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REBEL Cast — Government & Organizations
REBEL Cast

Rational Evidence-Based Evaluation of Literature

Latest Episodes:

REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes Sep 15, 2025

🧭 REBEL Rundown

🗝️ Key Points

💨 Master the 3 Types of Breaths
Control, Assist, and Spontaneous — know the difference before tackling ventilator modes.
📦 Breath Delivery: Volume vs. Pressure
Volume-Targeted = fixed volume → monitor pressure
📈 Pressure-Targeted = fixed pressure → monitor volume
🫁 Lung Compliance = Pressure-Volume Relationship
Volume mode: ↑ pressure = ↓ compliance (stiff lungs)
Pressure mode: ↓ tidal volume = ↓ compliance

Click here for Direct Download of the Podcast.

📝 Introduction

For many medical residents, the ICU can feel like stepping into a pressure cooker. At the heart of that stress often lies one intimidating machine: the ventilator. Rather than diving headfirst into complex ventilator modes, this episode lays a critical foundation by breaking down the basic building blocks of mechanical ventilation, something every clinician should master before moving on to more advanced concepts. Once you know the 3 types of breaths and how those breaths are delivered, you can more easily understand most of the mechanical ventilator modes.

🧮 The 3 Types of Breaths

To simplify things, we use a pull-up analogy to explain the types of ventilator breaths:

🫁 The 3 Types of Breaths…It's Like

😮‍💨 Breath Delivery: Volume vs. Pressure

Once you know the type of breath, the next key concept is how it’s delivered:
1. Volume-Targeted Delivery
The ventilator delivers a fixed tidal volume (e.g., 400 mL) with each control or assist breath.
What to monitor: Pressure. As lung compliance worsens, pressure increases.
Risk: Barotrauma if the pressure becomes too high.
2. Pressure-Targeted Delivery
The ventilator delivers air to a preset pressure (e.g., 15 cm H₂O).
What to monitor: Tidal volume. As compliance drops, so does delivered volume.
Adjustment: Modify pressure to maintain appropriate ventilation.

🧱 Putting It All Together: Lung Compliance

The relationship between pressure and volume is described by compliance:
📐 Compliance = Δ Volume / Δ Pressure
In volume mode:
Rising pressure to achieve the same volume = decreased compliance (stiff)
Decreasing pressure to achieve the same volume = increased compliance (loose)
In pressure mode:
Dropping tidal volume at a constant pressure = decreased compliance (stiff)
Rising tidal volume at a constant pressure = increased compliance (loose)

🚨 Clinical Bottom Line

Before tackling advanced ventilator modes, master these foundational concepts:
The three breath types
The two delivery methods
The role of lung compliance
Once you’ve got these down, the rest of mechanical ventilation becomes far easier to understand.
Stay tuned for Part 2, where we’ll build on this foundation and unpack the most commonly used ventilator modes.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Show Notes By: Nicole Ebalo, DO

👤 Guest Contributors

Eric Acker, MD
Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Nicole Ebalo, DO
Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes

For many medical residents, the ICU can feel like stepping ...
Thoracic and Respiratory Read More
REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine

The sicker the patient, the more likely an IO line ...
Procedures and Skills Read More
REBEL Core Cast 139.0: Pneumothorax Decompression

On this episode of the Rebel Core Cast, Swami takes ...
Procedures and Skills Read More
REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia

Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ...
Cardiovascular Read More
REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient

In this episode, we focus on the bedside evaluation of ...
Thoracic and Respiratory Read More
REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia)

In this episode, we break down a practical bedside approach ...
Resuscitation Read More
The post REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes Sep 15, 2025

🧭 REBEL Rundown

🗝️ Key Points

💨 Master the 3 Types of Breaths
Control, Assist, and Spontaneous — know the difference before tackling ventilator modes.
📦 Breath Delivery: Volume vs. Pressure
Volume-Targeted = fixed volume → monitor pressure
📈 Pressure-Targeted = fixed pressure → monitor volume
🫁 Lung Compliance = Pressure-Volume Relationship
Volume mode: ↑ pressure = ↓ compliance (stiff lungs)
Pressure mode: ↓ tidal volume = ↓ compliance

Click here for Direct Download of the Podcast.

📝 Introduction

For many medical residents, the ICU can feel like stepping into a pressure cooker. At the heart of that stress often lies one intimidating machine: the ventilator. Rather than diving headfirst into complex ventilator modes, this episode lays a critical foundation by breaking down the basic building blocks of mechanical ventilation, something every clinician should master before moving on to more advanced concepts. Once you know the 3 types of breaths and how those breaths are delivered, you can more easily understand most of the mechanical ventilator modes.

🧮 The 3 Types of Breaths

To simplify things, we use a pull-up analogy to explain the types of ventilator breaths:

🫁 The 3 Types of Breaths…It's Like

😮‍💨 Breath Delivery: Volume vs. Pressure

Once you know the type of breath, the next key concept is how it’s delivered:
1. Volume-Targeted Delivery
The ventilator delivers a fixed tidal volume (e.g., 400 mL) with each control or assist breath.
What to monitor: Pressure. As lung compliance worsens, pressure increases.
Risk: Barotrauma if the pressure becomes too high.
2. Pressure-Targeted Delivery
The ventilator delivers air to a preset pressure (e.g., 15 cm H₂O).
What to monitor: Tidal volume. As compliance drops, so does delivered volume.
Adjustment: Modify pressure to maintain appropriate ventilation.

🧱 Putting It All Together: Lung Compliance

The relationship between pressure and volume is described by compliance:
📐 Compliance = Δ Volume / Δ Pressure
In volume mode:
Rising pressure to achieve the same volume = decreased compliance (stiff)
Decreasing pressure to achieve the same volume = increased compliance (loose)
In pressure mode:
Dropping tidal volume at a constant pressure = decreased compliance (stiff)
Rising tidal volume at a constant pressure = increased compliance (loose)

🚨 Clinical Bottom Line

Before tackling advanced ventilator modes, master these foundational concepts:
The three breath types
The two delivery methods
The role of lung compliance
Once you’ve got these down, the rest of mechanical ventilation becomes far easier to understand.
Stay tuned for Part 2, where we’ll build on this foundation and unpack the most commonly used ventilator modes.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Show Notes By: Nicole Ebalo, DO

👤 Guest Contributors

Eric Acker, MD
Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Nicole Ebalo, DO
Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes

For many medical residents, the ICU can feel like stepping ...
Thoracic and Respiratory Read More
REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine

The sicker the patient, the more likely an IO line ...
Procedures and Skills Read More
REBEL Core Cast 139.0: Pneumothorax Decompression

On this episode of the Rebel Core Cast, Swami takes ...
Procedures and Skills Read More
REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia

Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ...
Cardiovascular Read More
REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient

In this episode, we focus on the bedside evaluation of ...
Thoracic and Respiratory Read More
REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia)

In this episode, we break down a practical bedside approach ...
Resuscitation Read More
The post REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine Sep 01, 2025

🧭 REBEL Rundown

📌 Key Points

💉 IO Lines Are Life-Saving in Extremis: IO access is fast, reliable, and can deliver nearly any resuscitative medication or fluid during cardiac arrest or hemorrhagic shock.
🧭 Location Matters for Flow. Sternal IO: 💨 Fastest (up to 500cc/5 min). Humerus IO: ⚡ Faster than tibia (300cc/5 min). Tibial IO: 🐢 Slower (200cc/5 min) but easier to place during CPR
⚠️ Watch for Contraindications: Avoid IO placement in bones with fractures, prior IO attempts, or compromised circulation proximal to the site.
🩸 Labs From IO = ❌: Labs drawn from IO lines are generally unreliable. Once stabilized, obtain bloodwork through IV access.
🎯 Stabilize or Lose It: IO dislodgement is common—always use a stabilizer or secure with gauze and tape if none is provided.
🧠 Don’t Forget Non-Trauma Uses: IO isn’t just for trauma—think about it in medical arrests, shocked pediatric patients, and patients with difficult IV access.

Click here for Direct Download of the Podcast.

⏰ Highlights

00:00 Introduction to the Podcast
00:07 First Encounter with Intraosseous Lines
01:09 Advantages of Intraosseous Lines
02:42 Intraosseous Lines in Pediatric Patients
03:34 Optimal Locations for Intraosseous Lines
06:17 Limitations and Considerations
07:34 Conclusion and Final Thoughts

📝 Introduction

Welcome to the Rebel Core Content blog, your go-to source for core medical concepts applicable to practitioners anywhere, anytime. Today, we delve into the world of Intraosseous (IO) lines—a crucial tool in emergency medicine. Swami shares insights into the effectiveness and limitations of IO usage in diverse clinical scenarios.

🧠 Background

The sicker the patient, the more likely an IO line is the right choice. In emergencies such as cardiac arrest or hemorrhagic shock, the speed and reliability of IO access outshine traditional intravenous (IV) or central line placements. There’s virtually no resuscitation medication or blood product that cannot be administered through an IO, making it indispensable in life-threatening situations.

🧭 Location

While proximal humerus site portents faster infusion rates than proximal tibia site, the main limitation of the proximal humerus site is that the arm must be held in internal rotation to avoid dislodgement of the IO
Proximal tibia may be easier to landmark than proximal humerus
Other sites include distal tibia, distal femur and sternum but are uncommonly employed in EDs

🚰 Flow Rates

Proximal Humerus IO
~300cc over 5 minutes
Faster than tibia
May be harder to access in some trauma or positioning scenarios
Tibial IO
~200cc over 5 minutes
Slower flow compared to humerus
Easier to access, especially during CPR or transport
Sternal IO
Up to 500cc over 5 minutes
Highest flow rate
Best for rapid volume resuscitation
Risk of dislodgement or interfering with CPR compressions

⚠️ Limitations

Placing an IO in a bone with a proximal fracture, a previous IO placement attempt or any circulatory compromise proximal to the site is contraindicated
Blood work drawn from an IO are generally not accurate, so once the patient has been resuscitated with the IO, intravenous blood draws are recommended
Dislodgement is common; it is best to use the stabilizer that comes with the IO kit; if the kit does not have a stabilizer, stack lots of gauze on both sides of the IO needle and tape it down

🚨 Clinical Bottom Line

Intraosseous lines are a powerful tool, particularly in acute resuscitation scenarios involving cardiac arrest or severe trauma. While they offer quick and effective access, Clinicians must remain vigilant about their limitations and be prepared to switch to more stable options as patients stabilize.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Associate Editor

Anand Swaminathan

MD, MPH

All Things REBEL EM
Meet The Team
🔎 Your Deep-Dive Starts Here

REBEL Core Cast 134.0 – Acetaminophen Toxicity

Acetaminophen (APAP) overdose remains one of the most common causes ...
Toxicology Read More
Street Medicine: Compassionate Care for the Unhoused

Introduction: In this episode of Rebel Cast, host Marco Propersi, ...
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REBEL Cast Ep91: Static Ultrasound vs Landmark Placement of Subclavian Central Lines

Background Information: Central venous catheterization is a common procedure performed in ...
Procedures and Skills Read More
REBEL Cast Ep82: Timing of Endoscopy for UGIB

Background: Upper endoscopy allows for the identification of the source ...
Abdominal and Gastroinstestinal Read More
REBEL Core Cast 1.0 – The Intro

REBEL EM-ers: Salim, Jenny and I would like to announce ...
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REBEL Cast Ep 46b: Vent Management in the Crashing Patient with Haney Mallemat

In Episode 46a we discussed respiratory failure and NIV. In ...
Thoracic and Respiratory Read More
The post REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 139.0: Pneumothorax Decompression Aug 18, 2025

🧭 REBEL Rundown

📌 Key Points

🧠 Think Beyond Trauma: Don’t forget to suspect tension pneumothorax in ventilated patients who suddenly crash or after a central line placement! 🫁⚠️
🔍 Confirm with Ultrasound: If the patient is stable enough, grab the probe! 🖐️📟Ultrasound can rapidly confirm tension PTX and avoid unnecessary delays.
💉🚫 Needles Are Out: Needle decompression? Meh. Finger thoracostomy is faster, more reliable, and more definitive. 🖐️🫁

Click here for Direct Download of the Podcast.

