REBEL Core Cast 138.0: A Simple Bedside Approach to Shock

🧭 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.

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📝 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

1. • 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

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