Shock is a life-threatening condition associated with impaired circulation that results in tissue hypoxia. Different types of shock have been defined based on the underlying cause: distributive (↑cardiac output [CO], ↓systemic vascular resistance [SVR]), cardiogenic (↓CO, ↑SVR), hypovolemic (↓CO, ↑SVR), obstructive (↓CO), and mixed. The most common symptoms include tachycardia, tachypnea, hypotension, altered mentation, and oliguria. Measures vary depending on the suspected cause of shock and may include mechanical ventilation, IV crystalloids, vasopressors, and blood transfusion.
Table of Contents
Definition and Classification
A life-threatening condition of organ dysfunction resulting from tissue hypoxia which is due to decreased oxygen delivery, increased oxygen consumption and/or defective oxygen utilization.
- Distributive: characterized by a reduction in systemic vascular resistance (SVR) and a compensatory increase in cardiac output (CO). (Table 1)
- Septic shock
- Severe burns
- Anaphylactic shock
- Neurogenic shock
- Endocrine shock
- Adrenal crisis
- Drug- and toxin-induced shock
- Cardiogenic: characterized by a reduced CO due to a primary cardiac problem
- Myocardial infarction
- Severe aortic valve insufficiency
- Severe mitral valve insufficiency
- Hypovolemic: characterized by a reduced CO due to reduced preload
- GI losses
- Diabetic ketoacidosis
- Diabetes insipidus
- Obstructive: characterized by a reduced CO due to an extracardiac obstruction
- Tension pneumothorax
- Pulmonary embolism
- Cardiac tamponade
- Aortic dissection
- Restrictive pericarditis
- Mixed/Multifactorial: often, one class does not exist in isolation.
- Undifferentiated: often, the etiology of shock is unknown when it is initially diagnosed.
|Type of Shock||CVP||PCWP||Cardiac Output||Systemic Vascular Resistance|
Table 1: Major types of shock based on hemodynamic characteristics. CVP, central venous pressure; PCWP, pulmonary capillary wedge pressure. Source: Harrison’s 2018
Pathophysiology and Stages of Shock
Pathophysiology of shock
- 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 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 cardiac output (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)
- CO = heart rate (HR) × stroke volume (SV)
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
- Preshock or compensated shock (also referred to as nonpregressive shock)
- Reversible with interventions
- Perfusion and oxygen delivery is 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 is abnormal
- Overt signs of organ dysfunction
- Irreversible shock
- Permanent organ dysfunction
- Progression to multisystem organ failure
History and Physical Examination
Always maintain a high suspicion for shock.! Suggestive features include tachycardia, hypotension, altered mentation, oliguria, weak peripheral pulses, and cool and clammy skin.
History is suggestive:
- 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 supports the presence and indicates the stage of shock.
- 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: CNS hypoperfusion
- Oliguria (< 0.5 mL/kg/hour) in a patient without a history of renal disease: renal hypoperfusion
Physical examination suggests the etiology of shock.
- 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
Physical examination indicates severity of specific types of shock.
- Shock index (SI): heart rate (HR; beats per minute)/systolic blood pressure (SBP; mm Hg)
- SI of 0.5-0.7: Normal
- SI > 0.9: indicates critical bleeding and transfusion requirement
- qSOFA-score: presence of 2 of the following 3 criteria indicates a worse outcome in a patient suspected of having sepsis and triggers immediate diagnostic workup and treatment as appropriate. (See Sepsis and Septic Shock)
- SBP < 100 mm Hg
- Respiratory rate > 22/minute
- Altered mental status
Laboratory Studies and Imaging
Laboratory studies further help with determining the stage and etiology of shock. The following laboratory studies are recommended in undifferentiated shock:
- Serial measurements are recommended to evaluate response to therapy.
- Elevations correlate with worse outcomes.
- Renal function tests: blood urea nitrogen and creatinine
- Liver functions tests: elevation of alkaline phosphatase (ALP) to more than 3 times may suggest biliary obstruction as the cause of sepsis and distributive shock.
- Cardiac enzymes: elevation may indicate infarction, myocarditis, or pulmonary embolism.
- Complete blood count (with differential): elevation of leukocytes with a left shift, although not diagnostic, may indicate infection.
- Prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR)
- 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
Additional laboratory and imaging workup that are often indicated:
- Cultures including blood, urine, and sputum
- Radiographic evaluation including chest X-ray and thoracoabdominal CT scan
- Point-of-care ultrasound:
- Heart: LV and RV function, valvular function, pericardium, 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
Approach and Management
Shock is a medical emergency! Initiate simultaneous treatment and evaluation for etiology, utilizing findings from history, physical examination, hemodynamic monitoring, and laboratory studies. (Image 1) This is best accomplished within a multidisciplinary team in a resourceful setting such as the ICU.
Endotracheal intubation and mechanical ventilatory support:
- May be indicated any time during the evaluation and management of a patient with shock.
- Common indications include: significant hypoxemia (PaO2 < 60 mm Hg or oxygen saturation < 90%), hypoventilation (rising PCO2), increased work of breathing, significant 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%
Obtaining appropriate monitoring and therapeutic access:
- Peripheral venous access: obtain large bore (16G or 18G) intravenous 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
Close monitoring of volume status with frequent adjustment of therapy is 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 red blood cells:
- Hypovolemic shock and ongoing hemorrhage
- Shock and Hb < 7 mg/dL
- Fresh frozen plasma (FFP) and platelets:
- Massive transfusions
- Packed red blood cells:
- Invasive methods such as Swan Ganz catheter for PCWP: no longer recommended for routine monitoring of volume status in shock
- 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 (Image 2)
- 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
Vasopressor and inotropic therapy:
The following drugs are indicated if hypotension remains despite restoration of intravascular volume with fluids:
- Distributive shock (most commonly septic shock): norepinephrine (1st line), vasopressin (2nd line)
- Cardiogenic shock: dobutamine (1st line)
- Mixed distributive and cardiogenic shock: norepinephrine + dobutamine
The most common cause of undifferentiated shock is sepsis:
- If etiology of shock is unknown:
- Obtain blood cultures
- Administer antibiotics within the 1st hour after diagnosis of shock (See Sepsis and Septic Shock)
- Discontinue antibiotics if sepsis is excluded.
- Distributive shock due to anaphylaxis:
- Removal of allergen
- 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 gastrointestinal 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