📝 Introduction

On this episode of the Rebel Core Cast, Swami takes a deep dive into pneumothorax decompression, focusing on the need for improvements beyond the classic teachings. Covering scenarios where immediate decompression is critical, particularly in tension pneumothorax, Swami discusses the limitations of needle decompression, especially in the second intercostal space at the midclavicular line. He highlights the importance of using POCUS for diagnosis and recommends skipping needle decompression in favor of finger thoracostomy for a more reliable and effective treatment. Key takeaways emphasize recognizing tension pneumothorax in various clinical situations and the advantages of finger thoracostomy over traditional techniques.

⏰ Highlights

00:00 Introduction to Pneumothorax Decompression
00:17 Recognizing Tension Pneumothorax
01:00 Common Scenarios for Pneumothorax
01:34 Confirming Diagnosis with POCUS
01:50 Issues with Needle Decompression
03:21 Advantages of Finger Thoracostomy
04:11 Key Takeaways and Conclusion

📚 References

Ferrie EP et al. The right place in the right space? Awareness of site for needle thoracentesis. Emerg Med J 2005; 22: 788-9 PMID: 16244336
Laan DV et al. Chest wall thickness and decompression failure: a systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Injury; 2016; 47(4): 797-804 PMID: 26724173
Terboven T et al. Chest wall thickness and depth to vital structures in paediatric patients – implications for prehospital needle decompression of tension pneumothorax. Scan J Trauma Resusc Emerg Med 2109; 27(1). PMID: 30992028

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Associate Editor

Anand Swaminathan

MD, MPH

All Things REBEL EM
Meet The Team
🔎 Your Deep-Dive Starts Here

REBEL Cast Ep 46a – Respiratory Failure and NIV with Haney Mallemat

Imagine you have a patient in respiratory failure sitting right ...
Thoracic and Respiratory Read More
REBEL Cast Ep 43: Pain Control and Opioid Sparing Options in the ED

Background: In the United States we are not only seeing ...
Trauma Read More
REBEL Cast Episode 42: Research From the Past Year – In the Pipeline

Welcome back to Episode 42 of REBEL Cast. In this ...
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REBEL Cast Episode 41: Research From the Past Year – Resuscitation

Welcome back to Episode 41 of REBEL Cast. In this ...
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REBEL Cast Episode 40: Research From the Past Year – Pain Control

Welcome back to Episode 40 of REBEL Cast. We have ...
Trauma Read More
February 2017 REBEL Cast: The All Hyperoxia Edition

Background: Many providers and health care workers place oxygen on ...
Resuscitation Read More
The post REBEL Core Cast 139.0: Pneumothorax Decompression appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 138.0: A Simple Bedside Approach to Shock Aug 04, 2025

🧭 REBEL Rundown

📌 Key Points

🧠 Shock is a Clinical Diagnosis — Not Just a Number
Patients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR.
🖐️ Start with the 4 L’s
Lucid (mental status), Limbs (warm/cold), Leak (urine output), and Lactate give you rapid bedside insight into perfusion status.
💡 Pulse Pressure Helps Pinpoint the Type
➡️ Narrow PP = Cardiogenic, Hypovolemic, or Obstructive shock
➡️ Wide PP = Distributive shock (Sepsis, Anaphylaxis, Neurogenic)
🚨 Be Systematic at the Bedside
Quick vitals, focused history, and targeted exam can reveal the etiology faster than invasive tools.

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we will dive into a simple yet effective bedside approach to a patient in shock. By using quick physical exam findings and bedside vitals (particularly pulse pressure), you can form a quick assessment of the likely underlying etiology of a critically ill patient.

🔑 Key Concepts

What is Shock?

Supply vs. Demand mismatch:
Inadequate perfusion relative to metabolic demands
Leading to tissue hypoxia and cell death
DO2 = CO x (Hb x Sat + (0.003 x paO2))
CO = Heart Rate x Stroke Volume
Determinants of Stroke Volume: Preload, Contractility, and Afterload
4 L’s of Hypotension
Lucid: What’s their mental status?
Limbs: Are they cold vs. warm? What is the cap refill?
Leak: Are they taking a “leak”? What is the urine output?
Lactate
Remember:
Shock DOES NOT equal hypotension
A patient in shock can still have normotensive pressures in “Compensated Shock”
Signs of Shock
Increased HR, increased RR, AMS, decreased urine output, cool to touch, weak pulses, slow capillary refill

Defining Blood Pressure

Systolic Blood Pressure
Stroke Volume: Main contributor to SBP ➡️ SV ≈ SBP
Aortic/Arterial Compliance
Diastolic Blood Pressure
Systemic Vascular Resistance
Maintains end-organ perfusion in diastole
Pulse Pressure
SBP – DBP
Mean Arterial Pressure
MAP < 60-65 can lead to end-organ damage

Narrow Pulse Pressure

Cardiogenic: “Cold Shock”
Low contractility ➡️low SV ➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Cold limbs, weak pulses, poor capillary refill
Hypovolemic
Hemorrhagic vs. Dehydration
Decrease preload ➡️ decreased SV ➡️ decreased SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Obstructive
“Obstruction of preload” ➡️ decreased SV➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Pneumothorax
Increased intrathoracic pressure ➡️ decrease IVC and SVC ➡️ decreased preload
Cardiac Tamponade
Fluid in pericardial space ➡️ decrease filling ➡️ decreased preload
Pulmonary Emboli: Obstruction of RV to LA flow ➡️ decreased preload

Wide Pulse Pressure: Distributive Shock

“Warm shock”: Vasodilatation ➡️ decreased SVR ➡️ Decreased DBP
Septic: Main cause of distributive shock
Neurogenic: Loss of sympathetic tone ➡️ unopposed parasympathetic / vagal tone ➡️ decreased SVR ➡️ decreased DBP
Anaphylaxis: histamine and other inflammatory mediators released ➡️ increased vascular permeability ➡️ decreased SVR ➡️ decreased DBP
Adrenal Crisis: Not secreting cortisol ➡️ not increasing vascular tone ➡️ decreased SVR ➡️ decreased DBP
Hepatic Failure: Increase in NOS ➡️ increases NO ➡️ vasodilatation

🛌 Practical Bedside Approach

When called to bedside:
Is the patient meeting any of the 4 “L’s” ?
Check the pulse pressure along with other vitals
Why are they here? What’s the brief history?
Narrow Pulse Pressure? Cardiogenic, hypovolemic, or obstructive shock
Wide Pulse Pressure? Distributive shock
Think: sepsis (most likely), neurogenic, anaphylaxis, adrenal crisis, hepatic failure

🚨 Clinical Bottom Line

A brief but thorough bedside exam remembering the 4 “L’s”, a quick history, and examining the pulse pressure can help a clinician form a quick differential into the underlying etiology for a critically ill patient in shock. Stay sharp, stay systematic!
💡 Shock is a clinical diagnosis based on bedside findings — not just blood pressure readings.
You don’t always need invasive monitoring to identify shock. Look at HR, RR, UOP, and mentation.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Micheal Bass DO
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
Frank J. Lodeserto MD
Associate Professor and Internal Medicine Residency Program Director Adult & Pediatric Critical Care Medicine, Cape Fear Valley Medical Center, Fayetteville, NC
🔎 Your Deep-Dive Starts Here

REBEL Core Cast 138.0: A Simple Bedside Approach to Shock

In this episode, we will dive into a simple yet ...
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REBEL Core Cast 131.0 – Traumatic Arthrotomy

Take Home points: Always suspect an open joint if there ...
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REBEL Core Cast 130.0 – Omphalitis

Take Home Points Early diagnosis: erythema and warmth of the ...
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REBEL Core Cast 129.0 – Gastric Lavage

Take Home Points Orogastric lavage may still play an important ...
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REBEL Core Cast 128.0 – Toxic Alcohols

Take Home Points Toxic alcohols generally refer to methanol and ...
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REBEL Core Cast 127.0 – Penetrating Neck Injuries

Take Home Points Anticipate anatomically challenging airways and consider early ...
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The post REBEL Core Cast 138.0: A Simple Bedside Approach to Shock appeared first on REBEL EM - Emergency Medicine Blog.

Eric Acker MD — REBEL Core Cast 138.0: A Simple Bedside Approach to Shock Aug 04, 2025

🧭 REBEL Rundown

📌 Key Points

🧠 Shock is a Clinical Diagnosis — Not Just a Number
Patients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR.
🖐️ Start with the 4 L’s
Lucid (mental status), Limbs (warm/cold), Leak (urine output), and Lactate give you rapid bedside insight into perfusion status.
💡 Pulse Pressure Helps Pinpoint the Type
➡️ Narrow PP = Cardiogenic, Hypovolemic, or Obstructive shock
➡️ Wide PP = Distributive shock (Sepsis, Anaphylaxis, Neurogenic)
🚨 Be Systematic at the Bedside
Quick vitals, focused history, and targeted exam can reveal the etiology faster than invasive tools.

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we will dive into a simple yet effective bedside approach to a patient in shock. By using quick physical exam findings and bedside vitals (particularly pulse pressure), you can form a quick assessment of the likely underlying etiology of a critically ill patient.

🔑 Key Concepts

What is Shock?

