1 PHYSIOLOGICAL CHANGES IN PREGNANCY
Chapter contents Blood and circulatory changes |
The following alterations occur in order to meet the increasing metabolic demands of the fetus and prepare the mother for delivery.
Coagulation
During pregnancy - there is increased activation of the coagulation system affecting the normal balance of intravascular coagulation and fibrinolysis. Platelet activity and consumption are increased but there is also a compensatory rise in production. The concentration of most coagulation factors including fibrinogen VII,VIII, IX, X and XII are significantly increased. By contrast factor XIII (fibrin stabilising factor) decreases. Increased levels of antithrombin III, an increase in fibrin degradation products and increased plasminogen concentrations reflect enhanced fibrinolysis. These changes are not detected in a routine coagulation screen which is usually reported as 'normal'
At delivery - placental separation prompts a further shift to increased coagulation but a fall in fibrinolysis. The risk of postpartum haemorrhage is reduced but this change is also linked to an increased risk of postpartum thromboembolism. Uterine contraction leading to closure of open placental vessels is also essential in reducing blood loss.
Blood volume - plasma volume increases by 45% while the red cell mass increases by only 20%. This results in the physiological anaemia of pregnancy (the haemoglobin falling from 15 g/dl to 12 g/dl at 34 weeks). The blood volume returns to normal 10 - 14 days post partum (Fig 1.1).
Haemodynamic changes - progesterone induced vasodilatation causes a 20% decrease in peripheral vascular resistance by term; consequently there is a fall in systolic and diastolic blood pressures. In the last trimester changes in posture may exert significant effects on cardiac output and blood pressure. Cardiac output rises to 50% above the non pregnant level during the third trimester; heart rate and stroke volume both rise by 25%. The central venous pressure, reflecting right ventricular filling pressure, shows no change during normal pregnancy - left ventricular hypertrophy and dilatation accounting for the increased cardiac output. During labour cardiac output rises by a further 15% in the latent phase, 30% in the active phase and up to 45% in the expulsive phase.
Fig 1.1 Changes in cardiac output, plasma volume and red blood cell (RBC) volume during pregnancy and the puerperium (modified from Obstetric Analgesia and Anesthesia: 1980 Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)
After 24 weeks the gravid uterus may compress the inferior vena cava when the patient lies supine thus reducing venous return and maternal cardiac output. Two compensatory mechanisms exist:
- An increase in sympathetic tone leading to venous and arterial constriction (this includes the utero-placental circulation) and an increase in heart rate.
- A collateral circulation allows blood from the lower limbs to flow through the vertebral venous plexus and reach the right side of the heart via the azygos veins.
In 10% of mothers these mechanisms are inadequate to maintain a normal blood pressure when supine (supine hypotensive syndrome). If the blood pressure fall is severe, consciousness may be lost. Turning the patient onto her side allows the cardiac output and blood pressure to return to normal as the IVC is decompressed. Falls in maternal cardiac output and blood pressure lead to a reduced placental flow with the risk of fetal hypoxia. By contrast the thicker walled aorta is less prone to compression; however, should it occur blood flow to the kidneys, uterus, placenta and the lower limbs may decrease - inadequate placental perfusion and fetal hypoxia may also follow. During labour uterine contractions displace most of the blood from the uterus and placenta into the azygos system; important consequences of this include intermittent increases in epidural venous pressure and cardiac output.
Significance to the anaesthetist
- Anaesthesia - The induction of general anaesthesia or the institution of epidural or spinal blockade reduce sympathetic tone and may unmask aortocaval compression; as a result there is likely to be a fall in maternal cardiac output, blood pressure and placental perfusion. A left lateral tilt should be maintained by appropriately wedging the mother's pelvis.
- Labour and delivery - The mother should be prevented from lying completely supine. This is especially important during fetal blood sampling or instrumental delivery.
- Venous distension - Distension of epidural veins increases the chance of vascular damage during performance of regional blocks. It also reduces the volume of the epidural and intrathecal spaces therefore a reduced dose of local anaesthetic is required at term.
- Resuscitation - During external cardiac massage tilting the patient is essential to allow refilling of the right side of the heart. Immediate delivery also improves venous return and offers the best chance of survival for both mother and baby.
