Types of Shock

Definition and Classification

Definition

Shock is a life-threatening condition of organ dysfunction resulting from tissue hypoxia due to decreased oxygen delivery, increased oxygen consumption, and/or defective oxygen utilization.

Classification

• Distributive: characterized by a reduction in systemic vascular resistance (SVR) and a compensatory increase in cardiac output (CO)
  • Septic shock
  • Pancreatitis
  • Severe burns
  • Anaphylactic shock
  • Neurogenic shock
  • Endocrine shock
  • Adrenal crisis
  • Drug- and toxin-induced shock 
• Cardiogenic: characterized by reduced CO due to a primary cardiac problem
  • Myocardial infarction
  • Myocarditis
  • Arrhythmic
  • Valvular
    • Severe aortic valve insufficiency
    • Severe mitral valve insufficiency
• Hypovolemic: characterized by reduced CO due to reduced preload
  • Hemorrhagic
  • Gastrointestinal (GI) losses
  • Burns
  • Polyuria
    • Diabetic ketoacidosis
    • Diabetes insipidus
• Obstructive: characterized by reduced CO due to an extracardiac obstruction
  • Tension pneumothorax
  • Pulmonary embolism
  • Cardiac tamponade
  • Aortic dissection
  • Restrictive pericarditis
• Mixed/multifactorial: Often, 1 class does not exist in isolation.

Pathophysiology and Stages

Pathophysiology

• Initial insult (most commonly resulting in circulatory failure) → impaired oxygen delivery (most common mechanism of tissue hypoxia) → tissue hypoxia → anaerobic metabolism (pyruvate to lactate conversion and reduced adenosine triphosphate (ATP) production) → failure of cells to maintain osmotic, ionic, and pH homeostasis → cellular swelling and death → activation of inflammatory cascades and microvascular alterations → organ dysfunction/shock  
• Determinants of oxygen delivery (DO₂) include CO and arterial oxygen content (CaO₂):
  DO₂ = CO × CaO₂
  • CO = heart rate (HR) × stroke volume (SV)
    • SV = (preload × contractility) / systemic vascular resistance (SVR)
  • CaO₂ ≈ hemoglobin (Hb) × 1.39 × arterial oxygen saturation (SaO₂); therefore, variables that affect DO₂ include CO (HR and SV (preload, contractility, and SVR)) and CaO₂ (Hb and SaO₂)
• Other mechanisms of tissue hypoxia (less common than impaired oxygen delivery): 
  • Increased oxygen consumption 
  • Impaired oxygen utilization (e.g., cyanide poisoning)

Stages of shock

1. Preshock or compensated shock
   • Reversible with interventions
   • Perfusion and oxygen delivery are relatively normal despite the insult.
   • No overt signs of organ dysfunction ± mild laboratory signs of organ dysfunction (e.g., mildly elevated creatinine, troponin, or lactate)
2. Shock or decompensated shock
   • Reversible with interventions
   • Perfusion and oxygen delivery are abnormal.
   • Overt signs of organ dysfunction are present.
3. Irreversible shock
   • Permanent organ dysfunction
   • Progression to multisystem organ failure

Diagnosis

Always maintain a high clinical suspicion for shock. Suggestive features include tachycardia, hypotension, altered mentation, oliguria, weak peripheral pulses, and cool and clammy skin.

History

• Fever and productive cough: distributive shock due to pneumosepsis
• Hives, dyspnea, and facial edema: distributive shock due to anaphylaxis
• Exertional chest pain and dyspnea: cardiogenic shock due to myocardial infarction
• Presyncope or syncope: cardiogenic shock due to arrhythmias
• Acute-onset dyspnea or chest pain and a history of malignancy, inactivity, or leg swelling: obstructive shock due to pulmonary embolism
• Severe diarrhea: hypovolemic shock due to gastrointestinal loss