Supply vs. Demand mismatch:
Inadequate perfusion relative to metabolic demands
Leading to tissue hypoxia and cell death
DO2 = CO x (Hb x Sat + (0.003 x paO2))
CO = Heart Rate x Stroke Volume
Determinants of Stroke Volume: Preload, Contractility, and Afterload
4 L’s of Hypotension
Lucid: What’s their mental status?
Limbs: Are they cold vs. warm? What is the cap refill?
Leak: Are they taking a “leak”? What is the urine output?
Lactate
Remember:
Shock DOES NOT equal hypotension
A patient in shock can still have normotensive pressures in “Compensated Shock”
Signs of Shock
Increased HR, increased RR, AMS, decreased urine output, cool to touch, weak pulses, slow capillary refill

Defining Blood Pressure

Systolic Blood Pressure
Stroke Volume: Main contributor to SBP ➡️ SV ≈ SBP
Aortic/Arterial Compliance
Diastolic Blood Pressure
Systemic Vascular Resistance
Maintains end-organ perfusion in diastole
Pulse Pressure
SBP – DBP
Mean Arterial Pressure
MAP < 60-65 can lead to end-organ damage

Narrow Pulse Pressure

Cardiogenic: “Cold Shock”
Low contractility ➡️low SV ➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Cold limbs, weak pulses, poor capillary refill
Hypovolemic
Hemorrhagic vs. Dehydration
Decrease preload ➡️ decreased SV ➡️ decreased SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Obstructive
“Obstruction of preload” ➡️ decreased SV➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP
Pneumothorax
Increased intrathoracic pressure ➡️ decrease IVC and SVC ➡️ decreased preload
Cardiac Tamponade
Fluid in pericardial space ➡️ decrease filling ➡️ decreased preload
Pulmonary Emboli: Obstruction of RV to LA flow ➡️ decreased preload

Wide Pulse Pressure: Distributive Shock

“Warm shock”: Vasodilatation ➡️ decreased SVR ➡️ Decreased DBP
Septic: Main cause of distributive shock
Neurogenic: Loss of sympathetic tone ➡️ unopposed parasympathetic / vagal tone ➡️ decreased SVR ➡️ decreased DBP
Anaphylaxis: histamine and other inflammatory mediators released ➡️ increased vascular permeability ➡️ decreased SVR ➡️ decreased DBP
Adrenal Crisis: Not secreting cortisol ➡️ not increasing vascular tone ➡️ decreased SVR ➡️ decreased DBP
Hepatic Failure: Increase in NOS ➡️ increases NO ➡️ vasodilatation

🛌 Practical Bedside Approach

When called to bedside:
Is the patient meeting any of the 4 “L’s” ?
Check the pulse pressure along with other vitals
Why are they here? What’s the brief history?
Narrow Pulse Pressure? Cardiogenic, hypovolemic, or obstructive shock
Wide Pulse Pressure? Distributive shock
Think: sepsis (most likely), neurogenic, anaphylaxis, adrenal crisis, hepatic failure

🚨 Clinical Bottom Line

A brief but thorough bedside exam remembering the 4 “L’s”, a quick history, and examining the pulse pressure can help a clinician form a quick differential into the underlying etiology for a critically ill patient in shock. Stay sharp, stay systematic!
💡 Shock is a clinical diagnosis based on bedside findings — not just blood pressure readings.
You don’t always need invasive monitoring to identify shock. Look at HR, RR, UOP, and mentation.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Micheal Bass DO
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
Frank J. Lodeserto MD
Associate Professor and Internal Medicine Residency Program Director Adult & Pediatric Critical Care Medicine, Cape Fear Valley Medical Center, Fayetteville, NC
🔎 Your Deep-Dive Starts Here

REBEL Core Cast 138.0: A Simple Bedside Approach to Shock

In this episode, we will dive into a simple yet ...
Cardiovascular Read More
REBEL Core Cast 131.0 – Traumatic Arthrotomy

Take Home points: Always suspect an open joint if there ...
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Take Home Points Orogastric lavage may still play an important ...
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The post REBEL Core Cast 138.0: A Simple Bedside Approach to Shock appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia Jul 21, 2025

🧭 REBEL Rundown

📌 Key Points

🩺 Sinus Tachycardia = Clinical Clue: Don’t just treat the number—it’s a sign of underlying physiologic stress.
🧮 Oxygen Delivery Equation: HR ↑ may compensate for ↓ hemoglobin, O₂ sat, or cardiac output. Know: 👉 DO₂ = CO x Hb x Sat + 0.003(pO₂)
🗂️ Systematic 8-Point Evaluation: 🫁 Airway/Hypoxia, 🌬️ Breathing , 💉 Circulation, 💊 Drugs,🩸 Erythrocytes (Anemia), 🌡️ Fever, 🍬 Glucose, 😖 “Holy Cow That Hurts”
🧠 Think Holistically: Tachycardia isn’t the problem—what’s causing it is.
🚫 Avoid Reflexive Beta Blockers: Don’t suppress a compensatory response before finding the cause.
🔁 Reassess Frequently: Clinical status can change—stay vigilant.

Click here for Direct Download of the Podcast.

📝 Introduction

Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ill patients, yet it often receives less attention than it warrants. While the rhythm itself is not inherently dangerous, it serves as a crucial indicator of underlying physiological disturbances that require prompt evaluation and management.

🔑 Key Concepts

Sinus Tachycardia as a Clinical Sign: Rather than focusing solely on the elevated heart rate, clinicians should interpret sinus tachycardia as a symptom pointing toward an underlying cause that needs to be identified and addressed.
Oxygen Delivery Equation: Understanding the components of oxygen delivery—hemoglobin concentration, oxygen saturation, and cardiac output—is essential. An increase in heart rate may be a compensatory mechanism to maintain adequate oxygen delivery when other components are compromised.

8 Causes of Sinus Tachycardia

Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia.
Breathing: Evaluate for respiratory distress or pulmonary pathology.
Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock.
Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states.
Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery.
Fever: Recognize that fever increases metabolic demand, leading to tachycardia.
Glucose: Identify hypoglycemia or hyperglycemia as potential contributors.
Holy Cow That Hurts: (Pain/Anxiety): Acknowledge that pain and emotional distress can elevate heart rate.

🛌 Practical Bedside Approach

Holistic Assessment: Always interpret sinus tachycardia within the broader clinical context.
Avoid Reflexive Treatment: Refrain from immediately administering rate-controlling medications without identifying and managing the underlying cause.
Continuous Monitoring: Regularly reassess the patient’s status, as the underlying cause of tachycardia may evolve over time.

🚨 Clinical Bottom Line

Sinus tachycardia is a vital clinical sign that necessitates a thorough and systematic evaluation to uncover and treat the root cause. By adopting this structured approach, clinicians can improve patient outcomes and avoid the pitfalls of symptomatic treatment without addressing underlying issues.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Thirumala “Keerthi” Kammaripalle, MD
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

It seems we can't find what you're looking for.

The post REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia Jul 21, 2025

🧭 REBEL Rundown

📌 Key Points

🩺 Sinus Tachycardia = Clinical Clue: Don’t just treat the number—it’s a sign of underlying physiologic stress.
🧮 Oxygen Delivery Equation: HR ↑ may compensate for ↓ hemoglobin, O₂ sat, or cardiac output. Know: 👉 DO₂ = CO x Hb x Sat + 0.003(pO₂)
🗂️ Systematic 8-Point Evaluation: 🫁 Airway/Hypoxia, 🌬️ Breathing , 💉 Circulation, 💊 Drugs,🩸 Erythrocytes (Anemia), 🌡️ Fever, 🍬 Glucose, 😖 “Holy Cow That Hurts”
🧠 Think Holistically: Tachycardia isn’t the problem—what’s causing it is.
🚫 Avoid Reflexive Beta Blockers: Don’t suppress a compensatory response before finding the cause.
🔁 Reassess Frequently: Clinical status can change—stay vigilant.

Click here for Direct Download of the Podcast.

📝 Introduction

Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ill patients, yet it often receives less attention than it warrants. While the rhythm itself is not inherently dangerous, it serves as a crucial indicator of underlying physiological disturbances that require prompt evaluation and management.

🔑 Key Concepts

Sinus Tachycardia as a Clinical Sign: Rather than focusing solely on the elevated heart rate, clinicians should interpret sinus tachycardia as a symptom pointing toward an underlying cause that needs to be identified and addressed.
Oxygen Delivery Equation: Understanding the components of oxygen delivery—hemoglobin concentration, oxygen saturation, and cardiac output—is essential. An increase in heart rate may be a compensatory mechanism to maintain adequate oxygen delivery when other components are compromised.

8 Causes of Sinus Tachycardia

Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia.
Breathing: Evaluate for respiratory distress or pulmonary pathology.
Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock.
Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states.
Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery.
Fever: Recognize that fever increases metabolic demand, leading to tachycardia.
Glucose: Identify hypoglycemia or hyperglycemia as potential contributors.
Holy Cow That Hurts: (Pain/Anxiety): Acknowledge that pain and emotional distress can elevate heart rate.

🛌 Practical Bedside Approach

Holistic Assessment: Always interpret sinus tachycardia within the broader clinical context.
Avoid Reflexive Treatment: Refrain from immediately administering rate-controlling medications without identifying and managing the underlying cause.
Continuous Monitoring: Regularly reassess the patient’s status, as the underlying cause of tachycardia may evolve over time.

🚨 Clinical Bottom Line

Sinus tachycardia is a vital clinical sign that necessitates a thorough and systematic evaluation to uncover and treat the root cause. By adopting this structured approach, clinicians can improve patient outcomes and avoid the pitfalls of symptomatic treatment without addressing underlying issues.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Thirumala “Keerthi” Kammaripalle, MD
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

It seems we can't find what you're looking for.

The post REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient Jul 07, 2025

🧭 REBEL Rundown

📌 Key Points

Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast ⚠️
Normal/large tidal volume: Compensation for metabolic/systemic cause
Use all tools: 👁 Eyes: Chest rise, ✋ Hands: Palpate,👂 Ears: Listen, 🧠 Brain: Synthesize

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside.

🔑 Key Concepts

First Priorities at the Bedside

Chest Rise:
Short, shallow respirations with poor chest rise are a major red flag.
Patients with minimal tidal volumes are often approaching respiratory failure.
Diaphoresis and Tachycardia:
Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse.
Immediate Action:
Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together)

Short, Shallow Breathing: Think Three Major Buckets

Neuromuscular Disease
Myasthenia gravis crisis, Guillain-Barré, myopathies, frailty.
Weak inspiratory effort leads to low tidal volumes.
Needs urgent positive pressure support (BiPAP, or intubation).
Severe Bronchospasm
Asthma, COPD, anaphylaxis.
Shallow, forced expirations signal airway obstruction.
Silent Chest = airway emergency.
Treat with bronchodilators, steroids, and positive pressure ventilation.
Avoid immediate intubation if reversible; trial NIPPV first.
Worsening Lung Compliance
“Stiff lungs” harder to ventilate.
Compliance (C) = Δ Volume / Δ Pressure
So if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is low
Causes include:
Chest Wall: Rigidity, burn eschar.
Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise).
Lung Parenchyma: Pneumonia, contusion, atelectasis.
Below the Lung: Abdominal distension, ascites.
Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen).

