TOPICS
With advances in medical and obstetric care, more and more women with cardiac disease are able to become pregnant and deliver a viable fetus. This chapter is divided into four main sections corresponding to four types of cardiac or cardiopulmonary disease that women may present with during pregnancy: valvular disease, congenital heart disease, cardiomyopathy, and pulmonary arterial hypertension. Although the incidence of ischemic/coronary heart disease may be increasing, we will not discuss it in this chapter, because there is much less experience and literature to guide therapeutic strategies in this area.
VALVULAR DISEASE
The prevalence of valvular disease in pregnant women is low and has decreased with the decline of rheumatic fever in developed countries. Although rare, clinically significant valvular disease increases the risk of adverse maternal, fetal, and neonatal outcomes. Risk to the pregnant patient and developing fetus depends on the severity of the valvular lesion and underlying cardiac function. Ideally, patients with known valvular heart disease should be evaluated prior to conception; this should include a detailed history and physical examination, 12-lead electrocardiogram (ECG), and an echocardiogram with Doppler study. Pregnancy outcome and complications in patients with valvular disease can be closely correlated to prepregnancy New York Heart Association (NYHA) functional status and further to any deterioration of NYHA status during the pregnancy. In general, stenotic lesions are much more poorly tolerated during pregnancy than regurgitant lesions, because pregnancy usually requires, or at least causes, an increase in cardiac output, a process impaired by stenotic lesions and potentially causing decompensation.
Mitral Stenosis
ETIOLOGY/RISK FACTORS
Mitral stenosis (MS) is the most commonly encountered valvular lesion in pregnancy.1 Mitral stenosis usually occurs secondary to childhood rheumatic disease but may also be seen in association with congenital heart disease.
PATHOPHYSIOLOGY
The normal mitral valve area determined by echocardiography is 4 to 5 cm2. A valve area of 1.5 to 2 cm2 is classified as mild stenosis, 1 to 1.5 cm2 as moderate, and less than 1 cm2 as severe. Stenosis of the mitral valve impedes blood flow from the left atrium to the left ventricle, creating a pressure gradient across the valve. As left ventricular filling is restricted, longer diastolic filling time is necessary to maintain ventricular preload and cardiac output. Accordingly, the left atrium enlarges and pulmonary venous and arterial pressures increase, eventually leading to pulmonary edema and right-sided heart failure. Left atrial enlargement can result in atrial dysrhythmias, particularly fibrillation, which can lead to significant sudden hemodynamic decompensation from the loss of the contribution of atrial contraction to ventricular filling.
The pressure gradient across the stenotic mitral valve will generally increase with pregnancy-associated increases in heart rate and blood volume. Tachycardia reduces diastolic filling time, which limits left ventricular filling through the stenotic valve, thus decreasing stroke volume. Increases in blood volume may lead to pulmonary edema. Many patients with mitral stenosis become symptomatic for the first time during pregnancy, and a majority of women will demonstrate symptomatic deterioration, particularly those with high-order functional impairment as classified by NYHA class during pregnancy.2 Symptoms include dyspnea, chest pain, palpitations, orthopnea, pulmonary edema, and decreased exercise capacity.
Parturients with mild stenosis (NYHA 1 or 2) tend to tolerate pregnancy well and have favorable outcomes. Those with moderate to severe stenosis experience a much higher incidence of morbidity, including development of dysrhythmias, heart failure, and the need to start and/or adjust medications, as well as the need for hospitalization. Whereas morbidity may be high, maternal mortality is rare in contemporary practice. Fetal risk, including preterm delivery and intrauterine growth retardation, is increased with moderate and severe stenosis.2
MANAGEMENT AND ANESTHETIC CONSIDERATIONS
Patients with severe mitral stenosis who are contemplating pregnancy should be offered percutaneous mitral balloon valvuloplasty or mitral valve replacement before conceiving. Management of the patient with mitral stenosis who is already pregnant should focus on control of heart rate (usually ≤ 80 beats/min) and left atrial pressure. Heart rate reduction is typically achieved with β-adrenergic receptor antagonists and restriction of physical activity. Digoxin may be necessary in patients with atrial fibrillation. Atrial fibrillation should be treated promptly with rate control or electrical cardioversion if the patient is hemodynamically unstable. Diuretics are used to treat volume overload but should be used cautiously to avoid hypovolemia and reduction of uteroplacental perfusion.1
For patients with severe symptoms despite maximal medical therapy, balloon mitral valvuloplasty may be necessary even during pregnancy, and it has been successfully performed. The risk of radiation exposure to the fetus can be reduced by minimizing fluoroscopy time, ensuring adequate abdominal and pelvic shielding of the mother and delaying the procedure until after the first trimester. The most common time for a parturient to undergo valvuloplasty is 28 to 32 weeks’ gestation, both because this is the safest time for the fetus, with delivery a reasonable option if absolutely necessary, and because this is when many women with severe stenosis develop symptoms. Balloon valvuloplasty has been shown to be safe and effective for pregnant women and carries a decreased risk of fetal mortality compared to valve repair or replacement with cardiopulmonary bypass.3,4
Vaginal delivery is preferred over cesarean delivery, which is associated with more blood loss and larger fluid shifts, particularly during the postoperative period when vigilance may be decreased and fluid shifts may be exaggerated. Cesarean delivery is reserved for obstetric indications or in patients too hemodynamically unstable to tolerate labor. Outlet forceps or vacuum extraction may be used to shorten the second stage of labor and to help avoid sudden increases in venous return associated with bearing down.
