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.
| Type of shock | Central venous pressure (CVP) | Pulmonary capillary wedge pressure (PCWP) | Cardiac output | Systemic vascular resistance |
|---|---|---|---|---|
| Distributive | ↓ | ↓ | ↑ | ↓ |
| Cardiogenic | ↑ | ↑ | ↓ | ↑ |
| Obstructive | ↑ | ↓↑ | ↓ | ↑ |
| Hypovolemic | ↓ | ↓ | ↓ | ↑ |
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)
- CO = heart rate (HR) × stroke volume (SV)
- Other mechanisms of tissue hypoxia (less common than impaired oxygen delivery):
- Increased oxygen consumption
- Impaired oxygen utilization (e.g., cyanide poisoning)
Stages of shock
- 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)
- Shock or decompensated shock
- Reversible with interventions
- Perfusion and oxygen delivery are abnormal.
- Overt signs of organ dysfunction are present.
- 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).
Approach to shock
Image by Lecturio.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
Passive leg raise. CO, cardiac output; SV, stroke volume.
Image by Lecturio.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
- Distributive shock due to anaphylaxis:
References
- Kasper DL, Fausi AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison’s Principles of Internal Medicine. New York, NY: McGraw-Hill Education; 2018.
- Gaieski DF, Mikkelsen ME. Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2020.
