Christopher F. Ciliberto & Gertie F. Marx,
Department of Anaesthesiology, Albert Einstein College of Medicine,
Jacobi 1226, 1300 Morris Park Avenue, Bronx, New York 10461, USA.

Introduction		Metabolism
Cardiovascular system		Renal system
Respiratory system		Drug responses
Gastrointestinal system

Physiological and anatomical alterations develop in many organ systems during the course of pregnancy and delivery. Early changes are due, in part, to the metabolic demands brought on by the fetus, placenta and uterus and, in part, to the increasing levels of pregnancy hormones, particularly those of progesterone and oestrogen. Later changes, starting in mid-pregnancy, are anatomical in nature and are caused by mechanical pressure from the expanding uterus. These alterations create unique requirements for the anaesthetic management of the pregnant woman. 
 
Cardiovascular System

The pregnancy-induced changes in the cardiovascular system develop primarily to meet the increased metabolic demands of the mother and fetus.

Blood Volume increases progressively from 6-8 weeks gestation (pregnancy) and reaches a maximum at approximately 32-34 weeks with little change thereafter. Most of the added volume of blood is accounted for by an increased capacity of the uterine, breast, renal, striated muscle and cutaneous vascular systems, with no evidence of circulatory overload in the healthy pregnant woman. The increase in plasma volume (40-50%) is relatively greater than that of red cell mass (20-30%) resulting in hemodilution and a decrease in haemoglobin concentration. Intake of supplemental iron and folic acid is necessary to restore hemoglobin levels to normal (12 g/dl).

The increased blood volume serves two purposes. First, it facilitates maternal and fetal exchanges of respiratory gases, nutrients and metabolites. Second, it reduces the impact of maternal blood loss at delivery. Typical losses of 300-500 ml for vaginal births and 750-1000 ml for Caesarean sections are thus compensated with the so-called "autotransfusion" of blood from the contracting uterus.

Blood Constituents. As mentioned above, red cell mass is increased 20-30%. Leukocyte counts are variable during gestation, but usually remain within the upper limits of normal. Marked elevations, however, develop during and after parturition (delivery). Fibrinogen, as well as total body and plasma levels of factors VII, X and XII increase markedly. The number of platelets also rises, yet not above the upper limits of normal. Combined with a decrease in fibrinolytic activity, these changes tend to prevent excessive bleeding at delivery. Thus, pregnancy is a relatively hypercoagulable state, but during pregnancy neither clotting or bleeding times are abnormal.

Cardiac Output increases to a similar degree as the blood volume. During the first trimester cardiac output is 30-40% higher than in the non-pregnant state. Steady rises are shown on Doppler echocardiography, from an average of 6.7 litres/minute at 8-11 weeks to about 8.7 litres/minute flow at 36-39 weeks; they are due, primarily, to an increase in stroke volume (35%) and, to a lesser extent, to a more rapid heart rate (15%). There is a steady reduction in systemic vascular resistance (SVR) which contributes towards the hyperdynamic circulation observed in pregnancy.

During labor, further increases are seen with pain in response to increased catecholamine secretion; this increase can be blunted with the institution of labour analgesia. Also during labour, there is an increase in intravascular volume by 300-500 ml of blood from the contracting uterus to the venous system. Following delivery this autotransfusion compensates for the blood losses and tends to further increase cardiac output by 50% of pre-delivery values. At this point, stroke volume is increased while heart rate is slowed.

Cardiac Size/Position/ECG. There are both size and position changes which can lead to changes in ECG appearance. The heart is enlarged by both chamber dilation and hypertrophy. Dilation across the tricuspid valve can initiate mild regurgitant flow causing a normal grade I or II systolic murmur. Upward displacement of the diaphragm by the enlarging uterus causes the heart to shift to the left and anteriorly, so that the apex beat is moved outward and upward. These changes lead to common ECG findings of left axis deviation, sagging ST segments and frequently inversion or flattening of the T-wave in lead III.

Blood Pressure. Systemic arterial pressure is never increased during normal gestation. In fact, by midpregnancy, a slight decrease in diastolic pressure can be recognized. Pulmonary arterial pressure also maintains a constant level. However, vascular tone is more dependent upon sympathetic control than in the nonpregnant state, so that hypotension develops more readily and more markedly consequent to sympathetic blockade following spinal or extradural anaesthesia. Central venous and brachial venous pressures remain unchanged during pregnancy, but femoral venous pressure is progressively increased due to mechanical factors.

Aortocaval Compression. From mid-pregnancy, the enlarged uterus compresses both the inferior vena cava and the lower aorta when the patient lies supine. Obstruction of the inferior vena cava reduces venous return to the heart leading to a fall in cardiac output by as much as 24% towards term. In the unanaesthetised state, most women are capable of compensating for the resultant decrease in stroke volume by increasing systemic vascular resistance and heart rate. There are also alternative venous pathways, the paravertebral and azygos systems. During anesthesia, however, these compensatory mechanisms are reduced or abolished so that significant hypotension may rapidly develop. Obstruction of the lower aorta and its branches causes diminished blood flow to kidneys, uteroplacental unit and lower extremities. During the last trimester, maternal kidney function is markedly lower in the supine than in the lateral position. Furthermore, the fetus is compromised by insufficient transplacental gas exchange.

Venous Distension increases approximately to 150% during the course of gestation and the venous ends of capillaries become dilated, causing reduced blood flow. These vascular changes contribute to delayed absorption of subcutaneously or intramuscularly injected substances. Distension of the extradural veins heightens the risk of vascular damage during institution of a regional block. The increased venous volume within the rigid spinal canal reduces the volume or capacity of the extradural and intrathecal spaces for local anaesthetic solutions. This will therefore increase the spread of injected drugs.

Clinical Implications. Despite the increased workload of the heart during gestation and labour, the healthy woman has no impairment of cardiac reserve. In contrast, for the gravida with heart disease and low cardiac reserve, the increase in the work of the heart may cause ventricular failure and pulmonary oedema. In these women, further increases in cardiac workload during labour must be prevented by effective pain relief, optimally provided by extradural or spinal analgesia. Since cardiac output is highest in the immediate postpartum period, sympathetic blockade should be maintained for several hours after delivery and then weaned off slowly.

Teaching Point. There is a 30% reduction in volume of local anaesthetic solution required at term when compared to the non-pregnant woman, to achieve the same block.

Aortocaval compression and its sequelae must be avoided. No woman in late pregnancy should lie supine without shifting the uterus off the great abdomino-pelvic vessels. During labour, the parturient should rest on her side, left or right. During Caesarean section and for other indications demanding the supine position, the uterus should be displaced, usually to the left, by placing a rigid wedge under the right hip and/or tilting the table left side down. 

(Continued ...)

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