Physiology of pregnancy

Figure 23.2

Changes in cardiac output through the trimesters of pregnancy



Patient posture has been found to influence cardiac output measurements during pregnancy (Figure 23.3). Measurements performed in the lateral position, to avoid aortocaval compression, demonstrate an increase in cardiac output by 5 weeks gestation.



Figure 23.3 The effect of position on cardiac output during pregnancy





















Position Change in cardiac output
Supine Baseline
Left lateral by 13.5%
Lithotomy by 17%
Steep Trendelenburg by 18%

A further transient rise in cardiac output occurs during labour, at delivery and in the immediate period after delivery as a result of uteroplacental transfusion of 300500 mL of blood from the intervillous space into the maternal intravascular volume (autotransfusion). Cardiac output increases by a further 45% during contractions, a further 60% in the second stage, and up to a further 80% immediately after delivery when compared with the pre-delivery state.





  • Cardiac output increases throughout pregnancy, to reach a level of 50% greater than in the non-pregnant state during the last trimester.



  • The increase in cardiac output in pregnancy is produced by a combination of increased heart rate, reduced systemic vascular resistance (SVR) and increased stroke volume.




Heart rate and stroke volume


Heart rate (HR) is increased above non-pregnant values by 15% at the end of the first trimester. This increases to 25% by the end of the second trimester, but there is no further change in the third trimester.


Stroke volume (SV) is increased by about 20% at 8 weeks and by up to 30% by the end of the second trimester, after which it remains level until term (Figure 23.2). Stroke volume and heart rate both increase during labour and immediately post delivery.



Systemic vascular resistance and blood flow to organs


Systemic vascular resistance (SVR) is reduced during pregnancy. The average SVR in pregnancy is about 980 dyne.s.cm−5, compared with about 1150 dyne.s.cm−5 in non-pregnant women. The decrease in the SVR results from the development of a low-resistance vascular bed (the intervillous space) and vasodilatory effects of oestrogens, prostacyclin and progesterone.


Distribution of the cardiac output during pregnancy is different from that of the non-pregnant state, with increased blood flow to the uterus, kidneys and skin. Uterine blood flow varies from 500 to 700 mL min−1 (about 1012% of the cardiac output) at term, of which > 80% perfuses the placenta. The flow to the kidneys is increased, as is the flow to the skin due to peripheral vasodilatation. Flow to the liver and brain remains unchanged.



Blood pressure


Blood pressure falls during pregnancy and returns towards the baseline near term. Systolic blood pressure is minimally affected, with a maximum decline of 8% during early and mid-gestation, returning to non-pregnant levels at term. Diastolic blood pressure falls to a greater extent, with early and mid-gestational decreases of 2025%, and returns to normal at term. In the supine position, 70% of mothers have a fall in blood pressure of at least 10%, and 8% have decreases of 3050%.



Aortocaval compression


Compression of the inferior vena cava (IVC) and aorta by the gravid uterus occurs during pregnancy and reduces cardiac output. The severity of this effect is dependent on:




  • Patient position



  • Gestation



  • Systemic blood pressure



  • Presence of sympathetic block


In the supine position during pregnancy, IVC obstruction occurs and venous blood bypasses this obstruction primarily via vertebral venous plexuses which empty into the azygos vein. IVC compression develops as early as 1316 weeks gestation, causing a 50% increase in femoral venous pressures. Near term, women in the supine position may experience a 1020% reduction in stroke volume and cardiac output. This effect becomes maximal between 36 and 38 weeks, after which it may decline as the fetal head descends into the pelvis. Moving from a supine to a lateral position reduces the femoral and IVC pressures, but these are still elevated above those of the non-pregnant woman, indicating that the compression of the IVC is not completely relieved by lateral positioning. In the supine position, 1520% of pregnant women experience a substantial drop in blood pressure (supine hypotension syndrome), and the patients develop systemic signs of shock, i.e. pallor, sweating, nausea, vomiting and syncope.


Obstruction of the aorta in the supine position has been demonstrated angiographically, but the higher pressures in the aorta prevent total obstruction. This does not cause maternal hypotension but causes arterial hypotension in the lower extremities and in the uterine arteries, which can lead to inadequate uterine blood flow resulting in fetal asphyxia and bradycardia.



Aortocaval compression can reduce cardiac output by up to 20% during pregnancy when the mother is supine at term. The left lateral position can correct this reduction by 60%.



Electrocardiogram (ECG) and echocardiogram


The ECG in pregnancy may show the following changes:




  • Sinus tachycardia, reduced PR interval and reduced uncorrected QT interval



  • Rotation of the electrical axis of the heart to the left



  • ST segment depression



  • T wave flattening


However, these changes are thought to be of no clinical significance.


Echocardiographic studies during pregnancy have shown:




  • Left ventricular hypertrophy from 12 weeks gestation.



