References

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

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

However, once resuscitation begins, the philosophy of care diverges.

Unlike many medical emergencies where organ failure results from progressive disease processes (e.g., myocardial infarction, sepsis), poisoning frequently represents a potentially reversible physiologic disturbance caused by a toxin interacting with receptors, ion channels, or metabolic pathways (Mégarbane et al., 2020).

If the toxin can be neutralised, eliminated, or outlasted with supportive care, full recovery may occur even after severe shock or prolonged cardiac arrest (Lavonas et al., 2023).

This fundamental difference alters how clinicians monitor, resuscitate, and determine prognosis in poisoned patients.

Conceptual Differences in Toxicologic Resuscitation

Poisoning therefore requires a different cognitive model:

Resuscitate aggressively because the underlying physiology may still be reversible (Lavonas et al., 2023; Mégarbane et al., 2020).

Monitoring Poisoned Patients: What Is Different?

Monitoring in toxicology is not purely supportive—it is diagnostic, prognostic, and therapeutic.

Clinical deterioration may occur abruptly due to delayed absorption, redistribution, or toxic metabolite formation. Therefore, continuous bedside observation and trend monitoring are essential (Vega et al., 2024; Hüser et al., 2025).

Standard parameters remain central:

• Heart rate

• Blood pressure

• Respiratory rate

• Oxygen saturation

• Temperature

• Level of consciousness (GCS)

However, clinicians focus heavily on trajectory rather than isolated measurements.

For example:

• Gradual bradycardia and hypotension may suggest β-blocker or calcium channel blocker toxicity.

• Increasing respiratory rate with metabolic acidosis may indicate salicylate poisoning.

• Progressive sedation may signal opioid or sedative ingestion.

These patterns emerge because toxicodynamics evolve with time through delayed absorption, redistribution, or metabolite toxicity (Mégarbane et al., 2020).

ECG Monitoring: The Toxicology Stethoscope

In poisoning, the ECG is both a monitoring tool and a diagnostic instrument.

Certain electrocardiographic findings strongly suggest specific toxin classes (Mégarbane et al., 2020).

Continuous telemetry is particularly important for exposures involving cardiotoxic drugs such as:

• Tricyclic antidepressants

• Antiarrhythmics

• Antipsychotics

• Cocaine

• Calcium channel blockers

• β-blockers (Mégarbane et al., 2020).

ECG abnormalities often precede hemodynamic deterioration, allowing earlier intervention.

Laboratory Monitoring: Targeted Rather Than Indiscriminate

Routine critical care investigations remain important:

• Arterial or venous blood gases

• Electrolytes

• Creatinine

• Glucose

• Lactate

However, interpretation focuses on toxicologic patterns.

Examples include:

Toxin-specific laboratory assays are ordered only when they influence management, such as:

• Acetaminophen levels

• Salicylate levels

• Lithium levels

• Toxic alcohol levels (Bechtel & Holstege, 2022).

Routine broad toxicology screens rarely change acute management.

ABCDE in Poisoning: Same Structure, Different Thresholds

Although the ABCDE framework remains identical, poisoning alters the thresholds and priorities within each step (Hoving et al., 2011; Hüser et al., 2025).

Airway

Airway protection is often required earlier due to:

• Rapid deterioration in consciousness

• Recurrent seizures

• High aspiration risk

Intubation is frequently indicated in:

• Sedative overdose

• Severe opioid intoxication

• Massive ingestion with expected deterioration (Parris & Calello, 2022).

Breathing

Standard oxygen and ventilation strategies are combined with toxin-specific reversal therapies.

Examples include:

• Naloxone for opioid-induced respiratory depression

• Bronchodilators for inhalational exposures

• Atropine and pralidoxime for organophosphate poisoning (Mégarbane et al., 2020).

Circulation

Circulatory failure in poisoning often requires toxin-directed therapy early in resuscitation.

Examples include:

These interventions are frequently initiated before diagnostic confirmation because delay may worsen outcomes (Lavonas et al., 2023).

Disability

Neurologic assessment using GCS, pupillary examination, and glucose measurement guides antidote therapy and toxidrome recognition (Hoving et al., 2011).

For example:

• Pinpoint pupils → possible opioid toxicity → naloxone trial

• Seizures → benzodiazepine therapy

• Anticholinergic syndrome → targeted management

Detoxification: Unique to Toxicology

Unlike most critical illness, poisoning may require active toxin removal.

Gastrointestinal decontamination

Selective use of:

• Activated charcoal

• Whole bowel irrigation

• Gastric lavage

Decision-making depends on:

• Time since ingestion

• Drug characteristics

• Airway protection (Hüser et al., 2025).

Enhanced elimination

Certain toxins can be removed through extracorporeal techniques.

Serial laboratory monitoring determines initiation and termination of therapy (Ghannoum & Roberts, 2023).

Cardiac Arrest in Poisoning: Why It Is Different

Toxicologic cardiac arrest differs from typical cardiac arrest in several important ways.

Many patients are:

• Younger

• Previously healthy

• Experiencing reversible pharmacologic toxicity

Therefore prognosis may be better than in non-toxic cardiac arrest (Lavonas et al., 2023).

Longer and More Aggressive Resuscitation

Termination rules used in standard cardiac arrest may not apply in poisoning.

Resuscitation often involves:

• Prolonged CPR

• Early antidote administration

• Aggressive supportive therapy

Successful neurologic recovery has been reported even after prolonged resuscitation in toxicologic arrests (Lavonas et al., 2023).

Antidotes During Resuscitation

Poisoning resuscitation incorporates toxin-specific therapies alongside standard ACLS medications.

These therapies address the underlying mechanism of arrest, rather than simply supporting circulation.

Extracorporeal Life Support

Extracorporeal membrane oxygenation (ECMO) plays a particularly important role in toxicologic resuscitation.

Because poisoning often represents a reversible physiologic insult, ECMO may function as a bridge to toxin clearance and organ recovery (Ng et al., 2023).