Blood loss
- During vaginal delivery this averages 300 ml, in Caesarean section 750 ml; normally this is well tolerated because of the increased blood volume
- Venous return increases immediately after delivery due to an autotransfusion secondary to uterine emptying and the removal of IVC occlusion. Normally this additional volume is accommodated by vasodilatation and an increase in cardiac output; however cardiac failure with pulmonary oedema may be precipitated in the following conditions: systemic or pulmonary hypertension, severe cardiac disease and the use of vasopressors including ergometrine.
- Regional analgesia reduces the large increase in cardiac output which occur during labour and following delivery. It may be of value in patients such as those above with a limited cardiac output
Utero-placental circulation
Fig 1.2 Diagram of the maternal blood supply to the human placenta
As pregnancy advances a fibrin matrix replaces the elastic lamina and smooth muscle of the spiral arteries ( Fig. 1.2). Consequently vascular resistance falls and placental blood flow increases. At term the uterine blood flow is around 700 ml/minute (10% of cardiac output); some 80% of this flows via the maternal spiral arteries into the intervillous space where exchange of gases and nutrients occurs between the villi containing the fetal capillaries and the maternal blood. Any reduction in uterine blood flow is therefore detrimental to the fetus.
Uterine blood flow = (uterine arterial pressure - uterine venous pressure)
uterine vascular resistance
An increase in uterine vascular resistance causes a reduction in uterine blood flow. The uterine vascular resistance and venous pressure rise with each contraction. The bigger the contraction the more profound the drop in uterine perfusion. When the intra-amniotic pressure rises above 50 - 60 mmHg intervillous perfusion ceases. Hence uterine hypertonus is clearly undesirable.
Likely causes of reduced uterine blood flow are -
- Hypotension:- aortocaval compression, blood loss, sympathetic block
- Hypertension:- essential or pregnancy-induced elevation of blood pressure
- Uterine Hypertonus:- excess oxytocin, placental abruption, high concentrations of local anaesthetic, ketamine in doses > 1.5 mg/kg, cocaine abuse
- Vasoconstriction:-sympathetic overactivity due to fear/anxiety or extreme hypoxia, sympathomimetic drugs (a1 adrenergic) with the exception of ephedrine (mainly ß1 adrenergic),
- Fall in cardiac output: - this is not necessarily accompanied by a fall in blood pressure - for example in pre-eclampsia
Anatomy - Capillary engorgement affects all the airways. In particular the false cords and arytenoids may be oedematous. There is a progesterone induced increase in ventilation with tracheal and bronchial dilatation. Although the uterus displaces the diaphragm upwards inspiration is still predominantly due to diaphragmatic contraction. There is a compensatory increase in both the anteroposterior and transverse diameters of the rib cage.
Fig 1.3 Changes in ventilatory parameters during pregnancy (modified from Obstetric Analgesia and Anesthesia: 1980 Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)
Lung volumes: A 20% reduction in functional residual capacity is present in the third trimester; this is due to a reduction in both expiratory reserve volume and residual volume. Inspiratory capacity increases and vital capacity is unchanged.
Ventilation and blood gases during pregnancy
Alveolar ventilation - increases by 70% during the second to third month of gestation. This is mainly due to an increase in tidal volume.
Oxygen consumption and carbon dioxide production - both increase progressively to reach 60% above non pregnant levels at term.
PaCO2 - falls and stabilizes at 4.1 kPa (31 mmHg) by the end of the first trimester; this is due to rising progesterone levels which reset the sensitivity of the respiratory centre to PaCO2
PaO2 - rises to 14 kPa (105 mmHg) during the third trimester in the erect position; this is due to the fall in PaCO2 plus a reduced arteriovenous oxygen difference. The PaO2 declines slightly by term - the rise in cardiac output does not keep pace with to the increased oxygen consumption and arteriovenous oxygen difference increases. In the supine position a fall in cardiac output and, in some patients, closure of dependant airways may lead to a fall in PaO2 to <13.5 kPa (100 mm Hg)
Ventilation during labour: Pain and anxiety during labour may induce significant further changes to some of the above values.