Normal to High Tidal Volumes with Tachypnea: Systemic Causes

Metabolic Acidosis (e.g., DKA)
Compensatory hyperventilation (Kussmaul breathing)
Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosis
Respiratory Alkalosis
Causes: Pain, anxiety, fever, early sepsis, CNS issues
Central drive increases respiratory rate
Again, ABG or VBG helps confirm
Dead Space Ventilation
Pulmonary embolism (PE) is the classic cause.
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.

🛌 Practical Bedside Approach

Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issue
Think: Impending respiratory failure, act quickly.
Normal to large tidal volumes? Systemic causes
Think: Compensation (acidosis, pain, anxiety, PE).
Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize).

🚨 Clinical Bottom Line

A careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic!

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Micheal Bass DO
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection

Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) ...
Cardiovascular Read More
REBEL Core Cast 126.0 – Peds Hem Onc Emergencies

Take Home Points Early administration of antibiotics (within 60 min) ...
Hematology and Oncology Read More
REBEL Core Cast 125.0 – Hyperkalemia

Take Home Points Always obtain an EKG in patients with ...
Endocrine, Metabolic, Fluid, and Electrolytes Read More
REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy

Take Home Points Management of severe beta-blocker and calcium-channel blocker ...
Toxicology Read More
REBEL Core Cast 123.0 – Posterior Epistaxis

Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. ...
Head, Eye, Ear, Nose, and Throat Read More
ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal

Background: In May of 2018, Andexanet alfa gained accelerated approval ...
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The post REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient appeared first on REBEL EM - Emergency Medicine Blog.

Eric Acker MD — REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient Jul 07, 2025

🧭 REBEL Rundown

📌 Key Points

Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast ⚠️
Normal/large tidal volume: Compensation for metabolic/systemic cause
Use all tools: 👁 Eyes: Chest rise, ✋ Hands: Palpate,👂 Ears: Listen, 🧠 Brain: Synthesize

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside.

🔑 Key Concepts

First Priorities at the Bedside

Chest Rise:
Short, shallow respirations with poor chest rise are a major red flag.
Patients with minimal tidal volumes are often approaching respiratory failure.
Diaphoresis and Tachycardia:
Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse.
Immediate Action:
Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together)

Short, Shallow Breathing: Think Three Major Buckets

Neuromuscular Disease
Myasthenia gravis crisis, Guillain-Barré, myopathies, frailty.
Weak inspiratory effort leads to low tidal volumes.
Needs urgent positive pressure support (BiPAP, or intubation).
Severe Bronchospasm
Asthma, COPD, anaphylaxis.
Shallow, forced expirations signal airway obstruction.
Silent Chest = airway emergency.
Treat with bronchodilators, steroids, and positive pressure ventilation.
Avoid immediate intubation if reversible; trial NIPPV first.
Worsening Lung Compliance
“Stiff lungs” harder to ventilate.
Compliance (C) = Δ Volume / Δ Pressure
So if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is low
Causes include:
Chest Wall: Rigidity, burn eschar.
Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise).
Lung Parenchyma: Pneumonia, contusion, atelectasis.
Below the Lung: Abdominal distension, ascites.
Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen).

Normal to High Tidal Volumes with Tachypnea: Systemic Causes

Metabolic Acidosis (e.g., DKA)
Compensatory hyperventilation (Kussmaul breathing)
Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosis
Respiratory Alkalosis
Causes: Pain, anxiety, fever, early sepsis, CNS issues
Central drive increases respiratory rate
Again, ABG or VBG helps confirm
Dead Space Ventilation
Pulmonary embolism (PE) is the classic cause.
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.

🛌 Practical Bedside Approach

Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issue
Think: Impending respiratory failure, act quickly.
Normal to large tidal volumes? Systemic causes
Think: Compensation (acidosis, pain, anxiety, PE).
Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize).

🚨 Clinical Bottom Line

A careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic!

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributors

Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Micheal Bass DO
Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC
🔎 Your Deep-Dive Starts Here

A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection

Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) ...
Cardiovascular Read More
REBEL Core Cast 126.0 – Peds Hem Onc Emergencies

Take Home Points Early administration of antibiotics (within 60 min) ...
Hematology and Oncology Read More
REBEL Core Cast 125.0 – Hyperkalemia

Take Home Points Always obtain an EKG in patients with ...
Endocrine, Metabolic, Fluid, and Electrolytes Read More
REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy

Take Home Points Management of severe beta-blocker and calcium-channel blocker ...
Toxicology Read More
REBEL Core Cast 123.0 – Posterior Epistaxis

Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. ...
Head, Eye, Ear, Nose, and Throat Read More
ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal

Background: In May of 2018, Andexanet alfa gained accelerated approval ...
Hematology and Oncology Read More
The post REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) Jun 16, 2025

🧭 REBEL Rundown

📌 Key Points

🫁 Hypoxemia = low blood oxygen
🧠 Hypoxia = low tissue oxygen
🔍 5 causes of hypoxemia, but most hospital cases are either:
🚫 Shunt = doesn’t improve with oxygen therapy
💨 Dead space = causes tachypnea but is easier to oxygenate
💡 Always start with maximizing oxygen delivery (💊💨),
but recognize quickly when positive pressure (🫁➡️) is needed
️ V/Q mismatch
🩸 Shunt (refractory to oxygen therapy)

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we break down a practical bedside approach to hypoxemia. We clarify the difference between hypoxemia (low oxygen in the blood) and hypoxia (low oxygen at the tissue level), and walk through the major causes of hypoxemia that you need to recognize quickly at the bedside.

🔑 Key Concepts

Hypoxemia vs. Hypoxia: Know the Difference

Hypoxemia = Low oxygen in the blood.
Measured indirectly by SpO₂ (pulse oximeter) or directly by PaO₂ (arterial oxygen tension) or SaO₂ (oxygen saturation).
Hypoxia = Low oxygen at the tissue level.
Can happen with or without hypoxemia.

Four Types of Hypoxia

Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia)
Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis)
Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock)
Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning)

Five Major Causes of Hypoxemia

Hypopnea/Apnea (Decreased Respiratory Drive)
Inadequate breaths (or no breaths) means lower oxygen intake.
Seen in cardiac arrest, drug overdose, severe brain injury.
Easy to recognize as patients are encephalopathic or apneic.
High Altitude
Lower barometric pressure = less available oxygen, despite 21% FiO₂.
Rarely relevant inside hospitals, but important to know.
Diffusion Defect
Impaired oxygen transfer across alveoli, often due to chronic lung disease.
Examples: interstitial lung disease, idiopathic pulmonary fibrosis.
Patients are usually known to have underlying disease.
V/Q Mismatch (Dead Space Disease)
Problem with perfusion relative to ventilation
Common examples:
Pulmonary embolism (classic dead space).
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but unperfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation.
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.
Key point: Patients often oxygenate “ok” at rest but are tachypneic
Shunt (Most Common and Most Concerning)
“Crap in the alveoli” blocks oxygen diffusion:
Pneumonia (pus)
Pulmonary edema (water)
Atelectasis (collapse)
Pulmonary hemorrhage (blood)
Blood moves from right to left without being oxygenated.
Refractory hypoxemia despite oxygen therapy = shunt physiology.
Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation).

🛌 Practical Bedside Approach

Give as much FiO₂ as possible (non-rebreather mask).
Watch SpO₂ response:
If it improves → V/Q mismatch or dead space more likely.
If it doesn’t improve → think shunt physiology.
If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation).

🚨 Clinical Bottom Line

Mastering the basics of hypoxemia helps you recognize dangerous physiology early — before your patient crashes. Keep in mind the four types of hypoxia and the five major causes of hypoxemia.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributor

Eric Acker

MD

Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Meet The Team
🔎 Your Deep-Dive Starts Here

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Infectious Disease Read More
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Background: The holy grail of outcomes in OHCA is survival ...
Resuscitation Read More
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Take Home Points Acute rhinosinusitis is a clinical diagnosis The ...
Head, Eye, Ear, Nose, and Throat Read More
REBEL EM Book Club – MicroSkills

Podcast Direct Download: Link Release Date: April 16th, 2024 Show ...
Read More
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REBEL Cast – EMTALA + Reproductive Health Click here for ...
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Background: The mainstay of treatment for symptomatic pulmonary embolism (PE) ...
Cardiovascular Read More
The post REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) Jun 16, 2025

🧭 REBEL Rundown

📌 Key Points

🫁 Hypoxemia = low blood oxygen
🧠 Hypoxia = low tissue oxygen
🔍 5 causes of hypoxemia, but most hospital cases are either:
🚫 Shunt = doesn’t improve with oxygen therapy
💨 Dead space = causes tachypnea but is easier to oxygenate
💡 Always start with maximizing oxygen delivery (💊💨),
but recognize quickly when positive pressure (🫁➡️) is needed
️ V/Q mismatch
🩸 Shunt (refractory to oxygen therapy)

Click here for Direct Download of the Podcast.

📝 Introduction

In this episode, we break down a practical bedside approach to hypoxemia. We clarify the difference between hypoxemia (low oxygen in the blood) and hypoxia (low oxygen at the tissue level), and walk through the major causes of hypoxemia that you need to recognize quickly at the bedside.

🔑 Key Concepts

Hypoxemia vs. Hypoxia: Know the Difference

Hypoxemia = Low oxygen in the blood.
Measured indirectly by SpO₂ (pulse oximeter) or directly by PaO₂ (arterial oxygen tension) or SaO₂ (oxygen saturation).
Hypoxia = Low oxygen at the tissue level.
Can happen with or without hypoxemia.

Four Types of Hypoxia

Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia)
Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis)
Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock)
Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning)

Five Major Causes of Hypoxemia

Hypopnea/Apnea (Decreased Respiratory Drive)
Inadequate breaths (or no breaths) means lower oxygen intake.
Seen in cardiac arrest, drug overdose, severe brain injury.
Easy to recognize as patients are encephalopathic or apneic.
High Altitude
Lower barometric pressure = less available oxygen, despite 21% FiO₂.
Rarely relevant inside hospitals, but important to know.
Diffusion Defect
Impaired oxygen transfer across alveoli, often due to chronic lung disease.
Examples: interstitial lung disease, idiopathic pulmonary fibrosis.
Patients are usually known to have underlying disease.
V/Q Mismatch (Dead Space Disease)
Problem with perfusion relative to ventilation
Common examples:
Pulmonary embolism (classic dead space).
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but unperfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation.
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.
Key point: Patients often oxygenate “ok” at rest but are tachypneic
Shunt (Most Common and Most Concerning)
“Crap in the alveoli” blocks oxygen diffusion:
Pneumonia (pus)
Pulmonary edema (water)
Atelectasis (collapse)
Pulmonary hemorrhage (blood)
Blood moves from right to left without being oxygenated.
Refractory hypoxemia despite oxygen therapy = shunt physiology.
Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation).

