Ch04: Shock（休克）

Preparatory Mindset

Shock = inadequate tissue perfusion and oxygen delivery → cellular hypoxia → organ dysfunction (CM exam tested). The lecture (Dr. Pan) covers pathophysiology (including ischemia-reperfusion injury), the patterns of shock (hypovolemic, cardiogenic, distributive), and the principles & priorities of resuscitation with monitoring endpoints. The case-driven teaching (75-yr-old woman with bright red rectal bleeding → hypovolemic shock) shows the exam's clinical style.

Exam mindset: classify shock, recognize the stages, and know the resuscitation algorithm (airway → bleeding control → fluids/blood → vasopressors → endpoint monitoring). The prep PDFs add the classic definitions (休克指数, 微循环变化) and treatment priorities.

Core Concepts

1. Definition & pathophysiology

• Shock: acute circulatory failure with inadequate tissue perfusion → cellular hypoxia → anaerobic metabolism (lactic acidosis) → organ dysfunction → MODS if uncorrected
• The final common pathway: ↓ perfusion pressure → ↓ O2 delivery → cellular ATP depletion → membrane failure → release of inflammatory mediators → capillary leak → further hypovolemia (vicious cycle)
• Ischemia-reperfusion injury: restoration of blood flow paradoxically causes further damage via reactive oxygen species (ROS), neutrophil infiltration, calcium overload — relevant to trauma, revascularization, organ transplant

2. Classification of shock (MUST KNOW)

3. Hypovolemic shock — the surgical archetype

| Class | Blood loss | HR | BP | RR | Urine | Mental state | |---|---|---|---|---|---|---| | I | <15% (~750 ml) | <100 | Normal | 14-20 | >30 | Slight anxiety | | II | 15-30% (750-1500) | 100-120 | Normal (↓ pulse pressure) | 20-30 | 20-30 | Mild anxiety | | III | 30-40% (1500-2000) | 120-140 | ↓ | 30-40 | 5-15 | Confused | | IV | >40% (>2000) | >140 | ↓↓ | >40 | Negligible | Lethargic |

• Causes: hemorrhage (GI bleed — the case!), trauma, surgery, burns, severe dehydration
• Hemorrhagic shock classes (ATLS):
• Clinical (compensated → decompensated): tachycardia (earliest sign), cold clammy skin, delayed capillary refill, hypotension (late), oliguria, altered mental status, weak thready pulse

4. Septic shock — the most common distributive cause

• Sepsis = infection + organ dysfunction (SOFA ↑); septic shock = sepsis + vasopressor requirement + lactate > 2 mmol/L (Sepsis-3)
• Pathophysiology: pathogen PAMPs (LPS) → cytokine storm → vasodilation, capillary leak, microthrombosis → distributive shock
• Clinical: fever/hypothermia, warm flushed skin (early) then cold (late), tachycardia, hypotension, tachypnea, altered mentation, oliguria; lactate elevated
• Surviving Sepsis bundle (1-hour): measure lactate; blood cultures before antibiotics; broad-spectrum antibiotics within 1 h; 30 ml/kg crystalloid for hypotension/lactate ≥4; vasopressors (norepinephrine) if hypotensive during/after fluids; reassess

5. Resuscitation principles & priorities (MUST KNOW)

- Start with warm crystalloid (balanced salt solution / Ringer's lactate) — 1-2 L bolus in adults (10-20 ml/kg) - Blood products early in hemorrhagic shock (balanced 1:1:1 RBC:FFP:platelets; massive transfusion protocol) - Avoid excessive crystalloid (dilutional coagulopathy, edema) — permissive hypotension in uncontrolled hemorrhage (SBP ~80-90 until bleeding controlled, except head injury) - Colloids (albumin, starches — starches avoided in sepsis/renal failure)

• ABC approach first (airway, breathing, circulation) — secure the airway, control external bleeding (direct pressure), obtain IV/IO access
• Fluid resuscitation:
• Vasopressors: norepinephrine (first-line) if fluid-refractory; add vasopressin
• Endpoints of resuscitation (MUST KNOW): MAP ≥ 65 mmHg; urine output ≥ 0.5 ml/kg/h (30 ml/h); lactate clearance; normalization of mentation & skin perfusion; ScvO2 ≥ 70%; base deficit improvement
• Monitoring: invasive arterial BP (accurate in shock), CVP (preload), lactate, ABG, urine output, ECG, pulse oximetry

6. Monitoring & endpoints

• Clinical endpoints: BP, HR, urine output, mentation, skin perfusion, capillary refill
• Lactate: best single prognostic marker; clearance reflects resuscitation adequacy
• CVP: reflects right heart preload (low in hypovolemic; high in cardiogenic/obstructive)
• Mixed/central venous oxygen saturation (ScvO2): low = inadequate O2 delivery
• Base deficit: reflects tissue acidosis in trauma

7. Complications / consequences

• Acute kidney injury (prerenal → ATN)
• ARDS (pulmonary edema, hypoxemia)
• DIC (coagulopathy, microthrombosis)
• MODS (multi-organ failure) — leading cause of late death
• Stress ulcers, ileus, hyperglycemia, immunosuppression

High-Yield Points

• Shock = inadequate tissue perfusion → cellular hypoxia → lactic acidosis → MODS
• Four types: hypovolemic, cardiogenic, distributive (septic/anaphylactic/neurogenic), obstructive (tension PTX, tamponade, PE)
• Hypovolemic (hemorrhagic) shock classes I-IV; tachycardia is the earliest sign; hypotension is LATE
• Sepsis-3: SOFA ↑ + infection; septic shock = vasopressor needed + lactate > 2
• Sepsis bundle: antibiotics within 1 h, 30 ml/kg crystalloid, norepinephrine, lactate
• Resuscitation: ABC first, warm crystalloid, blood 1:1:1 in hemorrhage, norepinephrine for fluid-refractory
• Endpoints: MAP ≥ 65, urine ≥ 0.5 ml/kg/h, lactate clearance, ScvO2 ≥ 70%
• Permissive hypotension in uncontrolled hemorrhage (unless head injury)
• Ischemia-reperfusion injury: ROS, neutrophils, calcium overload

Topic Summary

Shock is inadequate tissue perfusion → cellular hypoxia → lactic acidosis → MODS. Types: hypovolemic (hemorrhage/burns/dehydration — the surgical archetype, staged I-IV), cardiogenic (pump failure, ↑ CVP), distributive (septic most common, anaphylactic, neurogenic — ↓ SVR), obstructive (tension pneumothorax, tamponade, PE). Resuscitation: ABC, control bleeding, warm crystalloid then blood (1:1:1 in hemorrhage), norepinephrine if refractory, monitor endpoints (MAP ≥65, urine ≥0.5 ml/kg/h, lactate clearance, ScvO2). Sepsis bundle: lactate, cultures, antibiotics within 1 h, 30 ml/kg fluids, norepinephrine. Complications: AKI, ARDS, DIC, MODS. Ischemia-reperfusion injury adds ROS-mediated damage on reperfusion.