Critical Care Obstetrics part 66 potx

639 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 45 Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease Shobana Chandrasekhar & Maya S. Suresh Department of Anesthesiology, Baylor College of Medicine, Houston, TX, USA Introduction and e pidemiology Cardiac disease, a leading cause of non - obstetric mortality in pregnancy, occurs in 1 – 3% of pregnancies and accounts for 10 – 15% of maternal mortality [1,2] . Even though the incidence of rheumatic heart disease is declining in developing countries, it still accounts for a majority of mortality in obstetric cases. The incidence of congenital heart disease in pregnant women is increasing in developed countries because of advances in the diagnosis and treatment of congenital heart defects in childhood. Cardiovascular maternal morbidity and mortality during preg- nancy correlate strongly with maternal functional status [1 – 3] . Women with NYHA class I and II (no or minor symptoms) toler- ate pregnancy without major deterioration, whereas those with NYHA class III and IV during pregnancy are at risk for major morbidity resulting in mortality upwards of 50% [4] . Because of the physiologic changes in pregnancy, further deterioration in functional status in the range of 15 – 55% of symptomatic patients can be expected during pregnancy [2] . When a pregnant woman presents with onset of cardiorespiratory deterioration the main differential diagnoses include thromboembolism, cardiomyopa- thy, dysrhythmia, pre - eclampsia, hemorrhage, and sepsis. A less commonly considered differential is underlying heart disease, and this is something that should be excluded in all of these cases. Therefore the diagnosis of cardiac disease by history, physical exam, ECG, CXR, and echocardiogram is essential to obstetric and anesthetic management. In the United Kingdom Report of the Confi dential Enquiries into Maternal and Child Health (CEMACH; formerly Confi dential Enquiries into Maternal Deaths (CEMD)), cardiac disease was the second commonest cause of maternal mortality. Signifi cant and increasing numbers of deaths occur in women without previously known disease, either in those with risk factors or in those who develop conditions in the absence of risk factors [5] . Labor analgesic techniques and anesthetic management in the critically ill parturient are determined largely by the nature of the presenting illness. Issues dictating choice of anesthetic technique are the patient ’ s ability to maintain her airway, coagulation status, intravascular volume, and requirements for ventilatory support and intensive care. Fetal well - being is an important issue in the antepartum period. Uteroplacental blood fl ow should be main- tained and hypotension should be avoided. Maternal survival clearly takes priority. Anesthesia itself is associated with known hazards, and the risks of each technique must be balanced against the possible benefi ts to both mother and baby in the context of the presenting illness. Physiologic c hanges of p regnancy r elevant to the c ardiorespiratory s ystem Pregnancy - induced alterations of the cardiovascular and respira- tory systems are the result of both anatomic and functional changes. The cardiovascular changes that occur during pregnancy improve oxygenation and fl ow of nutrition to the fetus. Cardiac output increases up to 50% in the fi rst half of pregnancy due to increased stroke volume, and later in the pregnancy due to increased heart rate. Hypotension and decreased cardiac output can occur due to inferior vena cava compression by the enlarged uterus. Peripheral vascular resistance is decreased due to smooth muscle relaxation caused by increased circulating progesterone levels. Systolic murmurs are a normal occurrence due to increased blood fl ow. However, a diastolic murmur is not a normal fi nding during pregnancy. During labor, cardiac output increases an additional 45% above that found in late pregnancy. Mean arterial pressure increases 10 mmHg during each contraction. Immediately after delivery, cardiac output increases by as much as 80% due to autotransfusion. The autotransfusion results from an increase in preload secondary to release of vena caval obstruction by the enlarged uterus, and from autotransfusion of the blood during Chapter 45 640 Congenital h eart d isease ( CHD ) Congenital heart diseases with small left to right intracardiac shunts account for 60 – 80% of cardiac disease in pregnant patients in the United States [2] . Women with signifi cant uncorrected congenital heart lesions, signifi cantly dilated aortic root in Marfan ’ s disease, congestive heart failure (NYHA class III and IV) despite optimized medical treatment and palliative surgery, and those with increased pulmonary vascular resistance, are at increased risk for major morbidity and mortality and should be advised against pregnancy (Table 45.2 ) [6] . The risks to mother and fetus of congenital heart disease during pregnancy are shown in Table 45.3 . The two most important predictors of fetal mor- contraction and involution of the uterus. Simultaneously, sys- temic vascular resistance increases dramatically in the immediate postpartum period (Table 45.1 & Figure 45.1 ). Pulmonary anatomic and physiologic changes during preg- nancy place the pregnant patient at increased risk for hypoxemia. The anatomic changes occur to