Haemodynamic Shock

Core

Useful equations to remember for this article:

MaBP = CO x TPR
CO = SV x HR

Haemodynamic shock is an acute condition of inadequate blood flow throughout the body which may lead to organ failure due to poor perfusion.

Shock can be due to a fall in cardiac output (CO) or a fall in total peripheral resistance (TPR).

Shock due to a fall in CO can be put into three categories:

• Cardiogenic shock
• Mechanical shock
• Hypovolaemic shock

Shock due to a fall in TPR (profound vasodilation) is called distributive shock. The blood volume is constant, but the vasodilation of the peripheral vasculature reduces TPR massively. There are two types of distributive shock:

• Toxic/Septic shock
• Anaphylactic shock

The decreased CO or the decreased TPR causes a characteristic low blood pressure. The low blood pressure results in decreased tissue perfusion and this causes multi-organ failure as the organs are not supplied with enough oxygen.

Cardiogenic Shock

Cardiogenic shock is when there is pump failure, i.e. the heart fails as a pump and the ventricles do not empty properly.

As the heart can fill but has impaired contraction, blood is not ejected from the full heart. This results in a build-up of blood in the venous circulation, causing a raised central venous pressure.

Some causes of cardiogenic shock include:

• Following a myocardial infarction leading to a reduction in functioning tissue.
• Serious arrhythmia - the CO becomes very low as the ventricles either pump too slowly to maintain a good level of CO, or they pump too fast meaning little blood can enter the ventricles so little can be ejected.
• Acute worsening of heart failure.
• Severe dilatation of the left ventricle - also known as severe dilated cardiomyopathy.

Symptoms of cardiogenic shock include: tachypnoea (rapid breathing), tachycardia, shortness of breath, pale and clammy/sweaty skin. 

Cardiogenic shock can lead to cardiac arrest. In cardiac arrest, the heart has either stopped or has ceased to pump effectively. Cardiac arrest is characterised by unresponsiveness with a lack of pulse. Some causes of cardiac arrest:

• Asystole - loss of electrical and mechanical activity. There is no contraction and there is no activity whatsoever on an ECG.
• Pulseless Electrical Activity (PEA) - loss of mechanical activity but there is still some electrical activity that is detected on an ECG.
• Ventricular Fibrillation (VF)/ pulseless ventricular tachycardia (VT) - uncoordinated activity of the heart with minimal ejection. This can occur following a myocardial infarction, an electrolyte imbalance or after some arrhythmias.

Of the above causes of cardiogenic shock, only VF and pulseless VT are shockable rhythms. This means a defibrillator can be used in attempt to return the heart to sinus rhythm. The defibrillator sends an electric shock through the myocardium and depolarises all the cells. This places the cells into the refractory period. This effective reset of the heart is intended to terminate the arrhythmia and allow organised electrical activity to resume. 

Asystole and PEA are non-shockable rhythms and therefore should not be shocked as it will have no therapeutic benefit.

Mechanical Shock

Mechanical shock is where the ventricles cannot fill properly. As blood is not entering the heart effectively it will build up in the venous circulation causing a raised central venous pressure and jugular venous pressure (JVP). Mean arterial blood pressure falls as cardiac output is reduced due to the lack of preload on the heart as it is not effectively filling.

Two causes of mechanical shock are:

• Cardiac Tamponade - this is a build-up of fluid in the pericardial space. This restricts the heart from filling properly as pressure is being put on it from the outside.
  
  • Cardiac tamponade affects both the left and right side of the heart.
  • As blood cannot enter the right atrium, there is a build-up of blood within the venous circulation which is indicated by distended neck veins - raised JVP.
• Pulmonary Embolism - if an embolus blocks a large pulmonary artery, blood cannot move past the obstruction. This obstruction causes a raised pressure in the pulmonary circulation which the right ventricle cannot overcome. This means blood cannot exit the heart.
  
  • This causes blood to back up in the systemic venous circulation.
  • A pulmonary embolus will only cause this if it is big enough to occlude large pulmonary arteries.

Hypovolaemic Shock

Hypovolaemic shock is caused by reduced blood volume. This reduction in circulating volume means organs are less well perfused.

Hypovolaemic shock has several causes, including:

• Severe burns - the body’s response to injury is acute inflammation, and part of this response is to make the capillaries leakier. However, as the skin is burnt off, the fluid leaking out is not contained and is lost from the body.
• Extremely severe diarrhoea or vomiting.
• Loss of sodium - water follows sodium so if there is reduced sodium there is less water and hence a reduced blood volume.
• Haemorrhage with 30-40% blood loss.

The body can compensate for hypovolaemia to a certain extent. Pressure in the circulation falls due to the fluid loss, which is detected by baroreceptors. These increase sympathetic stimulation causing tachycardia, increased force of contraction of the heart, and vasoconstriction. This is an attempt to try and increase BP back to normal, and therefore the BP may be stable for a short period. 

This will be helped by a degree of ‘internal transfusion’. This is caused by a decreased capillary hydrostatic pressure due to blood loss, but a constant oncotic pressure between the capillary and tissue fluid. This leads to a net movement of fluid into the capillary from the tissue fluid causing a small increase in circulating volume helping to slightly recover blood pressure.

However if this continues for too long without restoring fluids, there is a risk of decompensation. This is because peripheral vasoconstriction can impair tissue perfusion causing hypoxia. The hypoxic tissue releases chemical mediators which cause vasodilation of the blood vessels in an attempt to maintain perfusion to organs. This widespread vasodilation 'undos' the actions of the sympathetic nervous system and decreases the BP massively. This means vital organs cannot be perfused and this causes multi-system failure.

Symptoms of hypovolaemic shock include: tachycardia, weak pulse, pale skin, cold and clammy extremities.

Distributive shock

Caused by reduced total peripheral resistance causing reduced BP. There are two main subdivisions of distributive shock:

Septic Shock

• Persisting hypotension requiring treatment to maintain BP despite fluid resuscitation.
• In septic shock, infection triggers a massive inflammatory response mediated by microbial products and host cytokines. This response causes profound vasodilation leading to a decrease in TPR and decreased arterial pressure.
• The capillaries also become leaky due to the inflammatory response so fluid will move out of the capillaries, reducing circulating volume and worsening the shock.
• Decreased arterial pressure impairs organ perfusion.
• Symptoms of septic shock include: tachycardia, red and warm extremities (this is in contrast to hypovolaemic shock where the patient will be peripherally shut down, however in septic shock they are systemically vasodilated).

Anaphylactic Shock

• Anaphylactic shock is a severe allergic reaction which results in a large amount of histamine released from mast cells.
• Histamine has a powerful vasodilatory effect which will decrease TPR which then decreases arterial pressure.
• The mediators released in anaphylaxis also cause bronchoconstriction and laryngeal oedema causes breathing difficulties.
• First line treatment of anaphylaxis is intramuscular adrenaline, commonly delivered using an EpiPen, alongside urgent emergency management. The high level of adrenaline administered causes vasoconstriction by its action on α1-receptors thus restoring normal TPR.
• Symptoms of anaphylactic shock include: difficulty breathing, tachycardia, red and warm extremities. 

Edited by: Dr. Ben Appleby

Reviewed by: Dr. Marcus Judge

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