Shock — Pathophysiology¶

Category: Concepts Sources: raw/protocols/nm-sop-guidelines-treatment-2022.pdf Last updated: 2026-04-05

Overview¶

Shock is not a disease — it is a physiological state. The core definition: inadequate tissue perfusion resulting in cellular hypoxia. When cells cannot receive sufficient oxygen to maintain aerobic metabolism, they shift to anaerobic pathways, accumulate metabolic waste, and begin to fail. If the process is not reversed, organ failure follows. If not corrected, death follows.

This article covers the pathophysiology of shock — the mechanism of what is happening at the cellular and organ system level. For clinical assessment findings and EMT-B management, see shock.

The Core Mechanism¶

Normal circulation delivers oxygen (O2) to tissues and removes CO2 and metabolic waste. This depends on:

Adequate circulating volume — enough blood to fill the vascular system
Adequate pump function — the heart contracts forcefully and at an appropriate rate
Appropriate vascular tone — vessels maintain resistance to distribute flow to the right tissues
Functional oxygen-carrying capacity — enough functional hemoglobin to carry O2

When any of these fails below a critical threshold, tissue perfusion becomes inadequate — shock begins.

Cellular Level¶

Under normal aerobic metabolism: - Glucose + O2 → 36–38 ATP (energy) + CO2 + H2O

In shock, O2 delivery falls: - Glucose → 2 ATP + lactic acid (anaerobic glycolysis)

The consequences: - Lactic acidosis — accumulating lactic acid drops blood pH → metabolic acidosis - ATP depletion — cells cannot maintain membrane pumps (Na+/K+ ATPase), leading to cellular swelling, ion imbalance, and eventually membrane failure - Inflammatory mediator release — damaged cells release cytokines and reactive oxygen species, which damage adjacent cells and accelerate organ dysfunction - End-organ failure — kidneys, brain, liver, lungs, gut — all are oxygen-dependent; prolonged hypoperfusion causes irreversible organ damage

This cascade explains why shock that is caught early (compensated) is reversible, and shock that progresses to organ failure may not be.

Four Types of Shock¶

1. Hypovolemic Shock¶

Mechanism: Loss of circulating volume → decreased preload → decreased stroke volume → decreased cardiac output → decreased tissue perfusion.

Subtypes: - Hemorrhagic: Blood loss — trauma, GI hemorrhage, ruptured ectopic pregnancy, aortic aneurysm, internal bleeding. Both volume and oxygen-carrying capacity are lost simultaneously. - Non-hemorrhagic: Plasma/fluid loss — severe burns (plasma leaks into damaged tissue), vomiting and diarrhea (dehydration), diabetic ketoacidosis (osmotic diuresis), third-spacing (fluid into tissues or body cavities).

Key finding: Tachycardia + hypotension + poor skin perfusion + volume history (trauma, vomiting, burns).

Why tachycardia comes first: See Compensation section below.

2. Distributive Shock¶

Mechanism: Massive vasodilation → relative hypovolemia. The circulating volume hasn't changed but the vascular bed has expanded beyond what the existing volume can fill — the pressure drops.

Subtypes:

Type	Trigger	Mechanism
Septic	Systemic infection (bacterial, viral, fungal)	Bacterial endotoxins trigger massive inflammatory response → vasodilation + capillary leak
Anaphylactic	Allergen exposure in sensitized patient	IgE-mediated mast cell degranulation → histamine release → bronchoconstriction + vasodilation + capillary leak
Neurogenic	Spinal cord injury (typically cervical)	Disruption of sympathetic outflow below the lesion → loss of vasomotor tone → vasodilation

Key finding in septic/anaphylactic: Early presentation often has warm, flushed skin (vasodilation is still delivering blood to the skin before decompensation). This is distinct from cold/clammy hypovolemic shock. See shock for clinical distinction.

Neurogenic shock: Hypotension with bradycardia (no sympathetic compensatory tachycardia). Warm, dry skin below injury level. This is the opposite of the typical shock presentation — a clinical trap for providers who assume all shock has tachycardia.

3. Cardiogenic Shock¶

Mechanism: Pump failure → inadequate stroke volume → decreased cardiac output → decreased tissue perfusion despite normal or elevated circulating volume.

