Approach to the Patient with Shock¶
Chapter 314 | Part 8: Critical Care Medicine
KEY CLINICAL POINTS¶
- Shock is a clinical syndrome of organ dysfunction due to impaired oxygen delivery, classified into four types: distributive, cardiogenic, hypovolemic, and obstructive.
- Early recognition and treatment are critical to prevent irreversible organ failure; key tools include the shock index (SI) and qSOFA score.
- ECMO (venoarterial or venovenous) is used for severe respiratory/circulatory failure, with specific indications for each type.
- Volume resuscitation, vasopressors (e.g., norepinephrine), and targeted interventions (e.g., antibiotics for sepsis) are core to management.
- Prognosis varies by shock type, with septic and cardiogenic shock having the highest mortality rates.
1. DEFINITION & OVERVIEW¶
Shock is a life-threatening condition characterized by inadequate oxygen delivery to tissues, leading to cellular hypoxia and organ dysfunction. It results from an imbalance between oxygen supply and demand, often progressing from a reversible to irreversible phase if untreated. The clinical presentation includes hypotension, tachycardia, and signs of end-organ hypoperfusion.
Table 313-4: Main Types and Key Features of Extracorporeal Gas Exchange¶
| TERM | DESCRIPTION | KEY FEATURES | IMPORTANT TECHNICAL NOTES |
|---|---|---|---|
| VA-ECMO | Deoxygenated blood drains via venous catheter to a pump and membrane oxygenator; blood is returned to the arterial system | Circulatory and respiratory support | Requires large vascular catheters (16–30 Fr); Higher blood flow rates (2–6 L/min) |
| VV-ECMO | Deoxygenated blood drains via venous catheter to a pump and membrane oxygenator; blood is returned to the venous system | Respiratory support | Requires large vascular catheters (20–30 Fr); Higher blood flow rates (2–5 L/min) |
| ECCOR | Venous catheter drains blood to a COn removal device; blood returns via a venous catheter | Partial respiratory support, COn removal only | Requires smaller vascular catheters (14–18 Fr); Lower blood flow rates (0.25–2 L/min) |
1.1 Pathophysiology¶
Shock arises from impaired oxygen delivery (CO × CaO I ) due to derangements in cardiac output (CO), arterial oxygen content (CaO I ), or both. The four main types reflect distinct hemodynamic profiles: distributive (reduced SVR), cardiogenic (reduced CO from cardiac failure), hypovolemic (reduced preload), and obstructive (mechanical obstruction).
1.2 Classification¶
Shock is categorized into four types based on pathophysiology: distributive (e.g., septic, anaphylactic), cardiogenic (e.g., myocardial infarction), hypovolemic (e.g., hemorrhage), and obstructive (e.g., tension pneumothorax).
2. EPIDEMIOLOGY¶
Shock is a common ICU admission reason, with septic shock being the most prevalent in ICUs. In a Danish ED study, 30.8% of shock cases were hypovolemic, 27.2% septic, and 23.4% distributive nonseptic. Mortality is highest in septic and cardiogenic shock (56.2% and 52.3% 90-day mortality, respectively).
2.1 Risk Factors¶
Infection (sepsis), trauma, hemorrhage, cardiac disease, and pulmonary embolism are leading causes. Patients with chronic illness, immunosuppression, or recent surgery are at higher risk.
2.2 Demographics¶
Sepsis is most common in ICU settings, while hypovolemic shock is prevalent in trauma or GI bleeding. Cardiogenic shock is more common in older adults with cardiovascular disease.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Shock results from derangements in oxygen delivery (CO × CaO I ). Distributive shock (e.g., sepsis, anaphylaxis) involves vasodilation and reduced SVR. Cardiogenic shock (e.g., MI, valvular disease) is due to cardiac pump failure. Hypovolemic shock (e.g., hemorrhage, dehydration) results from fluid loss. Obstructive shock (e.g., pulmonary embolism, tension pneumothorax) involves mechanical obstruction.
Table 314-1: Physiologic Classification of Shock¶
| TYPE OF SHOCK | DISEASES |
|---|---|
| Distributive | Sepsis, anaphylaxis, pancreatitis, severe burns |
| Cardiogenic | Myocardial infarction, valvular disease, arrhythmias |
| Hypovolemic | Hemorrhage, trauma, GI bleeding, burns |
| Obstructive | Pulmonary embolism, tension pneumothorax, cardiac tamponade |
3.1 Mechanisms¶
Distributive shock: Vasodilation and reduced SVR. Cardiogenic shock: Impaired cardiac output. Hypovolemic shock: Reduced preload. Obstructive shock: Mechanical obstruction of blood flow.