Indications include:

• Refractory toxic cardiogenic shock

• Poisoning-related cardiac arrest

• Severe cardiotoxic drug overdose.

When Should Resuscitation Stop?

Determining when to stop resuscitation is challenging in poisoning.

Delayed recovery may occur because:

• Drugs have long half-lives

• Sedatives delay neurologic recovery

• Metabolites remain active

Therefore many toxicology experts recommend delayed prognostication and consultation with poison centers or toxicologists before withdrawal of care (Lavonas et al., 2023).

The Practical Emergency Medicine Takeaway

For emergency physicians, toxicologic resuscitation requires a shift in mindset.

Key principles include:

• Apply standard ABCDE and ACLS frameworks.

• Monitor physiologic trends rather than isolated values.

• Use the ECG as an early diagnostic tool.

• Initiate toxin-specific therapies early.

• Consider detoxification strategies.

• Be prepared for prolonged resuscitation.

• Think of ECMO as a bridge to recovery rather than rescue therapy.

Because in toxicology:

What appears to be irreversible collapse may simply be physiology waiting for the toxin to clear.

References

1. Hüser N, et al. Management of poisoned patients in the emergency department: monitoring, risk stratification, and supportive care. Clinical Toxicology (Phila). 2025.

2. Lavonas EJ, Drennan IR, Gabrielli A, et al. 2023 American Heart Association focused update on toxicologic emergencies in cardiac arrest and resuscitation. Circulation. 2023;148(24):e___–e___.

3. Mégarbane B, Deye N, Bloch V, et al. Management of acute poisoning in intensive care: general principles and supportive care. Clinical Toxicology (Phila). 2020;58(6):487-502.

4. Bechtel LK, Holstege CP. Toxicologic testing in the emergency department: indications and limitations. Emergency Medicine Clinics of North America. 2022;40(2):345-360.

5. Ghannoum M, Roberts DM. Extracorporeal treatments in poisoning: indications and clinical applications. Clinical Journal of the American Society of Nephrology. 2023;18(3):467-479.

6. Ng PC, et al. Extracorporeal life support for poisoning and drug overdose. Circulation. 2023.

7. Vega RM, et al. Monitoring and early recognition of deterioration in poisoned patients. Clinical Toxicology (Phila). 2024.

8. Parris R, Calello DP. Initial approach to the poisoned patient in the emergency department. Emergency Medicine Clinics of North America. 2022;40(2):215-230.

9. Hoving S, et al. The ABCDE approach to the poisoned patient. Clinical Toxicology (Phila). 2011;49(6):517-524.

10. Ornillo TA, Harbord NB. Respiratory complications of poisoning and their management. Clinics in Chest Medicine. 2020;41(4):633-645.

11. Reyes JC, et al. Laboratory evaluation and risk stratification in acute poisoning. Clinical Toxicology (Phila). 2021.

12. El-Sarnagawy GN, et al. Clinical and laboratory predictors of outcomes in acute pediatric poisoning. Clinical Toxicology (Phila). 2023.

13. Elliott R, et al. Intraosseous access in emergency resuscitation. Resuscitation. 2017;121:1-6.

14. Upchurch CP, et al. Extracorporeal cardiopulmonary resuscitation in reversible causes of cardiac arrest. Circulation. 2021.

15. Von Ow D, Osterwalder J. Decontamination strategies in toxicologic emergencies. Clinical Toxicology (Phila). 2009.

16. Holstege CP, et al. Evaluation and management of the poisoned patient in critical care. Critical Care Clinics. 2008;24(1):103-119.

17. Pannu N. Toxicologic emergencies in the ICU: recognition and management. Critical Care Medicine. 2025.

• Pressure–time

• Flow–time

• Volume–time

These waveforms help identify problems such as airway obstruction, compliance changes, and ventilator asynchrony.

But the ventilator screen offers another powerful tool.

Loops.

Ventilator loops allow clinicians to visualize the relationship between pressure, flow, and volume during a single breath — providing deeper insight into lung mechanics.

Before interpreting loops, however, we must understand the mechanics of the ventilator circuit and the equation that governs ventilation.

The Ventilator Circuit

At its core, the mechanical ventilation system consists of two interacting pumps:

1. The ventilator

2. The patient’s respiratory system

These are connected by the endotracheal tube and ventilator circuit.

The ventilator generates positive pressure that pushes gas into the lungs, while the respiratory system offers resistance and elastic recoil.

The respiratory system can be simplified into two components:

1. Resistive Component

This includes:

• Endotracheal tube

• Airways

• Bronchi

Resistance determines how difficult it is for air to move through the airway.

Examples of increased resistance:

• Bronchospasm

• Secretions

• ET tube obstruction

2. Elastic Component

This includes:

• Lung tissue

• Chest wall

Elastic recoil determines how much pressure is required to expand the lungs.

Examples of reduced compliance:

• ARDS

• Pulmonary edema

• Pneumonia

The Equation of Motion for the Respiratory System

Mechanical ventilation follows a fundamental equation known as the equation of motion.

It describes the pressure required to inflate the lungs.

The equation is:

Airway Pressure = (Flow × Resistance) + (Volume ÷ Compliance)

This equation explains why airway pressure increases during ventilation.

Pressure generated by the ventilator must overcome:

1️⃣ Airway resistance
2️⃣ Elastic recoil of the lungs and chest wall

This explains a key ventilator concept:

Peak pressure reflects both resistance and compliance, while plateau pressure reflects compliance alone.

Understanding this equation is essential before interpreting ventilator loops.

What Are Ventilator Loops?

Unlike scalars, which plot variables against time, loops plot variables against each other.

This allows clinicians to visualize the relationship between pressure, flow, and volume during a breath.

The two most important loops are:

1️⃣ Pressure–Volume (PV) loop
2️⃣ Flow–Volume loop

These loops reveal information about:

• Lung compliance

• Airway obstruction

• Air trapping

• Overdistension

• Optimal PEEP

The Pressure–Volume Loop

The pressure–volume loop plots airway pressure on the X-axis and volume on the Y-axis.