Table 1.1 Ventilatory data for pregnancy and labour.
| Pregnancy | Labour | |
| Respiratory rate /min | 15 | 22 - 70 |
| Tidal volume ml | 480 - 680 | 650 - 2000 |
| Minute ventilation l/min | 7.5 - 10.5 | 9 - 30 |
| PaCO2 kPa | 4.1 (31 mmHg) | 2 - 2.7 (15 - 20 mmHg) |
| PaO2 kPa | 14 (105 mmHg) | 13.5 -14.4 (100-108 mmHg) |
Significance to the anaesthetist
- Airway obstruction at induction of general anaesthesia leads to a more rapid fall in oxygen saturation than in the non-pregnant patient because:
- oxygen consumption is increased at term; functional residual capacity is reduced - there is a reduced oxygen reservoir in the lungs, a fall in cardiac output and sometimes closure of dependant airways.
- The reduced functional residual capacity has other important consequences:
- during preoxygenation before induction of general anaesthesia (important in delaying the onset of hypoxia) the time for denitrogenation is reduced: 2-3 minutes is required
- during anaesthesia with volatile agents the alveolar anaesthetic concentration rises relatively rapidly to approach the inspired concentration.
- Airway obstruction is more likely to occur during sedation and anaesthesia. The airway mucosa is easily traumatised and may bleed profusely. A smaller endotracheal tube may be required especially if the larynx is oedematous (pre-eclampsia)
- There may be difficulty with laryngoscopy and tracheal intubation. Failed intubation rates of 1:280 compared to 1:2200 in the non pregnant population have been reported.
Materno-fetal respiratory gas exchange
Fig 1.4 Oxygen dissociation curves for human maternal and fetal blood, indicating the physiologic range of PO2 and O2 for mother and fetus. (Modified from Towell ME: Fetal respiratory physiology in Perinatal Medicine.1976 Edited by JW Goodwin, GW Chance: Longman; Toronto, Canada.)
Although fetal partial pressure of oxygen is much lower, the saturation is relatively higher than in the adult. This is because fetal haemoglobin (75% - 80% of the haemoglobin at birth) has a greater affinity for oxygen than adult haemoglobin. The fetal oxy-haemoglobin dissociation curve is displaced to the left (see fig 1.4).
Important shifts of the dissociation curves take place in the placenta. The maternal blood gains CO2, the pH falls and the curve shifts to the right releasing additional oxygen. On the fetal side of the placenta CO2 is lost, the pH rises and the curve shifts to the left allowing additional oxygen uptake (double Bohr effect).
Other important factors in delivery of oxygen to the fetal tissues are:
- A high maternal intervillous blood flow (almost double the fetal placental flow)
- The high fetal haemoglobin (16 - 17 g/dl)
- The high fetal cardiac output
- The fetal metabolic acidosis which shifts the curve to the right and thus aids delivery of oxygen to the tissues.
- The high oxygen affinity of fetal blood could limit oxygen unloading to the tissues although this is minimised by the steepness of the curve.
Significance to the anaesthetist
- An effective epidural block in labour may largely reverse the following detrimental, metabolic and respiratory changes:
- Maternal hyperventilation causes respiratory alkalosis and hypocapnia, causing cerebral and placental vasoconstriction. The oxyhaemoglobin dissociation curve is shifted to the left. This increases the affinity of maternal haemoglobin for oxygen and reduces the amount of oxygen available for transfer to the fetus.
- During a long labour with painful contractions an opposing change may also occur: there is an increase in the metabolic rate and oxygen consumption with a tendency to lactic acidosis thus causing a right shift of the curve and reducing maternal oxygen uptake.
As pregnancy progresses the intra abdominal pressure increases and the axis of the stomach is altered. The competence of the lower oesophageal sphincter (LOS) is reduced due to the relaxant effect of progesterone on smooth muscle; most pregnant women suffer from heartburn and some 80% have gastric reflux at term. There is no evidence of delayed gastric emptying during pregnancy. By contrast prolonged labour is associated with impaired gastric emptying and increased gastric volume. The administration of opioids aggravates these changes, and also reduce the tone of the LOS. These physiological changes can be expected to return to normal within 24 - 48 hours of delivery.
