Pregnancy and heart disease pathophysiology

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I. Pre-existing Cardiac Disease:
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II. Valvular Heart Disease:
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III. Cardiomyopathy:
Dilated Cardiomyopathy
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Peripartum Cardiomyopathy
IV. Cardiac diseases that may develop During Pregnancy:
Arrhythmias
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Anjan K. Chakrabarti, M.D. [2]

Overview

There are significant hemodynamic changes associated with pregnancy that begin early, reach their peak during the second trimester, and persist through delivery. These changes include blood volume expansion, reductions in blood pressure and vascular resistance, and a resultant increase in cardiac output. These changes can have a significant impact on both the mother and the fetus, particularly when there are maternal cardiac disorders.

Effect of Pregnancy on Maternal Physiology

The Corpus Luteum Produces Progesterone

Increased Estrogen Levels

  • Increased estrogen may increase the contractility of heart[2]

Increased Renin and Aldosterone Levels Caused by Increased Estrogen

  • Enhances Na and water retention
  • Compensates for the decreased SVR
  • By the middle trimester, plasma volume is increased by 40 to 45%
  • Hemodilution leads to anemia, but the total red cell mass is not decreased. The rate of rise in plasma 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%.[3]
  • Starts as early as 6 weeks
  • There is a greater increase in blood volume among multigravidas[3]

Cardiac Output Increases by 50%

  • There is a higher volume of more dilute blood to circulate[2]
  • There is the need for well oxygenated blood to circulate to the fetus
  • Cardiac output begins to rise at the 5th week, and the cardiac output increases until week 24 at which time it plateaus
  • The resting pulse rate increases by 10 to 15 beats per minute. Pregnancy with multiple fetuses is associated with even more rapid heart rates.
  • The blood pressure (BP) remains relatively unchanged when measured in the left lateral recumbent position
  • Hemodynamics measured in the supine position are erroneous because the uterus compresses the inferior vena cava (IVC) decreasing the return of blood from the lower extremities. Therefore the patient may experience syncope when they stand up from a supine position.
  • Much of the blood is shunted to the placenta where it may pass from arterioles to venules bypassing the capillaries. This may precipitate high cardiac output failure in some women.
  • Cardiac output increases in the lateral position and declines in the supine position owing to inferior vena caval compression by the gravid uterus.
  • The increase in cardiac output (CO) 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

Blood Pressure

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[5]

Other Changes in Pregnancy

  • Flared ribs
  • Breast hypertropy[6] (may impede effective cardiopulmonary resuscitation)

The Physiology of Labor and Delivery

The Hemodynamic Effect of Normal Vaginal 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 contractions with a greater augmentation during the second stage. The form of anesthesia may impact the blood pressure.[7]
  • By the time of delivery the cardiac output (CO) 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 CO by 60% over the baseline level.
  • During the second stage of labor, the patient is on her back there is venous stasis, the heart rate increases to > 120 beats per minute and the [[blood pressure may rise to > 150 mm Hg. [8]
  • 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.

The 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.[9]

Hemodynamic Changes Postpartum:

There can be a temporary increase in venous return immediately after delivery due to relief of inferior vena 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 (CO) that may lead to clinical deterioration.[10]

Both heart rate and cardiac output (CO) return to prelabor values by one hour after delivery and the blood pressure and stroke volume returns to normal at 24 hours following delivery.

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

References

  1. Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D; et al. (1998). "Temporal relationships between hormonal and hemodynamic changes in early human pregnancy". Kidney Int. 54 (6): 2056–63. doi:10.1046/j.1523-1755.1998.00217.x. PMID 9853271.
  2. 2.0 2.1 Robson SC, Hunter S, Boys RJ, Dunlop W (1989). "Serial study of factors influencing changes in cardiac output during human pregnancy". Am J Physiol. 256 (4 Pt 2): H1060–5. PMID 2705548.
  3. 3.0 3.1 Lund CJ, Donovan JC (1967). "Blood volume during pregnancy. Significance of plasma and red cell volumes". Am J Obstet Gynecol. 98 (3): 394–403. PMID 5621454.
  4. Almeida FA, Pavan MV, Rodrigues CI (2009). "The haemodynamic, renal excretory and hormonal changes induced by resting in the left lateral position in normal pregnant women during late gestation". BJOG. 116 (13): 1749–54. doi:10.1111/j.1471-0528.2009.02353.x. PMID 19781045.
  5. Jevon P, Raby M. Physiological and anatomical changes in pregnancy relevant to resuscitation. In: O'Donnell E, Pooni JS, editors. Resuscitation in Pregnancy. A practical approach. Oxford: Reed Educational and Professional Publishing Ltd.; 2001. p. 10-16.
  6. Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.
  7. PRITCHARD JA (1965). "CHANGES IN THE BLOOD VOLUME DURING PREGNANCY AND DELIVERY". Anesthesiology. 26: 393–9. PMID 14313451.
  8. Kjeldsen J (1979). "Hemodynamic investigations during labour and delivery". Acta Obstet Gynecol Scand Suppl. 89: 1–252. PMID 290123.
  9. Tihtonen K, Kööbi T, Yli-Hankala A, Uotila J (2005). "Maternal hemodynamics during cesarean delivery assessed by whole-body impedance cardiography". Acta Obstet Gynecol Scand. 84 (4): 355–61. doi:10.1111/j.0001-6349.2005.00489.x. PMID 15762965.
  10. Ueland K, Hansen JM (1969). "Maternal cardiovascular dynamics. II. Posture and uterine contractions". Am J Obstet Gynecol. 103 (1): 1–7. PMID 5761774.


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