Physical examination

• Compensated shock:
  • Tachycardia: to compensate for CO
  • Tachypnea: to compensate for metabolic acidosis
  • Hypotension: systolic blood pressure (SBP) < 90 mm Hg, mean arterial pressure (MAP) < 65 mm Hg in normotensive individuals or higher in patients with uncontrolled hypertension
  • Decreased capillary refill 
  • Cold and clammy skin
•  Decompensated shock: signs of organ failure
  • Confusion/altered mental status: central nervous system (CNS) hypoperfusion
  • Oliguria (< 0.5 mL/kg/hr) in a patient without a history of renal disease: renal hypoperfusion
• Specific findings:
  • Bilateral rales: pulmonary edema due to left heart failure or acute respiratory distress syndrome 
  • Warm distal extremities, capillary refill in < 2 seconds, and bounding pulses: high CO such as in distributive shock
  • Cool extremities, delayed capillary refill, weak pulses, and a narrow pulse pressure suggest low CO:
    • Elevated jugular venous pressure (JVP) and peripheral edema: cardiogenic shock with right heart failure
    • Elevated JVP and pulsus paradoxus (i.e., > 10 mm Hg drop in systolic blood pressure during inspiration): obstructive shock due to cardiac tamponade 
    • Reduced JVP (< 8 cm): hypovolemic shock
  • Infected skin/mucosal lesions: septic shock
  • Large ecchymosis suggests major internal bleeds: hypovolemic shock
  • Blood on digital rectal examination: hypovolemic shock due to GI bleeding
  • Unilateral absence of breath sounds with tympanic percussion, subcutaneous emphysema, and lateral deviation of trachea: obstructive shock due to tension pneumothorax

Laboratory studies

• Lactate: 
  • Serial measurements are recommended to evaluate response to therapy. 
  • Elevations correlate with worse outcomes. 
• Renal function tests: blood urea nitrogen (BUN) and creatinine
• Liver function tests: Elevation of alkaline phosphatase (ALP) to more than 3 times normal may suggest biliary obstruction as the cause of sepsis and distributive shock. 
• Cardiac enzymes: Elevations may indicate myocardial infarction, myocarditis, or pulmonary embolism.
• Complete blood count (with differential): Elevation of leukocytes with a left shift (immature granulocyte count > 3% by automated analyzer or manual band count > 10%), although not diagnostic, may indicate infection.
• Prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR): Elevations may indicate a coagulopathy related to septic shock.
• Cultures including blood, urine, and sputum
• Urinalysis: Pyuria indicates infection.
• Arterial blood gas: shows degree and type of acid-base disorder and hypoxemia
• Electrocardiogram (ECG) may suggest etiology of shock:
  • ST-segment elevation: myocardial infarction
  • Tachyarrhythmias or bradyarrhythmias
  • S1Q3T3 pattern: pulmonary embolism
  • Reduced QRS voltage + electrical alternans: pericardial tamponade

Imaging

• Radiographic evaluation including chest X-ray and thoracoabdominal computed tomography (CT) scan
• Point-of-care ultrasound: 
  • Heart: left ventricle (LV) and right ventricle (RV) function, valvular function, pericardium, inferior vena cava (IVC) diameter and collapsibility
  • Chest: pneumothorax, hemothorax, empyema, thoracic aortic aneurysm
  • Abdomen: peritoneal cavity for fluid accumulation and bleeding, abdominal aortic aneurysm
  • Proximal lower extremities: deep venous thrombosis

Scores and indices

• Shock index (SI): heart rate (HR; beats/min) / SBP (mm Hg)
  • SI of 0.5–0.7: Normal
  • SI > 0.9: indicates critical bleeding and transfusion requirement
• qSOFA (quick Sequential (sepsis-related) Organ Failure Assessments) score: Presence of 2 of the following 3 criteria indicates a worse outcome in a patient suspected of having sepsis and triggers an immediate diagnostic workup and treatment as appropriate.
  • SBP < 100 mm Hg 
  • Respiratory rate > 22/min
  • Altered mental status

Management

Shock is a medical emergency!
Initiate simultaneous treatment and evaluation for etiology, utilizing findings from history, physical examination, hemodynamic monitoring, and laboratory studies. This is best accomplished within a multidisciplinary team in a resource-equipped setting such as the intensive care unit (ICU).

