📌 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.
- 🧠 Shock is a Clinical Diagnosis — Not Just a Number
📝 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
- Supply vs. Demand mismatch:
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
- Systolic Blood Pressure
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
Micheal Bass DO
Frank J. Lodeserto MD
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