Causes: - Massive myocardial infarction (MI) — loss of ventricular muscle mass - Severe dysrhythmia (VT, VF, high-degree AV block, SVT with very high rate) - Valvular failure (acute mitral regurgitation, aortic stenosis) - Myocarditis, dilated cardiomyopathy

Key finding: Signs of shock + signs of pulmonary edema (pulmonary congestion from backup of fluid into the lungs). JVD (jugular venous distension) is present because fluid backs up. Crackles on auscultation. Do NOT aggressively fluid-load cardiogenic shock — it worsens pulmonary edema.

The distinction matters: Hypovolemic shock → give fluids. Cardiogenic shock → fluids can kill.

4. Obstructive Shock¶

Mechanism: Mechanical obstruction prevents adequate blood flow through the cardiovascular system, despite normal pump function and normal circulating volume.

Causes: - Tension pneumothorax: Air accumulates under pressure in the pleural space → compresses the heart and great vessels → reduces venous return → reduces cardiac output. Tracheal deviation away from the affected side, absent breath sounds, JVD, hypotension. See chest-trauma. - Cardiac tamponade: Blood accumulates in the pericardial sac (usually from penetrating trauma or aortic dissection) → compresses the heart → reduces cardiac filling and output. Beck's triad: hypotension + JVD + muffled heart sounds. - Massive pulmonary embolism (PE): Clot in the pulmonary arterial system obstructs blood flow from the right ventricle to the lungs → backs up right heart → reduces left heart output.

Key finding: JVD present (distinguished from hypovolemic shock, which does not have JVD). Specific mechanism diagnosis requires clinical and imaging context.

Stages of Shock¶

Compensated Shock¶

The body's homeostatic mechanisms are responding to the threat. The patient is in shock but the BP may still be normal. This is the window where prehospital intervention is most effective.

Compensation mechanisms:

Response	Mediator	Effect
Tachycardia	Catecholamines (epinephrine, norepinephrine)	Increases cardiac output (CO = HR × SV)
Peripheral vasoconstriction	Catecholamines, angiotensin II	Shunts blood away from skin/gut toward brain and heart
Increased respiratory rate	Hypoxia, acidosis	Increases O2 intake and blows off CO2 (respiratory compensation for metabolic acidosis)
ADH release	Hypothalamus	Retains water at the kidney; reduces urine output
RAAS activation	Kidney → aldosterone	Na+ and water retention; vasoconstriction

Why tachycardia comes before hypotension: Cardiac output (CO) = Heart Rate (HR) × Stroke Volume (SV). As SV falls (from blood loss, pump failure, or vasodilation), the body compensates by increasing HR to maintain CO. This can preserve BP for a significant time. By the time BP falls, the compensatory reserve has been exhausted — the patient is already in trouble.

In adults: BP may remain normal with 15–30% blood volume loss (roughly 750–1500 mL in a 70 kg adult). Tachycardia and anxiety appear first.

Clinical teaching point: The "classic" shock presentation of hypotension is a late finding in adults who are previously healthy. The early presentation is tachycardia + skin signs (pale, cool, diaphoretic) + anxiety/agitation + decreased cap refill.

Decompensated Shock¶

Compensatory mechanisms are overwhelmed. BP falls. Organ perfusion decreases below functional thresholds.

Clinical findings: - Hypotension — BP falls; systolic <90 mmHg in adults - Altered mental status — brain perfusion falls; patient becomes confused, then unresponsive - Oliguria — kidneys not receiving enough perfusion to filter; reduced or absent urine output - Worsening tachycardia or paradoxical bradycardia (profound shock or spinal injury) - Severe lactic acidosis — pH drops below 7.35; hyperventilation becomes pronounced as respiratory compensation maxes out

Irreversible Shock¶

Prolonged ischemia causes cellular death at scale. Organs cannot recover even if perfusion is restored.

