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Shock for the ABIM

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Shock for the American Board of Internal Medicine Exam
Shock is a life-threatening condition resulting from inadequate tissue perfusion and oxygenation, leading to cellular dysfunction and organ failure. It is classified into four main types: hypovolemic, distributive, cardiogenic, and obstructive.
signs and symptoms of shock
Types of Shock
Hypovolemic Shock
  • Etiology: Caused by a reduction in intravascular volume, typically from hemorrhage (trauma, gastrointestinal bleeding) or fluid losses (vomiting, diarrhea, burns).
  • Pathophysiology: Reduced preload decreases stroke volume and cardiac output, leading to poor perfusion.
  • Clinical Presentation:
    • Symptoms: Weakness, dizziness, confusion, and cool, clammy skin.
    • Physical Exam: Tachycardia, hypotension, narrowed pulse pressure, and delayed capillary refill.
  • Diagnosis:
    • Labs: Elevated hematocrit in dehydration; decreased hematocrit in hemorrhage.
    • Hemodynamic Monitoring: Low central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP).
  • Management:
    • Fluid Resuscitation: Isotonic crystalloids (e.g., normal saline) as the first-line therapy.
    • Blood Products: For hemorrhagic shock, initiate blood transfusion if there is significant blood loss or ongoing bleeding.
    • Hemorrhage Control: Surgical intervention or endoscopic techniques may be required.
Distributive Shock
  • Etiology: Characterized by vasodilation and maldistribution of blood flow. Main causes include septic shock, anaphylactic shock, and neurogenic shock.
Septic Shock
    • Etiology: Severe infection leading to systemic inflammatory response and widespread vasodilation.
    • Pathophysiology: Infection triggers a release of cytokines, causing vasodilation, capillary leakage, and decreased systemic vascular resistance (SVR).
    • Clinical Presentation:
    • Symptoms: Fever, chills, altered mental status, warm skin initially, progressing to cool extremities in later stages.
    • Physical Exam: Hypotension, tachycardia, and bounding pulses early in the disease.
    • Diagnosis:
    • Labs: Elevated lactate, leukocytosis or leukopenia, and procalcitonin levels may aid diagnosis.
    • Hemodynamic Monitoring: Increased cardiac output (CO) with low SVR in early stages.
    • Management:
    • Early Antibiotics: Broad-spectrum antibiotics within one hour of recognition.
    • Fluid Resuscitation: Initial 30 mL/kg of crystalloids.
    • Vasopressors: Norepinephrine as first-line if hypotension persists after fluids.
Anaphylactic Shock
    • Etiology: Severe allergic reaction to an antigen (e.g., food, medications, insect stings).
    • Pathophysiology: IgE-mediated release of histamine and other mediators causes massive vasodilation, increased capillary permeability, and airway obstruction.
    • Clinical Presentation:
    • Symptoms: Angioedema, urticaria, wheezing, stridor, and abdominal cramps.
    • Physical Exam: Hypotension, tachycardia, respiratory distress, and stridor.
    • Management:
    • Epinephrine: Intramuscular injection is first-line treatment.
    • Adjuncts: IV fluids, antihistamines, and corticosteroids to control symptoms and prevent recurrence.
Neurogenic Shock
    • Etiology: Often occurs after spinal cord injury, leading to loss of sympathetic tone.
    • Pathophysiology: Loss of vascular tone below the level of injury leads to unopposed vagal tone, resulting in hypotension and bradycardia.
    • Clinical Presentation: Warm, dry skin with hypotension and bradycardia.
    • Management:
    • IV Fluids: To restore intravascular volume.
    • Vasopressors: Norepinephrine for persistent hypotension.
    • Atropine: For bradycardia, if significant.
Cardiogenic Shock
  • Etiology: Failure of the heart to pump effectively, most commonly due to acute myocardial infarction (MI). Other causes include severe heart failure, valvular disease, and arrhythmias.
  • Pathophysiology: Reduced cardiac output leads to systemic hypoperfusion despite normal or high filling pressures.
  • Clinical Presentation:
    • Symptoms: Dyspnea, chest pain, and altered mental status.
