Pregnancy and heart disease pathophysiology
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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[1]
- Increased progesterone decreases smooth muscle tone which decreases the systemic vascular resistance (SVR)
- later in pregnancy the placenta produces progesterone
- Increased progesterone decreases smooth muscle tone which decreases the systemic vascular resistance (SVR)
- Increased Estrogen Levels
- may increase contractility of heart[2]
- may increase 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 -> 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%.[3]
- starts as early as 6 weeks
- greater increase in blood volume among multigravidas[3]
- enhances Na and water retention
- Cardiac Output Increases by 50%[2]
- have a higher volume of more dilute blood to circulate
- need well oxygenated blood to circulate to the fetus
- begins to rise at 5th week, and cardiac output increases until week 24 at which time it plateaus
- resting pulse rate increases by 10 to 15 beats per minute. Pregnancy with multiple fetuses is associated with even more rapid heart rates.
- 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 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 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.
- have a higher volume of more dilute blood to circulate
- Increased Respiratory Rate
- secondary to increased abdominal pressure, elevation of the diaphragm
- lowers carbon dioxide tension
- secondary to increased abdominal pressure, elevation of the diaphragm
- 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.[4]
- 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 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 contractions with a greater augmentation during the second stage. The form of anesthesia impacts 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, heart rate increases to > 120/min and the BP may be > 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.
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 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 CO that may lead to clinical deterioration.[10]
Both heart rate and CO 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.
References
- ↑ 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.
- ↑ 2.0 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.
- ↑ 3.0 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.
- ↑ 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.
- ↑ 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.
- ↑ Morris S, Stacey M. Resuscitation in pregnancy. BJM 2003;327:1277-1279.
- ↑ PRITCHARD JA (1965). "CHANGES IN THE BLOOD VOLUME DURING PREGNANCY AND DELIVERY". Anesthesiology. 26: 393–9. PMID 14313451.
- ↑ Kjeldsen J (1979). "Hemodynamic investigations during labour and delivery". Acta Obstet Gynecol Scand Suppl. 89: 1–252. PMID 290123.
- ↑ 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.
- ↑ Ueland K, Hansen JM (1969). "Maternal cardiovascular dynamics. II. Posture and uterine contractions". Am J Obstet Gynecol. 103 (1): 1–7. PMID 5761774.