Physiological Changes in Pregnancy

Part of the physiological adaptation to pregnancy includes an increase of about 40% in the circulating blood volume. This accommodates the increased utero-placental circulation and also prepares the woman, to some extent, to withstand haemorrhage at delivery. This is necessary because the ‘normal’ blood loss at vaginal delivery and caesarean section is about 500 ml and 1000 ml respectively, and such loss is accommodated well by the normal pregnant woman. However, obstetric haemorrhage is often rapid and may be poorly tolerated by the woman who is anaemic, dehydrated after prolonged labour, or with the reduced blood volume and contracted intravascular space associated with pre-eclampsia/eclampsia.

An additional important consideration is the size of the woman and therefore her circulating blood volume. In the non-pregnant woman the formula to calculate blood volume is about 70 ml/kg or her weight in kilograms divided by 14. Thus, the circulating blood volume of a 50 kg woman and an 80 kg woman would be about 3500 ml and 5600 ml, respectively. In pregnancy, with the 40% increase in blood volume, the formula is approximately 100 ml/kg; so in the same 50 kg and 80 kg weight categories the blood volume would be 5000 ml and 8000 ml respectively – a difference of 3 L. The woman of small stature who is anaemic may withstand poorly even a blood loss of 1000–1500 ml, which the larger, non-anaemic woman would tolerate with relative impunity.

Pathophysiological Response to Haemorrhage

Severe haemorrhage associated with hypotension causes an increased release of catecholamines and stimulation of the baroreceptors leading to increased sympathetic tone, with the following results:

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  Increased cardiac output due to an increase in the rate and force of myocardial contraction.

  
  
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  Maintenance of blood flow to the critical organs (heart and brain) by selective peripheral arteriolar constriction reducing blood flow to all the other organs.

  
  
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  Venous constriction causing, in effect, an autotransfusion from these capacitance vessels.

  
  
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  As a result of the peripheral vasoconstriction the reduced hydrostatic pressure in the capillaries causes them to imbibe extracellular fluid in an attempt to augment the intravascular volume. Increased levels of aldosterone and antidiuretic hormone cause sodium and water retention by the kidneys.

These mechanisms are aimed at improving cardiac output, sustaining the blood pressure, restoring the intravascular volume and maintaining tissue perfusion. At this stage, provided the haemorrhage is arrested and the circulation restored, the shock is completely reversible without sequelae. However, if the blood loss continues, the above mechanisms fail to sustain adequate circulation, leading to reduced tissue perfusion, tissue hypoxia, metabolic acidosis, cell damage and ultimately cell death. The hypoxic metabolites damage the capillary cells leading to more loss of intravascular volume as fluid leaks through the damaged capillary walls. Persistent hypoperfusion of peripheral organs may cause damage to the lung (‘shock lung’, adult respiratory distress syndrome), the kidney (acute tubular and cortical necrosis), the liver and to the pituitary (Sheehan’s syndrome).

As the diastolic blood pressure falls, coronary artery perfusion is compromised, leading to myocardial hypoxia and failure. Such extensive hypoxic tissue damage and release of metabolites may initiate disseminated intravascular coagulation (see Chapter 25 ).

Clinical Features

In the early phase of blood loss, peripheral arteriolar constriction will sustain normal maternal blood pressure but may lead to a reduction in utero-placental perfusion. Thus, abnormalities of the fetal heart rate may serve as an early warning sign of maternal vascular decompensation.

The classic early signs of haemorrhagic shock are changes in the vital signs with tachycardia, hypotension, tachypnoea and air hunger. In addition to these vital signs one can monitor the skin, brain and kidney for clinical manifestations of hypovolaemia as these are end-organs sensitive to reduced perfusion and hypoxia. The clinical manifestations of hypoperfusion and hypoxia in these end-organs are as follows:

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  Skin: sweating, cold, pallor, cyanosis. A clinically useful sign of skin perfusion is the capillary refill time. This is easily assessed by compressing a finger nail for 5 seconds; if normal, the colour in the nail bed returns within 2 seconds.

  
  
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  Brain: alteration in mental state including restlessness, anxiety, aggression, confusion and coma.

  
  
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  Kidney: oliguria and anuria.

Hypovolaemic shock can be classified into three categories:

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  Mild : 10–25% loss of blood volume. In cases of mild hypovolaemic shock there is tachycardia and possibly mild hypotension along with decreased perfusion of non-vital organs and tissue such as skin, fat and skeletal muscle. Provided bleeding stops at this stage the circulation is well compensated, will respond to intravenous crystalloid alone and does not require blood replacement.

  
  
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  Moderate : 25–40% loss of blood volume. With moderate shock there is decreased perfusion to the vital organs due to peripheral vasoconstriction and this is usually manifest by tachycardia, hypotension, tachypnoea, cool skin and oliguria. This requires intravenous crystalloid and blood replacement.

  
  
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  Severe : > 40% loss of blood volume. This is life threatening, with all of the clinical manifestations of shock present in their most extreme form. A working guide to the presence of severe haemorrhagic shock is when the radial pulse is impalpable, which means the systolic blood pressure is less than 70 mmHg – at which level perfusion to the vital organs (heart, brain and kidney) is critically reduced. Loss of more than 50% of blood volume results in loss of consciousness. These patients require immediate blood replacement and urgent measures to stop the bleeding.