  • A 50% increase in left ventricular mass at term. This is due to increase in the size of cardiomyocytes.



  • A 1214% increase in tricuspid, pulmonary and mitral valve annular diameters. The majority of pregnant women have tricuspid and pulmonary regurgitation, and 27% have mitral regurgitation.


Studies have demonstrated a high incidence of asymptomatic pericardial effusion during normal pregnancy.



Heart sounds


The apical impulse moves to the fourth intercostal space and mid-clavicular line. Most pregnant women develop a loud and sometimes split first heart sound. A third heart sound is common, and 16% of women have a fourth heart sound. A grade III early to mid-systolic heart murmur is commonly heard at the left sternal edge. This may be due to tricuspid regurgitation resulting from dilatation of the tricuspid valve.



Venous pressure


In the absence of IVC compression by the uterus, central venous pressure (CVP) and venous pressure in the upper limbs are normal. However, during late pregnancy when in the supine position, IVC compression by the gravid uterus occurs and CVP may decrease dramatically. IVC compression can also cause increased venous pressure in the lower limbs.


During labour various factors can cause an increase in CVP, including:




  • Contractions can increase CVP by about 5 cmH2O.



  • Expulsive efforts of the second stage can create a major rise in CVP by up to 50 cmH2O.



  • IV ergometrine 0.25 mg after delivery of the baby can produce a rise in CVP of 8 cmH2O, which can last up to 60 minutes.


There are no observed changes in pulmonary capillary wedge and pulmonary artery pressures during pregnancy.




Haematology


The haematological changes found at term are summarised in Figure 23.4.



Figure 23.4 Haematological changes at term, compared with non-pregnant values



















































































































Parameter Change
Blood volumes Total blood volume by 45%
Plasma volume by 50%
Blood cells Red blood cell volume by 18%
White cell count
Haematocrit by 15%
Haemoglobin by 15%
Plasma proteins Total plasma protein by 18%
Albumin by 14%
Globulin or
Plasma cholinesterase by 2025%
Colloid osmotic pressure by 18%
Coagulation Platelets by 0-5%
Prothrombin time by 20%
Bleeding time by 10%
Partial thromboplastin time by 20%
Antithrombin III by 10%
Fibrinogen from 2.5 to 4.6 g L−1
Fibrin degradation by 100%
Products
Plasminogen
Fibrinolysis
Thromboelastography Hypercoagulable state
Clotting factors I by 100%
VII by 100%
VIII by 150%
IX by 100%
X by 30%
XII by 30%
XI by 4050%
XIII by 50%
Antithrombin III by 10%
II
V


Blood volume


Plasma volume (PV), total blood volume (TBV) and red blood cell volume (RBCV) all increase during pregnancy. The development of these changes through the trimesters is illustrated in Figure 23.5. Plasma volume rises by 15% during the first trimester and can reach 50% above non-pregnant values by 32 weeks; it then remains at this level unchanged. Plasma volume returns to non-pregnant levels by 6 days post delivery. There is often a sharp rise of up to 1 litre in plasma volume 24 hours after delivery. This is of significant importance in patients with cardiac disease, such as those with fixed cardiac output. Such patients may develop pulmonary oedema during this period.



Figure 23.5

Changes in PV, TBV and RBCV through the trimesters of pregnancy


RBC volume falls during the first 8 weeks of pregnancy, increasing back to non-pregnant levels by 16 weeks and then rising to 30% above non-pregnant levels by term. This increase in RBC volume is due to raised erythropoietin levels that occur from 12 weeks gestation.



The physiological anaemia of pregnancy arises from the increase of only 30% in RBC volume, relative to an increase of 50% in plasma volume in the last trimester. This results in overall reductions of about 15% in haemoglobin (Hb) and haematocrit.


The above changes combine to give total blood volume increases of 10%, 30% and 45% at the end of the first, second and third trimester respectively (Figure 23.5). Oestrogens and progesterone appear responsible for the increase in plasma volume through their effect on the reninangiotensinaldosterone systems.



Immune system


The white blood cell (WBC) count rises progressively during pregnancy from non-pregnant levels to 911 × 109 L−1. This is predominantly an increase in polymorphonuclear cells. There is a further leucocytosis to about 15 × 109 L−1 during labour. White cell count returns to normal by 6 days post delivery. Serum levels of IgA, IgG and IgM remain unchanged.



Immunity during pregnancy

In spite of a leucocytosis during pregnancy, depressed neutrophil chemotaxis and adherence leads to reduced polymorphonuclear leucocyte function. This may account for the increased incidence of infection during pregnancy and the reduced incidence of symptoms in women with autoimmune diseases such as rheumatoid arthritis.