compensate for an enlarging uterus. The increased subcostal angle increases the chest circum- ference. There is increased diaphragmatic excursion and the dia- phragm is elevated 4 cm in late pregnancy. Pulmonary function is also altered in pregnancy. A 30% increase in tidal volume occurs, with a corresponding 30 – 40% increase in minute ventila- tion. The expiratory reserve volume and functional residual capacity decrease by 20%. Respiratory rate, vital capacity, and inspiratory reserve volume do not change. P a O 2 is increased while P a CO 2 and HCO 3 are decreased. PaCO 2 decreases to 27 – 32 mmHg in the second half of pregnancy as a result of the increased minute ventilation. Oxygen consumption increases progressively during pregnancy and is maximum during the stress of labor. Figure 45.1 Cardiac output increases during labor. Table 45.1 Comparison of hemodynamic parameters in pregnant and non - pregnant patients. Non - pregnant Pregnant Central venous pressure (mmHg) 1 – 10 Unchanged Pulmonary artery pressure (mean) (mmHg) 9 – 16 Unchanged Pulmonary capillary wedge pressure (mmHg) 3 – 10 Unchanged Cardiac output (L/min) 4 – 7 ↑ 30 – 45% Systemic vascular resistance (dyne - sec cm − 5 ) 770 – 1500 ↓ 25% Pulmonary vascular resistance (dyne - sec cm − 5 ) 20 – 120 ↓ 25% Heart rate 65 – 72/min ↑ 10 – 20% Table 45.2 Absolute contraindications to pregnancy. Severe primary and secondary pulmonary hypertension Marfan ’ s syndrome with aortopathy and ascending aorta diameter > 40 mmHg Eisenmenger syndrome (cyanosis due to R to L intracardiac shunt) Table 45.3 Risks of congenital heart disease to mother and fetus during pregnancy. Risk to the mother Risk to the fetus Pulmonary edema Intrauterine growth restriction Arrhythmias Prematurity Heart failure Congenital heart disease (inherited) Hemorrhage from anticoagulation Teratogenic effect of drugs administered to the mother Death Intracranial hemorrhage Fetal loss Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease 641 bidity in these parturients are the presence of congestive heart failure and persistent cyanosis in the mother. Left to r ight s hunts Pathophysiology The hemodynamic alterations depend on the size of the defect. Patients with atrial shunts, such as atrial septal defect (ASD) are at low risk of hemodynamic deterioration or onset of arrhyth- mias. In the rare case of a marked clinical deterioration, catheter - based closing of the shunt is the fi rst - line treatment. Ventricular septal defect (VSD), and persistent patent ductus arteriosus (PDA) are also usually well tolerated during pregnancy although arrhythmias should be anticipated in these conditions. The hemodynamic alterations, complications and prognosis are summarized in Table 45.4 . Anesthetic m anagement c onsiderations in l eft to r ight i ntracardiac s hunts With small shunts right ventricular (RV) and pulmonary artery (PA) pressures are unchanged and there is not much change in pulmonary blood fl ow. Risk of bacterial endocarditis is increased. With larger shunts, there is progressively increased pulmonary Table 45.4 Left to right shunts. Size of defect Hemodynamic alterations Pregnancy complications Prognosis Small RV and PA are unchanged Increased risk of endocarditis Usually uncomplicated course Moderate RV and PA pressures are increased but remain below systemic pressures Increased pulmonary blood fl ow Pulmonary vascular disease unlikely LV volume overload and failure CHF and arrhythmias are likely High chance of cardiac decompensation during pregnancy Large RV and LV pressures equalize Eisenmenger ’ s syndrome Pulmonary vascular disease likely Heart failure, fetal hypoxemia Mortality can reach as high as 50% Pregnancy is contraindicated RV, right ventricle; PA, pulmonary artery; LV, left ventricle; CHF, congestive heart failure. Table 45.5 Antibiotic Prophylaxis for Genitourinary/Gastrointestinal Procedures. Standard Regimen Ampicillin, gentamicin, and amoxicillin Intravenous or intramuscular administration of ampicillin, 2 g plus gentamicin 1.5 mg/kg (not to exceed 80 mg), 30 min before procedure; followed by amoxicillin, 1.5 g orally 6 h after initial dose; alternatively the parenteral regimen may be repeated once 8 h after initial dose Ampicillin/Amoxicillin/Penicillin Allergic Patient Region Vancomycin and gentamicin Intravenous administration of vancomycin, 1 g over 1 hr plus intravenous or intramuscular administration of gentamicin 1.5 mg/kg (not to exceed 80 mg), 1 hr before procedure; may be repeated once 8 hr after initial dose Alternative Low - risk Patient Regimen Amoxicillin 3 g orally 1 hr before procedure; then 1.5 g 6 hr after initial dose blood fl ow with resultant increase in RV and PA pressures. Ultimately RV and left ventricular (LV) pressures equalize, leading to pulmonary vasoconstriction and irreversible vascular changes resulting in pulmonary hypertension and Eisenmenger ’ s syndrome. One of the primary goals in the anesthetic management of these women is to avoid pain thus mitigating the hemodynamic increases in pulmonary and systemic vascular resistance. Avoidance of sudden decrease in systemic vascular resistance is also of paramount importance because it increases the L to R shunt thus increasing the incidence of hypoxemia. Because of hemodynamic responses secondary to increased stress hormones and catecholamines seen during labor and deliv- ery, parturients