Cardiology and Cardiothoracic Surgery/Pregnancy and Cardiovascular Disease
- 1 Introduction: The Importance of Maternal Health and Fetal Vulnerability
- 2 Physiologic Cardiovascular and Respiratory Changes During Gravity and Parturition
- 3 Clinical Cardiovascular and Respiratory Manifestations of Normal Pregnancy
- 4 Cardiovascular and Respiratory Disease Processes During Pregnancy
- 4.1 General Clinical Presentation
- 4.2 Pregnancy in the Context of Existing Congenital and/or Valvular Heart Disease
- 4.3 Infective Endocarditis
- 4.4 Cardiac Arrest and Hemodynamic Collapse
- 4.5 Hematological Disease
- 5 References
Introduction: The Importance of Maternal Health and Fetal Vulnerability
Fetal health parallels maternal health during gestation. Normal fetal development highly depends on the ability of the maternal cardiovascular system to provide sufficient oxygen and nutrients. If the mother has impaired cardiac function or significant vascular redistribution to areas other than the utero-placento-fetal complex, the supply of oxygen and nutrients to the fetus, as well as the capacity for waste and heat removal will be compromised. Furthermore, treatment and diagnostic workup of maternal heart disease may also jeopardize fetal development or viability.
|Table 1. Cardiovascular Abnormalities Placing a Mother and Infant at Extremely High Risk|
|Advise avoidance or interruption of pregnancy|
Congestive heart failure secondary to dilated cardiomyopathy
Marfan syndrome with a dilated aortic root
Cyanotic congenital heart disease
|Pregnancy Counseling and Close Clinical Follow-Up Required|
Coarctation of the aorta
Asymptomatic dilated cardiomyopathy
|Source: Hurst's The Heart 12th Ed.|
Physiologic Cardiovascular and Respiratory Changes During Gravity and Parturition
Recall from the "Cardiac Physiology" section of this WikiBook that the primary determinant of cardiac output is the oxygen requirement of peripheral tissues: during pregnancy the maternal VO2 increases to levels greater than 30% of the values before pregnancy. Stroke volume and heart rate therefore increase throughout pregnancy, elevating the cardiac output by more than 40%; cardiac output reaches its zenith at approximately the 20th week of gestation. This may be compounded by the concomitant fall in total peripheral resistance which also peaks at 20 weeks of gestation (maintenance of stable mean arterial pressure would require the increase in cardiac output; see the "Cardiac Physiology" section.) Left ventricular preload, however, is compromised later in pregnancy due to fetal compression of the inferior vena cava, reducing venous return from the lower extremities. Positional changes, especially the supine position, can result in supine hypotensive syndrome of pregnancy, a condition which can be relieved by placement of a thin pillow underneath the right buttocks whilst the mother is in the supine position.
The mechanism of increased cardiac output during pregnancy may be caused by fluid overload (over 5 L of total body water gained.) This increase may be partially mediated by sodium retention, which begins as early as 6 weeks post-conception. Marked increases in activity of the renin-angiotensin-aldosterone system result in sodium retention. A consequence of this increase in fluid volume (most is extracellular, e.g. plasma volume) is a decrease in hematocrit to as low as 30%. Increases in cardiac stroke volume (although without change in ejection fraction) may be an intrinsic cardiac adaptation to pregnancy which increases cardiac output: this is likely due to a primary cardiac remodeling process. The maternal vasculature contributes to increased cardiac output via increased venous capacitance (we will discuss the contribution of this change to maternal thromboembolic risk,) tone, and arterial compliance4.
During labor, cardiac output increases with each subsequent uterine contraction due to a muscle pump effect on venous return (see "Cardiac Physiology" section in this WikiBook,) and an increase in heart rate. Note that the administration of anaesthesia (epidural or general) will reduce the cardiac output. Postpartum, the cardiac output reaches approximately 10L/min1. This level of output reverts to nonpregnant levels within weeks postpartum.
