Cardiac disease in pregnancy pathophysiology

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Cardiac disease in pregnancy Microchapters




Epidemiology and Demographics

Risk Factors


History and Symptoms

Physical Examination


Exercise Testing

Radiation Exposure

Chest X Ray





Pulmonary artery catheterization
Cardiac catheterization
Cardiac Ablation


Cardiovascular Drugs in Pregnancy

Labor and delivery

Resuscitation in Late Pregnancy

Contraindications to pregnancy

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:
Acute Myocardial Infarction

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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]; Anjan K. Chakrabarti, M.D. [3]; Lakshmi Gopalakrishnan, M.B.B.S. [4]


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 a 40% increase in blood volume expansion, reductions in both the systemic vascular resistance and pulmonary vascular resistance, a 30% rise in cardiac output and little change in the blood pressure. 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

I. Hormonal Changes

Increased Progesterone Levels
Increased Estrogen Levels
  • Elevated estrogen levels may increase myocardial contractility.[2]
Increased Renin and Aldosterone Levels

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 → hemodilutionanemia
  • 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-weeks of gestation and is referred to as the physiologic anemia of pregnancy.
  • The hematocrit may drop to 33-38%.[3]
  • A greater increase in blood volume may be observed among multigravidas.[3]
  • An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.[1]

III. Cardiac Output

  • There is a higher volume of more dilute blood to circulate.[2]
  • There is approximately a 50% increase in cardiac output which is required to oxygenate the fetus.
  • The increase in cardiac output begins as early as the 5th week of gestation and steadily increases up to the 24th week of gestation after which time it plateaus.[2][4]
  • 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.[2] Higher rates of increase in heart rate is observed with multiple gestation.
  • Several factors influence the changes observed in cardiac output during pregnancy. Serial hemodynamic measurements performed in the supine position may be erroneous secondary to the compression of the inferior vena caval by the enlarging uterus which subsequently decreases the venous return from the lower extremities. Therefore, owing to the caval compression, cardiac output has been shown to decline in the supine position whereas the cardiac output increases in the left lateral position.[5][6]

IV. Blood Pressure

  • Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 10 mm Hg below baseline) and returns toward pre-gestational levels before term.[7][8]
  • The blood pressure remains relatively unchanged when measured in the left lateral recumbent position. However, the supine hypotensive syndrome of pregnancy occurs in approximately 11% of pregnant women and is often associated with weakness, lightheadedness, nausea, dizziness and even syncope. Acute compression of the inferior vena cava by the gravid uterus is a possible explanation for this syndrome. Symptoms usually subside when the patient changes from the supine position.[13]

V. Respiratory Rate

  • An increased respiratory rate is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
  • An increased respiratory rate subsequently lowers the carbon dioxide tension.

VI. Gastrointestinal Changes

  • Reduced gastric emptying secondary to reduced gastrointestinal motility is observed during pregnancy.
  • Intra-gastric pressure increases during the last trimester.[14]

VII. Hematologic Changes in Pregnancy

  • There is an increase in clotting factor concentration
  • There is an increase in platelet adhesiveness
  • There is a decrease in fibrinolysis and protein S activity
  • As a result of all of the above, there is an increased risk of thormbosis and embolism

VIII. Other Changes in Pregnancy

  • Flared ribs.
  • Breast hypertropy which may impede effective resuscitation.[15]

Physiology of Labor and Delivery

Hemodynamic Changes During Labor and Delivery:

  • Hemodynamics are altered substantially during labor and delivery secondary to increased sympathetic tone caused by anxiety, pain, and uterine contractions.
  • These changes include:
  • By the time of delivery, cardiac output has increased by 50%, the plasma volume has increased by 40% and the red cell mass has increased by 25% to 30%.

Hemodynamic effects of Cesarean Section:

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.[19]
  • Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to pre-gestational 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.


  1. 1.0 1.1 1.2 1.3 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 2.2 2.3 2.4 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. Robson SC, Hunter S, Moore M, Dunlop W (1987). "Haemodynamic changes during the puerperium: a Doppler and M-mode echocardiographic study". British Journal of Obstetrics and Gynaecology. 94 (11): 1028–39. PMID 3322367. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. KERR MG (1965). "THE MECHANICAL EFFECTS OF THE GRAVID UTERUS IN LATE PREGNANCY". The Journal of Obstetrics and Gynaecology of the British Commonwealth. 72: 513–29. PMID 14341106. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  6. Metcalfe J, Ueland K (1974). "Maternal cardiovascular adjustments to pregnancy". Progress in Cardiovascular Diseases. 16 (4): 363–74. PMID 4368892. Retrieved 2012-04-17.
  7. Pitkin RM, Perloff JK, Koos BJ, Beall MH (1990). "Pregnancy and congenital heart disease". Annals of Internal Medicine. 112 (6): 445–54. PMID 2178537. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  8. Weiss BM, Atanassoff PG (1993). "Cyanotic congenital heart disease and pregnancy: natural selection, pulmonary hypertension, and anesthesia". Journal of Clinical Anesthesia. 5 (4): 332–41. PMID 8373615. Retrieved 2012-04-17.
  9. Willcourt RJ, King JC, Queenan JT (1983). "Maternal oxygenation administration and the fetal transcutaneous PO2". American Journal of Obstetrics and Gynecology. 146 (6): 714–5. PMID 6869444. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  10. Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR (1987). "Congenital heart disease in pregnancy: short- and long-term implications". American Journal of Obstetrics and Gynecology. 156 (2): 313–22. PMID 3826166. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  11. McFaul PB, Dornan JC, Lamki H, Boyle D (1988). "Pregnancy complicated by maternal heart disease. A review of 519 women". British Journal of Obstetrics and Gynaecology. 95 (9): 861–7. PMID 3191059. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  12. Selzer A (1977). "Risks of pregnancy in women with cardiac disease". JAMA : the Journal of the American Medical Association. 238 (8): 892–3. PMID 577983. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  13. 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.
  14. 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.
  15. Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.
  16. PRITCHARD JA. CHANGES IN THE BLOOD VOLUME DURING PREGNANCY AND DELIVERY, Anesthesiologyvolume 26, pages 393–9, 1965.
  17. Kjeldsen J (1979). "Hemodynamic investigations during labour and delivery". Acta Obstet Gynecol Scand Suppl. 89: 1–252. PMID 290123.
  18. 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.
  19. 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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