Epidural anesthesia should be used for relief of labor pain using a dilute local anesthetic and opioid infusion. Small incremental boluses of 2% lidocaine or 3% 2-chloroprocaine may be necessary and desirable for planned instrumental delivery to control bearing-down reflex. Careful infusion of fluid and vasoconstrictors should be used to treat hypotension from sympathetic blockade.
In women with moderate to severe mitral stenosis and most other cardiovascular lesions that limit cardiac output and forward flow (eg, some congenital lesions, pulmonary hypertension, cardiomyopathy, aortic coarctation), a common strategy is to increase the “density” of epidural analgesia as the parturient approaches full dilation (5-10 mL 2% lidocaine, with or without additional fentanyl, occasionally 50-100 μg clonidine). This allows for the fetus to descend passively and deliver with outlet forceps while minimizing pushing (Valsalva) that can impair venous return. Reversible vasoconstriction with phenylephrine infusions, rather than fluid to treat hypotension from sympathetic blockade will prevent fluid overload, particularly after delivery of the infant. Epidural anesthesia (or combined spinal-epidural [CSE] anesthesia with a very low dose initial spinal) is also the preferred anesthetic for cesarean delivery, allowing for incremental titration of surgical blockade. Single-shot surgical spinal anesthesia should be avoided, because abrupt hypotension is poorly tolerated and may be more likely in these patients given their dependence on preload. If general anesthesia is necessary for cesarean delivery, a short-acting β-adrenergic receptor antagonist (esmolol) and/or opioid (remifentanil) are reasonable options during induction to limit sympathetic response to laryngoscopy and intubation.
The level of monitoring for labor or cesarean delivery depends on the severity of the lesion and symptoms. There should be a low threshold for continuous ECG monitoring in any laboring woman susceptible to dysrhythmias and a low threshold for arterial line placement during labor or cesarean delivery, because the benefits (even simply multiple blood draws) probably outweigh the risks in most women with significant mitral stenosis or other significant cardiac abnormalities. The indications, if any, for pulmonary artery (PA) catheters are unclear, as in most other clinical scenarios in obstetrics and elsewhere in medicine. If used at all, the PA catheter should probably be reserved for the most severely ill women undergoing cesarean delivery or those with severe pulmonary edema of unclear etiology. Many of these patents might benefit more from echocardiography rather than a PA catheter to clarify the pathophysiology leading to the hemodynamic abnormalities.
POSTPARTUM CARE
Patients with significant/symptomatic mitral stenosis are at risk for hemodynamic compromise and pulmonary edema due to peripartum blood loss and fluid shifts, irrespective of the mode of delivery. Mild to moderate pulmonary edema is often seen in the first few hours postpartum or postoperatively and usually responds to diuresis. Oxytocin, methylergonovine, and 15-methylprostaglandin F2α should be used with caution and with appreciation of their potential cardiovascular effects, because these agents can alter systemic and pulmonary vascular resistance. Patients with severe mitral stenosis should be monitored in an intensive care or similar high-dependency setting after delivery for 1 to 2 days, especially after cesarean delivery.
Aortic Stenosis
ETIOLOGY/RISK FACTORS
Aortic stenosis in pregnancy occurs most commonly secondary to congenitally stenotic aortic valves, including bicuspid aortic valve and supravalvular or subvalvular stenosis. Rheumatic aortic stenosis is much less common.