Total Peripheral Resistance and Blood Flow Redistribution
The total peripheral resistance in the pregnant woman decreases markedly. This may be the result of progesterone, increased diversion of blood from the arterial to the venous system as a result of the placental "arterio-venous shunt," and/or a decreased vascular responsiveness to vasopressors such as angiogensin II. Failure of the pregnant female's vascular system to decrease responsiveness to systemic vasopressors leads to pre-eclampsia.
The most obvious redistribution of blood flow that occurs with pregnancy is the increase in vascular supply to the pregnant uterus (increase from 100mL/min to approximately 1200mL/min at full term.2, 3)
The venous pressure in the pregnant female increases, especially in the lower limbs. This may manifest as varicose veins, hemorrhoids, and thromboembolic events. The mechanism of increased lower limb venous pressure is likely due to aorto-caval compression and the placental arterio-venous shunt.
During pregnancy, blood volume increases 40-50%. This increase is comprised of a 40-50% increase in plasma volume and a 30-40% increase in red blood cell (RBC) volume. The increase in RBC volume is not as large in magnitude as the increase in plasma volume. This may be due to the high concentrations of sex steroids and atrial natriuretic peptide, and constant activation of the renin-angiotensin-aldosterone system.
White blood cell (WBC) count increases, with normal values reaching as high as 20,000/mL.
|In evaluating inflammatory/infectious disease with the white blood cell count, differential analysis is more valuable than total WBC count.|
Estrogen is known to stimulate hepatic protein synthesis. This results in greater levels of circulating factors II, VII, IX, X, and proteins C & S.
During pregnancy, lung capacities do not change with the exception of residual volume decreasing approximately 20%. Tidal volume increases in parallel with minute ventilation, which is greater than non-pregnant levels by 40-50% (arterial blood gas analysis does in fact demonstrate compensated respiratory alkalosis).
Clinical Cardiovascular and Respiratory Manifestations of Normal Pregnancy
Mothers may present with symptoms of dyspnea and fatigue.
Signs such as the third heart sound (significant for a volume overloaded left ventricle best heard during early diastole,) peripheral edema (recall that the majority of fluid overload is extracellular.) Normal auscultatory signs during pregnancy may include internal mammary souffles and venous hums (see the physical examination section of this WikiBook.)
Physiological Anemia of Pregnancy
Cardiovascular and Respiratory Disease Processes During Pregnancy
General Clinical Presentation
Patients presenting with dyspnea interfering with activities of daily living (or at rest,) orthopnea, hemoptysis, exertional syncope and/or angina pectoris, central or peripheral cyanosis, systolic murmurs greater than or equal to a grade 3 murmur (see the physical examination section of this WikiBook,) or any diastolic murmur should be thoroughly evaluated for cardiac pathology.
Pregnancy in the Context of Existing Congenital and/or Valvular Heart Disease
Existing, albeit previously undiagnosed maternal cardiac disease may be unmasked by the gravid state. Certain time points during pregnancy present the greatest probability for cardiovascular decompensation.
- The zenith in blood volume increase with pregnancy at the end of the second trimester.
- During labor due to increased activity.
- Relief of vena caval compression post delivery + placental auto-transfusion
- Post-partum fluid shifts.
The pathophysiology of valvular disease exacerbation during pregnancy is the result of changes in systemic vascular resistance in the maternal vasculature. As previously discussed, systemic vascular resistance decreases dramatically in the pregnant female, with the end target of increasing cardiac output and oxygen delivery to a greater number of tissues. It is therefore logical that
- In stenotic valvular disease, symptoms are exacerbated. Furthermore, the greater blood volume compounded with stenotic disease increases the probability of morbidity.
