Cardiac disease in pregnancy pathophysiology

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Special Scenarios: I. Pre-existing Cardiac Disease: Congenital Heart Disease Repaired Congenital Heart Disease Pulmonary Hypertension Rheumatic Heart Disease Connective Tissue Disorders II. Valvular Heart Disease: Mitral Stenosis Mitral Regurgitation Aortic Insufficiency Aortic Stenosis Mechanical Prosthetic Valves Tissue Prosthetic Valves III. Cardiomyopathy: Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Peripartum Cardiomyopathy IV. Cardiac diseases that may develop During Pregnancy: Arrhythmias Acute Myocardial Infarction Hypertension
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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]

Effect of Pregnancy on Maternal Physiology

Corpus uteum produces progesterone

• increased progesterone → decreased smooth muscle tone → therefore decreased systolic vascular resistance.
• later in pregnancy the placenta produces progesterone.

Increased estrogen levels

• may increase contractility of heart.

Increased renin and aldosterone levels caused by increased estrogen

• enhances Na and water retention.
• compensates for the decreased systemic vascular resistance.
• by the middle trimester, plasma volume is increased by 40 to 45%.
• hemodilution → anemia, but total red cell mass is not decreased. Rate of rise in volume is more rapid than rate of rise in red cell mass. This occurs until week 30 and is referred to as the physiologic anemia of pregnancy. The hematocrit can be as low as 33% to 38%.
• starts as early as 6 weeks.
• greater increase in blood volume among multigravidas.

Cardiac output increases by 50%

• have a higher volume of more dilute blood to circulate.
• need well oxygenated blood to circulate to the fetus.
• begins to rise at 5^th week, and cardiac output increases until week 24 at which time it plateaus.
• resting heart rate increases by 10 to 15 beats per minute. Pregnancy with multiple fetuses is associated with even more rapid heart rates.
• blood pressure remains relatively unchanged when measured in the left lateral recumbent position.
• hemodynamics measured in the supine position are erroneous because the uterus compresses the IVC decreasing the return from the lower extremities. Therefore may have syncope when a gravid stands up from a supine position.
• keep in mind that much of the blood is shunted to the placenta where it may pass from arterioles to venules bypassing the capillaries. May precipitate high cardiac output failure in some women.
• cardiac output increases in the lateral position and declines in the supine position owing to caval compression by the gravid uterus.
• the increase in cardiac output in early pregnancy is due to an increase in stroke volume early on, but in the third trimester it is due to an increase in heart rate.

Increased respiratory rate

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

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.

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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