Coagulation


Pregnancy is associated with enhanced platelet turnover, clotting and fibrinolysis (Figure 23.4). Thrombocytopenia (platelets < 100 × 109 L−1) occurs in 0.80.9% of normal pregnant women, while increases in platelet factor and β-thromboglobulin suggest elevated platelet activation and consumption. Since there is no change in platelet count in the majority of women during pregnancy, there is probably an increase in platelet production to compensate for the increased consumption. Platelet function, however, remains normal during pregnancy.


The concentrations of most coagulation factors (I, VIIX and XII) are increased, and a few (XI and XIII) are reduced. The levels of factors II and V remain the same during pregnancy. There are increases in fibrin degradation products (FDP) and plasminogen concentrations which indicate increased fibrinolytic activity during pregnancy.



Plasma proteins


The plasma concentration of albumin is reduced to 3439 g L−1, but fibrinogen levels are increased. Globulin is reduced in the first trimester then increases to 10% above the pre-pregnancy level at term. These reductions in plasma proteins are associated with the following changes (Figure 23.4):




  • Total colloid osmotic pressure is reduced by 5 mmHg.



  • Drug-binding capacity of the plasma is altered, with consequent changes in pharmacokinetics and dynamics (e.g. a reduction in plasma α-acid glycoprotein concentration reduces the lidocaine binding capacity).



  • Plasma concentration of plasma cholinesterase is reduced by 2025% at term.



  • Erythrocyte sedimentation rate (ESR) and blood viscosity are increased.



Fluid compartments


As described above, plasma volume increases by up to 50% in pregnancy. Extravascular interstitial water also increases, but this increase is variable, from 1.7 litres in women without oedema to 5 litres in women with oedema.



Oedema and plasma protein levels in pregnancy




  • Extravascular interstitial fluid volume increases by a variable amount during pregnancy depending on the presence of oedema.



  • Total plasma protein concentration falls to 6570 g L−1.



Respiratory system



Anatomical changes


Capillary engorgement and oedema of the mucosa of nasal cavity, pharynx and larynx begin early in the first trimester. This may explain why many pregnant women complain of difficulty in nasal breathing, have more episodes of epistaxis and experience voice changes. The thoracic cage increases in circumference by 57 cm because of the increase in both the anteroposterior and transverse diameters from flaring of the ribs. Flaring of the ribs begins early in pregnancy, and is therefore not entirely due to pressure from the enlarging uterus. The enlarging uterus displaces the diaphragm upwards in the later weeks of pregnancy, but the internal volume of the thoracic cavity remains unchanged (Figure 23.6).



Figure 23.6 Respiratory changes at term during pregnancy.




































































































Parameter Change
Anatomy Capillary engorgement
Upper airway swelling
Airways Dilated
Diaphragm Elevated
Thoracic circumference by 57cm
Lung volumes Tidal volume by 45%
Inspiratory reserve volume by 5%
Expiratory reserve volume by 25%
Residual volume by 20%
Functional residual capacity by 30%
Total lung capacity by 05%
Vital capacity Nil
Closing capacity Nil
Ventilation Minute ventilation (MV) by 50%
Alveolar ventilation (AV) by 70%
Respiratory rate (RR) by 015%
Dead space by 45%
Lung mechanics Diaphragm movement
Chest wall movement
Total pulmonary resistance by 50%
Lung compliance nil
FEV1 nil
FEV1/VC nil
Flow volume loop nil
Arterial blood gases PaCO2 to 3.74.2kPa
PaO2 to 13.314.6 kPa
pH to 7.44
HCO3 to 1821 mmol L−1


Lung mechanics and volumes


Inspiration is mainly as a result of diaphragmatic movement, since flaring of the ribs reduces chest wall movement. Bronchial smooth muscle relaxation decreases airway resistance but lung compliance remains unchanged. Factors contributing to airway dilatation include direct effects of progesterone, cortisone and relaxin.


Forced expiratory volume at 1 second (FEV1), the ratio of FEV1 to forced vital capacity (FVC), and the flowvolume loop remain unchanged, demonstrating that large airway function is not impaired during pregnancy.


The following changes in lung volumes occur during pregnancy, relative to non-pregnant values:




  • Tidal volume (TV) increases steadily from the first trimester, by up to 45% at term (Figure 23.7).



  • Functional residual capacity (FRC) is decreased by 2030% at term due to reductions of 25% in expiratory reserve volume (ERV) and 15% in residual volume (Figure 23.6).



  • Closing capacity can encroach on FRC, increasing ventilation/perfusion mismatch and leading to the ready occurrence of hypoxia, particularly in supine and Trendelenburg positions.



  • Inspiratory capacity increases by 15% at term due to increases in inspiratory reserve and tidal volumes.


Jan 18, 2017 | Posted by in ANESTHESIA | Comments Off on Physiology of pregnancy

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