- In regurgitant valvular disease,the decrease in systemic vascular resistance favours blood flow into the systemic vasculature, therefore reducing regurgitant valvular symptomatology.
|Management of labour in the context of maternal valvular disease|
|Minimize cardiac preload, careful to avoid low cardiac output syndrome|
|Careful management of heart rhythm. This involves aggressive pain control to prevent tachycardia and maximize diastolic filling time.|
|Careful education with breathing techniques (no valsalva)|
|Assist in the second stage of labour|
Congenital Heart Disease
Females with repaired congenital heart disease fare better than those with unrepaired adult congenital heart disease. Offspring of mothers with congenital heart disease have an increased risk of congenital heart lesions, intrauterine growth retardation, in-utero death, and prematurity. Therefore, all women with congenital heart disease should be offered a prenatal echocardiogram.
Several risk factors for maternal and fetal complications have been elucidated:
- Right to left shunting lesion
- NYHA symptom class III-IV
- Maternal cyanosis
- Maternal erythrocytosis
- Stenotic congenital heart lesions
The ACC/AHA guidelines on the prevention of infective endocarditis indicate that antibiotic prophylaxis is not required for standard vaginal or cesarian sectional deliveries. Antibiotic prophylaxis is suggested when the mother is harboring an active infection in the context of a "high risk" valve (prostetic, previous endocarditis, complex congenital heart disease or valvular structural abnormalities). It is suggested that any antibiotic prophylaxis delivered cover enterococcus sp.
Cardiac Arrest and Hemodynamic Collapse
Cardiopulmonary resuscitation is an important link in the chain of survival. In a pregnant woman undergoing an episode of cardiovascular collapse for whom cardiopulmonary resuscitation is indicated, the uterus should be manually held to the left side to improve venous return during chest compressions.
Cesarian section should be attempted to improve maternal and fetal outcomes following 5 minutes of unresponsive cardiopulmonary resuscitation.
Cardioversion may be attempted (DC) following disconnection of fetal monitoring devices.
As opposed to the physiological anemia of pregnancy, medically significant anemias of iron and folate deficiency may develop.
Risk factors. In addition to the standard risk factors for venous thromboembolism (VTE), pregnancy bears a 6-fold fisk in the incidence of VTE. Specific modifiers of this risk include preeclampsia, peripartum hemorrhage, instrumental or cesarian delivery, and multiparity.
Pathophysiology and Clincal Features. Most (90%) of VTEs occur on the left side, and in the pelvic veins, during pregnancy. Ovarian vein thrombosis is not uncommon.
Management. The mainstay of management for VTE during pregnancy is low molecular weight heparin or intravenous heparin administration for a minimum of six months. Many caretakers use unfractionated heparin due to familiarity and low cost. However, this therapy carries a greater risk of heparin induced thrombocytopenia (~3%) and iatrogenic hemorrhage compared to low molecular weight heparins. The latter, however are more expensive, cause fewer cases of osteopenia compared to UFH. Furthermore, the risk of heparin induced thrombocytopenia and iatrogenic hemorrhage are <1% in patients treated with low molecular weight heparins. The heparin level is the best monitoring measure for unfractionated heparin; for low molecular weight heparins, anti-Xa levels should be monitored. Low molecular weight heparins should be discontinued within 12 hours of potential epidural anaesthetic delivery. Therapy with unfractionated heparin is a better option for women who request regional anaesthetic administration, which is contitional on a normal prothrombin time. Warfarin therapy should be avoided at all costs.
Folate Deficiency Anemia
Epidemiology. The incidence of folate deficiency is geographically variable and considerably less than the incidence of iron deficiency anemia; it is typically responsible for <25% of clinically significant anemias in pregnancy.
Risk Factors, Etiology, Pathophysiology, and Complications. Folate deficiency anemias occur most often with iron deficiency anemias. Decreased intake of folic acid, increased requirements (multiple gestation), chronic hemolytic anemias, malabsorption, and drug use (e.g. methotrexate) can induce folate deficiency anemias.
Folic acid is necessary for neural tube closure. Complications of folate deficiency anemia in pregnancy therefore include neural tube defects, placental abruption, and spontaneous abortion6.