MODS (Multiple Organ Dysfunction Syndrome): kidneys fail (dialysis), lungs fail (ARDS, ventilator), liver fails, coagulation fails (DIC — disseminated intravascular coagulation)
Reperfusion injury: Paradoxically, restoring circulation to ischemic tissue releases a surge of inflammatory mediators and reactive oxygen species that cause additional damage
Irreversible cellular death: Beyond a threshold of ischemia time, cell membranes cannot be restored regardless of treatment

Prehospital providers rarely encounter true irreversible shock before death occurs. The goal is to prevent progression from compensated → decompensated → irreversible by early recognition and aggressive treatment.

Pediatric Considerations¶

Children compensate for shock more effectively than adults and for longer. A child in significant hemorrhagic shock may maintain a normal blood pressure until they are near cardiovascular collapse. The tachycardia and skin signs (pale, mottled, cool periphery) appear first and may be the only clinical signal.

Do not be falsely reassured by a normal BP in a child with other shock signs. Pediatric BP maintenance in the face of hemorrhage is a physiological trap — when it finally fails, it fails fast.

Normal pediatric BP thresholds (NM protocol): - <1 year: SBP <60 mmHg = hypotension - 1–10 years: (age × 2) + 70 = minimum SBP - >10 years: SBP <90 mmHg

Shock vs. Syncope¶

Vasovagal syncope is a transient, self-limited neurally-mediated event that causes brief loss of consciousness — it is not shock. However, syncope can be the presenting symptom of serious underlying conditions that do cause shock: hemorrhage (ruptured ectopic pregnancy, GI bleed), cardiac dysrhythmia, massive PE. Any patient with syncope requires evaluation; do not assume benign etiology. See syncope.

Why This Matters for the EMT-B¶

Understanding the pathophysiology of shock matters clinically because:

Tachycardia before hypotension — Early recognition requires acting on tachycardia and skin signs, not waiting for BP to fall.
Type determines treatment — Hypovolemic: fluid resuscitation and hemorrhage control. Cardiogenic: no aggressive fluids. Neurogenic: may require vasopressors (ALS). Obstructive: treat the obstruction (needle decompression, pericardiocentesis — ALS).
Pediatric compensation — Normal BP in a child does not rule out shock.
Time sensitivity — The transition from compensated to decompensated to irreversible is time-dependent. Every minute of cellular hypoxia advances the process.

NM Protocol Notes¶

NM EMS shock recognition criteria include: AMS, delayed capillary refill, SpO2 <94%, ETCO2 <25 mmHg, tachycardia, weak/decreased pulses, cool/mottled or flushed skin. Notably, hypotension is not required — the protocol explicitly recognizes compensated shock.

Fluid resuscitation (isotonic, 20 mL/kg max 1 L bolus, up to 3 boluses) is authorized at the EMT level but establishing IV access should not delay transport in trauma. The mantra: treat the shock, transport the patient, don't wait.

For anaphylactic shock: epinephrine IM is first-line — not fluids. The mechanism (histamine-mediated vasodilation + bronchoconstriction) responds to epinephrine faster than volume.

NREMT Relevance¶

Foundational topic for the cognitive exam:

Classify each type of shock: hypovolemic, distributive (3 subtypes), cardiogenic, obstructive
Know that tachycardia precedes hypotension in compensated shock — this is a specific NREMT question pattern
Know that children compensate longer than adults — normal BP does not rule out shock in pediatric patients
Know the clinical distinction between hypovolemic (cold/clammy, no JVD) and cardiogenic (JVD, pulmonary edema) and obstructive (JVD, absent breath sounds)
Know that neurogenic shock presents with hypotension AND bradycardia (loss of sympathetic tone) — this is unique among shock types
Know that fluid resuscitation is appropriate for hypovolemic but not cardiogenic shock

shock — clinical assessment and EMT-B management of shock
bleeding-control-shock — hemorrhage control procedure; primary intervention for hypovolemic shock
anaphylaxis — anaphylactic (distributive) shock mechanism and epinephrine treatment
chest-trauma — obstructive shock from tension pneumothorax
acs-chest-pain — cardiogenic shock from massive MI
spinal-injury — neurogenic shock from cervical spinal cord injury
start-triage — perfusion assessment (radial pulse / cap refill) in START reflects shock physiology

Sources¶

raw/protocols/nm-sop-guidelines-treatment-2022.pdf — Shock protocol (p. 57–58)