with NYHA class III and IV may require invasive monitoring to note the beat to beat changes. In such cases con- tinuous arterial blood pressure monitoring with an arterial line, continuous ECG and central venous pressure (CVP) monitoring may be useful during both labor and cesarean section. Antibiotic prophylaxis for prevention of bacterial endocarditis, particularly in patients with ASD for uncomplicated delivery, is not advocated by the American Heart Association [4] . (See Table 45.5 .) Chapter 45 642 Anesthetic m anagement Goals of anesthetic management include: • avoiding decreases in systemic vascular resistance, thus mini- mizing the magnitude of the right to left shunt • maintaining adequate intravascular volume and venous return. Amongst the neuraxial anesthesia labor analgesic techniques the combined spinal/epidural (CSE) technique is most preferable. Early establishment of CSE in labor with the use of intrathecal narcotics followed by epidural infusion of ultra low concentra- tions of local anesthetics can provide excellent analgesia without decreasing the systemic vascular resistance. Phenylephrine is the drug of choice for managing hypotension in these patients. The advantage of a CSE technique for labor analgesia is the ability to provide surgical anesthesia if a cesarean section is needed. In the event that general anesthesia becomes necessary (due to lack of time to establish a regional block or if there are contraindications to regional anesthesia), it is important to avoid decreases in SVR with intravenous induction and inhalational agents, and increases in pulmonary vascular pressures. Following acid aspiration pro- phylaxis, controlled induction with ketamine, or short - acting narcotics such as remifental is preferable in order to prevent large hemodynamic perturbations, and to minimize adverse effects on the fetus. Consultation with the neonatologist and plans for neonatal resuscitation are also important. Eisenmenger ’ s s yndrome Pathophysiology Eisenmenger ’ s complex is described as pulmonary hypertension with a reversible or bidirectional shunt through a large VSD. The systemic and pulmonary circulations are in open communica- tion. When the pulmonary vascular resistance rises or systemic vascular resistance falls, severe hypoxemia ensues due to blood bypassing the lungs. When fl ow through the pulmonary vascular bed is increased, as in patients with congenital intracardiac (left to right) shunts, the vasculature is initially able to compensate for the increased volume. However, over a prolonged period, there is thickening of the vessel walls, resulting in an increase in pulmonary vascular resistance. Eventually, as a result of the increased pulmonary vascular resistance, right - sided cardiac pressures become elevated leading to reversal in the intracardiac shunt. The conversion or reversal to a right to left shunt with longstanding atrial or ven- tricular septal defect or a patent ductus arteriosus results in Eisenmenger ’ s syndrome. A retrospective analysis (1978 – 1996) [9] , showed an increase in pulmonary artery pressure and pul- monary vascular resistance during gestation in some patients with moderate pulmonary hypertension at the beginning of the pregnancy. The maternal death rate was 36% in a series of 73 patients with Eisenmenger syndrome. Three women died during pregnancy and 23 died at the time of delivery or within 1 month postpartum. Mortality was strongly associated with late diagnosis and late hospital admission, while severity of pulmonary hyper- tension was also found to be a contributing factor. Neither the In parturients with left to right shunts, the primary consider- ations are alleviation of pain during labor and therefore the use of a combined spinal/epidural (CSE) technique in early labor is particularly advantageous. Intrathecal lipophilic narcotics such as fentanyl can be used to alleviate pain without causing any changes in the hemodynamics (specifi cally the SVR). Furthermore, this can be followed with ultra - low dose epidural infusion which pro- vides continuous labor analgesia without any adverse effects on the hemodynamics or progress of labor [7] . The technique of loss of resistance to saline should be used during epidural placement in order to prevent air entry into an epidural vein which can lead to paradoxical air embolism [8] . In addition, in those patients with potential intracardiac shunts air fi lters should be used on all venous and arterial lines. Decompensation in the cardiac status is most likely immedi- ately after delivery due to the autotransfusion that occurs from the uteroplacental unit. Close monitoring of the hemodynamics are important. Prevention of the Vasalva maneuver in the second stage is important and decreasing the duration of the second stage of labor by operative vaginal delivery and provision of adequate analgesia is important. Supplemental oxygen is helpful to increase oxygen reserves and to enhance oxygen delivery to both mother and fetus (Table 45.6 ). Cyanotic h eart d isease Tetralogy of Fallot Pathophysiology Tetralogy of Fallot (TOF) is the commonest congenital heart disease associated with the following conditions: right to left shunt, VSD, right ventricular hypertrophy, pulmonary stenosis with right ventricular outfl ow tract obstruction, and an overrid- ing aorta. Most women have correction in childhood but some