During mechanical ventilation, the loop moves counterclockwise.

The loop begins at the end of expiration and moves upward as the lungs fill with air.

As pressure increases, volume increases.

During expiration, the curve follows a different path back to the starting point.

This difference between inspiratory and expiratory curves is called hysteresis.

It reflects the surface tension and recruitment dynamics of the lung.

Key Points on the Pressure–Volume Loop

Several important landmarks can be identified on the PV loop.

Lower Inflection Point

This point represents the pressure at which alveoli begin to open.

Below this pressure, many alveoli remain collapsed.

Clinically, this helps guide PEEP selection.

Upper Inflection Point

This represents the point where alveoli begin to overdistend.

Beyond this point, additional pressure produces little increase in volume.

This region increases the risk of ventilator-induced lung injury.

Detecting Over-distension

When the upper part of the PV loop flattens or bends outward, it suggests that the lungs are being overinflated.

Common causes include:

• Excessive tidal volume

• High inspiratory pressures

• Inadequate lung protective ventilation

Management:

• Reduce tidal volume

• Reduce driving pressure

• Optimize PEEP

The Flow–Volume Loop

The flow–volume loop plots:

• Flow (Y-axis)

• Volume (X-axis)

The loop consists of:

• Inspiratory limb (above baseline)

• Expiratory limb (below baseline)

Changes in the loop shape provide clues about airway resistance, obstruction, and air trapping.

1. Normal Flow–Volume Loop

Characteristics:

• Smooth inspiratory limb

• Rapid peak expiratory flow

• Gradual return to baseline

• Loop closes completely

Clinical meaning:

Normal airway resistance and lung compliance.

2. Obstructive Lung Disease (COPD / Asthma)

Classic pattern:

Scooped-out expiratory limb

Features:

• Reduced peak expiratory flow

• Concave expiratory curve

• Prolonged expiration

Seen in:

• COPD

• Asthma

• Bronchospasm

• Airway obstruction

Clinical interpretation:

Airflow limitation prevents rapid emptying of the lungs.

3. Fixed Airway Obstruction

Pattern:

Flattened inspiratory AND expiratory limbs

Seen in:

• Tracheal stenosis

• Endotracheal tube obstruction

• Large airway tumor

Clinical interpretation:

Airflow is limited during both inspiration and expiration.

4. Variable Extrathoracic Obstruction

Pattern:

Flattened inspiratory limb

Examples:

• Vocal cord dysfunction

• Laryngeal edema

• Upper airway obstruction

Reason:

Negative intrathoracic pressure during inspiration collapses the airway.

5. Variable Intrathoracic Obstruction

Pattern:

Flattened expiratory limb

Examples:

• Tracheomalacia

• Intrathoracic airway tumor

• Bronchial compression

Reason:

Airways collapse during expiration.

6. Air Trapping / Auto-PEEP

Pattern:

Loop does not return to baseline before next breath

Seen in:

• COPD

• Asthma

• High respiratory rates

• Inadequate expiratory time

Clinical implications:

• Dynamic hyperinflation

• Increased work of breathing

• Hemodynamic compromise

7. Circuit Leak

Pattern:

Loop fails to close

Inspiratory and expiratory volumes do not match.

Causes:

• ETT cuff leak

• Circuit disconnection

• Bronchopleural fistula

Why Ventilator Loops Matter

Ventilator loops allow clinicians to move beyond simple ventilator settings.

They provide a visual understanding of:

• Lung mechanics

• Patient–ventilator interaction

• Recruitment and overdistension

When combined with waveform analysis, loops help clinicians optimize ventilation and prevent complications such as:

• Ventilator-induced lung injury

• Dynamic hyperinflation

• Patient–ventilator asynchrony

The Takeaway

Ventilator waveforms tell us what is happening over time.

Ventilator loops show how pressure, flow, and volume interact during a breath.

Together, they transform the ventilator screen into a real-time window into respiratory physiology.

For clinicians managing critically ill patients, learning to read ventilator loops is not optional — it is an essential skill.

Creator

Dr Arihant Jain, MD
lifeonthefrontline.com

Follow on Instagram: @humans.of.em

• Tidal volume

• Respiratory rate

• PEEP

• FiO₂

But the real story is told by the ventilator waveforms.

Pressure, flow, and volume curves show the interaction between the patient and the ventilator in real time. Learning to read them allows clinicians to detect problems such as:

• Airway obstruction

• Poor lung compliance

• Auto-PEEP

• Ventilator asynchrony

Often before the patient deteriorates clinically.

The Three Fundamental Waveforms

Every ventilator screen shows three basic scalars:

• Pressure vs time

• Flow vs time

• Volume vs time

These waveforms display how gas moves into and out of the lungs with every breath. Ventilators directly measure airway pressure and flow, while volume is derived from the flow signal

1. The Flow–Time Waveform

The Most Informative Curve

The flow waveform represents how quickly gas moves into and out of the lungs.

Two phases exist in every breath:

Inspiratory phase

• Active

• Controlled by ventilator settings

• Pattern depends on ventilation mode

Expiratory phase

• Passive

• Determined by lung recoil and airway resistance.

Square Flow Pattern (Volume Control)

In volume-controlled ventilation, inspiratory flow is usually constant.

Clinical implications:

• Short inspiratory time

• Higher peak airway pressure

• Lower mean airway pressure

This pattern is commonly used in volume assist-control ventilation.

Decelerating Flow Pattern (Pressure Control)

Pressure-controlled ventilation produces a decelerating flow pattern.

Flow starts high and gradually decreases as alveoli fill.

Clinical implications:

• Lower peak airway pressure

• Better gas distribution

• Frequently used in ARDS ventilation strategies

Recognizing Air Trapping

One of the most important things to check:

Does expiratory flow return to zero?

If it does not, the lungs have not fully emptied before the next breath.

This indicates dynamic hyperinflation or auto-PEEP.

Common causes:

• COPD

• Asthma

• High respiratory rate

• Short expiratory time

2. The Pressure–Time Waveform

The pressure waveform shows airway pressure throughout the respiratory cycle.

