Intro

This chapter explores the concept of shock, highlighting its definition as a supply and demand mismatch and the risks associated with it. The hosts provide insights on key equations and the significance of maintaining tissue oxygenation in patients experiencing shock.

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🧭 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

- 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)