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By Dr. Thomas Burnell and Dr. Bethany Turner
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Contents
Abstract
- Haemodynamic shock is inadequate blood flow throughout the body.
- There are two main causes of this: reduced cardiac output (how much blood the heart pumps each minute) and/or reduced total peripheral resistance (how much the blood vessels resist blood flow).
- The four types of shock are cardiogenic, obstructive (also called mechanical), hypovolaemic and distributive.
- In hypovolaemic shock, decompensation (the point where the body's compensating responses fail) is when peripheral vasoconstriction impairs tissue perfusion (blood supply), causing hypoxia (too little oxygen in the tissues). Hypoxic tissues release vasodilators (chemicals that widen blood vessels), causing vasodilation, which causes a further rapid decrease in BP and organ hypoperfusion (too little blood reaching the organs). This results in multi-system failure.
Core
Useful equations to remember for this article:
MaBP = CO x TPR
CO = SV x HR
MaBP is mean arterial blood pressure (the average pressure in the arteries during one heartbeat). CO is cardiac output (the volume of blood the heart pumps each minute), TPR is total peripheral resistance (how much the blood vessels resist blood flow), SV is stroke volume (the volume pumped with each beat) and HR is heart rate. In shock, blood pressure falls because the heart pumps less or the blood vessels widen.
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
- Obstructive shock (also called mechanical shock)
- Hypovolaemic shock
Shock due to a fall in TPR (profound vasodilation) is called distributive shock. The blood volume is initially unchanged, but the vasodilation (widening) of the peripheral blood vessels reduces TPR massively. Fluid can then leak out of the capillaries into the surrounding tissues, which reduces the circulating volume further. There are two main types of distributive shock:
- Septic shock (shock caused by infection)
- 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 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 (the blood pressure in the large veins near the heart).
Some causes of cardiogenic shock include:
- A myocardial infarction (heart attack), which destroys heart muscle so that less is left to pump.
- Serious arrhythmia (an abnormal heart rhythm) - the CO becomes very low. The ventricles either pump too slowly to maintain a good level of CO, or they pump so fast that little blood can enter them, so little can be ejected.
- Acute worsening of heart failure.
- Severe dilatation of the left ventricle - also known as severe dilated cardiomyopathy (a disease of the heart muscle in which the chamber is stretched and the muscle is weak).
Symptoms of cardiogenic shock include: tachypnoea (rapid breathing), tachycardia (a fast heart rate), 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 abnormal breathing and a lack of pulse. The heart rhythms seen in cardiac arrest are:
- 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) - in VF the electrical activity is disorganised, so the ventricles contract in an uncoordinated way instead of pumping. In pulseless VT the ventricles beat extremely fast but ineffectively. In both, little or no blood is ejected. These rhythms can occur following a myocardial infarction, an electrolyte imbalance (abnormal levels of salts in the blood) or after some arrhythmias.
Of the above rhythms, only VF and pulseless VT are shockable. This means a defibrillator can be used in an attempt to return the heart to sinus rhythm (the heart's normal rhythm). The defibrillator sends an electric shock through the myocardium and depolarises all the cells. This places the cells into the refractory period (a short phase in which they cannot be triggered again). 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.
Obstructive (Mechanical) Shock
Obstructive shock (also called mechanical shock) is where a problem outside the heart muscle stops the ventricles from filling or emptying properly. Blood then builds 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 (how much the ventricles are stretched as they fill with blood) on the heart, as it is not filling effectively.
Three common causes of obstructive (mechanical) shock are:
- Cardiac Tamponade - this is a build-up of fluid in the pericardial space (the gap between the heart and the pericardium, its outer sac). 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 be pumped out of the right ventricle.
- 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.
- Tension pneumothorax - air becomes trapped in the pleural space (the gap between the lung and the chest wall) and the pressure builds up.
- The raised pressure compresses the blood vessels that bring blood to the heart, so the heart cannot fill and cardiac output falls.
- It is a reversible cause of cardiac arrest, so it must be identified and treated immediately.
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 (pressure sensors in the walls of large arteries). The baroreceptors then 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.
The compensation is helped by a degree of ‘internal transfusion’. This happens because the capillary hydrostatic pressure (the pressure pushing fluid out of the capillary) falls with blood loss, while the oncotic pressure (the pull of plasma proteins that draws fluid into the capillary) stays constant. 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 (the point at which the body's compensating responses fail). This is because peripheral vasoconstriction can impair tissue perfusion causing hypoxia (too little oxygen in the tissues). The hypoxic tissue releases chemical mediators which cause vasodilation of the blood vessels in an attempt to maintain perfusion to organs. This widespread vasodilation 'undoes' 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.
Caused by reduced total peripheral resistance causing reduced BP. There are two main subdivisions of distributive shock:
- Persisting hypotension needing a vasopressor (a drug that tightens blood vessels) to keep the mean arterial pressure at 65 mmHg or more, with a serum lactate (a blood marker of poorly perfused tissue) above 2 mmol/L, despite adequate fluid resuscitation.
- In septic shock, infection triggers a massive inflammatory response mediated by microbial products and host cytokines (chemical signals released by the body's own immune cells). 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 blood vessels in the skin tighten and the hands and feet are cold and pale, whereas in septic shock the blood vessels are widened throughout the body). Not every patient looks flushed: mottled (patchy, blotchy) or ashen (grey) skin, a non-blanching rash (one that does not fade when pressed) and blue skin, lips or tongue (cyanosis) are warning signs of severe illness.
- Anaphylactic shock is a severe allergic reaction which results in a large amount of histamine (a chemical messenger that widens blood vessels) released from mast cells (immune cells found in the tissues).
- Histamine has a powerful vasodilatory effect which will decrease TPR which then decreases arterial pressure.
- The mediators released in anaphylaxis also cause bronchoconstriction (narrowing of the airways in the lungs) and laryngeal oedema (swelling of the larynx), which cause breathing difficulties.
- First line treatment of anaphylaxis is intramuscular adrenaline, commonly given using an auto-injector such as an EpiPen, alongside calling 999 for urgent emergency help. The high level of adrenaline administered causes vasoconstriction by its action on α1-receptors (receptors on blood vessel muscle that make it contract), which helps to restore TPR towards normal.
- Symptoms of anaphylactic shock usually start within minutes of contact with the trigger. They include: difficulty breathing (with wheeze, or swelling of the throat and tongue), tachycardia, feeling faint or dizzy, and a swollen, raised or itchy rash. The skin may be red and warm, but it can also be cold, pale, grey or blue.
Edited by: Dr. Ben Appleby
Reviewed by: Dr. Marcus Judge
Quiz
- 14160