PATHOPHYSIOLOGY
Normal aortic valve area is 3 to 4 cm2. As valve area decreases, pressure in the left ventricle increases, and the left ventricle hypertrophies to maintain cardiac output. With disease progression, stroke volume becomes relatively fixed, and alterations in cardiac output become dependent on heart rate. Symptoms, including angina, dyspnea, and syncope, are related to the degree of stenosis and are usually not present until late in the course of the disease. Severe aortic stenosis, defined as a valve area less than 1 cm2, is rare in pregnancy.
Two decades ago, it was thought that the presence of aortic stenosis was a much more serious problem in pregnancy than mitral stenosis, but more recent reports suggest similar outcomes with either, dependent on severity. Patients with mild to moderate aortic stenosis tend to tolerate pregnancy reasonably well with close attention and follow-up. Patients with severe disease are often unable to accommodate the increase in blood volume and cardiac output associated with pregnancy. These patients are more likely to develop congestive heart failure and pulmonary edema. In addition, severe disease is associated with premature delivery and small-for-gestational age infants. Despite an increase in morbidity, mortality due to aortic stenosis in pregnancy is now rare.
MANAGEMENT AND ANESTHETIC CONSIDERATIONS
Ideally, patients with severe aortic stenosis should undergo balloon valvuloplasty or valve replacement before conceiving. Medical management of patients who become pregnant despite severe aortic disease includes diuretics and sometimes β-adrenergic blocking agents. Patients with severe symptoms despite optimal medical therapy may require termination of pregnancy or repair of the valve. As with mitral stenosis, valvuloplasty is associated with much lower risk to the fetus and is preferred over valve replacement.1
Goals in the management of the laboring patient with aortic stenosis include maintenance of normal heart rate and sinus rhythm, avoidance of hypotension and aortocaval compression, and maintenance of intravascular volume and venous return. Bradycardia may significantly decrease cardiac output in patients with aortic stenosis due to a fixed stroke volume. Tachycardia results in increased myocardial oxygen consumption and decreased diastolic perfusion time.
Vaginal delivery with an assisted second stage of labor as previously described with mitral stenosis is preferred over cesarean section. As with mitral stenosis, epidural anesthesia using a dilute local anesthetic and opioid infusion is recommended early for relief of labor pain. Cesarean delivery is reserved for obstetric indications or for patients too hemodynamically unstable to tolerate labor. Single-shot spinal anesthesia is contraindicated in women with severe aortic stenosis and relatively contraindicated in those with moderate disease. Many reports describe the successful use of incrementally dosed epidural or spinal catheters for cesarean delivery in patients with severe disease. Careful vasopressor (typically phenylephrine) infusion and intravenous fluids should be administered to avoid decreases in systemic vascular resistance (SVR) and preload. Local anesthetics without epinephrine are preferable because of the risk of severe tachycardia if injected intravascularly and mild tachycardia and hypotension when absorbed systemically. Many general anesthetic induction strategies have been suggested in the presence of aortic stenosis, typically involving moderate to high-dose rapid-acting opioids (fentanyl, alfentanil, remifentanil) to limit sympathetic activation and tachycardia with induction, intubation, incision, and delivery.
Blood pressure monitoring with an arterial line is recommended in patients with moderate to severe aortic stenosis. Use of pulmonary artery catheters is controversial and now rarely used; monitoring of central venous pressure (CVP) with a central line may be considered for monitoring volume status. The potential for hypovolemia is of greater concern than pulmonary edema in severe aortic stenosis, and CVP should be maintained at high-normal levels. Transesophageal echocardiography (TEE) should be considered in patients receiving general anesthesia.
POSTPARTUM CARE
Patients with aortic stenosis may be unable to accommodate the further increase in blood volume and cardiac output seen after delivery as the uterus involutes; this may lead to pulmonary edema requiring diuresis in the early postpartum period. Conversely, hypovolemia from postpartum hemorrhage is very poorly tolerated and should be managed aggressively; again, mild hypervolemia is probably preferable to hypovolemia. Patients with severe aortic stenosis or those with symptoms during the puerperium should be monitored in an intensive care setting after delivery for 1 to 2 days.
Mitral Regurgitation
ETIOLOGY/RISK FACTORS
Mitral regurgitation (MR) in women of reproductive age is usually due to myxomatous degeneration or rheumatic disease. In general, MR is well tolerated during pregnancy because the pregnancy-induced decrease in SVR tends to promote forward blood flow. Acute MR, usually caused by endocarditis or papillary muscle rupture, is much more problematic but is rarely seen in pregnancy.