Baseline pressure corresponds to PEEP, while inspiratory pressure rises during tidal volume delivery.

Distinguishing Resistance vs Compliance

Waveforms allow rapid bedside diagnosis.

Increased Airway Resistance

Pattern:

• High peak pressure

• Normal plateau pressure

Causes:

• Secretions

• Bronchospasm

• ET tube obstruction

Reduced Lung Compliance

Pattern:

• High peak pressure

• High plateau pressure

Causes:

• ARDS

• Pulmonary edema

• Pneumonia

The Stress Index

Detecting Overdistension

The shape of the pressure-time curve during constant flow ventilation provides insight into lung mechanics.

This concept is often used during lung-protective ventilation in ARDS.

3. The Volume–Time Waveform

Volume waveforms show how tidal volume changes over time.

Interestingly, ventilators do not measure volume directly. Instead, volume is calculated from the area under the flow-time curve.

This waveform helps detect:

• Air leaks

• Hyperinflation

• Active expiration

Ventilator Waveforms Reveal Asynchrony

Waveforms also help identify patient–ventilator asynchrony.

Common patterns include:

Ineffective triggering

Patient effort fails to trigger the ventilator.

Often caused by:

• Auto-PEEP

• Weak respiratory muscles

Double triggering

Two breaths delivered for one patient effort.

Seen in:

• ARDS

• High respiratory drive

Auto-triggering

Ventilator delivers breaths without patient effort.

Possible causes:

• Circuit leaks

• Water in tubing

• Cardiac oscillations

What Comes Next

In this article, we focused on the three ventilator scalars:

• Pressure–time

• Flow–time

• Volume–time

These waveforms allow clinicians to quickly recognize changes in airway resistance, lung compliance, air trapping, and patient–ventilator interaction.

But the ventilator screen offers even deeper physiological insight.

In Part 2, we will decode the ventilator loops — including:

• Pressure–Volume loops

• Flow–Volume loops

These loops help identify:

• Overdistension

• Recruitment

• Optimal PEEP

• Airway obstruction

Understanding loops transforms ventilator interpretation from pattern recognition into true respiratory physiology.

Creator

Dr Arihant Jain, MD
lifeonthefrontline.com

Follow on Instagram: @humans.of.em

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

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

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

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

Let’s break this down pragmatically.

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

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

Early recognition hinges on identifying:

• Suspected infection plus

• Evidence of organ dysfunction

Not just shock.

Red flags at the front door:

• Altered mentation

• Tachypnea

• Rising oxygen requirement

• Oliguria

• Cool or mottled extremities

• Elevated lactate despite preserved BP

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

This is cryptic shock — where hypoperfusion precedes hypotension.

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

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

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

Excess fluid leads to:

• Pulmonary edema

• Delayed extubation

• Worsened renal outcomes

• Increased mortality in some subgroups

The emerging model is dynamic:

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

Use physiology to guide you:

• Passive leg raise

• Stroke volume change

• Bedside echo (LV function)

• Capillary refill

• Urine output

• Lactate trend (not single value)

Sepsis resuscitation should be a loop:

Resuscitate → Reassess → Redirect.

Not a one-time fluid event.

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

3️⃣ Earlier Vasopressors Prevent Fluid Creep

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

When hypotension persists after limited fluid resuscitation:

• Start norepinephrine early.

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

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

Earlier vasopressors:

• Restore perfusion sooner

• Limit excess fluid accumulation

• Shorten time to hemodynamic stability

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

4️⃣ Antibiotics Are Urgent — But Source Control Is Definitive

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

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

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

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

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

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

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

Definitive therapy often requires :- Source Control

• Drainage

• Debridement

• Decompression

• Device removal

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

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

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

5️⃣ Point-of-Care Ultrasound Is Now Foundational

Sepsis is hemodynamically heterogeneous.

Some patients are:

• Pure vasoplegia

• Septic cardiomyopathy

• Mixed shock

• Fluid responsive

• Fluid intolerant

Without ultrasound, we are often guessing.

POCUS allows rapid differentiation:

• LV systolic function

• RV strain

• IVC variability

• B-lines (early pulmonary edema)

• Pericardial effusion

• Intra-abdominal source clues

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

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

Many decisive interventions occur before ICU transfer:

• High-flow nasal oxygen

• Noninvasive ventilation

• Early intubation with hemodynamic preparation

• Lung-protective ventilation

• Vasopressor titration

• Renal function surveillance

Disposition is not administrative. It is physiological triage.

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

Clear handovers must include:

• Fluids administered

• Current vasopressor dose

• Lactate trajectory

• POCUS findings

• Source control plan

7️⃣ Stewardship and Individualization Matter

Sepsis pathways must balance urgency with precision.

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

Clinical decisions must incorporate:

• Age

• Co-morbidities

• Functional baseline

• Patient preferences

• Resource realities

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

The Shift We Must Embrace

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

Sepsis is not a protocol problem.

It is a physiology problem.

And physiology demands continuous reassessment.

Reference -

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

1. SGLT-2 Inhibitors as Foundational Therapy

What has changed

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

• No comorbidity

• Heart failure

• ASCVD

• CKD (down to eGFR 20)

• Early-onset T2DM

• Obesity

Acute Care Relevance

1.1 Expect near-universal exposure

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

• Empagliflozin

• Dapagliflozin

This includes patients with:

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

  type-2-diabetes-in-adults-manag…

• Heart failure with preserved or reduced EF

• ASCVD on triple therapy

1.2 Increased Risk of Eu-glycaemic DKA

The guideline explicitly:

• Requires DKA risk assessment before starting SGLT-2

• Advises suspension during ketogenic diets and intercurrent illness

EM/ICU Translation

Lower threshold to:

• Check blood ketones in:

  • Sepsis

  • Major surgery

  • AKI

  • Reduced oral intake

  • Steroid therapy

• Diagnose DKA despite glucose <250 mg/dL

• Stop SGLT-2 immediately on admission if:

