Shock

A syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement

Aetiology

• Hypovolaemic: caused by loss of plasma or blood volume
• Examples: acute haemorrhage, fluid deplete states (severe dehydration, burns)
• Volume depletion leads to reduced SVR
• Reduced volume returning to the heart → reduced pre-load and hence reduced CO

• Cardiogenic: ‘pump failure’ causes reduced CO
• Reduced contractility - ‘stroke volume’
• Reduced heart rate
• Primarily caused by ischaemia induced myocardial dysfunction
• Other causes include cardiomyopathies, valvular problems, dysrhythmias
• If due to MI suggests that >40% of LV is involved
• Unless correctable pathology (e.g. valvular), mortality >75%

• Distributive: caused by disruption of normal vascular autoregulation, and profound vasodilation, resulting in poor perfusion (despite increased CO)
• Regional perfusion differences
• Alteration of oxygen extraction
• Can be seen in sepsis, anaphylaxis, acute livery failure, spinal cord injuries

• Obstructive: mechanical obstruction to normal cardiac output in an otherwise normal heart
• Direct obstruction to cardiac output - PE, air/fat/amniotic fluid embolism
• Restriction of cardiac filling - tamponade, tension pneumothorax

• Endocrine: severe uncorrected hypothyroidism, Addisonian crisis - both cause reduced CO and vasodilation
• Paradoxically can also be caused by thyrotoxicosis

Pathophysiology

• Pathophysiology is more complex than simply poor perfusion

• Multiple aetiologies, same end pathway
• Cascade of inflammatory mediators as a consequence of cellular ischaemia cause a vicious cycle of vasoconstriction and oedema (worsening cellular ischaemia) as well as direct cytotoxic damage

The inflammatory response

• Can be part of the pathological process (sepsis), or a consequence of (persisting hypoperfusion) and often both

• A protective reflex - of benefit when targeted appropriately, but when disseminated causes widespread harm

• Often followed by secondary immune suppression, leading predisposition to secondary infection

• Activation of complement cascade - attraction and activation of leucocytes

• Cytokine release - interleukins, TNF-alpha

• Platelet activating factor - increased vascular permeability, platelet aggregation

• Lysosomal enzymes - myocardial depression, coronary vasoconstriction

• Adhesion molecules - damage to vessel walls, further leucocyte attraction

• Endothelium derived mediators - nitric oxide

• Imbalance between antioxidents and oxidents

Sympatho-adrenal response to shock

• Pathways to preserve normal cardiac output, and hence BP

Neuroendocrine response to shock

• Release of pituitary hormones - adrenocorticotrophic hormone, ADH, endogenous opiods

• Release of cortisol - fluid retention, antagonises insulin

• Release of glucagon

• Suggestion that some shock states (sepsis) blunts the response to ACTH

Haemodynamic changes

• Vascular abnormalities - vasodilation, or constriction

• Maldistribution of blood flow

• Microcirculatory abnormalities - AV shunting, ‘stop-flow’ or ‘no-flow’ capillary beds, failure of capillary recruitment, increased capillary permeability

• Inappropriate activation of coagulation system

• DIC

Loss of vascular reactivity

• The failure of smooth muscle constriction, primarily due to nitric oxide
• NO is important in regulation of blood flow, coagulation, neural activity and immune function
• Produced in minute concentrations in endothelial and other cells by cNOS
• Inflammation pathways induce its inducible isoform iNOS in vessel smooth walls, leading to 1000 fold increase in NO production

Myocardial dysfunction

• Reversible biventricular systolic diastolic dysfunction caused by:
• Circulating cytokines with direct myocardial effect
• Beta receptor downregulation
• Decreased cardiomyofilament calcium sensitivity
• NOT due to reduced coronary blood flow - usually preserved

Clinical presentation

• Common clinical feature: hypotension

Cardiogenic

• Signs of myocardial failure

Obstructive

• Raised JVP

• Pulsus paradoxus

• Signs of cause

Distributive

• Septic: pyrexia, vasodilation, rapid capillary refill

• Anaphalaxis: profound vasodilation, erythema, bronchospasm, oedema

Hypovolaemia

• Pale, cold skin, prolonged capillary refill

Investigations

• Surrogate markers used to measure normal perfusion:
• Blood pressure
• Consciousness (brain perfusion)
• Urine output (renal perfusion)
• Lactate (general tissue perfusion)

• Pulse contour analysis used to measure cardiac output

Management

Fluids

• Rapid fluid replacement (over minutes)

• Balance between rapid volume replacement and risk of fluid overload
• Shocked patients are more susceptible to pulmonary oedema due to microvascular dysfunction

• Use fluid challenge - rapid administration of a fluid with an assessment of response
• Rapid enough to get a response, but not so fast as to provoke a stress response, typically 300-500ml over 10-20 mins

Pharmacological

• Used in severe cases - when fluids don’t work, or stop working, can be used as a bridge to adequate filling

• Adrenaline - alpha/beta adrenergic agonist, at low dose primarily beta (heart rate, contractility, vasodilation)

• Noradrenaline - predominantly alpha agonist

• Others:
• Vasopressin - ADH
• Dopamine - natural predursor to the above, complex dose-dependent effects
• Dobutamine/dopexamine - analogues of domapine

Mechanical support options

• When drugs fail

• In cardiogenic shock: balloon pumps, L-VADs, R-VADs, VA-ECHMO (severe cases)

Hypovolaemic

• Assessment of bleeding - estimation of volume loss and speed of ongoing loss

• Establish source - may require imaging if stable

• Temporisation - direct pressure, tourniquets

• Damage limitation resuscitation - until definitive control

• Damage limitation surgery

De-escalation/’de-resucitation’

• Importance of removing extra fluid from a patient once their shock has resolved

• Various means - spontaneous, diuretic, dialysis