may present with residual defects. The degree of intracar- diac shunting, severity of right ventricular outfl ow obstruction, and right ventricular function are primary determinants of outcome. Table 45.6 Anesthetic management principles in left to right intracardiac shunts. Management principles Rationale Supplemental oxygen Increases oxygen reserves, especially in second stage of labor Loss of resistance to saline technique for epidural anesthesia Decreases risk of venous air embolism and paradoxic air embolism Early combined spinal epidural technique with intrathecal narcotics and ultra - low concentration of epidural infusion analgesia for good pain control throughout labor Avoid increases in maternal catecholamines Cut short second stage of labor with forceps/vacuum assist Avoids Valsalva and hemodynamic changes associated with pushing Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease 643 48 hours after delivery due to the increased risk of thromboem- bolism in these patients. Stenotic l esions Pathophysiology Congenital a ortic s tenosis Congenital aortic stenosis is usually associated with a bicuspid aortic valve [11] . Patients with aortic stenotic lesions, functional class NYHA > 2, cyanosis, severe left ventricular outfl ow obstruc- tion (aortic valve area < 1.5 cm 2 ) resulting in decreased cardiac output and uteroplacental blood fl ow, or impaired left ventricu- lar function are considered at high risk for morbidity and mortal- ity during pregnancy. Severe aortic stenosis (a peak transvalvular gradient greater than 50 mmHg) must be corrected before pregnancy. Severe aortic stenosis carries a high risk of mortality during pregnancy. Siu et al. reported a maternal mortality rate of 11% and a peri- natal mortality rate of 4% [3] . A Canadian study described 49 cases with a 10% risk of complications in patients with severe stenosis [12] . Conservative medical management is acceptable for mild to moderate aortic stenosis. However, once surgical valve replace- ment for severe aortic stenosis is required during pregnancy, there is an increased (30%) fetal mortality [13] . Intrapartum balloon valvuloplasty has been reported, but it is not widely available and needs to be done in centers with the necessary experience [14] . Pulmonary s tenosis Pulmonic valve stenosis is rare as an isolated condition. Untreated severe/symptomatic pulmonary stenosis causes arrhythmias and right heart failure leading to high maternal and fetal morbidity and mortality. The right ventricular failure is a result of an inabil- ity to compensate for the increases in heart rate, right ventricular preload, and oxygen delivery and consumption associated with pregnancy. Management of isolated pulmonic stenosis by percutaneous balloon valvuloplasty has been shown to improve the outcome of pregnancy and has been used in some institutions with success [14;15] . Beta - blockade and diuretics, as well as close hemody- namic monitoring, should be continued throughout the pregnancy. Pain control during labor is often inadequate with the systemic analgesics that have been recommended by some authors, and fetal cardiorespiratory depression is an unwanted side effect when high - dose narcotic analgesia is used. Anesthetic m anagement Epidural/spinal local anesthetics should be avoided due to the risk of hypotension and the risk of decreasing preload which may not be well tolerated in patients with mild to moderate aortic and pulmonary stenosis. However, epidural and intrathecal narcotics using fentanyl or sufentanil are very effective for pain control with minimal hemodynamic consequences. The disadvantage of mode and timing of delivery, nor the type of anesthesia and monitoring correlated with maternal outcome. Most fatalities were described as sudden death or therapy - resistant heart failure. Because maternal and fetal mortality can be as high as 50% in parturients with Eisenmenger ’ s syndrome, this condition is con- sidered an absolute contraindication to pregnancy. If the patient decides to continue pregnancy despite counseling then the fol- lowing modalities should be implemented: bed rest, hospital admission by second trimester, continuous pulse oximetry, sup- plemental oxygenation, and prophylactic antithrombotic pro- phylaxis with heparin. Anesthetic m anagement The important considerations in patients with large VSD and severe symptoms are: • avoidance of decrease in SVR and increase in PVR • prevention of hypercarbia, hypoxemia, acidosis and high airway pressures. Invasive monitoring should include continuous invasive blood pressure measurement. Assessment of central venous pressure (CVP) is equally important to monitor the trends in right ven- tricular fi lling pressures and the intravascular volume status. Continuous supplemental oxygen must be used throughout labor. Perioperative risk in Eisenmenger ’ s syndrome is high for patients undergoing non - cardiac surgery, and regional anesthesia should be avoided because of the potential deleterious hemody- namic effects. Spinal or epidural anesthesia could decrease the afterload, causing an increase in the magnitude of the right to left shunt. A review of 57 articles describing 103 anesthetic proce- dures in patients with Eisenmenger ’ s syndrome showed the overall perioperative mortality based on anesthetic management to be 14%. Patients receiving regional anesthesia had a mortality