The upper oesophageal sphincter (UOS) is formed mainly from the striated cricopharyngeus muscle. Its pressure varies from 40 mmHg when awake to 8 mmHg during deep sleep. Regurgitation will occur when this pressure falls below that of the oesophageal contents. The UOS may retain sufficient tone to prevent regurgitation of oesophageal contents during general anaesthesia with volatile agents in the absence of neuromuscular blockade: however this cannot be relied upon.
Significance to the anaesthetist
- Pulmonary aspiration of gastric acid with a pH of less than 2.5 and a volume of between 25 - 50 ml may lead to the development of a severe aspiration pneumonitis (Mendelson's Syndrome).
- Obesity, multiple pregnancy, hydramnios and the lithotomy position increase the likelihood of gastric reflux and possible pulmonary aspiration
- Neutralisation of gastric acid and a technique of rapid sequence induction of general anaesthesia are mandatory because of these changes
- The application of cricoid pressure compensates for the reduction in UOS pressure which occurs during induction of general anaesthesia
- The evidence suggests that 24 - 48 hours after delivery and during early pregnancy the above precautionary techniques are unnecessary unless the woman has symptomatic reflux or severe obesity
Glomerular filtration rate and renal plasma flow increase rapidly in the first trimester. There is an increase in urine production and frequency of micturition. The clearances of urea, creatinine and urate are correspondingly increased and serum levels are below non pregnant levels (table 1.2).
Table 1.2 Pregnant and non pregnant parameters of renal function
| Investigation | Pregnant | Non Pregnant |
|---|---|---|
| Plasma creatinine µmol/l | 50 - 73 | 73 |
| Plasma urea mmol/l | 2.3 - 4.3 | 4.3 |
| Plasma urate mmol/l | 0.15 - 0.35 | 0.2 - 0.35 |
| Plasma bicarbonate mmol/l | 18 - 26 | 22 - 26 |
Aldosterone, progesterone and renin-angiotensin activity increase and there is a rise in total body water and sodium. The reabsorptive capacity for glucose and lactose is reduced (glycosuria is present in 40% of pregnancies). Progesterone causes ureteric dilatation; the associated urinary stasis may precipitate infection.
Significance to the anaesthetist
- Renal problems are usually encountered with pre-eclampsia. Proteinuria occurs due to glomerular damage. Oliguria may be a consequence of arteriolar damage and spasm which may lead to acute tubular necrosis.
- Non-steroidal anti-inflammatory drugs (NSAID) may be used as tocolytics and for post delivery pain relief. They are prostaglandin synthetase inhibitors and may reduce renal blood flow when renal function is compromised e.g. pre-eclampsia or following major blood loss.
- Increased doses of renally excreted drugs may be required to obtain adequate therapeutic levels.
Slight elevations in aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and alkaline phosphatase occur during pregnancy. Serum cholinesterase activity is reduced by 25% at term and by 33% three days postpartum. This appears to be due to haemodilution rather than decreased synthesis. In practice the duration of action of suxamethonium is increased by 2-3 minutes in the first week postpartum; this is not a clinical problem.
FURTHER READING
Bonica JJ. Maternal Anatomic and Physiological Alterations during Pregnancy and Parturition. In: Bonica JJ, McDonald JS eds. Principles and Practice of Obstetric Analgesia. Baltimore:Williams & Wilkins, 1995;45-83.
Conclin KA. Physiologic changes of pregnancy. In:Chestnut DH ed. Obstetric Anesthesia.St Louis: Mosby,1994;17-76.
Chamberlain G and Pipkin B.F. Clinical Physiology in Obstetrics; Blackwell Science, 1998.
Bourne T, Ogilvy AJ, Vickers R, Williamson K. Nocturnal hypoxaemia in late pregnancy. British Journal of Anaesthesia 1995;75: 678-682.Click here for Medline link
Bassell GM and Marx GF. Optimisation of fetal oxygenation. International Journal of Obstetric Anesthesia 1995;4:238-243.
Pilkington S, Carli F, Dakin MJ, Romney M, Dewitt KA, Dore CJ, Cormack RS. Increase in Mallampati score during pregnancy. British Journal of Anaesthesia 1995; 74: 638-642.Click here for Medline link
Vanner RG. Mechanisms of regurgitation and its prevention with cricoid pressure. International Journal of Obstetric Anesthesia 1993; 4:207-215.
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