Definition of Shock
Shock is a state of acute circulatory failure resulting in inadequate delivery of oxygen and nutrients to tissues, leading to cellular dysfunction, end-organ hypoperfusion, and if untreated, multi-organ failure and death. 1
Core Pathophysiologic Concept
- Shock fundamentally represents an imbalance between cellular oxygen supply and demand, resulting in tissue hypoperfusion and metabolic dysfunction 2, 3
- The circulatory system fails to adequately deliver required substrates to maintain end-organ perfusion, tissue homeostasis, and cellular metabolism 4
- This leads to anaerobic metabolism, lactic acidosis, and progressive cellular and organ dysfunction 5
Clinical Manifestations of Inadequate Perfusion
Shock manifests through multiple clinical signs reflecting end-organ hypoperfusion:
- Hypotension - typically systolic blood pressure <90 mmHg or mean arterial pressure <65 mmHg 1
- Altered mental status - confusion or decreased level of consciousness from cerebral hypoperfusion 1, 6
- Peripheral vasoconstriction - cold extremities, delayed capillary refill 1
- Oliguria - decreased urine output from renal hypoperfusion 1
- Elevated lactate - serum lactate >2 mmol/L indicating cellular metabolic dysfunction 1
- Tachycardia - compensatory increase in heart rate 1
Four Primary Categories of Shock
The mechanisms producing shock are classified into four distinct categories based on underlying pathophysiology 2, 5:
1. Hypovolemic Shock
2. Distributive Shock
- Characterized by profound vasodilation and increased vascular permeability 7, 8
- Septic shock is the most common form, defined by vasopressor requirement to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate fluid resuscitation 1, 7, 6
- Involves microcirculatory dysfunction leading to tissue hypoperfusion despite potentially normal macrocirculatory parameters 8
3. Cardiogenic Shock
- Represents inability of the heart to maintain effective cardiac output commensurate to metabolic demands due to primary cardiac pathology 1
- The central pathophysiologic derangement is diminished cardiac output leading to systemic hypoperfusion 1
- Typically presents with pulmonary edema and specific cardiac symptoms, distinguishing it from other shock types 6
- Defined by sustained hypotension (systolic BP <90 mmHg), cardiac index <2.2 L·min⁻¹·m⁻² secondary to cardiac dysfunction, or requirement for inotropic/vasopressor support 1
4. Obstructive Shock
- Results from mechanical obstruction to cardiac output (e.g., pulmonary embolism, cardiac tamponade, tension pneumothorax) 2, 5
Critical Cellular and Metabolic Consequences
- Altered cellular metabolism leads to lactate accumulation, which serves as both a diagnostic marker and indicator of severity 1, 7, 8
- Severe lactic acidosis impairs cellular enzyme activity, reduces myocardial contractility, and diminishes vascular responsiveness to catecholamines 8
- Prolonged shock beyond critical time thresholds leads to irreversible cellular injury; once cells reach this point, restoration of perfusion cannot prevent cell death 8
Common Diagnostic Pitfalls
- Failing to recognize "preshock" states where compensatory vasoconstriction maintains near-normal blood pressure despite tissue malperfusion 1
- Patients receiving vasopressors may still have profound perfusion abnormalities despite normalized blood pressure 7, 6
- Not measuring lactate levels, which are essential for identifying cellular metabolic dysfunction and shock severity 7, 6
- Confusing different shock types can lead to inappropriate management strategies 6
Clinical Urgency and Reversibility
- Shock is reversible in earlier stages but transitions to an irreversible phase if left untreated, resulting in multi-organ failure and death 9
- Rapid recognition and intervention are of utmost importance to reverse the shock state before irreversible cellular damage occurs 4, 9
- Early identification is crucial for improving outcomes across all shock types 7