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Shock

 

Definition of shock

  • Circulatory shock: an abnormality of the circulatory system that results in reduced organ perfusion and tissue oxygenation
  • Emotional shock: an acute stress reaction arising in response to a traumatic event, often erroneously used interchangeably with the term ‘shock’ in popular culture; this will not be discussed further

 

Causes of shock

  • Reduced cardiac output (CO):
    • Hypovolaemic shock
      • Haemorrhage
        • External, including gastrointestinal
        • Internal (Chest; abdomen; pelvis; retroperitoneum; long bones)
      • Vomiting
      • Diarrhoea
      • Diuresis
      • Burns
    • Cardiogenic shock
      • Myocardial infarction
      • Myocardial contusion
      • Myocarditis
      • Cardiac arrhythmia
      • Negatively inotropic drug overdose (e.g. beta blockers or calcium channel blockers)
    • Obstructive shock
      • Tension pneumothorax
      • Massive PE
      • Cardiac tamponade
  • Reduced systemic vascular resistance (SVR):
    • Septic shock
    • Anaphylactic shock
    • Neurogenic shock

 

Pathophysiology of shock

  • Blood pressure (BP) is related to cardiac output (CO) and systemic vascular resistance (SVR) by the following equation:
    • BP = CO x SVR
  • CO is the volume of blood pumped by the heart per minute and is in turn related to heart rate (HR) and stroke volume (SV) as follows:
    • CO = HR x SV
  • SV is the volume of blood pumped by the heart per contraction and is determined by
    • Preload
    • Myocardial contractility
    • Afterload
  • Preload is the ventricular wall tension at the end of diastole and reflects the degree of myocardial muscle fibre stretch; it is determined by volume status, venous capacitance and the difference between mean venous pressure and right atrial pressure
  • Preload is related to SV by the Frank-Starling mechanism; increased fibre length initially leads to an increased SV but above a certain point, the fibres become overstretched and further filling results in a decreased SV, as is the case in cardiac failure
  • Myocardial contractility is the intrinsic ability of the heart to work independently of preload and afterload; positive inotropes increase the contractility, shifting the Frank-Starling curve upwards
  • Afterload is the ventricular wall tension at the end of systole and is the resistance to anterograde blood flow
  • Regardless of the cause of shock, inadequate organ perfusion and tissue oxygenation results in cells switching from aerobic to anaerobic metabolism
  • This generates a lactic acidosis that disrupts the cellular environment and causes myocardial depression

 

 

History in a shocked patient

  • Assessment of severity
    • Dyspnoea
    • Confusion
    • Light-headedness
    • Drowsiness
    • Oliguria/anuria
  • Symptoms of the cause

 

Examination of the shocked patient

  • Airway
    • May be compromised by reduced conscious level
  • Breathing
    • Hypoxia secondary to:
      • Cause
      • Airway compromise
      • Apparent hypoxia due to ineffective pulse oximetry from peripheral shutdown
    • Tachypnoea
    • Kussmaul’s breathing: hyperventilation to compensate for metabolic acidosis manifesting as ‘air hunger’
  • Circulation
    • Cold, pale peripheries
    • Prolonged capillary refill times (CRT >2 s)
    • Tachycardia
    • Hypotension
    • Oliguria
    • Anuria
  • Disability
    • Confusion
    • Drowsiness
    • Unconsciousness
  • Signs of the cause

 

Classification of haemorrhagic shock

  • Type I
    • Volume of blood loss (ml): <750
    • Percentage blood loss (%): <15
    • Heart rate (beats/min): <100
    • Blood pressure: normal
    • Pulse pressure: normal/increased
    • Respiratory rate (breaths/min): 14-20
    • Urine output (ml/hour): >30
    • Mental state: slightly anxious
  • Type II
    • Volume of blood loss (ml): 750-1500
    • Percentage blood loss (%): 15-30
    • Heart rate (beats/min): 100-120
    • Blood pressure: normal
    • Pulse pressure: decreased
    • Respiratory rate (breaths/min): 20-30
    • Urine output (ml/hour): 20-30
    • Mental state: mildly anxious
  • Type III
    • Volume of blood loss (ml): 1500-2000
    • Percentage blood loss (%): 30-40
    • Heart rate (beats/min): 120-140
    • Blood pressure: decreased
    • Pulse pressure: decreased
    • Respiratory rate (breaths/min): 30-40
    • Urine output (ml/hour): 5-15
    • Mental state: anxious, confused
  • Type IV
    • Volume of blood loss (ml): >2000
    • Percentage blood loss (%): >40
    • Heart rate (beats/min): >140
    • Blood pressure: decreased
    • Pulse pressure: decreased
    • Respiratory rate (breaths/min): >35
    • Urine output (ml/hour): negligible
    • Mental state: confused, lethargic

 

Investigation of shock

  • Bloods including blood gas to check pH and lactate
  • Electrocardiogram (ECG)
  • Chest radiograph (CXR)
  • Echocardiography
  • In trauma
    • Pelvic XR
    • CT chest/abdo/pelvis as indicated
    • FAST

 

Initial management of shock

  • Assess the patient from an ABCDE perspective
  • Maintain a patent airway
    • Use manoeuvres, adjuncts, supraglottic or definitive airways as indicated and suction any sputum or secretions
  • Deliver high flow oxygen 15L/min via reservoir mask to keep sats over 94%
  • Attach monitoring
    • Pulse oximetry and non-invasive blood pressure
    • Three-lead cardiac monitoring
  • Request 12 lead ECG and portable CXR
  • Obtain large-bore intravenous (IV) access and take bloods including blood gas to check pH and lactate
  • Fluid resuscitation IV
  • Urethral catheterisation and fluid balance monitoring aiming for a urine output >0.5 ml/kg/hour
  • If BP fails to respond consider referral to HDU/ICU for
    • Central line insertion with central venous pressure (CVP) and central venous oxygen saturation (ScvO2) monitoring
    • Arterial line insertion and invasive arterial BP monitoring
    • Vasopressor and/or inotrope infusion

 

Further management of shock

  • Identify and treat the cause
    • Haemorrhagic shock
      • Identify the source(s) of bleeding and achieve haemorrhage control e.g. direct compression, pelvic binder, splinting of long bone fractures, surgical ligation of bleeding vessels
      • Restoration of adequate circulating volume
        • Cross-match blood and activate the major haemorrhage protocol
        • Transfuse O negative blood initially, followed by type-specific and fully cross-matched blood as soon as it is available; aim for permissive hypotension
      • Correct coagulopathy by transfusion of platelets, fresh frozen plasma and cryoprecipitate as appropriate
      • RBC: FFP ratio should be between 1:1 and 1:2, the optimum ratio is uncertain. The key is to give FFP early with RBC. Cryo if fibrinogen<1.5.
    • Antibiotics and source control for septic shock
    • Adrenaline 0.5 mg intramuscular (IM) for anaphylactic shock
    • Needle thoracocentesis and intercostal chest drain insertion for tension pneumothorax
    • Pericardiocentesis and thoracotomy for cardiac tamponade
    • Thrombolysis for massive PE
    • Synchronised direct current (DC) cardioversion for unstable tachyarrhythmias
    • Pacing for unstable bradyarrhythmias

 

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