of 5%, whereas those receiving general anesthesia had a mortality of 18%. This trend favored the use of regional anesthesia but was not statistically signifi cant [10] . Since the primary objectives involve maintaining cardiac output, preserving systemic vascular resistance and lowering pul- monary vascular resistance, general anesthesia is the preferred technique for parturients with Eisenmenger ’ s syndrome who are undergoing cesarean section delivery. However there are anec- dotal case reports of the use of regional anesthesia for both opera- tive and vaginal delivery. As mentioned earlier, combined/spinal epidural is the pre- ferred technique for labor analgesia in these high - risk patients. A combination of 10 – 15 µ g of fentanyl and bupivacaine 2.5 mg intrathecally provides excellent analgesia with minimal hemody- namic perturbation. This is followed by a low - dose epidural infu- sion of bupivacaine 0.0625 mg/mL and fentanyl 2 µ g/mL at 10 – 15 mL/hour. If cesarean section is needed the authors recommend general anesthesia with ketamine as an induction agent and the use of short - acting narcotics such as remifental. Close monitoring in the intensive care unit is recommended post operatively for at least Chapter 45 644 dose narcotic induction offers good hemodynamic stability and invasive monitors should be used to guide fl uid management. The mild chronotropic effect of vasopressors like ephedrine and dopamine is helpful in managing decreases in blood pressure. In general neuraxial blockade (particularly spinal anesthesia) for cesarean section is not recommended. There have been some case reports showing success using titrated epidural analgesia for vaginal delivery [19] . Vaginal delivery has been reported in uncomplicated coarcta- tion [17] . When cesarean section is needed for obstetric indica- tions, or in patients with poorly controlled blood pressure, general anesthesia is administered with invasive hemodynamic monitoring, intravenous antihypertensive drugs, including β - blockade, and postoperative intensive care management. Aortic d issection Pathophysiology Patients with Marfan syndrome or bicuspid aortic valve may proceed to aortic root dilatation and dissection, secondary to the hyperdynamic and hypervolemic condition associated with preg- nancy. There is an increased chance of acute Type A dissection in parturients with Marfan syndrome, particularly when aortic root dilatation is greater than 4 cm, or if an increase in aortic size is detected during pregnancy [20] . Numerous case series have been reported with favorable out- comes in the mother, but fetal outcome, in majority of the cases (especially when acute aortic dissection occurred necessitating emergency surgery), is relatively poor [21,22] . It is hard to draw conclusions from so few patients, but it seems logical that emergent delivery of a viable fetus is preferable before emergent repair of aortic dissection. In situations where, based on gestational age, fetal viability is not assured, the mother ’ s condition takes priority and emergent repair of the dissection should be performed with the knowledge that the fetus will be unlikely to tolerate cardiopulmonary bypass and deep hypother- mic circulatory arrest. Fetal protection can be attempted with pulsatile perfusion and minimizing the circulatory arrest time. Anesthetic m anagement The considerations are similar to those in non - pregnant patients who undergo emergent cardiac surgery and cardiopulmonary bypass. Acquired h eart d isease Rheumatic m itral s tenosis Pathophysiology (Figure 45.2 & Table 45.7 ) Rheumatic mitral valve stenosis is the most frequent rheumatic heart disease (RHD) encountered in the pregnant population worldwide. Mitral stenosis is the lesion that most frequently requires therapeutic intervention during pregnancy. In severe mitral stenosis the valve area reduction decreases left ventricular fi lling and causes a fi xed cardiac output state, elevated this technique is the short duration of action of the neuraxial narcotics, necessitating repeated lumbar punctures with the sin- gle - shot technique. A successful case using continuous spinal anesthesia with narcotics (sufentanil) has been reported and other lipid - soluble narcotics like fentanyl may also be used [16] . Left v entricular o utfl ow t ract o bstruction Aortic c oarctation Pathophysiology Aortic coarctation is a fi xed left ventricular outfl ow obstruction, causing elevated blood pressure proximal to the lesion and hypo- perfusion distally. The decreased left ventricular outfl ow causes decreased uteroplacental perfusion with a fetal mortality that can approach 20% [12] . Parturients with uncorrected coarctation are usually unable to meet the increased hemodynamic demands of pregnancy. Complications include left ventricular failure, aortic rupture, aortic dissection and endocarditis due to associated bicuspid aortic valve [11] . These patients are also prone to cere- brovascular accidents due to an association with aneurysms in the circle of Willis. Uncomplicated uncorrected coarctation carries a maternal mortality risk of less than 3%. Severe complications include aortic dissection and rupture (particularly in the third trimester), con- gestive heart failure secondary to the increased pressure load on the left ventricle, and bacterial endocarditis. The increased demands of pregnancy predispose