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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.
6.2 Aortocaval compression and supine hypotension syndrome
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.
To prevent the effects of aortocaval compression, the pregnant woman should lie in the lateral position. Although a 15° tilt to the left (Figure 6.1b) is advocated there is evidence that the effects of compression still occur. Manual displacement of the uterus off the inferior vena cava up and to the left, relieves compression more effectively (Figure 6.1a). It is important to remember to relieve aortocaval compression in the initial management of the shocked woman to not exacerbate hypotension from other causes.
Figure 6.1 (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?’
6.3 Types of shock
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
This form of shock is due to a drop in the effective circulating volume resulting in a decrease in venous return. This causes a drop in stroke volume. There is usually a compensatory increase in heart rate to preserve cardiac output and also a compensatory increase in vascular resistance. This vasoconstriction, mediated by endogenous catecholamine release, increases the diastolic pressure without having the same effect on the systolic pressure thus there is a narrowed pulse pressure. Compensatory fluid shifts occur from the extravascular space into the vascular compartment, resulting in intracellular dehydration and a sensation of thirst.
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