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