PATHOPHYSIOLOGY
In acute MR, the left atrium experiences a sudden increase in volume load; this inhibits pulmonary venous return and leads to pulmonary congestion and edema. Cardiac output is decreased as a portion of the stroke volume flows backward through the incompetent mitral valve. If MR develops slowly over months to years (as is seen with myxomatous degeneration or rheumatic disease), the left atrium is able to gradually dilate to accommodate the increase in volume. Atrial dilation predisposes the patient to developing atrial fibrillation and thrombus formation. With disease progression, patients eventually develop left ventricular dysfunction and signs of congestive heart failure. Even if severe, MR is usually well tolerated unless the patient is symptomatic prior to pregnancy.
MANAGEMENT AND ANESTHETIC CONSIDERATIONS
Patients who are asymptomatic do not require medical therapy during pregnancy; those who develop heart failure usually benefit from diuretics and vasodilators (such as hydralazine). Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor antagonists (commonly used for afterload reduction) are contraindicated during pregnancy due to teratogenicity.
General goals in anesthetic management include the following: (1) prevent increases in SVR, (2) maintain sinus rhythm and avoid bradycardia, and (3) maintain venous return. Epidural analgesia helps minimize pain-related increases in SVR and is strongly recommended. Epidural anesthesia and spinal anesthesia for cesarean delivery are usually tolerated well because decreases in SVR favor forward blood flow. However, decreases in venous return should be treated with careful titration of intravenous fluids and vasopressor (phenylephrine) infusion. Invasive monitoring is usually reserved for patients with severe, symptomatic MR.
POSTPARTUM CARE
As noted above, most patients do not require much more than fairly routine care. Symptomatic patients, or those with known dysrhythmias, may need a more monitored setting for 1 to 2 days.
Aortic Insufficiency
ETIOLOGY/RISK FACTORS
Aortic insufficiency (AI) is often due to rheumatic disease and may occur with mitral valve disease. Other causes include congenital abnormalities of the aortic valve, endocarditis, and collagen vascular disease.
PATHOPHYSIOLOGY
AI leads to a state of volume overload and progressive left ventricular dilation and hypertrophy. Disease progression leads to left ventricular failure. Symptoms, such as dyspnea, orthopnea, palpitations, and angina, are usually not seen until disease is severe. Pregnancy and labor are typically well tolerated in patients with AI. The decrease in SVR with pregnancy promotes forward blood flow, and the concomitant increase in heart rate reduces time for regurgitation across the incompetent valve during diastole.
MANAGEMENT AND ANESTHETIC CONSIDERATIONS
Goals in the management of AI during labor and delivery primarily consist of maintaining a normal to slightly elevated heart rate and avoiding increases in SVR. Epidural analgesia is recommended during labor to avoid pain-induced increases in SVR. As with MR, epidural anesthesia and spinal anesthesia are usually tolerated well for cesarean delivery; decreases in SVR promote forward blood flow. However, abrupt hemodynamic changes associated with spinal anesthesia may be poorly tolerated in patients with severe disease, and epidural anesthesia is usually a better choice for these patients. Bradycardia (eg, from thoracic levels of regional anesthesia) may lead to an increase in regurgitant fraction; this may be problematic and should be treated promptly. Invasive monitoring is typically not needed.
POSTPARTUM CARE
Increases in blood volume and changes in SVR after delivery may lead to volume overload and left ventricular failure. Aggressive diuresis and afterload reduction (with nitrates and/or hydralazine) may be required.
Mitral Valve Prolapse
Mitral valve prolapse (MVP) is a variant of mitral valve disease, occurring commonly in women of childbearing age. MVP is usually asymptomatic, but some women may experience chest pain or palpitations and a small percentage of women will develop progressive mitral regurgitation. In the absence of coexisting cardiovascular disease, analgesic and anesthetic management rarely needs to be altered.
Pulmonary Stenosis
Pulmonary stenosis (PS) is one of the more common congenital cardiac defects and many patients remain asymptomatic well into adult life. Although severe PS can lead to right ventricular failure, it is very rare during pregnancy. It is important to understand that these patients do not behave like women with pulmonary vascular disease (pulmonary arterial hypertension), who are at grave risk during pregnancy and delivery. Isolated PS is usually well tolerated in pregnancy and labor, and cesarean delivery should be reserved for patients with obstetrical indications. Anesthetic and obstetric management in a stable patient with isolated PS does not usually need to be altered.