to aortic dissection. Coarctation of aorta is also associated with a high incidence of bicuspid aortic valve, aneurysms of the circle of Willis, ventricular septal defects, and Turner syndrome. An MRI of the brain in such patients is not unreasonable to exclude berry aneurysms. Recent data on the outcome of pregnancy in patients with this rare condition is limited. A Mayo clinic review included a com- parison of 50 women who underwent repair of aortic coarctation before pregnancy and parturients who had unrepaired lesions. In 118 pregnancies the miscarriage rate was 9% and the preterm delivery rate was 3%. One third of the women who had uncor- rected coarctation had signifi cant hypertension during preg- nancy. There was one maternal death and a very low incidence of cardiovascular complications [17] . Anesthetic m anagement Patients with corrected coarctation and no arm/leg blood pres- sure discrepancy; and those with an arm to leg residual gradient of less than 20 mmHg, usually can expect a good pregnancy outcome. In these patients, both vaginal delivery with neuraxial labor analgesia, and cesarean section with neuraxial anesthesia, have been conducted with minimal morbidity [18] . Pregnant patients with uncorrected coarctation are, however, at much greater risk, and anesthetic goals should focus on main- taining a normal or high cardiac preload, SVR and heart rate. In most situations, abdominal delivery by cesarean section under general anesthesia is recommended. This includes pre - and post- ductal arterial catheters in the upper and lower extremities and PA catheter monitoring with intravenous β - blockade. A high - Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease 645 delivery due to the auto transfusion from uterine contraction, with resultant augmentation in cardiac output. Mitral stenosis with chronic left ventricular failure can result in pulmonary hypertension by causing back - pressure distal to the pulmonary vasculature in either the left atrium or left ventricle. This condition eventually causes structural changes in the vascu- lature and an increase in pulmonary vascular resistance. Tolerance of pregnancy when a woman has mitral disease depends upon the severity of the valve disease, the heart rate and rhythm, atrial compliance, circulating blood volume, and pulmonary vascular response. Patients with a mitral orifi ce area > 1.5 cm 2 can usually be treated medically, whereas parturients with more advanced mitral stenosis often require percutaneous mitral balloon valvotomy, a procedure with a very low complication rate in experienced hands. Closed and open mitral commissurotomy has been per- formed with low maternal risk and a fetal survival of greater than 90% [23] . Closed or open mitral commissurotomy, balloon val- vuloplasty, and valve replacement, are usually considered in patients with a valve area < 1.2 cm 2 , a poor response to medical therapy, and the absence of valve calcifi cation [25] . Percutaneous balloon valvuloplasty of the mitral valve is the preferred method left atrial and pulmonary arterial pressures, and eventually pul- monary edema. Compensatory RV hypertrophy leads to right heart failure. During gestation and labor, the increased cardiac output and demands, plus the increased heart rate and decreased left ventricular fi lling, increase the risk for pulmonary edema. The time of highest risk for pulmonary edema is immediately after Pathophysiology NlMVA 4–6 cm 2 Mild MS=1.6–2.0 cm 2 Mod MS=1.1–1.5 cm 2 Severe MS==1.0 cm 2 Increased LA pressures Pulmonary congestion RV failure Symptoms initially only noted during exercise or when during AF Reduced stroke volume Reduced LVEDV and LVEDP Impaired filling of LV congestion Chronic underfilling results in cardiomopathy Impaired contractility Mitral Stenosis Normal Mitral valve stenosis Mitral valve CCF Figure 45.2 Pathophysiology of mitral stenosis. MS, mitral stenosis; Nl MVA, normal mitral valve area; LV, left ventricle; LVEDV, left ventricle end - diastolic volume; LVEDP, left ventricle end - diastolic pressure; RV, right ventricle; CCF, congestive cardiac failure; AF, atrial fi brillation. Table 45.7 Interaction of Hemodynamic Changes on Pregnancy and Mitral Stenosis. • Mitral stenosis limits ability to increase CO during pregnancy • The increase in HR during pregnancy limits the time available for fi lling of the LV & results in LAP & PAP pulmonary edema • With the increase in HR, blood volume, and demands for increase in CO( late trimester and L & D) causes the pressure gradient across the valve to quadruple – thus increasing the functional cardiac status ( NYHAC) • Approximately 80% off cases of systemic emboli occur in patients with atrial fi brillation CO, cardiac output; HR, heart rate; LV, left ventricle; LAP, left atrial pressure; PAP, pulmonary artery pressure; L & D, labor and delivery; NYHAC, New York Heart Association classifi cation. Chapter 45 646 when intervention is needed during pregnancy [24] . Kasb et al. [25] have shown that pregnant patients with symptomatic mitral stenosis can be safely treated with β - blockade which signifi cantly reduces the incidence of pulmonary edema. It has also been shown that patients with severe symptoms who undergo valvu- loplasty or valve surgery before pregnancy have fewer complica- tions than those treated medically. Early preconceptional counseling regarding management and