Shock

Shock is acute circulatory failure, with inadequate tissue perfusion causing cellular hypoxia

• Can't be defined using systemic parameters, as it is possible to have inadequate perfusion with normal blood pressure

Aetiology

Hypovolaemia

• • Haemorrhage
  • Fluid loss
  • Dehydration

Cardiogenic

• • MI
  • Heart failure
  • Arrhythmia

Obstructive

• • PE
  • Cardiac tamponade
  • Pneumothorax

Distributive

• • Sepsis
  • Neurogenic
  • Anaphylaxis
  • Adrenal insufficiency

Pathophysiology

Haemorrhagic/hypovolaemic

• • Tachycardia and increase in cardiac contractility - attempt to preserve cardiac output (usually first signs)
  • Endogenous catecholamines increase PVR, which increases DBP and reduces pulse pressure, but does not increase tissue perfusion
  • Vasoconstriction of cutaneous, muscular and visceral circulation - preserve flow to kidneys, heart and brain - increases PVR
  • Contraction of volume of blood in venous system
  • Shift to anaerobic metabolism - lactic acid forms, and metabolic acidosis - which can progress to end-organ damage/MODS
  • Stress hormone activation
  • Systemic inflammatory response from wounds, treatment, stress hormones

Cardiogenic

• • Primary cardiac disorder characterised by low cardiac output resulting in end-organ hypoperfusion and tissue hypoxia
  • Myocardial ischaemia results in depressed myocardial contractility, reducing cardiac output and blood pressure
  • Compensatory action of the SNS leads to peripheral vasoconstriction, preserving coronary perfusion at the cost of increased afterload
  • Tachycardia increases myocardial oxygen demand

Obstructive

• • Tamponade
    • Rapid accumulation of pericardial fluid results in compression to cardiac chambers and subsequent diastolic failure (reduced preload)
    • Cardiac output reduces
    • Compensatory tachycardia to attempt to overcome the reduced output
  • Tension pneumothorax
    • Increased intra-thoracic pressure compresses the mediastinal structures and prevents filling of SVC and IVC, leading to reduced preload
    • There is also increased pulmonary vascular resistance
    • Cardiac output is compromised
  • PE
    • Increased pulmonary vascular resistance due to a combination of mechanical obstruction and hypoxic vasoconstriction
    • Increased right ventricular afterload compromises right-sided output, and prevents downstream left ventricular filling, which results in reduced overall cardiac output

Distributive

• • Sepsis/anaphylaxis
    • Inflammatory cytokines induce systemic vasodilation and capillary leak, and sometimes a direct cardiomyopathy
    • See separate topic 'Sepsis/SIRS'
  • Neurogenic
    • Loss of sympathetic outflow beneath the level of injury means reduced catecholamine delivery and subsequent vasodilation
    • Similar condition can be seen with epidurals
    • Differentiate from spinal shock - a neurological phenomenon where there is immediate temporary loss of power, reflexes and sensation below the level of the injury
  • Adrenal insufficiency
    • Decreased alpha-1 receptor expression on arterioles secondary to cortisol deficiency, resulting in vasodilation
    • Seen with sudden withdrawal of chronic steroids
  • Common pathway
    • Reduced venous return and reduced cardiac output
    • Reduced perfusion to vital organs

Clinical features of subtypes of shock, in addition to generic features of hypo-perfusion

• Cardiogenic
  • Similar to hypovolaemic shock
  • Elevated CVP or JVP and pulmonary oedema, but low arterial pressure
• Obstructive
  • Tachycardia
  • Elevated JVP
• Septic
  • Warm peripheries early
  • Lower SVR meaning lower diastolic pressure
  • Tachycardia
  • Confusion
• Hypovolaemic
  • Tachycardia
  • Cool peripheries
  • Decreased pulse pressure

Clinical features of decreased tissue perfusion

• Cool peripheries
• Poor filling of peripheral veins
• Increased RR
• Increased core-peripheral temperature gradient
• Prolonged CRT
• Poor signal on pulse oximeter
• Poor urine output (<0.5mL/kg/hr)
• Anxiety/restlessness
• Decreased consciousness level
• Metabolic acidosis or raised serum lactate

Treatment

• Diagnose and treat the underlying cause
• For hypovolaemic/vasodilatory shock:
  • 10mL/kg crystalloid if normotensive
  • 20mL/kg crystalloid if hypotensive
  • Oxygen in high flow via non-rebreather bag
• Venous access
• IDC
• ECG monitoring
• Pulse oximetry monitoring
• CVC
• Assess response after 30 minutes, and change plan if the patient is not improving