SHOCK

Recognize the physiology. Treat the cause. Reassess the response.

Shock is not just hypotension.

A normal blood pressure does not exclude shock, and a low blood pressure does not tell you the mechanism.

The bedside task is to determine whether tissue perfusion and oxygen delivery are adequate — and if not, why.

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SHOCK IS NOT JUST HYPOTENSION

Blood pressure is important, but it is only one part of the circulation.

A patient can maintain arterial pressure through compensatory vasoconstriction while tissue perfusion and oxygen delivery continue to deteriorate.

Conversely, a patient may have a relatively low MAP and still maintain adequate organ perfusion.

The more useful clinical question is not:

“What is the blood pressure?”

It is:

“Is oxygen delivery sufficient for tissue demand — and if not, why?”

THINK IN FOUR BUCKETS

VOLUME

Hypovolemic / hemorrhagic physiology

Think:

  • bleeding

  • fluid loss

  • reduced venous return

  • inadequate preload

Bedside clues:

  • small hyperdynamic LV

  • reduced filling

  • dynamic evidence of preload responsiveness where appropriate

  • occult hemorrhage

PUMP

Cardiogenic physiology

Think:

  • LV failure

  • RV failure

  • myocardial ischemia

  • myocarditis

  • severe dysrhythmia

Bedside clues:

  • reduced contractility

  • pulmonary edema

  • elevated filling pressures

  • RV dilation or dysfunction

FLOW

Obstructive physiology

Think:

  • tension pneumothorax

  • cardiac tamponade

  • massive pulmonary embolism

The core problem:

Blood cannot move effectively through the circulation.

TONE

Distributive physiology

Think:

  • sepsis

  • anaphylaxis

  • neurogenic shock

  • vasoplegia

The core problem:

  • loss of vascular tone

  • maldistribution of flow

MIXED SHOCK IS COMMON

Critically ill patients often do not fit neatly into a single category.

Common combinations include:

  • septic shock with myocardial depression

  • hemorrhage with vasoplegia

  • RV failure with distributive physiology

  • post-arrest myocardial dysfunction with vasodilation

Do not force the patient into one diagnosis if the physiology does not fit.

Identify the dominant mechanism, treat it, and reassess.

OXYGEN DELIVERY

DO₂ = CO × CaO₂

Cardiac output depends on:

Heart Rate × Stroke Volume

Oxygen delivery is determined by:

  • cardiac output

  • hemoglobin concentration

  • arterial oxygen saturation

Shock occurs when oxygen delivery becomes inadequate relative to metabolic demand.

This is why simply chasing a MAP may fail.

POCUS IN SHOCK

Use ultrasound to answer a clinical question.

Not:

“Can I perform a complete echo?”

Instead ask:

  • Is the LV severely impaired?

  • Is the RV enlarged or failing?

  • Is there pericardial fluid with tamponade physiology?

  • Is there severe hypovolemia?

  • Is there pulmonary edema?

  • Is there a pneumothorax?

  • Is there free intraperitoneal fluid?

POCUS is most useful when it changes the next decision.

FLUID RESPONSIVENESS ≠ FLUID REQUIREMENT

A patient may increase stroke volume after a fluid challenge and still not benefit from more volume.

Ask three questions:

1. Will stroke volume increase?

2. Will additional volume improve clinically meaningful perfusion?

3. What is the risk of congestion?

Use tools such as:

  • passive leg raise

  • dynamic stroke-volume assessment

  • focused echocardiography

  • repeated bedside reassessment

Avoid assuming that fluid responsiveness automatically means:

Give more fluid.

DON’T CHASE THE MAP

MAP is a target.

It is not the endpoint.

Increasing arterial pressure only matters if it improves organ perfusion.

After any intervention, reassess:

  • mentation

  • skin perfusion

  • capillary refill

  • urine output

  • lactate trajectory

  • hemodynamics

  • cardiac function

  • venous congestion

  • respiratory status

Treat the physiology, not just the monitor.

THE FIRST 5–10 MINUTES

1. RECOGNIZE

Is this shock?

Look for evidence of impaired perfusion:

  • altered mentation

  • cool or mottled skin

  • delayed capillary refill

  • oliguria

  • rising lactate

  • increasing work of breathing

  • tachycardia

  • narrowing pulse pressure

  • worsening metabolic acidosis1. RECOGNIZE

    Is this shock?

    Look for evidence of impaired perfusion:

    • altered mentation

    • cool or mottled skin

    • delayed capillary refill

    • oliguria

    • rising lactate

    • increasing work of breathing

    • tachycardia

    • narrowing pulse pressure

    • worsening metabolic acidosis

4. TREAT

Match the intervention to the mechanism.

Possible interventions may include:

  • hemorrhage control

  • blood products

  • fluid

  • vasopressors

  • inotropes

  • decompression

  • treatment of tamponade

  • treatment of pulmonary embolism

  • source control

  • treatment of anaphylaxis

2. STABILIZE

Address immediate threats to:

  • airway

  • breathing

  • circulation

Establish:

  • monitoring

  • vascular access

  • focused laboratory assessment

  • early POCUS

5. REASSESS

Ask:

Did perfusion improve?

Not simply:

Did the blood pressure improve?

3. PHENOTYPE

Ask:

Volume?

Pump?

Flow?

Tone?

Or mixed?

6. ESCALATE

If the patient is not improving:

  • reconsider the diagnosis

  • reassess the shock phenotype

  • look for mixed physiology

  • reassess cardiac function

  • look again for an obstructive cause

  • reconsider occult hemorrhage or uncontrolled source

DO NOT MISS

In any patient with unexplained shock, keep these diagnoses front of mind:

  • occult hemorrhage

  • tension pneumothorax

  • cardiac tamponade

  • massive pulmonary embolism

  • RV failure

  • myocardial infarction

  • sepsis

  • anaphylaxis

  • mixed shock