🛌 Practical Bedside Approach

Give as much FiO₂ as possible (non-rebreather mask).
Watch SpO₂ response:
If it improves → V/Q mismatch or dead space more likely.
If it doesn’t improve → think shunt physiology.
If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation).

🚨 Clinical Bottom Line

Mastering the basics of hypoxemia helps you recognize dangerous physiology early — before your patient crashes. Keep in mind the four types of hypoxia and the five major causes of hypoxemia.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

👤 Guest Contributor

Eric Acker

MD

Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC
Meet The Team
🔎 Your Deep-Dive Starts Here

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Take Home Points: There are many causes of neutropenia, chemotherapy ...
Infectious Disease Read More
REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA?

Background: The holy grail of outcomes in OHCA is survival ...
Resuscitation Read More
REBEL Core Cast 121.0 – Acute Sinusitis

Take Home Points Acute rhinosinusitis is a clinical diagnosis The ...
Head, Eye, Ear, Nose, and Throat Read More
REBEL EM Book Club – MicroSkills

Podcast Direct Download: Link Release Date: April 16th, 2024 Show ...
Read More
REBEL Cast – EMTALA + Reproductive Health Rights

REBEL Cast – EMTALA + Reproductive Health Click here for ...
Ethical and Legal Read More
REBEL Cast Ep125: 1st 48 Hours of PE Management – How Good Is Unfractionated Heparin?

Background: The mainstay of treatment for symptomatic pulmonary embolism (PE) ...
Cardiovascular Read More
The post REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 134.0 – Acetaminophen Toxicity Jun 02, 2025

Acetaminophen (APAP) overdose remains one of the most common causes of acute liver failure in the United States. While its therapeutic use is widespread and generally safe, unintentional overdoses and delayed presentations can lead to devastating outcomes. In this episode of REBEL Cast, we break down the pathophysiology, clinical course, diagnostic approach, and evidence-based management of APAP toxicity—including when to initiate NAC, how to apply the Rumack-Matthew nomogram, and the evolving role of adjunctive therapies like fomepizole. Whether you’re in the ED or elsewhere , this is core content every clinician should know.

Click here for Direct Download of the Podcast.

Definition and Physiology

After ingestion of a therapeutic dose, immediate release APAP is absorbed with a time to peak concentration anywhere between 30-45 minutes. In the context of extended-release, formulations, full absorption is typically reached by 4 hours post-ingestion.¹

In therapeutic dosing, the vast majority of APAP undergoes hepatic conjugation with glucuronide or sulfate to form benign metabolites that ultimately get excreted in the urine. The remaining ~5% is oxidized by CYP2E1 to form N-acetyl-p-benzoquinoeimine (NAPQI). NAPQI is hepatotoxic. Glutathione combines with NAPQI to generate non-toxic metabolites that are also eliminated in the urine.

In overdose, the amount of NAPQI that is generated is increased as the typical metabolic pathways become saturated. The NAPQI that remains leads to hepatocellular death in Zone 3 of the liver (or the centrilobular location) which is the area with the largest degree of oxidative metabolism.

Clinical Manifestations and Diagnostic Evaluation

The clinical course of acute APAP toxicity is classically broken into four different stages.

Stage1: this is generally within 24 hours. Patients are either asymptomatic or have non-specific GI symptoms (nausea, vomiting, malaise). At this point, hepatic function testing is normal.

Stage2: ~24-72 hours. The onset of hepatic injury marks this stage. Aspartate aminotransferase (AST) is the most sensitive marker to detect hepatic dysfunction; AST elevated is nearly universal by 36 hours post-ingestion.

Stage3: defined as peak hepatotoxicity; generally between 72-96 hours post-ingestion. Patients may manifest hepatic encephalopathy or coma. AST and/or ALT might rise above 10,000 IU/L. Other lab abnormalities include: INR/PT, glucose, lactate, pH, and creatinine. Death from fulminant hepatic failure usually occurs anywhere between 3-5 days after an acute ingestion. Mortality is often secondary to multiorgan failure, ARDS, sepsis, or cerebral edema.

Stage4: often called the “recovery phase.” Patient who survive demonstrate complete hepatic generation without any evidence of hepatic dysfunction.

The following labs should be obtained for severe APAP ingestions:

APAP Concentration, hepatic panel, pH, coagulation panel, renal function, lactate and phosphate. These labs will ultimately dictate disposition (see King’s College Criteria below)

Management

Consider GI decontamination with activated charcoal as this can reduce systemic absorption and limit subsequent clinical sequalae.

Ingestions should be classified as acute or repeated supratherapeutic (“chronic” ingestions)

Single Acute Ingestion

If feasible, obtain a 4 hour post-ingestion APAP concentration. Any concentration earlier than 4 hours is uninterpretable as subsequent concentrations may increase or decrease depending on the clinical scenario.

Concentrations between 4-8 hour post-ingestion can be plotted on the Rumack-Matthew nomogram to determine when NAC should be initiated.

If the APAP concentration is above the plotted line, NAC should be started.

NAC is nearly 100% effective if started within 8 hours post-ingestion.²

If an APAP concentration is unable to be drawn before 8 hours or if LFTs are already elevated, NAC should be empirically started if the pre-test probability is high enough for clinical concern.

Repeated Supratherapeutic/Chronic Ingestions

Cannot apply the Rumack-Matthew Nomogram

If LFTs are elevated or if there is a positive APAP concentration, NAC should generally be started however consultation with a toxicologist or Poison Control Center is advised as these cases are often complicated.

N-Acetyl-Cysteine (NAC) Dosing

“3 Bag Protocol” – 21 hour regimen

150mg/kg over 1 hour loading dose

50mg/kg over 4 hours = 12.5 mg/kg/hr

100mg/kg over 16 hours = 6.25 mg/kg/hr

Risk: anaphylactoid reaction

Reaction is rate related and typically occurs during the loading dose

Symptoms: flushing, urticaria.

NAC should be continued until all of the following criteria are met:

Negative APAP concentration

“Significant Decreased in AST”: defined as either <1000 IU/L or a 25-50% drop from the peak.

No evidence of hepatic failure

If criteria are not met, the third bag should be extended indefinitely.

The King’s College Criteria should be used as this set of lab work is used to determine which patients should be referred for possible liver transplant evaluation.^{3, 4}

Arterial pH < 7.30

INR > 6.5 (PT >100 sec)

Creatinine > 3.4

Grade III or IV hepatic encephalopathy

Hyperlactatemia

Hyperphosphatemia

Fomepizole (traditionally used for the treatment of toxic alcohols) has been used as an adjunctive treatment for massive acetaminophen toxicity as it has demonstrated efficacy in mitigating serum transaminase elevation, hepatic necrosis, and oxidative stress in both mouse and human models.^5-8

As large scale human studies have yet to be published, fomepizole should NOT be routinely administered for APAP toxicity.

Take Home Points

Acetaminophen (APAP), most commonly referred to as “Tylenol” in the United States, is in a variety of pharmaceuticals. Medications like Excedrin, Fioricet, Percocet, Vicodin, and Day/Nyquil all contain acetaminophen.

Given the lack of a toxidrome, there should be a low threshold to obtain a screening acetaminophen concentration in the undifferentiated poisoned patient.

In overdose, acetaminophen leads to generation of NAPQI which is hepatotoxic. N-Acetylcysteine (NAC) is the antidote of choice and ideally should be administered within 8 hours of an acute ingestion.

To determine which patients should be treated with antidotal therapy, the Rumack-Matthew Nomogram should be utilized. Of note, this nomogram was validated for a single concentration obtained at or greater than 4 hours after a single, acute ingestion. (i.e. patients with repeated ingestions cannot be applied to the nomogram).

In patients with a high pre-test probability of APAP poisoning, the King’s College Criteria should be considered; this is a set of lab markers that help determine when patients should be immediately referred for liver transplant.

While physiologic plausibility exists for the use of fomepizole to treat severe APAP toxicity, no large scale human studies exist at this time to suggest that it should be routinely given for toxicity. As with all cases of toxicity, please call your local poison control center for assistance.

References

Hendrickson RG, McKeown NJ. Chapter 33. Acetaminophen. In: Nelson LS, et al., editors. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019.

Smilkstein MJ, Knapp GL, Kulig KW, Rumack BH. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose: Analysis of the National Multicenter Study (1976 to 1985). N Engl J Med. 1988;319(24):1557-1562. PMID: 3059186

O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97(2):439-445. PMID: 2490426

King’s College Criteria for Acetaminophen Toxicity. Available at: https://www.mdcalc.com/calc/532/kings-college-criteria-acetaminophen-toxicity#next-steps

Akakpo JY, Ramachandran A, Duan L, et al. Delayed treatment with 4-methylpyrazole protects against acetaminophen hepatotoxicity in mice by inhibition of c-jun N-terminal kinase. Toxicol Sci. 2019;170(1):57-68. PMID: 30903181

Akakpo JY, Ramachandran A, Kandel SE, et al. 4-Methylpyrazole protects against acetaminophen hepatotoxicity in mice and in primary human hepatocytes. Hum Exp Toxicol. 2018;37(12):1310-1322. PMID: 29739258

Shah KR, Beuhler MC. Fomepizole as an adjunctive treatment in severe acetaminophen toxicity. Am J Emerg Med.2020;38(2):410.e5-410.e6. PMID: 31785979

Kang AM, Padilla-Jones A, Fisher ES, et al. The effect of 4-methylpyrazole on oxidative metabolism of acetaminophen in human volunteers. J Med Toxicol. 2020;16(2):169-176. PMID: 31768936

The post REBEL Core Cast 134.0 – Acetaminophen Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 134.0 – Acetaminophen Toxicity Jun 02, 2025

Acetaminophen (APAP) overdose remains one of the most common causes of acute liver failure in the United States. While its therapeutic use is widespread and generally safe, unintentional overdoses and delayed presentations can lead to devastating outcomes. In this episode of REBEL Cast, we break down the pathophysiology, clinical course, diagnostic approach, and evidence-based management of APAP toxicity—including when to initiate NAC, how to apply the Rumack-Matthew nomogram, and the evolving role of adjunctive therapies like fomepizole. Whether you’re in the ED or elsewhere , this is core content every clinician should know.

Click here for Direct Download of the Podcast.

Definition and Physiology

After ingestion of a therapeutic dose, immediate release APAP is absorbed with a time to peak concentration anywhere between 30-45 minutes. In the context of extended-release, formulations, full absorption is typically reached by 4 hours post-ingestion.¹

In therapeutic dosing, the vast majority of APAP undergoes hepatic conjugation with glucuronide or sulfate to form benign metabolites that ultimately get excreted in the urine. The remaining ~5% is oxidized by CYP2E1 to form N-acetyl-p-benzoquinoeimine (NAPQI). NAPQI is hepatotoxic. Glutathione combines with NAPQI to generate non-toxic metabolites that are also eliminated in the urine.

