Cardiac disease in pregnancy pathophysiology: Difference between revisions
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:*[[Peripheral vasodilation]] subsequently causes [[vasodilation|renal vasodilation]] and activation of the [[renin-angiotensin-aldosterone system]],<ref name="pmid9853271">{{cite journal |author=Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D, Johnson A, Osorio F, Goldberg C, Moore LG, Dahms T, Schrier RW |title=Temporal relationships between hormonal and hemodynamic changes in early human pregnancy |journal=[[Kidney International]] |volume=54 |issue=6 |pages=2056–63 |year=1998 |month=December |pmid=9853271 |doi=10.1046/j.1523-1755.1998.00217.x |url=http://dx.doi.org/10.1046/j.1523-1755.1998.00217.x |accessdate=2012-04-17}}</ref> which results in: | :*[[Peripheral vasodilation]] subsequently causes [[vasodilation|renal vasodilation]] and activation of the [[renin-angiotensin-aldosterone system]],<ref name="pmid9853271">{{cite journal |author=Chapman AB, Abraham WT, Zamudio S, Coffin C, Merouani A, Young D, Johnson A, Osorio F, Goldberg C, Moore LG, Dahms T, Schrier RW |title=Temporal relationships between hormonal and hemodynamic changes in early human pregnancy |journal=[[Kidney International]] |volume=54 |issue=6 |pages=2056–63 |year=1998 |month=December |pmid=9853271 |doi=10.1046/j.1523-1755.1998.00217.x |url=http://dx.doi.org/10.1046/j.1523-1755.1998.00217.x |accessdate=2012-04-17}}</ref> which results in: | ||
:::*Increased sodium and water retention. | :::*Increased sodium and water retention. | ||
:::*Compensation for the decreased [[systemic vascular resistance]]. | :::*Compensation for the decreased [[systemic vascular resistance]]. | ||
:*Increased [[renin]] and [[aldosterone]] levels are caused by increased [[estrogen]] | |||
===II. Plasma volume expansion=== | ===II. Plasma volume expansion=== |
Revision as of 17:00, 18 April 2012
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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.
- Increased progesterone decreases smooth muscle tone which decreases the systemic vascular resistance (SVR).[1]
Increased estrogen levels
- Elevated estrogen levels may increase myocardial contractility.[2]
Increased renin and aldosterone levels
- Peripheral vasodilation subsequently causes renal vasodilation and activation of the renin-angiotensin-aldosterone system,[1] which results in:
- Increased sodium and water retention.
- Compensation for the decreased systemic vascular resistance.
- Increased renin and aldosterone levels are caused by increased estrogen
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%.[3]
- Higher increase in blood volume may be prevalent among multigravidas.[3]
- An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.[1]
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 5th week of gestation and steadily increases up to 24th week of gestation following which it plateaus.[2][4]
- 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.[2]
- 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 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.[5][6]
- 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.
IV. Blood pressure
- Widened pulse pressure is present because there is a substantial reduction in the diastolic blood pressure greater than the systolic blood pressure.
- Drop in blood pressure is caused by a decline in systemic vascular resistance secondary to reduced vascular tone.[9][10] This is mediated by gestational hormone activity, increased circulating levels of prostaglandins and atrial natriuretic peptides,[1] as well as endothelial nitric oxide.[11][12]
- Blood pressure remains relatively unchanged when measured in the left lateral recumbent position. However, 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 the possible explanation for this syndrome. Symptoms usually subside when the supine position is abandoned.
V. Respiratory rate
- Increased respiratory rate is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
- Increased respiratory rate subsequently lowers carbon dioxide tension.
VI. Gastrointestinal changes
- Reduced gastric emptying secondary to reduced gastrointestinal motility is observed during pregnancy.
- An incompetent gastro-oesophageal sphincter leads to gastro-oesophageal reflux with increased risk of aspiration of gastric contents into the trachea.
- Intra-gastric pressure increases during late trimester.[13]
VII. Other changes in pregnancy
- Flared ribs.
- Breast hypertropy which may impede effective resuscitation.[14]
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:
- Oxygen consumption increases by threefold.
- Cardiac output rises progressively during labor owing to an increase in both stroke volume and heart rate. The work of labor has also shown to increase cardiac output by 60% over the baseline.
- Blood pressure is higher in the left lateral position. During uterine contractions, marked increase in both the systolic and diastolic blood pressure is observed with a greater augmentation during the second stage of labor. The form of anesthesia impacts the blood pressure.
- During the second stage of labor, an increase in venous stasis, heart rate (greater than 120 beats/min) and blood pressure (more than 150 mmHg) is observed.
- 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%.
- 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 patients with heart disease.
Hemodynamic effects of Cesarean Section:
- To avoid the hemodynamic changes associated with vaginal delivery, cesarean section is frequently recommended for women with cardiovascular disease.
- Cesarean section is also associated with hemodynamic fluctuations that are related to intubation, analgesia and the choice of anesthesia. Most common form of anesthesia used is epidural which significantly reduces pain but is also associated with significant peripheral vasodilation and subsequent hypotension.
- Cesarean section is associated with greater extent of blood loss as well as provides 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.
- Effective increase in venous return and blood volume, despite the blood loss occurred during delivery, results in a substantial increase in ventricular filling pressures, stroke volume, and cardiac output that may lead to clinical deterioration.
- Both heart rate and cardiac output return to pre-gestational values by an hour after delivery. However, it takes about 24-hours for the blood pressure and stroke volume to return to baseline.
- 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.
References
- ↑ 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.
- ↑ 2.0 2.1 2.2 2.3 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.
- ↑ 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
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(help) - ↑ 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
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(help) - ↑ Metcalfe J, Ueland K (1974). "Maternal cardiovascular adjustments to pregnancy". Progress in Cardiovascular Diseases. 16 (4): 363–74. PMID 4368892. Retrieved 2012-04-17.
- ↑ 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
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(help) - ↑ 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.
- ↑ 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
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(help) - ↑ 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
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(help) - ↑ 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
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(help) - ↑ 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
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(help) - ↑ 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.