  • Shock

  • Hypoxia

  • AKI

  • Severe infection

  • Peri-operative state

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

2. Sick-Day Rules Become Mandatory Documentation

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

• Metformin

• SGLT-2 inhibitors

Acute Care Implication

In ED/ICU you are now:

• Justified in holding these agents in:

  • Dehydration

  • Hypotension

  • Sepsis

  • Contrast exposure

• Expected to document:

  • When to restart

  • Under what renal/hemodynamic parameters

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

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

The update allows:

• Dapagliflozin or empagliflozin down to eGFR 20

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

EM/ICU Implications

You will encounter:

• Dialysis-adjacent patients still taking SGLT-2

• Lower baseline glucose but ongoing osmotic diuresis risk

Monitor for:

• Volume depletion

• Hypotension

• AKI worsening

• Electrolyte shifts

4. Early Triple Therapy is Now Common

For ASCVD, obesity, and early-onset T2DM:

• Metformin

• SGLT-2 inhibitor

• GLP-1 RA or tirzepatide

ICU Implications

Expect:

• Lower HbA1c but polypharmacy

• Reduced insulin requirements at baseline

• Higher GI side-effect burden

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

Recommended strongly for ASCVD and obesity

Acute Care Consequences

5.1 Delayed Gastric Emptying

Implications:

• Increased aspiration risk

• Nausea/vomiting complicating NIV tolerance

• Enteral feeding delays

5.2 Peri-intubation considerations

Consider:

• Full stomach assumption

• RSI preference in unstable patients

6. Glucose Monitoring: Acute Illness and Steroids

The guideline emphasizes:

• Acute intercurrent illness increases hyperglycaemia risk

• Short-term capillary monitoring is appropriate during steroid initiation

EM/ICU Translation

Expect:

• Marked steroid-induced hyperglycaemia

• Rapid escalation of insulin requirements

• Need for structured monitoring post-discharge

Steroid-treated pneumonia/COPD patients will frequently require:

• Basal-bolus insulin

• Escalated capillary monitoring

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

Clear endorsement of:

• isCGM

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

Acute Care Implications

You will see:

• CGM sensors in admitted patients

Important:

• Do NOT rely solely on CGM in:

  • Shock

  • Rapid glucose change

  • Vasopressor states

• Capillary testing remains required for accuracy confirmation.

Ensure:

• Backup strips are available

• Device knowledge confirmed at discharge

8. Organ-Protection Bias Over Glycaemia

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

Critical Care Reframing

When rationalising medications in ICU:

Do not interpret normal HbA1c as overtreatment.

Instead:

• Distinguish glycaemic drugs from organ-protective drugs

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

  • Hemodynamically stable

  • Renal function recovered

  • Oral intake adequate

These are now secondary prevention agents.

9. Frailty and Hypotension Risk

For frail adults:

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

ED/ICU Implication

In elderly septic patients:

• SGLT-2 may contribute to:

  • Pre-existing volume contraction

  • Orthostatic collapse

  • AKI

High vigilance for polypharmacy-related hypotension.

10. Peri-Operative and Critical Care Protocol Adjustments

Because SGLT-2 use is now foundational:

Every diabetic ICU admission should trigger:

• Medication reconciliation focused on SGLT-2

• Ketone surveillance if acidosis

• Clear peri-operative cessation plan

The era of “metformin only” diabetics is over.

Start/stop decision plan in EM/Acute care

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

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

It kills by right ventricular failure.

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

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

This is where classification becomes action.

Step 1: Immediate ED Stabilization

COR 1, LOE B-NR

Initial management priorities in suspected or confirmed PE:

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

Key immediate assessments:

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

Patients in Category D or E require immediate resuscitation.

Oxygen and Respiratory Support

COR 1, LOE C-LD

Indicated in hypoxemic patients.

Target:

SpO₂ ≥ 90%-94%

Preferred escalation:

1. Nasal cannula

2. High-flow nasal oxygen

3. Non-invasive ventilation

Avoid unnecessary intubation.

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

If intubation unavoidable:

• Use hemodynamically stable induction agents
• Initiate vasopressors first

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

Circulatory Support

COR 1, LOE B-NR

Hypotension reflects RV failure and impaired cardiac output.

First-line vasopressor:

Norepinephrine

Benefits:

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

Avoid aggressive fluid boluses.

Excess fluid worsens RV dilation and reduces LV filling.

Step 2: Anticoagulation — The Foundation of Treatment

Anticoagulation prevents clot propagation and allows endogenous fibrinolysis.

COR 1, LOE A

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

Choice of Anticoagulant

DOACs preferred in stable patients

COR 1, LOE A

Preferred agents:

• Apixaban
• Rivaroxaban

Advantages:

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

LMWH preferred when inpatient management required

COR 1, LOE B-R

Preferred in:

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

Advantages:

• Predictable anticoagulation
• Lower HIT risk

UFH preferred in unstable patients

COR 1, LOE B-NR

Indications:

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

Reason:

Rapid reversibility.

Step 3: Reperfusion Therapy

Indicated in RV failure and shock

Reperfusion reduces RV afterload and restores circulation.

Systemic Thrombolysis

COR 1, LOE B-R

Indicated in:

Category E1 — cardiogenic shock
Category E2 — cardiac arrest¹

Reduces mortality and improves hemodynamics.

Consider thrombolysis in Category D

COR 2a, LOE B-NR

Indicated if evidence of:

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

These patients are at high risk of deterioration.

Not recommended routinely in Category C

COR 3, LOE B-R

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

Alteplase (tPA) Dose for Acute Pulmonary Embolism

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

Dose: 100 mg IV over 2 hours

Regimen:

• 100 mg alteplase IV infusion over 120 minutes

• No bolus required (standard regimen)

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

Alternative accelerated regimen (commonly used in ED / ICU)

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

Used when:

• Rapid hemodynamic collapse

• Need for faster reperfusion

• Peri-arrest or severe shock

Evidence shows similar efficacy with potentially lower bleeding risk.