    • Physical Exam: Hypotension, cool, clammy skin, elevated jugular venous pressure (JVP), and pulmonary crackles.
  • Diagnosis:
    • Labs: Elevated cardiac biomarkers (e.g., troponin) suggest MI; BNP or NT-proBNP may be elevated in heart failure.
    • Hemodynamic Monitoring: High PCWP and low cardiac output.
    • Echocardiogram: Useful for assessing left ventricular function and identifying structural causes.
  • Management:
    • Inotropes: Dobutamine or milrinone to improve contractility.
    • Vasopressors: Norepinephrine for blood pressure support.
    • Revascularization: Percutaneous coronary intervention (PCI) or thrombolysis for MI.
Obstructive Shock
  • Etiology: Mechanical obstruction to blood flow; common causes include pulmonary embolism (PE), tension pneumothorax, and cardiac tamponade.
  • Pathophysiology: Obstruction limits blood flow to or from the heart, reducing cardiac output and tissue perfusion.
  • Clinical Presentation:
    • PE: Sudden dyspnea, pleuritic chest pain, and signs of right heart strain.
    • Tension Pneumothorax: Unilateral chest pain, tracheal deviation, absent breath sounds on the affected side.
    • Cardiac Tamponade: Beck’s triad (hypotension, distended neck veins, muffled heart sounds).
  • Diagnosis:
    • PE: D-dimer, CT pulmonary angiography.
    • Tension Pneumothorax: Clinical diagnosis, confirmed by imaging if stable.
    • Cardiac Tamponade: Echocardiogram showing pericardial effusion and diastolic collapse of the right ventricle.
  • Management:
    • PE: Anticoagulation and, in massive cases, thrombolysis.
    • Tension Pneumothorax: Immediate needle decompression followed by chest tube insertion.
    • Cardiac Tamponade: Urgent pericardiocentesis.
Hemodynamic Monitoring
  • Central Venous Pressure (CVP): Reflects right atrial pressure and preload; low in hypovolemic shock, high in cardiogenic and obstructive shock.
  • Pulmonary Capillary Wedge Pressure (PCWP): Estimates left atrial pressure; low in hypovolemic shock, high in cardiogenic shock.
  • Systemic Vascular Resistance (SVR): High in hypovolemic and cardiogenic shock, low in distributive shock.
  • Cardiac Output (CO): Decreased in all forms of shock except early septic shock (hyperdynamic phase).
Management Principles
1. Identify the Underlying Cause: Perform rapid assessment to determine the type of shock. 2. Fluid Resuscitation: First-line treatment for hypovolemic and distributive shock; use cautiously in cardiogenic and obstructive shock. 3. Vasopressors and Inotropes: Essential for cardiogenic and septic shock if hypotension persists after fluid resuscitation. 4. Oxygenation and Ventilation: Supplemental oxygen for all patients; consider mechanical ventilation if respiratory failure is present. 5. Monitor Hemodynamics: Use parameters like CVP, PCWP, SVR, and CO to guide therapy and assess response.
Key Points
  • Types of Shock:
    • Hypovolemic Shock: Due to volume loss; managed with fluid resuscitation and blood products if necessary.
    • Distributive Shock: Includes septic, anaphylactic, and neurogenic shock, characterized by vasodilation. Septic shock is managed with fluids, antibiotics, and vasopressors.
    • Cardiogenic Shock: Due to heart pump failure, often from MI. Managed with inotropes, vasopressors, and revascularization.
    • Obstructive Shock: Caused by mechanical obstruction (e.g., PE, tension pneumothorax, cardiac tamponade); managed by addressing the obstruction.
  • Hemodynamic Monitoring:
    • CVP: Low in hypovolemic shock, elevated in cardiogenic and obstructive shock.
    • SVR: Low in distributive shock, elevated in hypovolemic and cardiogenic shock.
  • Management Principles:
    • Fluid Resuscitation: Mainstay in hypovolemic and distributive shock.
    • Vasopressors: Norepinephrine is first-line for septic and neurogenic shock.
    • Treat the Cause: Rapidly identify and address the underlying cause to improve outcomes.

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