Cardiac disease in pregnancy pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]

Effect of Pregnancy on Maternal Physiology

I. Hormonal Changes

Increased progesterone levels

• During early stages of pregnancy, prior to full placentation, progesterone is produced by the corpus luteum.
• Elevated progesterone levels → decreased smooth muscle tone → reduced systemic vascular resistance.

Increased estrogen levels

• Elevated estrogen levels may increase myocardial contractility.

Increased renin and aldosterone levels

• Peripheral vasodilation subsequently causes renal vasodilation and activation of the renin-angiotensin-aldosterone system, which results in:

• Increased sodium and water retention.
• Compensation for the decreased systemic vascular resistance.

II. Plasma volume expansion

• Plasma volume expansion starts as early as 6-weeks of gestation and is increased to approximately 40-45% by the mid trimester.
• Plasma volume expansion → hemodilution → anemia
• Despite the development of anemia, the total red cell mass is not decreased because the rate of rise in plasma volume is more than rate of rise in red cell mass. This occurs until 30-week of gestation and is referred to as the physiologic anemia of pregnancy.
• The hematocrit may drop to 33-38%.
• Higher increase in blood volume may be prevalent among multigravidas.
• An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.

III. Cardiac output

• Approximately 50% increase in cardiac output is observed which is required to well oxygenate the fetus.
• The increase in cardiac output begins as early as the 5^th week of gestation and steadily increases up to 24^th week of gestation following which it plateaus.

• The initial increase in cardiac output is attributed to an increase in stroke volume, whereas during late trimesters, it is attributed to an increase in heart rate and reduction in systemic vascular resistance.

• Increase in resting heart rate by 10 to 15 beats per minute is observed during the first and second trimester suggesting an initial increase in venous return. Higher rates of increase in heart rate is observed with multiple gestation.

• Blood pressure remains relatively unchanged when measured in the left lateral recumbent position.

• Several factors influence the changes observed in cardiac output during pregnancy. Serial hemodynamic measurements performed in supine position are erroneous secondary to the inferior vena caval compression by the enlarging uterus which subsequently decreases the venous return from the lower extremities. Therefore, owing to the caval compression, cardiac output has shown to decline in supine position whereas increases in the left lateral position.

• Precipitation of high cardiac output failure may be observed in a few patients secondary to the shunting of blood to the placenta where it may pass from arterioles to venules bypassing the capillaries.

Blood pressure

• arterial pressure begins to fall during the first trimester reaches a nadir in mid pregnancy and returns toward pregestational levels before term.
• because diastolic blood pressure decreases substantially more than systolic blood pressure, the pulse pressure widens.
• reduction blood pressure is caused by a decline in systemic vascular resistance due to reduce vascular tone. This is mediated by gestational hormone activity, increased circulate levels of prostaglandins and atrial natriuretic peptides, as well as endothelial nitric oxide. Increased heat production by the developing fetus small and the creation of a lower resistance circulation in the uterus also play a role.
• supine hypotensive syndrome of pregnancy: occurs in 11% of women. Associated with weakness, lightheadedness, nausea, dizziness and even syncope. This is often explained by acute occlusion of the inferior vena cava by the enlarged uterus. Symptoms usually subside when the supine position is abandoned.

Increased respiratory rate

• secondary to increased abdominal pressure, elevation of the diaphragm.
• lowers carbon dioxide tension.

Gastrointestinal changes

• Gastric emptying is slower – in pregnancy women have reduced gastrointestinal motility.
• An incompetent gastro-oesophageal sphincter leads to gastro-oesophageal reflux with greater danger of aspiration of gastric contents into the trachea.
• Increased intragastric pressure in late pregnancy

Other changes in pregnancy

• Flared ribs.
• Breast hypertropy (may impede effective resuscitation).

Physiology of Labor and Delivery

• Hemodynamics are altered substantially during labor and delivery secondary to anxiety, pain, and uterine contractions. Oxygen consumption increases threefold, and cardiac output rises progressively during labor owing to increases in both stroke volume and heart rate. Blood pressure is higher in the lateral position. Both the systolic and diastolic blood pressure increase markedly during uterine contractions with a greater augmentation during the second stage. The form of anesthesia impacts the blood pressure.
  

• By the time of delivery the cardiac output has increased by 50%, the plasma volume has increased by 40% and the red cell mass has increased by 25 to 30%.
  

• The work of labor may increase the cardiac output by 60% over the baseline level.
  

• During the second stage of labor the patient is on her back there is venous stasis, heart rate increases to greater than 120/min and the blood pressure may be more than 150 mm Hg.
  

• Immediately following delivery, the uterus contracts and delivers a sudden bolus of 500-750 cc of blood to the circulatory system which may result in pulmonary edema in the patient with heart disease.

Hemodynamic effect of Cesarean Section:

To avoid the hemodynamic changes assocaited with vaginal delivery, cesarean section is frequently recommended for women with cardiovascular disease. This form of delivery can also be associated with hemodynamic fluctuations related to intubation, analgesic as well as anesthetic use. There can be a greater extent of blood loss as well as relief of caval compression.

Hemodynamic changes Postpartum:

There can be a temporary increase in venous return immediately after delivery due to relief of caval compression in addition to blood shifting from the contracting uterus into the systemic circulation. This change and effective blood volume occurs despite blood loss during delivery and can result in a substantial rise in ventricular filling pressures, stroke volume, and cardiac output that may lead to clinical deterioration.

Both heart rate and cardiac output returned to prelabor values by one hour after delivery and the blood pressure and stroke volume at 24 hours after delivery.

Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to prepregnancy values within 12-24 weeks after delivery.

Fetal Physiology

• Uterine blood flow increases by a factor of 50 during pregnancy.
• The uterine blood vessels remain dilated throughout pregnancy.
• Transfer of oxygen across the placenta is flow-limited.
• Fetal oxygen tension is normally quite low (30 to 40 mmHg).
• Supplemental oxygen to the mother is quite effective in increasing fetal oxygen, particularly with fetal distress.
• Normal fetal pH is 7.35. Fetal scalp pHs <7.25 are abnormal.
• Labor can precipitate fetal distress because during uterine contractions, uterine blood flow is nearly occluded.
• In a mother with cyanosis, it is easier for problems to arise during labor because of the reduced reserve in oxygen delivery.
• With contractions, there may normally be a reduction or deceleration in the fetal heart rate, but this rapidly returns to normal.
• In fetal distress, the decelerations are later in the contraction and persist, i.e. late decelerations.
• Fetuses do not die suddenly during labor, and there are many minutes or hours of fetal distress before death so that there is time to intervene.
• Placing the mother in the left lateral recumbent position and oxygen will relieve many cases of fetal distress.
• Fetal monitoring should be used in the presence of maternal heart disease, cardiac surgery, cardioversion.

References

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