Alteplase Dose During Cardiac Arrest due to PE

When PE is suspected or confirmed cause of arrest:

Recommended regimen (AHA cardiac arrest guidance)

50 mg IV bolus over 2–5 minutes

Then:

• Continue CPR for at least 15–30 minutes

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

Maximum total dose: 100 mg

Most commonly used cardiac arrest protocol in emergency medicine

Option 1 (most widely used):

• Alteplase 50 mg IV push

• Continue CPR 15–30 min

• Repeat 50 mg if needed

Option 2 (alternative):

• Alteplase 100 mg IV bolus over 10 minutes

Used less commonly due to bleeding risk.

Catheter-Directed Therapy

COR 2a, LOE B-NR

Indicated when:

• Thrombolysis contraindicated
• Failed thrombolysis
• Progressive deterioration¹

Advantages:

• Lower bleeding risk
• Targeted therapy

Mechanical Thrombectomy

COR 2a, LOE B-NR

Indications:

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

Improves hemodynamics rapidly.

Increasingly used in modern PE management.

ECMO

COR 2a, LOE C-LD

Indicated in refractory shock or cardiac arrest.

Provides circulatory support until reperfusion effective.

Step 4: Treatment and Disposition by A–E Group

This is the most important ED decision.

Category A — Incidental PE

Mortality risk: <1%

Treatment:

Anticoagulation or observation depending on risk factors¹

Disposition:

Discharge with outpatient follow-up

Category B — Symptomatic, Low Risk

Mortality risk: ~1%

Treatment:

DOAC preferred¹

Disposition:

Outpatient management recommended

Criteria:

• Stable vitals
• No hypoxia
• Reliable follow-up¹

Category C1 — Intermediate Risk, No RV Injury

Mortality risk: 3–5%

Treatment:

Anticoagulation¹

Disposition:

Hospital admission, telemetry

Category C2 — RV Injury or Biomarker Elevation

Mortality risk: 5–15%

Treatment:

Anticoagulation

Disposition:

Hospital admission with monitoring¹

Category C3 — RV Injury + Biomarker Elevation

Mortality risk: 15–30%

Treatment:

UFH preferred
Consider reperfusion if deterioration¹

Disposition:

Step-down or ICU

PERT consultation recommended.

Category D — Normotensive Shock

Mortality risk: 20–40%

Treatment:

UFH
Consider thrombolysis or thrombectomy¹

Disposition:

ICU

Immediate specialist consultation required.

Category E — Cardiogenic Shock or Arrest

Mortality risk: >40%

Treatment:

Immediate reperfusion therapy¹

Options:

• Thrombolysis
• Thrombectomy
• ECMO

Disposition:

ICU

Medical emergency.

Step 5: Monitoring

COR 1, LOE B-NR

Monitor for deterioration:

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

Serial reassessment essential.

Patients may deteriorate rapidly.

Step 6: Complications and Sequelae

Acute complications

Right ventricular failure
Cardiogenic shock
Cardiac arrest

Primary causes of death.

Chronic thromboembolic pulmonary hypertension (CTEPH)

Occurs in 2–4% of patients.¹

Caused by persistent pulmonary vascular obstruction.

Symptoms:

• Progressive dyspnea
• Exercise intolerance

Post-PE syndrome

Occurs in up to 50% of patients.¹

Symptoms:

• Dyspnea
• Reduced exercise tolerance
• Functional impairment

Step 7: Duration of Anticoagulation

COR 1, LOE A

Minimum duration:

3 months¹

Extended anticoagulation recommended if:

• Unprovoked PE
• Persistent risk factors¹

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

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Reference

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

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

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

The difference is not clot size.

It is physiology of clot against RV.

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

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

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

Definition of Acute Pulmonary Embolism

Acute pulmonary embolism is defined as:

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

The clinical consequences depend on the interaction between:

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

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

Epidemiology: The ED Reality

Pulmonary embolism presents a paradox in emergency medicine.

It is common—but rarely confirmed.

Key ED statistics:

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

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

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

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

This defines the core emergency medicine challenge:

Identify dangerous PE while safely excluding PE in the majority.

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

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

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

GROUP A: Subclinical (Incidental) PE

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

These patients have no physiological compromise.

Mortality risk: <1%

Subgroups

A1: Subsegmental incidental PE

Features:

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

Physiology intact.

Lowest-risk group.

A2: Segmental or proximal incidental PE

Features:

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

Anatomical clot present—but physiological compensation intact.

GROUP B: Symptomatic PE, Low Clinical Severity

Definition:
Symptomatic PE with low severity scores:

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

RV function preserved.

Mortality risk: ~1%

Subgroups

B1: Symptomatic sub-segmental PE

Features:

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

B2: Symptomatic segmental or proximal PE

Features:

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

These represent compensated pulmonary embolism physiology.

Many can be safely treated as outpatients.

GROUP C: Symptomatic PE with Elevated Clinical Severity

RV injury present, but no shock

Definition:

Symptomatic PE with elevated clinical severity scores:

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

Represents early RV dysfunction.

Mortality risk increases progressively across subgroups.

Subgroups

C1: Elevated clinical severity score only

Features:

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

Risk driven by co-morbid vulnerability.

Mortality risk: ~3–5%

C2: RV dysfunction OR biomarker elevation

Features:

Either:

• RV dilation on imaging
OR
• Elevated troponin or BNP

Indicates early RV myocardial stress.

Mortality risk: ~5–15%

C3: RV dysfunction AND biomarker elevation

Features:

• RV dilation present
• Elevated troponin
• Elevated BNP

Represents established RV injury.

Blood pressure still preserved due to compensation.

Mortality risk: 15–30%

This is the highest-risk normotensive subgroup.

Equivalent to old ‘Intermediate - High Risk Group’

Respiratory Modifier: “R”

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

Examples:

C3R
D2R
E1R

Defined by:

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

Pulm Embolism new guidelines

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

GROUP D: Incipient Cardiopulmonary Failure

Shock physiology emerging

Most important group to identify

These patients demonstrate circulatory compromise without persistent hypotension.

