REBEL Core Cast 138.0: A Simple Bedside Approach to Shock

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Aug 4, 2025

Discover the intriguing nature of shock as a clinical diagnosis, emphasizing that it's more than just a number. Learn to assess patients rapidly using the 'four L's' — mental status, limb temperature, urine output, and lactate levels. Find out how pulse pressure can reveal shock type, from narrow pressures indicating cardiogenic issues to wide pressures pointing towards distributive shock. The hosts stress the importance of systematic bedside evaluation, reinforcing that even basic techniques can uncover critical insights.

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ADVICE

Four L's Bedside Assessment

Use the Four L's at the bedside: Lucid (mental status), Limbs (warm/cold), Leak (urine output), Lactate.
This quick assessment helps determine if a patient with low blood pressure is truly in shock or compensated and appearing well.

INSIGHT

Pulse Pressure Explains Shock Types

Systolic BP reflects stroke volume while diastolic BP reflects systemic vascular resistance.
Pulse pressure (systolic minus diastolic BP) helps differentiate shock types based on stroke volume and vascular tone changes.

INSIGHT

Narrow Pulse Pressure Means Cold Shock

Narrow pulse pressure indicates low stroke volume with compensatory increased systemic vascular resistance.
This pattern occurs in cardiogenic, hypovolemic, and obstructive shock, commonly described as cold shock.

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📌 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

- 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)