Prosthetic Valves
Management of pregnant women with prosthetic heart valves is extremely challenging. These women are at high risk for both fetal and maternal complications. These complications include thromboembolism, valve failure, endocarditis, and fetal hemorrhage and teratogenicity due to anticoagulation. The advantage of bioprosthetic valves in young women is the reduced risk of thromboembolism and need for anticoagulation during pregnancy. However, these valves are less durable than mechanical valves.5 Mechanical valves seldom require replacement but require lifelong anticoagulation, which can be difficult to maintain due to hypercoagulable state during pregnancy and may complicate hemorrhage of delivery.
Warfarin crosses the placenta and is associated with a higher risk of spontaneous abortion, stillbirth, and fetal hemorrhage. Although considered safe during the first 6 weeks of pregnancy and after the first trimester, a fetus exposed to warfarin during weeks 6 through 12 of gestation is at risk for warfarin embryopathy. Unfractionated heparin (UFH) does not cross the placenta and is generally considered safer for the fetus regarding risk of embryopathy and hemorrhage. However, the incidence of thromboembolic disease, including fatal valve thrombosis, is higher.6 Low-molecular-weight heparin (LMWH) also does not cross the placenta, and it has a longer half-life and more predictable dose-response pattern. Although LMWH at relatively high doses is now frequently being used in more women with prosthetic heart valves, treatment failures have been reported.
According to the American College of Chest Physicians, there is no single accepted treatment option for pregnant women with mechanical prosthetic valves, and the decision as to which regimen to use should be made after discussing risks and options with the patient. Possible regimens include (1) warfarin throughout pregnancy with LMWH or UFH substitution close to term, (2) either LMWH or UFH between 6 weeks and 12 weeks and close to term only and warfarin at other times, (3) aggressive dose-adjusted UFH throughout pregnancy, or (4) aggressive adjusted dose LMWH throughout pregnancy.7
Anticoagulation therapy may be discontinued prior to, or during labor, but occasionally therapy will need to be continued during this period and increases the risk of postpartum hemorrhage. The use of neuraxial anesthesia may be contraindicated based on the type and timing of anticoagulation doses, prolonged activated partial thromboplastin time (aPTT), elevated international normalized ratio (INR), or thrombocytopenia associated with heparin administration.
CONGENITAL HEART DISEASE
In the United States, congenital heart disease (CHD) is the most common form of heart disease in pregnant women. The majority of women with CHD now reach childbearing age because of advances in medical and surgical management, and many of these women will desire pregnancy. In general, asymptomatic patients with mild defects, or who underwent definitive repair as children, will tolerate pregnancy and labor well; these patients can usually be managed with routine or moderately advanced care. Patients with uncorrected or partially corrected anomalies, and those with residual defects, are less likely to tolerate the physiologic changes of pregnancy and can pose challenges to the obstetrician and anesthesiologist.
In patients who underwent corrective or palliative surgery as children, it is extremely important to understand the patient’s anatomy. A discussion with the patient’s cardiologist may be invaluable, and recent echocardiography or cardiac catheterization records should be reviewed. It is surprising (and concerning) how often the physicians caring for such patients do not fully understand the current cardiac anatomy/function of the patient (ie, “where does the blood flow actually go?”). Knowledge of complex anatomy, residual defects, and current functional status can guide decision making regarding anesthetic technique and invasive hemodynamic monitoring.
Although maternal mortality during pregnancy is rare generally, many patients with CHD will experience adverse events. Risk factors for complications during pregnancy include the following8,9:
• NYHA functional class greater than II
• Cyanosis
• Left heart obstruction
• Prior cardiac event or dysrhythmia
• Systemic ventricular dysfunction
Specific congenital cardiac abnormalities to be discussed in this section include: left-to-right shunts, tetralogy of Fallot, single ventricle with Fontan physiology, transposition of the great vessels, coarctation of the aorta, and Marfan syndrome. Bicuspid aortic valve and pulmonic stenosis have been discussed in the “valve disease” section.