Mortality risk: 20–40%

Subgroups

D1: Transient hypotension

Features:

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

Represents unstable compensation.

D2: Normotensive shock

Features:

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

Shock present despite preserved blood pressure.

Extremely high risk.

GROUP E: Cardiopulmonary Failure

Established shock or cardiac arrest

Highest-risk group.

Mortality risk: >40%

Pulm Embolism new guidelines

Subgroups

E1: Cardiogenic shock

Features:

• Persistent hypotension
• Vasopressor requirement
• RV failure present

E2: Refractory shock or cardiac arrest

Features:

• Persistent shock despite therapy
• Cardiac arrest

Highest mortality subgroup.

Emergency Department Diagnostic Approach (COR and LOE)

The guideline recommends a structured, stepwise approach.

Step 1: Clinical Assessment

COR 1, LOE A

Pulm Embolism new guidelines

Includes:

Symptoms:

• Dyspnea
• Chest pain
• Syncope
• Hemoptysis

Signs:

• Tachycardia
• Hypoxia
• Hypotension
• Signs of DVT

Risk factors:

• Prior VTE
• Surgery
• Immobilization
• Cancer
• Pregnancy

Step 2: Clinical Probability Assessment

COR 1, LOE A

Pulm Embolism new guidelines

Validated tools:

• Wells Score
• Revised Geneva Score
• PERC Rule

These determine need for testing.

Step 3: D-Dimer Testing

COR 2a, LOE B-R

Pulm Embolism new guidelines

Indicated in low or intermediate probability patients.

Age-adjusted D-dimer improves diagnostic efficiency.

Failure rate: 0.3%

Step 4: Imaging with CTPA

COR 1, LOE A

Pulm Embolism new guidelines

CTPA is diagnostic standard.

Advantages:

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

Step 5: RV Assessment and Biomarkers

COR 1, LOE B-R

Pulm Embolism new guidelines

Critical prognostic parameters include:

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

These identify RV dysfunction.

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

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

Pulm Embolism new guidelines

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

Highest-Value Echo Findings Ranked by Likelihood Ratio

From strongest to weakest diagnostic strength:

1. McConnell sign → LR+ up to 12

2. Septal flattening → LR+ up to 10

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

4. TAPSE <1.6 cm → LR+ up to 6

5. RV dilation → LR+ up to 4

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

POCUS for diagnosis

COR 3 (No Benefit), LOE B-NR

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

Reason: poor sensitivity.

Cardiac POCUS for risk stratification

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

Pulm Embolism new guidelines

Multiple parameters improve accuracy

Guideline explicitly states:

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

Pulm Embolism new guidelines

Emergency Medicine Interpretation Algorithm Using Likelihood Ratios

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

Example: Moderate probability patient

Pretest probability: 30%

McConnell sign present
LR+ = 10

Post-test probability → ~80–90%

Strongly supports PE diagnosis and high-risk physiology.

Example: Echo normal

LR− ~0.6

Post-test probability drops modestly.

Cannot exclude PE.

CTPA still required.

Most Important ED Clinical Insight

POCUS is not sensitive enough to exclude PE.

highly valuable for identifying dangerous PE.

identifies physiology—not clot.

answers the question:

Is the right ventricle failing?

Not:

Is there a clot?

Highest-Yield Bedside Rule for Emergency Physicians

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

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

Post-test probability becomes very high.

Why Classification Matters in the Emergency Department

This classification determines:

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

This decision begins in the emergency department.

Not after admission.

Critical Emergency Medicine Insight

The most dangerous PE is not the hypotensive patient.

It is the normotensive patient with failing RV physiology.

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

This is the true purpose of classification.

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

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

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

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

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

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

If you found this useful, follow for more visual emergency medicine breakdowns.
I regularly share clinical algorithms, airway physiology, and critical care insights on Instagram:
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More visual explainers and ED-focused pearls are posted there.

Coming Next: Part 2

Part 2 will cover:

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

All mapped directly to A–E classification.

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References

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

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

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

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

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

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

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

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

The patient is hypoxic. SpO₂ is 82%. Agitated. Diaphoretic.

You push induction.

First attempt fails.

Second attempt fails.

The saturation falls faster than your confidence.

The room gets quieter.

This is the moment that defines airway management.

Not when you intubate.

But when you decide what to do next.

Because modern airway management is not about intubation.

It is about oxygenation.

The Most Important Airway Principle Ever Written

The goal of airway management is not to place a tube.

The goal is to maintain oxygenation.

This distinction seems subtle.

It is not.

It is the difference between controlled progression and catastrophic fixation.

Modern airway guidelines consistently emphasise this shift: prioritising oxygen delivery, limiting attempts, and progressing early through rescue strategies improves outcomes (Ahmad et al., 2025; Myatra et al., 2025).

Hypoxia kills.

Ego does not oxygenate.

Persistence does not oxygenate.

Only oxygenation oxygenates.

The Three Types of Difficult Airway

Every difficult airway belongs to one—or more—of three categories:

1. Anatomically difficult airway

2. Physiologically difficult airway

3. Situationally difficult airway

Understanding this framework changes everything.

Because in emergency medicine, anatomy is rarely the real problem.

Physiology and context are.

The Anatomically Difficult Airway: The Traditional Fear

Defined as difficulty with facemask ventilation, supraglottic airway, laryngoscopy, or surgical airway access (Myatra et al., 2025).

This is the airway we are trained to recognise:

• Limited mouth opening

• Cervical spine immobility

• Facial trauma

• Obesity

• Airway tumours

This airway is technically difficult.

But often physiologically stable.

These patients can tolerate attempts.

Critically ill patients often cannot.

Won’t discuss much about this.

The Physiologically Difficult Airway: The Airway That Kills

The most dangerous airway is not difficult to intubate.

It is difficult to survive.

The physiologically difficult airway is defined as an airway in which physiological or pathophysiological alterations increase the risk of hypoxaemia, cardiovascular collapse, or death during intubation and transition to positive pressure ventilation (Mosier et al., 2015; Myatra et al., 2022; Ahmad et al., 2025).

