Types of Shock
Hypovolaemic shock (figure 4)
Inadequate circulation volume. The most common causes of this type of shock being any cause of fluid loss; haemorrhage, salt and water loss, sepsis, burns, etc.
A poor venous return to the heart will decrease the stroke volume and cardiac output (see Starling curve on previous page). The patient will attempt to compensate by tachycardia and increased systemic vascular resistance (SVR). They become cold peripherally (shut down).
Figure 4. Pathophysiological changes in hypovolaemic shock.
Cardiogenic shock (figure 5)
Pump failure. The patient will have a poor cardiac output and will therefore attempt to maintain a blood pressure by increasing SVR. Blood pressure can be low, normal or high, but organ perfusion is compromised, peripheries are cold and the patient is prone to pulmonary oedema.
Early echocardiography is important to assess contractility, valve function and exclude significant pericardial effusion.
Figure 5. Pathophysiological changes in cardiogenic shock.
Distributive shock (figure 6)
Peripheral vasodilatation and subsequent maldistribution of blood flow. This leads to a relative hypovolaemia. (There is more space in which to put the same volume of fluid). Common examples of this type being septic, anaphylactic and neurogenic shock.
Septic shock is the commonest of these you will see in the ICU and frequently includes vasodilatation, high cardiac output, and loss of intravascular volume due to ‘leaky capillaries’. The patient may start with a low cardiac output due to the leaky capillaries with loss of fluid and because the vasodilated arterial tree requires a larger blood volume to fill it (relative hypovolaemia).
With appropriate fluid volume replacement the heart will pump against lower resistance and therefore there will often be an increase in cardiac output in order to compensate for the reduction in SVR. The patient may remain hypotensive but will have warm peripheries and a bounding pulse. The bounding pulse is a reflection of the wide pulse pressure which is due to a low diastolic pressure. However it is possible, due to toxins and acidosis, for sepsis to have a negative inotropic affect on the heart as well as causing vasodilatation and the patient can therefore have a low cardiac output and a low SVR.
Neurogenic shock occurs when there is damage to the spinal cord and a subsequent loss of the sympathetic tone. Features of this shock are hypotension, bradycardia, warm peripheries, venous pooling and sometimes priapism. Seek senior help if this type of shock is suspected. Please note that bradycardia is an important feature of this shock; if hypotension and tachycardia are present, e.g. in an RTA victim, look for other causes of shock like external or internal haemorrhage.
Figure 6. Pathophysiological changes in distributive shock.
Obstructive shock (figure 7)
Caused by extra-cardiac obstruction to blood flow. For example, in pulmonary embolism, aortic stenosis, pericardial effusion and tension pneumothorax.
As a result of the low cardiac output the patient will be tachycardic and have an increase in SVR to compensate. The patient becomes cold and shut down. They may demonstrate raised JVP and venous congestion of the face and body due to the obstruction.
Figure 7. Pathophysiological changes in obstructive shock.