In overdose, the amount of NAPQI that is generated is increased as the typical metabolic pathways become saturated. The NAPQI that remains leads to hepatocellular death in Zone 3 of the liver (or the centrilobular location) which is the area with the largest degree of oxidative metabolism.

Clinical Manifestations and Diagnostic Evaluation

The clinical course of acute APAP toxicity is classically broken into four different stages.

Stage1: this is generally within 24 hours. Patients are either asymptomatic or have non-specific GI symptoms (nausea, vomiting, malaise). At this point, hepatic function testing is normal.

Stage2: ~24-72 hours. The onset of hepatic injury marks this stage. Aspartate aminotransferase (AST) is the most sensitive marker to detect hepatic dysfunction; AST elevated is nearly universal by 36 hours post-ingestion.

Stage3: defined as peak hepatotoxicity; generally between 72-96 hours post-ingestion. Patients may manifest hepatic encephalopathy or coma. AST and/or ALT might rise above 10,000 IU/L. Other lab abnormalities include: INR/PT, glucose, lactate, pH, and creatinine. Death from fulminant hepatic failure usually occurs anywhere between 3-5 days after an acute ingestion. Mortality is often secondary to multiorgan failure, ARDS, sepsis, or cerebral edema.

Stage4: often called the “recovery phase.” Patient who survive demonstrate complete hepatic generation without any evidence of hepatic dysfunction.

The following labs should be obtained for severe APAP ingestions:

APAP Concentration, hepatic panel, pH, coagulation panel, renal function, lactate and phosphate. These labs will ultimately dictate disposition (see King’s College Criteria below)

Management

Consider GI decontamination with activated charcoal as this can reduce systemic absorption and limit subsequent clinical sequalae.

Ingestions should be classified as acute or repeated supratherapeutic (“chronic” ingestions)

Single Acute Ingestion

If feasible, obtain a 4 hour post-ingestion APAP concentration. Any concentration earlier than 4 hours is uninterpretable as subsequent concentrations may increase or decrease depending on the clinical scenario.

Concentrations between 4-8 hour post-ingestion can be plotted on the Rumack-Matthew nomogram to determine when NAC should be initiated.

If the APAP concentration is above the plotted line, NAC should be started.

NAC is nearly 100% effective if started within 8 hours post-ingestion.²

If an APAP concentration is unable to be drawn before 8 hours or if LFTs are already elevated, NAC should be empirically started if the pre-test probability is high enough for clinical concern.

Repeated Supratherapeutic/Chronic Ingestions

Cannot apply the Rumack-Matthew Nomogram

If LFTs are elevated or if there is a positive APAP concentration, NAC should generally be started however consultation with a toxicologist or Poison Control Center is advised as these cases are often complicated.

N-Acetyl-Cysteine (NAC) Dosing

“3 Bag Protocol” – 21 hour regimen

150mg/kg over 1 hour loading dose

50mg/kg over 4 hours = 12.5 mg/kg/hr

100mg/kg over 16 hours = 6.25 mg/kg/hr

Risk: anaphylactoid reaction

Reaction is rate related and typically occurs during the loading dose

Symptoms: flushing, urticaria.

NAC should be continued until all of the following criteria are met:

Negative APAP concentration

“Significant Decreased in AST”: defined as either <1000 IU/L or a 25-50% drop from the peak.

No evidence of hepatic failure

If criteria are not met, the third bag should be extended indefinitely.

The King’s College Criteria should be used as this set of lab work is used to determine which patients should be referred for possible liver transplant evaluation.^{3, 4}

Arterial pH < 7.30

INR > 6.5 (PT >100 sec)

Creatinine > 3.4

Grade III or IV hepatic encephalopathy

Hyperlactatemia

Hyperphosphatemia

Fomepizole (traditionally used for the treatment of toxic alcohols) has been used as an adjunctive treatment for massive acetaminophen toxicity as it has demonstrated efficacy in mitigating serum transaminase elevation, hepatic necrosis, and oxidative stress in both mouse and human models.^5-8

As large scale human studies have yet to be published, fomepizole should NOT be routinely administered for APAP toxicity.

Take Home Points

Acetaminophen (APAP), most commonly referred to as “Tylenol” in the United States, is in a variety of pharmaceuticals. Medications like Excedrin, Fioricet, Percocet, Vicodin, and Day/Nyquil all contain acetaminophen.

Given the lack of a toxidrome, there should be a low threshold to obtain a screening acetaminophen concentration in the undifferentiated poisoned patient.

In overdose, acetaminophen leads to generation of NAPQI which is hepatotoxic. N-Acetylcysteine (NAC) is the antidote of choice and ideally should be administered within 8 hours of an acute ingestion.

To determine which patients should be treated with antidotal therapy, the Rumack-Matthew Nomogram should be utilized. Of note, this nomogram was validated for a single concentration obtained at or greater than 4 hours after a single, acute ingestion. (i.e. patients with repeated ingestions cannot be applied to the nomogram).

In patients with a high pre-test probability of APAP poisoning, the King’s College Criteria should be considered; this is a set of lab markers that help determine when patients should be immediately referred for liver transplant.

While physiologic plausibility exists for the use of fomepizole to treat severe APAP toxicity, no large scale human studies exist at this time to suggest that it should be routinely given for toxicity. As with all cases of toxicity, please call your local poison control center for assistance.

References

Hendrickson RG, McKeown NJ. Chapter 33. Acetaminophen. In: Nelson LS, et al., editors. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019.

Smilkstein MJ, Knapp GL, Kulig KW, Rumack BH. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose: Analysis of the National Multicenter Study (1976 to 1985). N Engl J Med. 1988;319(24):1557-1562. PMID: 3059186

O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97(2):439-445. PMID: 2490426

King’s College Criteria for Acetaminophen Toxicity. Available at: https://www.mdcalc.com/calc/532/kings-college-criteria-acetaminophen-toxicity#next-steps

Akakpo JY, Ramachandran A, Duan L, et al. Delayed treatment with 4-methylpyrazole protects against acetaminophen hepatotoxicity in mice by inhibition of c-jun N-terminal kinase. Toxicol Sci. 2019;170(1):57-68. PMID: 30903181

Akakpo JY, Ramachandran A, Kandel SE, et al. 4-Methylpyrazole protects against acetaminophen hepatotoxicity in mice and in primary human hepatocytes. Hum Exp Toxicol. 2018;37(12):1310-1322. PMID: 29739258

Shah KR, Beuhler MC. Fomepizole as an adjunctive treatment in severe acetaminophen toxicity. Am J Emerg Med.2020;38(2):410.e5-410.e6. PMID: 31785979

Kang AM, Padilla-Jones A, Fisher ES, et al. The effect of 4-methylpyrazole on oxidative metabolism of acetaminophen in human volunteers. J Med Toxicol. 2020;16(2):169-176. PMID: 31768936

The post REBEL Core Cast 134.0 – Acetaminophen Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

Street Medicine: Compassionate Care for the Unhoused Apr 02, 2025
Introduction: In this episode of Rebel Cast, host Marco Propersi, along with co-hosts Steve Hochman and Kim Baldino, delve into the practice and importance of street medicine—the direct delivery of healthcare to homeless and unsheltered individuals. Special guests Dr. Jim O’Connell, a pioneer of street medicine, and Dr. Ed Egan, a recent street medicine fellowship graduate, share their experiences and insights on serving this vulnerable population. They discuss the origins, scope, and challenges of street medicine, the ethical dilemmas faced, and the profound impact of building trust and community with patients. The conversation underscores the necessity of integrating street medicine with mainstream healthcare systems and emphasizes that small acts of kindness and persistence can significantly improve the lives of those experiencing homelessness.
REBEL Cast – Street Medicine: Compassionate Care for the Unhoused

Click here for Direct Download of the Podcast.

00:00 Introduction to Rebel Cast

00:18 Meet the Hosts and Guests

00:47 Understanding Street Medicine

02:22 Origins and Early Challenges

07:23 Street Medicine in Practice

20:11 Barriers to Care

22:23 Housing First Experiment

26:56 Ethical Dilemmas in Street Medicine

27:52 Challenges of Providing Care on the Streets

29:56 The Role of Street Medicine Teams

31:17 The Importance of Building Trust

33:55 Limitations and Realities of Street Medicine

37:37 The Future of Street Medicine

41:42 Integrating Street Medicine with Emergency Medicine

43:36 Personal Reflections and Lessons Learned

48:56 Advice for Aspiring Street Medicine Practitioners

53:03 Final Thoughts and Encouragement

Links:

Street Medicine Institute

National Healthcare for the Homeless Council EMRA Fellowship Guide: Opportunities for Emergency Physicians, 3rd ed.

The post Street Medicine: Compassionate Care for the Unhoused appeared first on REBEL EM - Emergency Medicine Blog.

Street Medicine: Compassionate Care for the Unhoused Apr 02, 2025
Introduction: In this episode of Rebel Cast, host Marco Propersi, along with co-hosts Steve Hochman and Kim Baldino, delve into the practice and importance of street medicine—the direct delivery of healthcare to homeless and unsheltered individuals. Special guests Dr. Jim O’Connell, a pioneer of street medicine, and Dr. Ed Egan, a recent street medicine fellowship graduate, share their experiences and insights on serving this vulnerable population. They discuss the origins, scope, and challenges of street medicine, the ethical dilemmas faced, and the profound impact of building trust and community with patients. The conversation underscores the necessity of integrating street medicine with mainstream healthcare systems and emphasizes that small acts of kindness and persistence can significantly improve the lives of those experiencing homelessness.
REBEL Cast – Street Medicine: Compassionate Care for the Unhoused

Click here for Direct Download of the Podcast.

00:00 Introduction to Rebel Cast

00:18 Meet the Hosts and Guests

00:47 Understanding Street Medicine

02:22 Origins and Early Challenges

07:23 Street Medicine in Practice

20:11 Barriers to Care

22:23 Housing First Experiment

26:56 Ethical Dilemmas in Street Medicine

27:52 Challenges of Providing Care on the Streets

29:56 The Role of Street Medicine Teams

31:17 The Importance of Building Trust

33:55 Limitations and Realities of Street Medicine

37:37 The Future of Street Medicine

41:42 Integrating Street Medicine with Emergency Medicine

43:36 Personal Reflections and Lessons Learned

48:56 Advice for Aspiring Street Medicine Practitioners

53:03 Final Thoughts and Encouragement

Links:

Street Medicine Institute

National Healthcare for the Homeless Council EMRA Fellowship Guide: Opportunities for Emergency Physicians, 3rd ed.