You see the cords easily.

You pass the tube easily.

And the patient arrests.

Not because of anatomy.

Because of physiology.

The Five Physiological Phenotypes That Kill Patients

1. Hypoxaemic phenotype

Examples:

• ARDS

• Severe pneumonia

• Pulmonary edema

These patients have no oxygen reserve.

Apnea leads to rapid desaturation.

Peri-oxygenation

— pre , apneic and oxygenation during multiple attempts.

—including head-up positioning, NIV, and high-flow nasal oxygen—prolongs safe apnoea time and reduces hypoxaemia risk (Ahmad et al., 2025; Myatra et al., 2025).

2. Hypotensive / Shock phenotype

Examples:

• Septic shock

• Hemorrhagic shock

Induction removes sympathetic tone.

Positive pressure ventilation reduces venous return.

Cardiac output collapses.

Cardiovascular collapse during intubation occurs in a substantial proportion of critically ill patients, especially without haemodynamic optimisation (Mosier et al., 2015; Karamchandani et al., 2024).

3. Severe metabolic acidosis phenotype

Examples:

• DKA

• Septic acidosis

• Salicylate poisoning

These patients survive through compensatory hyperventilation.

Apnea removes compensation.

Acidosis worsens.

Cardiac arrest follows.

Preserving spontaneous ventilation may be life-saving.

4. Right ventricular failure phenotype

Examples:

• Pulmonary embolism

• Severe pulmonary hypertension

Positive pressure ventilation increases pulmonary vascular resistance.

RV fails.

Cardiac output collapses.

5. Neurologic / intracranial hypertension phenotype

Examples:

• Severe traumatic brain injury

• Intracranial hemorrhage

Even brief hypoxia or hypotension worsens neurologic outcomes.
Attempt to intubation can increase ICP

Physiology must be protected throughout airway management.

The Most Important Question Before Intubation

Not:

Can I intubate this patient?

But:

Can this patient survive intubation?

This single question separates safe airway management from catastrophic airway management.

The Situationally Difficult Airway: When Context Makes the Airway Dangerous

Sometimes anatomy is easy.

Physiology is stable.

But the environment makes the airway dangerous.

This is the situationally difficult airway.

Defined as airway difficulty caused by environmental, logistical, or resource constraints—even when anatomy and physiology are normal (Hung & Murphy, 2010; Karamchandani et al., 2021).

Situational factors that create airway risk

Environment

• Emergency department resuscitation

• ICU

• Prehospital care

• Remote locations

Airway management outside controlled environments carries higher complication risk (Lavery & McCloskey, 2008; Karamchandani et al., 2021).

Physical constraints

• Confined space

• Limited positioning

• Poor lighting

These impair visualisation and limit rescue options (Thoeni et al., 2015; Rudolph et al., 2025).

Resource limitations

• No videolaryngoscope

• Limited assistance

• No surgical airway expertise

Operator skill, equipment, and access to help directly influence airway outcomes (Law et al., 2021; Burgess et al., 2022).

Urgency and competing priorities

• Active cardiac arrest

• Ongoing CPR

• Simultaneous resuscitation

These increase cognitive load and reduce airway success.

Human factors contribute significantly to airway complications (Myatra et al., 2025).

The Airway Algorithm That Saves Lives: Plans A, B, C, and D

Airway management is not a single plan.

It is a sequence of oxygenation strategies.

Plan A: Tracheal Intubation

Maximise first-pass success:

• Videolaryngoscopy preferred (Ahmad et al., 2025)

• Optimal positioning

• Neuromuscular blockade

• Preoxygenation

First-pass success reduces complications and improves outcomes (Mosier et al., 2015).

Plan B: Supraglottic Airway

Rapid restoration of oxygenation.

Guidelines emphasise switching early between airway devices without fixation on intubation (Myatra et al., 2025).

Plan C: Face Mask Ventilation

Life-saving oxygenation strategy.

Buys time.

Allows physiological stabilisation.

Plan D: Emergency Front-of-Neck Access

Not failure.

Survival.

Emergency cricothyroidotomy is indicated when oxygenation cannot be achieved through other methods (Ahmad et al., 2025; Myatra et al., 2025).

The Vortex Approach: The Cognitive Framework That Prevents Airway Catastrophe

In a true airway crisis, the greatest threat is not anatomy. It is indecision. The Vortex Approach provides a simple, high-stakes cognitive framework designed for these exact moments. Instead of viewing airway management as a rigid sequence, the Vortex conceptualises three non-surgical oxygenation lifelines—facemask ventilation, supraglottic airway, and tracheal intubation—as interchangeable pathways, all aimed at a single goal: effective alveolar oxygen delivery (Nichols et al., 2017; Myatra et al., 2025).

Each attempt should be deliberate and optimised, but fixation on any one technique must be avoided. If oxygenation cannot be achieved despite best efforts in all three lifelines, the Vortex makes the decision clear and immediate: proceed to emergency front-of-neck access.

This framework removes hesitation, reduces cognitive overload, and prioritises oxygenation over procedural persistence. Modern guidelines increasingly emphasise similar principles—early recognition of failure, limiting repeated attempts, and rapid progression to rescue strategies—to prevent hypoxic injury and death (Ahmad et al., 2025; Myatra et al., 2025).

The Vortex does not replace airway skill. It protects decision-making when skill alone is not enough.

The Most Important Intervention Happens Before Induction

Preparation.

Not speed.

Preparation.

Optimise oxygenation.

Optimise hemodynamics.

Prepare equipment.

Prepare backup plans.

Communicate clearly.

Airway strategy must account for anatomy, physiology, environment, operator skill, and resources (Ahmad et al., 2025; Law et al., 2021).

The Most Dangerous Airway Error Is Fixation

One more attempt.

One more try.

Meanwhile, physiology collapses.

Human factors—including fixation and cognitive overload—are major contributors to airway complications (Myatra et al., 2025).