risk of adverse cardiac outcomes is important, especially in patients with severe mitral stenosis (Tables 45.8 & 45.9 ). Anesthetic m anagement (Tables 45.10 & 45.11 ) Principles of anesthetic management include: • prevention of pain and avoidance of increased sympathetic stimulation which can result in tachycardia and augmentation of cardiac output • judicious preload with crystalloids • invasive hemodynamic monitoring with a pulmonary artery pressure catheter. In laboring parturients an early epidural can be placed and boluses of medication can be given slowly. Combined spinal/ epidural labor analgesia with a lipophilic narcotic and ultralow concentration of bupivacaine as described above and in Tables 45.12 and 45.13 is the preferred technique. Figure 45.3 shows a technique of combining a lipophilic narcotic (fentanyl), given intrathecally, with a hydrophilic narcotic like morphine, which provides longer - lasting labor analgesia than a single narcotic. This technique also offers hemodynamic stability with reasonable Table 45.8 Impact of Pregnancy - Induced Hemodynamic Changes and Complications with Mitral Stenosis. An anatomically moderate stenosis become functionally severe • NYHAC during pregnancy • Pulmonary congestion • Atrial fi brillation ᭺ Systemic emboli • Paroxysmal tachycardia NYHAC, New York Heart Association Classifi cation. Table 45.9 Preanesthetic evaluation. Clinical Physical examination • Fatigue • Dyspnea on exertion, paroxysmal nocturnal dyspnea • Orthopnea • Dyspnea • Hemoptysis ᭺ Rupture of bronchopulmonary varices • Arrhythmias (atrial fi brillation) • Pulmonary embolism • Congestive heart failure Murmur • Presystolic accentuation or mid - diastolic murmur ᭺ Opening snap Signs of failure ᭺ Pulmonary edema ᭺ Jugular venous distension ᭺ Liver enlargement ᭺ Ascites Table 45.10 Maternal Monitoring. • EKG ᭺ Maintain NSR ᭺ Detect arrhythmias • Arterial catheterization ᭺ Beat - to - Beat monitoring( Labor & Delivery a dynamic state) ᭺ ABGs ᭺ Laboratory studies • Swan Ganz catheter ᭺ Following trends ᭺ PAP & PCWP ᭺ Calculate parameters PVR, (R/O Pulmonary HTN), SVR, Assess CO, CI, EKG, electrocardiogram; ABGs, arterial blood gases; NSR, normal sinus rhythm; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; HTN, hypertension; SVR, systemic vascular resistance; CO, cardiac output; CI, Cardiac Index. Table 45.11 Anesthetic Considerations and Challenges in Mitral Stenosis. • Prevent rapid ventricular rates • Maintain sinus rhythm • Minimize decreases in systemic vascular resistance • Minimize or prevent increases in central blood volume • Prevent increases in pulmonary artery pressure ᭺ Immediate postpartum ᭺ Avoid hypoxemia/hypoventilation Table 45.12 Selection of Anesthetic Technique - Pros & Cons. • Combined Spinal – Epidural technique ᭺ Optimal technique ᭺ Intrathecal opioids during stage I ( excellent analgesia without sympathetic block) ᭿ 15 – 25ugs fentanyl+0.25 – 0.5mgs morphine (preservative - free) ᭺ Dilute local anesthetics for late 1st stage and second stage of labor ᭿ 0.625 – 0.125% bupivacaine + fentanyl 2 – 2.5ugs/ml • Epidural with dilute local anesthetics ᭺ 0.625 – 0.125% bupivacaine + fentanyl 2 – 2.5ugs/ml ugs/ml: micrograms per milliliter. Table 45.13 Advantages of anesthetic techniques. Intraspinal Narcotic Epidural Local Anesthetics • Quick onset • Selective analgesia • No sympathetic block • No motor block Titratability of block • Unlimited duration analgesia (catheter) • Relative hemodynamic stability • Ability to use different Local Anesthetics/ different situation – 1st stage labor – 2nd stage labor – c/section – post op Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease 647 been attempted in some centers as a temporizing procedure. Aortic valve replacement performed antenatally has a maternal mortality of up to 11% [28] . Anesthetic m anagement The goals of anesthetic management include maintenance of a slow heart rate, preservation of adequate preload and circulating blood volume, and control of systemic vascular resistance. Oxygen supplementation, hemodynamic monitoring (continu- ous ECG, arterial catheter, central venous catheter/PA catheter), careful preloading and fl uid management strategies, left uterine displacement and cesarean delivery under general anesthesia, have all been recommended in patients with severe disease. Phenylephrine is the vasopressor of choice to restore coronary perfusion pressure in patients with severe aortic stenosis when under general anesthesia [29] . In patients with milder aortic stenosis who are undergoing cesarean section single - shot spinal anesthesia is contraindicated. However epidural anesthesia with incremental and careful titra- tion of local anesthetic has been administered with good maternal and fetal outcomes [30,31] . In a case of mitral stenosis with pul- monary hypertension undergoing general anesthesia for urgent cesarean section, Batson and Longmire [32] demonstrated that alfentanil provided cardiovascular stability and allowed immedi- ate postoperative extubation, and that subsequent epidural mor- phine provided excellent postoperative analgesia. Currently, ultra short - acting remifentanil is also used for induction of anesthesia in pregnant patients with cardiac disease. The combination of general anesthesia followed by postoperative epidural morphine allows early ambulation and helps with the prevention of