The post Street Medicine: Compassionate Care for the Unhoused appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 131.0 – Traumatic Arthrotomy Nov 13, 2024
Take Home points:

Always suspect an open joint if there is a laceration, regardless of size, the lies over joint

CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances.

Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients

REBEL Core Cast 131.0 – Traumatic Arthrotomy

Click here for Direct Download of the Podcast.

Definition: a deep laceration that extends into the joint capsule, exposing the intra-articular surface to the environment

A laceration into the joint exposes the normally sterile intra-articular contents to external contamination

Inoculation of the joint often results in septic arthritis

Physical Exam:

Laceration over joint (can be variable in size)

Local wound exploration may be sufficient in identifying the open joint

Exam findings suspicious for joint capsule involvement:

Air bubbles

Extravasation of joint fluid – straw colored, viscous, sometimes oily in appearance

Diagnostic testing:

Imaging:

X-ray

Limited ability to see air in joints but a reasonable first test

CT scan

Intra-articular air visualized on CT (Konda 2013)

May be up to 100% sensitive for joint violation

Study limited by small numbers, inclusion bias + inadequate gold standard

May be considered the standard evaluation modality in many settings.

Saline load test

Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test.

Useful if physical examination equivocal or plain radiographs non-diagnostic

Technique (Video)

Perform arthrocentesis of the joint with a large bore needle (18-20 gauge)

Sterile saline is injected into the joint while passive movement is applied to the joint

The laceration site is watched for saline extravasation indicating communication between the joint and external environment

Sensitivity ranges from 34%-99% depending on the study, joint, and the amount of saline used to load the joint (Browning 2016)

Methylene blue

Aids in distinguishing a true positive from additional bleeding from the wound

Recent studies suggest that the addition of methylene blue does not increase sensitivity if a sufficient amount of saline is used (Metzger 2012)

Volume of fluid injected

Varies depending on the joint in which you are injecting

Higher volumes increase sensitivity but also increase pain for the patient

Knee Joint (Keese 2007)

50 ml: Sensitivity of about 46%

194 ml: sensitivity of 95%

Elbow Joint (Feathers 2011)

20 ml: Sensitivity of 86%

40 ml: Sensitivity of 95%

Ankle Joint (Bariteau 2013)

7 ml: Sensitivity of 50%

30 ml: Sensitivity of 95%

ED Management:

Reduce open fractures if present

Irrigate grossly contaminated wounds in the ED

Immobilize the joint to prevent further injury

Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours

Tetanus prophylaxis

Prophylactic antibiotics (best if given within 6 hours)

Staph/strep coverage: 1^st generation cephalosporin (i.e. cefazolin or cefuroxime)

If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin)

If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin)

If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn)

If seawater contamination and concern for vibrio vulnificus, add doxycycline

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

The post REBEL Core Cast 131.0 – Traumatic Arthrotomy appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 131.0 – Traumatic Arthrotomy Nov 13, 2024
Take Home points:

Always suspect an open joint if there is a laceration, regardless of size, the lies over joint

CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances.

Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients

REBEL Core Cast 131.0 – Traumatic Arthrotomy

Click here for Direct Download of the Podcast.

Definition: a deep laceration that extends into the joint capsule, exposing the intra-articular surface to the environment

A laceration into the joint exposes the normally sterile intra-articular contents to external contamination

Inoculation of the joint often results in septic arthritis

Physical Exam:

Laceration over joint (can be variable in size)

Local wound exploration may be sufficient in identifying the open joint

Exam findings suspicious for joint capsule involvement:

Air bubbles

Extravasation of joint fluid – straw colored, viscous, sometimes oily in appearance

Diagnostic testing:

Imaging:

X-ray

Limited ability to see air in joints but a reasonable first test

CT scan

Intra-articular air visualized on CT (Konda 2013)

May be up to 100% sensitive for joint violation

Study limited by small numbers, inclusion bias + inadequate gold standard

May be considered the standard evaluation modality in many settings.

Saline load test

Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test.

Useful if physical examination equivocal or plain radiographs non-diagnostic

Technique (Video)

Perform arthrocentesis of the joint with a large bore needle (18-20 gauge)

Sterile saline is injected into the joint while passive movement is applied to the joint

The laceration site is watched for saline extravasation indicating communication between the joint and external environment

Sensitivity ranges from 34%-99% depending on the study, joint, and the amount of saline used to load the joint (Browning 2016)

Methylene blue

Aids in distinguishing a true positive from additional bleeding from the wound

Recent studies suggest that the addition of methylene blue does not increase sensitivity if a sufficient amount of saline is used (Metzger 2012)

Volume of fluid injected

Varies depending on the joint in which you are injecting

Higher volumes increase sensitivity but also increase pain for the patient

Knee Joint (Keese 2007)

50 ml: Sensitivity of about 46%

194 ml: sensitivity of 95%

Elbow Joint (Feathers 2011)

20 ml: Sensitivity of 86%

40 ml: Sensitivity of 95%

Ankle Joint (Bariteau 2013)

7 ml: Sensitivity of 50%

30 ml: Sensitivity of 95%

ED Management:

Reduce open fractures if present

Irrigate grossly contaminated wounds in the ED

Immobilize the joint to prevent further injury

Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours

Tetanus prophylaxis

Prophylactic antibiotics (best if given within 6 hours)

Staph/strep coverage: 1^st generation cephalosporin (i.e. cefazolin or cefuroxime)

If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin)

If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin)

If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn)

If seawater contamination and concern for vibrio vulnificus, add doxycycline

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

The post REBEL Core Cast 131.0 – Traumatic Arthrotomy appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 130.0 – Omphalitis Oct 30, 2024
Take Home Points Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating If the patient appears toxic or has systemic symptoms, the simply omphalitis has ... Read more

The post REBEL Core Cast 130.0 – Omphalitis appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 129.0 – Gastric Lavage Oct 16, 2024
Take Home Points Orogastric lavage may still play an important role in treatment of the overdose patient. Do not perform lavage if the ingestion has limited toxicity at any dose or the ingested dose is unlikely to cause significant toxicity. Strongly consider orogastric lavage in a patient who has taken an overdose of drugs that ... Read more

The post REBEL Core Cast 129.0 – Gastric Lavage appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 128.0 – Toxic Alcohols Oct 02, 2024
Take Home Points Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage. Patient who present shortly after ingestion will simply look inebriated – no different than ethanol intoxication. At this point, patients will have an elevated osmolar gap and little to no anion gap. Patient ... Read more

The post REBEL Core Cast 128.0 – Toxic Alcohols appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 127.0 – Penetrating Neck Injuries Sep 18, 2024
Take Home Points Anticipate anatomically challenging airways and consider early intubation prior to loss of airway anatomy. Skip the zones of the neck and focus on hard signs of vascular (Shock w/o another source, Pulsatile bleeding, Expanding hematoma, Audible bruit, Signs of stroke) or aerodigestive (Airway compromise, Bubbling wound, Extensive SubQ air, Stridor, Significant hemoptysis/hematemesis). ... Read more

The post REBEL Core Cast 127.0 – Penetrating Neck Injuries appeared first on REBEL EM - Emergency Medicine Blog.

A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection Jul 22, 2024
Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) criteria is founded on aging data and requires evolution. In the “Occlusive Myocardial Infarction (OMI) Manifesto,” emergency physicians Dr. Steve Smith, Dr. Pendell Meyers, and Dr. Scott Weingart introduced a new paradigm —OMI vs. non-occlusive myocardial infarction (NOMI). The OMI/NOMI paradigm focuses on the presence ... Read more

The post A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 126.0 – Peds Hem Onc Emergencies Jul 10, 2024
Take Home Points Early administration of antibiotics (within 60 min) in patients with fever and neutropenia is life saving. Fever in sickle cell is an emergency and always requires cultures and antibiotics even if the child appears well. Avoid sedation and lying supine and steroids in patients with mediastinal masses. Red flags in patients with ... Read more

The post REBEL Core Cast 126.0 – Peds Hem Onc Emergencies appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 125.0 – Hyperkalemia Jun 26, 2024
Take Home Points Always obtain an EKG in patients with ESRD upon presentation Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts In patients who are anuric, early mobilization ... Read more

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REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy Jun 12, 2024
Take Home Points Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone ... Read more

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REBEL Core Cast 123.0 – Posterior Epistaxis May 29, 2024
Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. The key is in identifying and rapidly gaining control with a posterior pack or foley catheter. These patients often require surgical intervention so get ENT to the bedside and admit to a place with a higher level of monitoring. REBEL Core Cast 123.0 – Posterior ... Read more

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ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal May 23, 2024
Background: In May of 2018, Andexanet alfa gained accelerated approval by the FDA for the reversal direct oral anticoagulants (DOACs) despite a lack of robust evidence for use. The 2022 AHA/ASA guidelines give the drug a level 2A recommendation and recommend it over the use of 4F-PCC (Greenberg 2022). FDA approval alongside guideline endorsement has ... Read more

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REBEL Core Cast 122.0 – Neutropenic Fever May 15, 2024
Take Home Points: There are many causes of neutropenia, chemotherapy being by far the most dangerous. Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality. For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but ... Read more

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REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? May 13, 2024
Background: The holy grail of outcomes in OHCA is survival with good neurologic outcome. The only interventions proven to increase this outcome are high quality CPR and defibrillation in shockable rhythms. Ventilation is also an important component of resuscitation in OHCA. Excess minute ventilation can adversely affect hemodynamics due to increased intrathoracic pressure (i.e. decreased ... Read more

The post REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 121.0 – Acute Sinusitis May 01, 2024
Take Home Points Acute rhinosinusitis is a clinical diagnosis The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement. REBEL Core Cast 121.0 – Acute Sinusitis Click here for Direct Download of ... Read more

The post REBEL Core Cast 121.0 – Acute Sinusitis appeared first on REBEL EM - Emergency Medicine Blog.

