Shock is a state of life threatening, generalised,acute circulatory failure associated with inadequate oxygen utilisation by the tissues of the body. (ESICM task force definition)
The result is that the circulation is unable to deliver adequate oxygen to the tissues of the body and cellular dysfunction starts to occur.
Understanding shock is made easier if we know the normal physiology. The key components of normal physiology relate to the cardiovascular system. The key parts to remember are:
Cardiac output = stroke volume x heart rate
Stroke volume is determined by:
Blood pressure is proportional to cardiac output and systemic vascular resistance
Given that there are several aspects of the physiology which can be disrupted, there are several different pathophysiological processes that generate shock. These can perhaps be best highlighted through the different classification of shock.
Shock can be classified into 4 groups:
These 4 classes can be seen to relate to the physiology of the CVS, and therefore to the pathophysiology of shock.
Hypovolaemic Here there is inadequate circulating volume. This means that there is inadequate venous return to the right side of the heart, impairing preload and stroke volume, and subsequently reducing cardiac output. Possible causes include:
Capillary leakage e.g. sepsis, burns
Cardiogenic Here the problem lies with the pump of the cardiovascular system i.e. the heart. Within our physiology we can see that this can arise from a few main areas:
An abnormal heart rate e.g. bradycardia, arrhythmia, may impair cardiac output. Similarly, an impairment of myocardial contractility will limit the ability of the heart to generate an effective stroke volume, resulting is similar problems. Abnormalities of the valves or other structures of the heart may similarly impair its ability to generate a stroke volume (or at least one going in the right direction). Possible causes include:
Arrhythmias e.g. VT
Ventricular septal defect
Obstructive Here there is a mechanical obstruction to the generation of an effective stroke volume by the heart. Causes may include:
Cardiac tamponade/constrictive pericarditis
Acute pulmonary hypertension
Distributive Here there is loss of the SVR that is required to generate a driving blood pressure to perfuse the different tissues. Cause may include:
Loss of sympathetic tone
CNS depression e.g. general anaesthesia, overdose
As can be readily appreciated, there is the potential for significant crossover between classes of shock for the same pathology, with sepsis being a good example. The classification of shock in this way can help the investigative process and also guide management, as the class of shock will often indicate a aspect of pathophysiology that is amenable to treatment e.g. volume replacement in hypovolaemia.
This can be very varied depending on the cause of the shock. The underlying pathology may be quite overt in the presentation or not e.g. chest pain with MI, pneumonia with sepsis.
Making a diagnosis of shock requires combining clinical features with investigations. The ESICM recommends looking at 3 clinical windows to provide insight into the perfusion aspect of shock:
Peripheral changes will often occur in shock, representing poor peripheral perfusion. Skin may be cold, pale, mottled or clammy.
The kidneys are very sensitive to perfusion and so may provide another window. Shock will often manifest as oliguria (defined as urine output <0.5ml/kg/hr).
Similarly, the brain can be very sensitive to alterations in perfusion. Effects may include confusion, drowsiness or obtundation.
Observations Heart rate - will be raised in most types as part of compensatory reflexes. BP - often low but not a requirement.
This may be to help better identify a diagnosis or assess severity.
Almost by definition, shock will result in elevated lactate levels due to the physiological response to tissue hypoperfusion/hypoxia. This is not the only cause of elevated lactate. There is some associated between the magnitude of lactate elevation and its trend, although this varies with pathology. Lactate as a measurement is looked at in more detail elsewhere.
Signs of ischaemia
Pulmonary vascular changes
Pericardial effusion/features of tamponade
This will be dependent on the underlying cause. In general there will be some common themes.
Replace volume as appropriate e.g. fluid, blood
Stop further losses e.g. haemostasis
Treat rhythm abnormalities
Optimise myocardial function e.g. PCI in acute MI
Cardiac support e.g. aortic balloon pump, GTN
Relieve obstruction e.g. thrombolysis, pericardiocentesis
Ensures adequately ‘filled’
Specific treatments e.g. adrenaline for anaphylaxis