Clinical Features. Always be alert for the potential consumption of alcohol in pregnancy: there is no safe level of alcohol consumption in pregnant women. Patients may complain of anorexia, nausea, vomiting, abdominal pain, and postprandial diarrhea. Dorsal digital, palmar, and solar pigmentation may present as a physical finding of folate deficiency. Aseptic temperature increases are also common, and typically resolve within 1-3 days.
Diagnosis. Routine hematology (complete blood count), serum folate, serum cobalamin, and a blood smear should be performed.
- Rule out cobalamin deficiency because treatment of folate deficiency will not be effective unless cobalamin deficiency is addressed.
- Megaloblastic anemia will be seen on blood smear. However, be cognizant of the fact that cobalamin and folate deficiencies may not be differentiated by megaloblastic erythrocytes found on smear.
Management. Preconception supplementation is recommended for 1-3 months with folic acid 0.4-1mg qd PO. This regiment should be continue throughout the first trimester.
Iron Deficiency Anemia
Epidemiology. Approximately 80% of nonphysiologic anemia during pregnancy is iron deficiency related.
Risk Factors, Etiology, and Pathophysiology. The iron requirements during pregnancy are significantly increased. Placental and fetal growth account for an increased requirement of 500mg; the 30-40% increase in erythrocyte volume accounts for another 500mg; finally, iron losses create an additional requirement of approximately 200g. Beyond this increased requirement from growth, maternal dietary insufficiency, malabsorption, or blood losses may induce a clinical iron deficiency anemia.
Clinical Presentation and Potential Complications. The presenting symptoms for iron deficiency anemia of pregnancy are the same as iron deficiency anemia in the non-pregnant state. Patients may be fatigued, pale, dyspneic, and tachycardic; they may also experience palpitations.
Anemia may induce angina and congestive heart failure in the mother, along with impaired response to injury and infection. The risk of preterm labour is increased, and the fetus may experience intrauterine growth retardation, hydrops fetalis, and low birth weight due to hypoxia.
Diagnosis. Diagnosis is done through analyses of serum iron, ferritin, and a blood smear. Assessing total iron binding capacity ratios is not valuable in pregnant patients because this number is increased due to physiological processes. Furthermore, investigation for a gastrointestinal source of bleeding should be done.
- Serum ferritin <45μg/dL is diagnostic of iron deficiency with a likelihood ratio >35. A serum ferrigin <100μg/dL suggests that further investigation of this patient's anemia should be done.
- Peripheral blood smear will show a hypochromic, microcytic anemia with an increased red-cell distribution width (anisocytosis).
Management. The essential philosophy of management of iron deficiency anemia in pregnancy is adequate iron intake and monitoring for potential blood loss. Every pregnant woman should be receiving (prophylactically)
- Ferrous sulfate 150mg and ferrous gluconate 300mg qd,
- Or ferrous iron 30mg qd.
If the woman is currently anemic, ferrous sulfate 1g qd should be prescribed.
1. Robson, S., Dunop, W., Boys, R., Hunter, S. Cardiac output during labor. BMJ. 1987;295:1169-1172.
2. Thoresen, M., Wesche, J., Doppler measurements of changes in human mammary and uterine blood flow during pregnancy and lactation. Acta Obstet Gynecol Scand. 1988;67:741-745
3. Thaler, I., Manor, D., Itskovitz, J., et al. Changes in uterine blood flow during human pregnancy. Am J Obstet Gynecol.1990;162:121-125.
4. Manor, A., Alpan, G., Specificity of creatine kinase MB isozyme for myocardial injury. Clin Chem. 1978;24:2206.
5. Guyatt, GH., Patterson, C., Ali, M., Singer, J., Levine, M., Turpie, I., Meyer, R.. Diagnosis of iron-deficiency anemia in the elderly. Am J Med. 1990; 88: 205-9.
6. Casey GJ, Phuc TQ, Macgregor L, et al. A free weekly iron-folic acid supplementation and regular deworming program is associated with improved hemoglobin and iron status indicators in Vietnamese women. BMC Public Health. Jul 24 2009;9:261