Left-to-Right Shunts (Atrial Septal Defect, Ventricular Septal Defect, and Patent Ductus Arteriosus)
Left-to-right shunts include atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). Large defects are associated with congestive heart failure and are typically detected and repaired in childhood. Patients with small defects may be asymptomatic into adulthood and usually tolerate pregnancy well. ASDs account for about one-third of congenital heart defects in adults and occur more commonly in women.10 ASDs typically do not spontaneously close and may be associated with other cardiac abnormalities (mitral valve prolapse, MR, partial anomalous pulmonary venous return). VSDs are the most common congenital heart defect and occur with similar frequency in males and females. Up to 40% of VSDs close spontaneously by 2 years of age, and 90% close spontaneously by 10 years of age. PDA accounts for about 10% of congenital heart defects; lesions that persist past infancy are unlikely to close spontaneously.
PATHOPHYSIOLOGY
The overall physiologic effect of an ASD is shunting of blood from the left atrium to the right atrium regardless of anatomic location of the defect (ostium primum, ostium secundum, or sinus venosus). Most ASDs are initially asymptomatic and may not be detected for years. The size of the defect ultimately determines the hemodynamic consequences of this lesion. Patients with small defects (less than 0.5 cm in diameter) typically remain asymptomatic and do not require closure. Those with moderate to large (greater than 2 cm in diameter) defects may have severe hemodynamic consequences that may not be apparent until the third to fourth decade of life.10 With time, the increased blood flow to the right side of the heart leads to right atrial and ventricular dilation and pulmonary hypertension. Patients with an ASD are at risk of developing dysrhythmias and paradoxical embolism. Severe disease may lead to Eisenmenger syndrome, although the latter is rare and more likely to occur with VSD.
VSDs may occur in isolation or with other congenital heart defects, such as tetralogy of Fallot. VSDs may occur at various locations within the ventricular septum and are classified a: membranous, subpulmonic (outlet), atrioventricular canal (inlet), or muscular. As with ASD, the size of the defect determines the hemodynamic consequences of this lesion. Small defects lead to minimal increases in pulmonary blood flow. Large defects, however, lead to sizable increases in pulmonary blood flow and ultimately result in left ventricular volume overload and dilation. With time, pulmonary vascular resistance (PVR) increases. As PVR exceeds systemic resistance, reversal of flow across the defect and cyanosis results (Eisenmenger syndrome). Large VSDs rarely persist into adulthood without surgical intervention. Surgical closure typically is performed in childhood; this involves a right atrial or ventricular incision and can lead to significant conduction abnormalities.
PDA occurs when the ductus arteriosus fails to close shortly after birth. In the fetus, the ductus arteriosus connects the aorta and pulmonary artery allowing blood to bypass the lungs. Failure of the ductus to close after birth results in continued blood flow from the aorta to the pulmonary artery. As with a VSD, the resultant left-to-right shunt results in left ventricular volume overload and dilation. When uncorrected, pulmonary vascular changes may lead to reversal of flow and cyanosis. Infants with PDA are typically diagnosed with symptoms of heart failure or failure to thrive; rarely, uncorrected adults may present with heart failure or cyanosis.
MANAGEMENT AND ANESTHETIC CONSIDERATIONS
The balance between SVR and PVR determines the amount of shunt flow. Acute changes in either can alter amount or direction of flow. Early epidural anesthesia is recommended to avoid pain-induced increases in SVR during labor. An increase in SVR is likely to worsen left-to-right shunting and can lead to right ventricular failure. Large decreases in SVR should also be avoided, because direction of flow through the defect may reverse and create a right-to-left shunt and hypoxemia. Thus, incrementally dosed epidural anesthesia is favored over spinal anesthesia in patients with large defects requiring cesarean delivery. Increases in PVR should be avoided with the use of supplemental oxygen and avoidance of hypercarbia. Routine monitors include pulse oximetry and ECG. CVP and arterial line monitoring should be considered in symptomatic patients. PA catheters are typically not used and are often difficult or dangerous to position in the setting of left-to-right shunting.
Air embolism poses a particularly serious potential risk in these patients, and intravenous lines should be meticulously monitored and cleared of air. In addition, saline is recommended for loss of resistance during epidural placement, because paradoxical embolism can occur if air enters an epidural vein. Uterotonics that increase SVR, such as methylergonovine (Methergine), should be used cautiously or not at all.
Tetralogy of Fallot
Tetralogy of Fallot (TOF) accounts for 10% of CHD and is the most common cause of cyanotic CHD.11 TOF is typically diagnosed prenatally or during infancy with manifestation of cyanosis. The majority of patients who have undergone corrective repair are asymptomatic, and the long-term survival rate at 35 years following repair is approximately 85%.11
PATHOPHYSIOLOGY
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