3.2 Molecular Basis¶
Cyanide poisoning uncouples oxidative phosphorylation, leading to anaerobic metabolism and lactate accumulation. Sepsis triggers systemic inflammation and endothelial dysfunction.
4. CLINICAL FEATURES¶
Early signs include tachycardia, tachypnea, and altered mental status. Advanced stages present with hypotension, oliguria, cold/clammy skin, and organ dysfunction (e.g., respiratory failure, renal failure).
4.1 Symptoms¶
Weakness, confusion, hypotension, tachycardia, dyspnea, and chest pain. Altered mental status may indicate cerebral hypoperfusion.
4.2 Signs¶
Cold extremities, mottled skin, decreased urine output (<0.5 mL/kg/h), jugular venous distension, and abnormal heart sounds (e.g., S3 gallop).
5. DIFFERENTIAL DIAGNOSIS¶
Distinguish between shock types based on hemodynamic profiles. Distributive shock (sepsis, anaphylaxis) vs. cardiogenic (MI, valvular disease) vs. hypovolemic (hemorrhage) vs. obstructive (pulmonary embolism).
5.1 Key Differentiators¶
Distributive: Low CVP/PCWP, high CO. Cardiogenic: High CVP/PCWP, low CO. Hypovolemic: Low CVP/PCWP, low CO. Obstructive: Normal/variable CVP/PCWP, low CO.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnostic workup includes history, physical exam, and lab tests (lactate, CBC, renal function, cardiac enzymes). Imaging (CXR, ultrasound, CT) and hemodynamic monitoring (CVP, Swan-Ganz) guide diagnosis.
Table 314-2: Hemodynamic Characteristics of the Major Types of Shock¶
| TYPE OF SHOCK | CVP | PCWP | CARDIAC OUTPUT | SYSTEMIC VASCULAR RESISTANCE |
|---|---|---|---|---|
| Distributive | fl | fl | › | fl |
| Cardiogenic | › | › | fl | › |
| Hypovolemic | fl | fl | fl | › |
| Obstructive | › | fl› | fl | › |
6.1 Laboratory Tests¶
Lactate levels, BUN/creatinine, electrolytes, CBC, PT/INR, cardiac enzymes, and arterial blood gas analysis.
6.2 Imaging¶
Chest X-ray for pulmonary edema, pneumothorax, or infiltrates. CT for pulmonary embolism or trauma. Point-of-care ultrasound (POCUS) for IVC assessment, pleural effusion, or cardiac function.
7. MANAGEMENT & TREATMENT¶
Immediate interventions include volume resuscitation, vasopressors, and addressing the underlying cause (e.g., antibiotics for sepsis). ECMO may be used for refractory cases.
Table 314-3: Key Principles in the Treatment of Shock¶
| PRINCIPLE |
|---|
| Recognize shock early |
| Assess type of shock present |
| Initiate therapy simultaneously with evaluation |
| Involve multidisciplinary team |
| Restore oxygen delivery |
| Identify etiologies requiring lifesaving interventions |
7.1 Volume Resuscitation¶
Crystalloids or blood products for hypovolemic shock. Early goal-directed therapy (EGDT) in septic shock (30 mL/kg initial fluid resuscitation).
7.2 Vasopressors¶
Norepinephrine as first-line for septic shock. Dopamine for cardiogenic shock. Vasopressin may be adjunctive in septic shock.
7.3 Specific Interventions¶
Antibiotics for sepsis, epinephrine for anaphylaxis, surgical intervention for hemorrhage or pulmonary embolism.
8. PROGNOSIS & COMPLICATIONS¶
Mortality is highest in septic and cardiogenic shock. Complications include multiorgan failure, arrhythmias, and infections. Early intervention improves outcomes.
8.1 Mortality Rates¶
Septic shock: 56.2% 90-day mortality; Cardiogenic shock: 52.3% 9,0-day mortality; Hypovolemic shock: lower mortality.
8.2 Long-Term Effects¶
Chronic organ dysfunction, post-traumatic stress, and increased risk of recurrent shock.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: Risk of hypovolemic shock from placental abruption. Pediatrics: Higher risk of distributive shock from sepsis. Elderly: Frailty and comorbidities increase mortality.
9.1 Pregnancy¶
Monitor for uterine bleeding and fetal distress. Avoid certain medications (e.g., NSAIDs).
9.2 Pediatrics¶
Higher risk of septic shock; use of qSOFA and POCUS for assessment.
10. KEY POINTS & CLINICAL PEARLS¶
- Use qSOFA and shock index to identify septic shock early. 2. Initiate volume resuscitation with crystalloids or blood products. 3. Administer norepinephrine as first-line vasopressor in septic shock. 4. Consider ECMO for refractory cases. 5. Address underlying causes (e.g., antibiotics, surgery).