Cardiac disease in pregnancy pathophysiology

Cardiac disease in pregnancy Microchapters
Home
Overview
Pathophysiology
Epidemiology and Demographics
Risk Factors
Diagnosis
History and Symptoms
Physical Examination
Electrocardiogram
Exercise Testing
Radiation Exposure
Chest X Ray
Echocardiography
MRI
CT
Catheterization: Pulmonary artery catheterization Cardiac catheterization Cardiac Ablation
Treatment
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: Arrhythmias Acute Myocardial Infarction Hypertension
Cardiac disease in pregnancy pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Cardiac disease in pregnancy pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Cardiac disease in pregnancy pathophysiology
CDC on Cardiac disease in pregnancy pathophysiology
Cardiac disease in pregnancy pathophysiology in the news
Blogs on Cardiac disease in pregnancy pathophysiology
Directions to Hospitals Treating Cardiac disease in pregnancy
Risk calculators and risk factors for Cardiac disease in pregnancy pathophysiology

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).

Increased estrogen levels

• Elevated estrogen levels may increase myocardial contractility.

Increased renin and aldosterone levels

• Peripheral vasodilation subsequently causes renal vasodilation and activation of the renin-angiotensin-aldosterone system, 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%.
• Higher increase in blood volume may be prevalent among multigravidas.
• An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.

III. Cardiac output

• There is a higher volume of more dilute blood to circulate
• 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 5^th week of gestation and steadily increases up to 24^th week of gestation following which it plateaus.

• 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.

• 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. 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.

• 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

• Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 100 mmHg below baseline) and returns toward pre-gestational levels before term.

• 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. This is mediated by gestational hormone activity, increased circulating levels of prostaglandins and atrial natriuretic peptides, as well as endothelial nitric oxide.

• 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.

VII. Other changes in pregnancy

• Flared ribs.
• Breast hypertropy which may impede effective resuscitation.

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.ref name="pmid290123">Kjeldsen J (1979). "Hemodynamic investigations during labour and delivery". Acta Obstet Gynecol Scand Suppl. 89: 1–252. PMID 290123. </ref>

• 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

Template:WikiDoc Sources