REBEL EM Book Club – MicroSkills Apr 09, 2024
Podcast Direct Download: Link Release Date: April 16th, 2024 Show Notes The Visible Voices Podcast Dr. Glaucomflecken: Power of Ultrasound with Emergency Medicine Dr. Resa Lewiss Adaira I Landry MD Resa E Lewiss MD is a Professor of Emergency Medicine at the University of Alabama at Birmingham. A TEDMED speaker and TimesUp Healthcare founder, she’s ... Read more

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REBEL Cast – EMTALA + Reproductive Health Rights Apr 03, 2024
REBEL Cast – EMTALA + Reproductive Health Click here for Direct Download of the Podcast. Dr. Dara Kass is a practicing emergency medicine physician who was most recently as the Regional Director of Region 2 for the US Department of Health and Human Services. She currently works with organizations and institutions to advance and implement ... Read more

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REBEL Cast Ep125: 1st 48 Hours of PE Management – How Good Is Unfractionated Heparin? Apr 01, 2024
Background: The mainstay of treatment for symptomatic pulmonary embolism (PE) is anticoagulation (AC). Patients with higher-risk PE may require advanced interventions such as thrombolytic therapy, surgical thrombectomy, or even extracorporeal membrane oxygenation (ECMO). Because of its short half-life and availability of a reversal agent, unfractionated heparin (UFH) is commonly used when percutaneous or surgical interventions ... Read more

The post REBEL Cast Ep125: 1st 48 Hours of PE Management – How Good Is Unfractionated Heparin? appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep124: Nitrates in Right Sided MIs? Mar 18, 2024
Background: Nitrates can help improve symptoms and ischemia in the setting of acute myocardial infarction. Current teaching holds that nitrates should be avoided in patients with potential right ventricular myocardial infarction (RVMI), due to the risk of decreasing preload and precipitating hypotension. This belief is based on a single 1989 study of 40 patients with ... Read more

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REBEL Core Cast 119.0 – Sleep Hygiene Mar 06, 2024
REBEL Core Cast 119.0 – Sleep Hygiene Click here for Direct Download of the Podcast Employ sleep strategies: Anchor sleep: a period of sleep that overlaps each day regardless of your night shift schedule to provide a guidepost for your body clock. Ideally would overlap with when you would normally be asleep if you were ... Read more

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REBEL Core Cast 118.0 – IM vs PO NSAIDs Feb 21, 2024
REBEL Core Cast 118.0 – IM vs PO NSAIDs Click here for Direct Download of the Podcast Bottom Line Up Top: There is no difference in analgesic efficacy between oral and intramuscular NSAIDs. Clinical Scenario: A 34-year-old woman presents to the ED with back pain. After your history and physical, you conclude that the patient’s ... Read more

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REBEL Core Cast 117.0 – Infections of Pregnancy Feb 07, 2024
Take Home Points Infections are a leading cause of maternal mortality worldwide. Prompt recognition is critical in management. Most infectious processes will require admission and close observation for improvement or decompensation. REBEL Core Cast 117.0 – Infections of Pregnancy Click here for Direct Download of the Podcast Urinary Tract Infection/Pyelonephritis Epidemiology: Occurs in as many ... Read more

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REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE? Jan 29, 2024
Background: Massive pulmonary embolism defined as sustained hypotension (SBP Read more

The post REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE? appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 116.0 – Achilles Tendon Rupture Jan 24, 2024
Take Home Points Achilles tendon rupture is a clinical diagnosis. The Thompson Test should be applied in all suspected cases. Remember to brace or splint a rupture, even if suspected, in the resting equinus position for optimal healing and prevention of further injury. Schedule follow up with orthopedics within 1 week for discussion of operative ... Read more

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REBEL Core Cast 115.0 – Cardiogenic Shock Dec 27, 2023
Take Home Points: Know clinical (cold extremities, oliguria, confusion, dizziness, narrow pulse pressure) and laboratory markers (metabolic acidosis, elevated creatinine, lactic acidosis) of hypoperfusion. An elevated lactate is a danger sign and requires explanation. Norepinephrine is a great first line vasopressor in Cardiogenic shock. Dobutamine is useful for inotropic support in Cardiogenic shock. Use POCUS ... Read more

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REBEL Core Cast 114.0 – Carbon Monoxide Toxicity Dec 13, 2023
Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of ... Read more

The post REBEL Core Cast 114.0 – Carbon Monoxide Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 113.0 – ACS Therapies and Management Nov 29, 2023
Take Home Points: All STEMIs should be loaded with dual antiplatelet therapy. Prasugrel (Effient) is avoided as there is an increase in bleeding complications if the patient requires a CABG. NSTEMI cases can be challenging to manage. Consult Cardiology early and use all available data. The appropriate medical treatment for ACS patients is as important ... Read more

The post REBEL Core Cast 113.0 – ACS Therapies and Management appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 112.0 – Awareness During Paralysis Nov 15, 2023
Take Home Points: Dose your RSI meds correctly. Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic. Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor! REBEL Core Cast 112.0 – Awareness During ... Read more

The post REBEL Core Cast 112.0 – Awareness During Paralysis appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 111.0 – Cardiac Testing Oct 25, 2023
Take Home Points: A CCTA is an anatomic test to determine if a patient has normal coronary arteries, non-obstructive disease, or obstructive disease. The warranty period for a CCTA is anywhere from 3-10 years depending on the characteristics of the plaque. A nuclear stress test is a functional study that allows for ischemia-driven management. The ... Read more

The post REBEL Core Cast 111.0 – Cardiac Testing appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 110.0 – On Shift Learning Pearls Oct 11, 2023
Take Home Points: Patients with recent onset atrial fibrillation can safely be cardioverted if they are 1) on anticoagulation 2) Low risk based on CHADS-VASC with onset Read more

The post REBEL Core Cast 110.0 – On Shift Learning Pearls appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 109.0 – Na Channel Blocker Poisoning Sep 27, 2023
Take Home Points: In the context of poisoning, a “wide QRS” is anything greater than 100 milliseconds. A newly “wide QRS”, especially with hemodynamic instability, should prompt consideration of sodium channel blockade and not ventricular tachycardia. Treatment is guided by administration of sodium-bicarbonate. Recall that the resultant alkalemia driven by sodium-bicarbonate will shift potassium intracellularly. ... Read more

The post REBEL Core Cast 109.0 – Na Channel Blocker Poisoning appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 108.0 – Angioedema Sep 13, 2023
Take Home Points: Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise. Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management. Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction. REBEL Core Cast ... Read more

The post REBEL Core Cast 108.0 – Angioedema appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 107.0 – Vertebral Osteomyelitis Aug 30, 2023
Take Home Points Clinical presentation is very nonspecific; evaluate all patients presenting with back pain for infectious risk factors. Baseline labs should not guide diagnosis, but may assist in later management. MRI is key to diagnosis, obtain this imaging in all patients who raise clinical suspicion Patients with hemodynamic instability and neurologic compromise warrant empiric ... Read more

The post REBEL Core Cast 107.0 – Vertebral Osteomyelitis appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 106.0 – Nerve Block Basics Aug 16, 2023
Take Home Points REBEL Core Cast 106.0 – Nerve Block Basics Click here for Direct Download of the Podcast Resources REBEL EM: Local Anesthetic Systemic Toxicity Sono in Staten Blog: https://www.statenislandem.com/sono-in-staten Core Ultrasound: https://www.coreultrasound.com/ POCUS Atlas: https://www.thepocusatlas.com/ Highland Ultrasound: http://highlandultrasound.com/ Post Created By: Billy Caputo MD Post Peer Reviewed By: Anand Swaminathan MD, MPH (Twitter ... Read more

The post REBEL Core Cast 106.0 – Nerve Block Basics appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep122 – Delayed vs Rapid Sequence Intubation in Agitated Trauma Patients Aug 07, 2023
Background: Getting a definitive airway in a critically ill trauma patient can be a stressful situation. The potential for soiled airways, cervical spine injuries, maxillofacial injuries and head injuries combined with agitation/delirium, altered mental status and hypoxemia can make securing a definitive airway both an anatomic and physiologic challenge. Traditional RSI entails preoxygenation followed by ... Read more

The post REBEL Cast Ep122 – Delayed vs Rapid Sequence Intubation in Agitated Trauma Patients appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep121: The Battle of the Blades – Video Laryngoscopy vs. Direct Laryngoscopy Jul 31, 2023
Background: The ongoing debate between video laryngoscopy (VL) and direct laryngoscopy (DL) has ignited intense debate within the emergency medicine and critical care communities. A recent pragmatic, randomized, multicenter trial (The DEVICE Trial) compared the two techniques to determine if VL outperformed DL in first-pass success (FPS). In this blog post, we explore the study’s ... Read more

The post REBEL Cast Ep121: The Battle of the Blades – Video Laryngoscopy vs. Direct Laryngoscopy appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 105.0 – Methylxanthine Toxicity Jul 26, 2023
Take Home Points Methylxanthines are a drug class that includes caffeine, theophylline, and theobromine. The three main mechanisms that account for the clinical presentation of methylxanthine toxicity are: catecholamine release, adenosine antagonism, and phosphodiesterase inhibition. Beta agonism will lead to hyperlactatemia, hypokalemia, hyperglycemia, and tachycardia. Adenosine antagonism may lead to seizures and/or supraventricular tachycardia that ... Read more

The post REBEL Core Cast 105.0 – Methylxanthine Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep120: Etomidate vs Ketamine for RSI in the ED? Jul 17, 2023
Background: Standard rapid sequence intubation (RSI) in the emergency department involves administration of an induction agent and a neuroblocking agent in quick succession. RSI inherently carries with it risks of complications such as post-intubation hypotension and cardiac arrest in the most extreme cases. It is possible that the induction agent used could play an important ... Read more

The post REBEL Cast Ep120: Etomidate vs Ketamine for RSI in the ED? appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 104.0 – Subtle ECGs in Acute Coronary Occlusion Jul 05, 2023
Take Home Points Provider assessment of how the patient looks is extremely important. If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. POCUS has been a phenomenal tool in the management and early diagnosis of a lot of abnormal ECG and chest pain presentations. Isolated elevation in aVR ... Read more

The post REBEL Core Cast 104.0 – Subtle ECGs in Acute Coronary Occlusion appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep119: A Discussion with Scott Weingart on the CT FIRST Trial Jun 29, 2023
Back on June 1st, 2023, Swami wrote a blog post on REBEL EM titled, The CT FIRST Trial, Should We Pan-CT After ROSC?. This stemmed a lot of discussion in the background between Swami, myself, and Scott. We felt it was worthwhile to record this as a podcast to better flush out some nuanced points. ... Read more

The post REBEL Cast Ep119: A Discussion with Scott Weingart on the CT FIRST Trial appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Cast Ep 118: The PROCOAG Trial – 4F-PCC for Trauma Patients? Jun 26, 2023
Background: Hemorrhage is the leading cause of mortality in trauma patients. Interventions such as early application of hemorrhage control, tranexamic acid, reduction of crystalloid fluid administration and balanced ratio blood product transfusion have improved many patients’ outcomes. However, mortality still remains high due to trauma-induced coagulopathy. Some clinicians have advocated for early administration of 4-factor ... Read more

The post REBEL Cast Ep 118: The PROCOAG Trial – 4F-PCC for Trauma Patients? appeared first on REBEL EM - Emergency Medicine Blog.

REBEL Core Cast 103.0 – Caustic Ingestions Jun 07, 2023
Take Home Points Caustics are substances that injure tissue upon physical contact. Caustic potential is not purely a function of pH. The decision to admit is dependent on the history and physical. Vomiting, drooling, and stridor are concerning. Stridor alone or 2/3 symptoms should warrant admission and gastroenterology consultation for potential endoscopy. The lack of ... Read more

The post REBEL Core Cast 103.0 – Caustic Ingestions appeared first on REBEL EM - Emergency Medicine Blog.

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