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strength) and the afterload (vascular resistance – the resistance against which the myocardium has to pump). Shock may result if any of the these components are compromised.

      During normal homeostasis, organ perfusion is regulated by local metabolic and microcirculatory factors within a set range of arterial pressures. This is called autoregulation. Beyond this range, blood flow to the organ is primarily determined by the pressure differential between the arterial and venous systems.

      The blood supply to vital organs is maintained at lower blood pressures than that to non‐vital organs. In shocked states, blood is preferentially supplied to the brain and the heart at the expense of perfusion elsewhere. Unfortunately for the fetus, the uterus does not count as one of the woman’s vital organs, hence placental blood supply is not maintained in the presence of a life‐threatening challenge to the mother. The resulting fetal compromise is an early and important indicator of maternal shock.

      In the pregnant woman in a supine position, the uterus compresses the vena cava, reducing venous return to the heart from 20 weeks’ gestation. Vena caval obstruction and aortic compression can reduce cardiac output by up to 30%. The woman may experience symptoms such as nausea, vomiting or lightheadedness. This is known as supine hypotension syndrome. The reduction in venous return impacts on placental blood flow, which lacks autoregulation.

Photos depict (a) Manual uterine displacement in the pregnant woman. (b) Fifteen degrees of left lateral tilt.

      Source: (a) Courtesy of Trauma Victoria – Obstetric Trauma guideline. http://trauma.reach.vic.gov.au/

      To prompt manual uterine displacement (MUD) early in the process of resuscitation, remember:

       ‘Hello. How are you Ms MUD?’

      Shock can be classified into four types:

       Hypovolaemic shock

       Cardiogenic shock

       Distributive shock

       Obstructive shock

      In order to differentiate between these types of shock, clues can be gained from the history, examination, selected additional tests and the response to treatment.

      Hypovolaemic shock: insufficient preload

        Absolute loss of fluid: e.g. haemorrhage

        Relative loss of fluid: vasodilatation, e.g. spinal/epidural anaesthesia

       Absolute hypovolaemia – blood loss, fluid loss

      Important implications of pregnancy physiology in haemorrhage

      During pregnancy there is an increase in circulating blood volume of approximately 40% due to increases in both plasma and red cell volume. In a 70 kg woman, blood volume in pregnancy increases from 70 to 100 ml/kg (from 4900 to 7000 ml). This circulating volume enables the pregnant woman to lose 1200–1500 ml of blood before demonstrating any signs of hypovolaemia (35% of her circulating blood volume). This enhanced ability to compensate for blood loss increases our risk of underestimating the severity of blood loss, occasionally even until the point of maternal collapse.

       Relative hypovolaemia – vasodilatation due to regional blockade

      Intrathecal and to a lesser extent epidural local anaesthetics block the sympathetic nervous system, resulting in vasodilatation and hypotension. Usually there is a compensatory tachycardia associated with a fall in diastolic pressure. Subsequently, systolic blood pressure falls earlier than would occur during actual blood loss.

      This sympathetic blockade exacerbates other simultaneous causes of hypotension such as haemorrhage and results in earlier decompensation.

      A ‘high’ spinal will also affect the sympathetic nerves controlling the heart rate, causing a bradycardia and profound hypotension.

      Cardiogenic shock – reduced cardiac contractility

      Causes of cardiogenic shock include:

       Ischaemic heart disease

       Cardiomyopathy

       Arrhythmias

      The distinguishing features of cardiogenic shock include orthopnoea and signs of pulmonary congestion, such as a raised jugular venous pressure, reduced oxygen saturation and basal pulmonary crackles. Symptoms and signs such as shortness of breath, chest pain, syncope, sweating, cool peripheries and tachycardia occur but are not specific to cardiogenic shock.

      Distributive shock – abnormal vascular resistance and fluid distribution

      The following pathologies can result in distributive shock:

       Sepsis

       Anaphylaxis

       Burns

       Sepsis

      In this form of shock (see Chapter 7), the patient will have signs and symptoms of systemic inflammation as well as those of the disease causing the sepsis. The pathological process is profound vasodilatation and hence these patients may have warm peripheries, particularly early in the process, despite being in shock. There is a compensatory tachycardia and increase in cardiac output to maintain perfusion pressure.

      Varying degrees of organ dysfunction are seen, depending on the duration and degree of sepsis. In advanced stages of shock, the septic patient will become vasoconstricted, with cold extremities.

       Anaphylaxis

      Anaphylaxis is a severe, life‐threatening, generalised, systemic hypersensitivity

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