Respiratory support

• Indications for endotracheal intubation and mechanical ventilatory support: 
  • Significant hypoxemia (PaO₂ < 60 mm Hg or oxygen saturation < 90%)
  • Hypoventilation (rising partial pressure of carbon dioxide (pCO₂)) 
  • Significantly altered level of consciousness 
  • Inability to protect airways with risk of aspiration 
  • Persistent metabolic acidosis with pH < 7.20
• Goal: arterial oxygen saturation of 92%–95%

Monitoring

• Peripheral venous access: for possible fluid and antibiotic therapy
• Central venous catheter placement: 
  • Consider if resuscitation is inadequate through peripheral access.
  • Applications: aggressive fluid administration, vasopressor therapy, hemodynamic monitoring, means to measure central venous oxygenation and pulmonary capillary wedge pressure through a Swan-Ganz catheter, if indicated 
• Intraosseous device: for rapid central venous access in critically ill patients
• Arterial line: 
  • For continuous monitoring of arterial pressure 
  • For continuous monitoring of oxygen tension as peripheral oximetry may be unreliable during hypoperfusion
  • For repeated measurements of acid-base status and lactate
•  Urinary catheter placement: for hemodynamic monitoring through hourly urinary output

Volume resuscitation

• Close monitoring of volume status with frequent adjustment of therapy as necessary
• Intravenous fluids (mainly crystalloids): most patients with undifferentiated shock 
  • All patients with hypovolemic and distributive shock (e.g., 30 mL/kg in septic shock)
  • Some patients with cardiogenic shock (e.g., acute right ventricular infarction)
• Blood products:
  • Packed RBCs: hypovolemic shock and ongoing hemorrhage 
  • Fresh frozen plasma (FFP) and platelets:
    • Massive transfusions
    • Coagulopathy
• Non-invasive monitoring methods indicating a volume-responsive state:
  • Passive leg raise: significant change in pulse pressure or CO (not blood pressure!) after administering a fluid bolus and repositioning the patient from a recumbent position with a 45-degree head elevation to Trendelenburg with a 45-degree leg elevation 
  • Significant variation of pulse pressure or SV during the respiratory cycle in an intubated patient
  • Echocardiography: reduced IVC diameter and IVC collapse, serial LV function assessment
• Invasive methods such as Swan-Ganz catheter for PCWP: no longer recommended for routine monitoring of volume status in shock because hemodynamic assessment can generally be made non-invasively

Pharmacologic treatment

• Vasopressor and inotropic therapy:
  • If hypotension remains despite restoration of intravascular volume with fluids
  • Distributive shock (most commonly septic): norepinephrine (1st line), vasopressin (2nd line)
  • Cardiogenic shock: dobutamine 
  • Mixed distributive and cardiogenic shock: norepinephrine + dobutamine
• Antibiotics:
  • Obtain blood cultures.
  • Administer antibiotics within the 1st hour after diagnosis of shock. 
  • Discontinue antibiotics if sepsis is excluded.
• Specific therapies:
  • Distributive shock due to anaphylaxis: 
    • Removal of allergen
    • Epinephrine
    • IV fluids and vasopressors
  • Distributive shock due to adrenal insufficiency: high-dose steroids
  • Cardiogenic shock due to myocardial infarction: revascularization
  • Cardiogenic shock due to arrhythmias: advanced cardiac life support including cardioversion and placement of temporary pacemakers
  • Hypovolemic shock due to GI bleeding: endoscopic and/or surgical intervention  
  • Obstructive shock due to tension pneumothorax: immediate decompression with placement of a chest tube
  • Obstructive shock due to massive pulmonary embolism: thrombolytic therapy or surgical removal of clot
  • Obstructive shock due to pericardial tamponade: pericardial window