Shock
Last updated 30th January 2019 - Tom Heaton
This is a key topic for critical care.
This is a nice introductory podcast on the topic from the guys at the resus room: https://theresusroom.co.uk/shock/
This is a nice introductory podcast on the topic from the guys at the resus room: https://theresusroom.co.uk/shock/
Definition
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.
The result is that the circulation is unable to deliver adequate oxygen to the tissues of the body and cellular dysfunction starts to occur.
Pathophysiology
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:
These can perhaps be best highlighted through the different classification of shock.
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:
- Preload
- Contractility
- Afterload
- Preload
- Blood pressure is proportional to cardiac output and systemic vascular resistance
These can perhaps be best highlighted through the different classification of shock.
Classification
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:
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:
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:
Obstructive
Here there is a mechanical obstruction to the generation of an effective stroke volume by the heart.
Causes may include:
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:
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.
- Hypovolaemic
- Cardiogenic
- Obstructive
- Distributive
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:
- Bleeding
- Dehydration
- Diarrhoea/vomiting
- Burns
- 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:
- Heart rate
- Contractility
- Structural
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:
- Heart rate
- Bradycardias
- Arrhythmias e.g. VT
- Contractility
- Cardiomyopathy
- MI
- Structural
- Valvular abnormality
- Ventricular septal defect
Obstructive
Here there is a mechanical obstruction to the generation of an effective stroke volume by the heart.
Causes may include:
- Pulmonary embolism
- Cardiac tamponade/constrictive pericarditis
- Tension pneumothorax
- Valvular stenosis
- 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
- Spinal anaesthesia
- Spinal trauma
- CNS depression e.g. general anaesthesia, overdose
- Anaphylaxis
- Sepsis
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.
Presentation
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.
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
- Renal
- Neurological
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.
Investigation
This may be to help better identify a diagnosis or assess severity.
Bloods:
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.
ECG:
CXR
Echo
Bloods:
- FBC
- U&E
- LFTs
- Lactate
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.
ECG:
- Any arrhythmia
- Signs of ischaemia
CXR
- Pneumothorax
- Pulmonary vascular changes
Echo
- Pericardial effusion/features of tamponade
- Myocardial contractility
- Volume status
Management
This will be dependent on the underlying cause.
In general there will be some common themes.
Hypovolaemic
Cardiogenic
Obstructive
Distributive
In general there will be some common themes.
Hypovolaemic
- Replace volume as appropriate e.g. fluid, blood
- Stop further losses e.g. haemostasis
Cardiogenic
- Treat rhythm abnormalities
- Optimise myocardial function e.g. PCI in acute MI
- Inotropes
- Cardiac support e.g. aortic balloon pump, GTN
Obstructive
- Relieve obstruction e.g. thrombolysis, pericardiocentesis
Distributive
- Ensures adequately ‘filled’
- Vasopressors
- Specific treatments e.g. adrenaline for anaphylaxis
Links & References
- The Resus Room. Shock; Roadside to Resus. 2019. https://theresusroom.co.uk/shock/
- Bewley, J. Classification of shock. e-LFH. 2016.
- Nickson, C. Shock. LITFL. 2017. https://lifeinthefastlane.com/ccc/shock-ddx/
- Cecconi, M. et al. Consensus on circulatory shock and haemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014. 40(12):1795-1815. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778/