throm- boembolism. Any neonatal respiratory depression that occurs as a result of this technique can usually be reversed with naloxone. Management of a trial fi brillation in p arturients with m itral s tenosis New - onset atrial fi brillation must be treated aggressively in preg- nant patients with mitral stenosis because of the increased reli- ance on the atrial component for cardiac output during pregnancy. pain control in this high - risk group of parturients (personal expe- rience of senior author). Clark et al. have previously suggested preloading with 5% albumin, but this is no longer routinely advo- cated [26] . Phenylephrine is the vasopressor of choice to manage hypotension rather than ephedrine which causes tachycardia and decreases the ventricular fi lling time, resulting in decreased cardiac output. Epinephrine - containing epidural solutions must be avoided because of the potential for accidental epidural intra- vascular injection and the associated adverse maternal hemody- namic and uteroplacental blood fl ow effects. Avoidance of the Valsalva maneuver, and shortening the second stage of labor with forceps or vacuum, are strategies that have been used successfully in these patients. Another advantage of an epidural analgesia for delivery is the increased venous capacitance caused by the sym- pathetic blockade. This is analogous to the effect of nitroglycer- ine, and helps to accommodate the autotranfused fl uid from the uterus, mitigating the increased preload and preventing the development of pulmonary edema. In our institution, when cesarean section is needed, gradual titration of an epidural block with continuous monitoring of blood pressure, pulmonary artery pressure and cardiac output is performed. A general anesthesia with a balanced anesthetic that includes a high - dose narcotic and β - blocker has been used suc- cessfully with intense invasive and/or transesophageal echocar- diography hemodynamic monitoring. Aortic s tenosis Pathophysiology Amongst the acquired cardiac lesions, advanced aortic stenosis is rare in patients of childbearing age. If the aortic valve orifi ce area is > 1.5 cm 2 , the hemodynamic changes of pregnancy are usually well tolerated. In those cases of more advanced aortic stenosis, there is considerable risk of myocardial decompensation. The development of symptoms such as dyspnea, chest pain, syncope, and arrhythmias are indicators of a complicated course. Patients with severe stenosis of < 0.5 cm 2 and a fl ow gradient greater than 60 mmHg are at high risk for left ventricular failure [27] . Balloon valvuloplasty, which carries the risk of severe regurgitation, has Figure 45.3 Cardioversion in pregnancy. Chapter 45 648 some of the indications for anticoagulation in a pregnant cardiac patient. Oral anticoagulation with warfarin has been associated with the lowest maternal mortality and rate of thromboembolism during pregnancy. However, it is well known that warfarin use in the fi rst trimester can cause fetal growth restriction, spontaneous abortion, embryopathy and premature birth, and fetal and pla- cental hemorrhage in the third trimester [36] . Any decision to use warfarin or its derivatives in pregnancy should be accompanied by an in - depth informed consent discus- sion with the patient and her family, in which the relative fetal and maternal risks are outlined. Unfractionated heparin and low molecular weight heparin do not cross the placenta, and are thought to have no fetal tera- togenic effects. These drugs may not be as effective as warfarin in preventing thrombosis. One accepted strategy is to use heparin in the fi rst trimester of pregnancy, switch to warfarin or enoxa- parin until 35 – 36 weeks, and then restart heparin until delivery. A special concern in the anesthetic management of anticoagu- lated patients is the risk of epidural or spinal hematoma develop- ment during neuraxial anesthesia. The American Society for Regional Anesthesia Consensus on anticoagulation and neuraxial anesthesia has stated that the decision to administer a neuraxial anesthetic in a patient receiving anticoagulants, particularly LMWH, should be based on an individual assessment of the risks and benefi ts for each patient. Table 45.15 discusses some of these recommendations [37] . Ischemic h eart d isease Pathophysiology Ischemic heart disease occurs in 1 in 10,000 pregnancies. Risk factors in pregnancy include older age, smoking, hypercholester- olemia, hypertension, class H diabetes, intravenous administra- tion of ergometrine, pheochromocytoma, cocaine and other drug Parturients with moderate mitral stenosis have an increased inci- dence of atrial fi brillation and an associated increased maternal mortality [33] (Table 45.14 ). Pharmacologic therapy includes β - blockers, calcium channel blockers and digoxin for heart rate control. Procainamide and quinidine are the preferred drugs for suppressive antiarrhythmic therapy because of their safety profi le in pregnancy [34] . Although the safety of other antiarrhythmic drugs such as sotalol and fl ecainide has not been established in pregnancy they have been used in the management of fetal tachycardia and no obvious maternal or fetal morbidity has been recognized. Amiodarone, on the other hand, has been asso- ciated with neonatal hypothyroidism, congenital anomalies and teratogenicity. Direct cardioversion should be considered if the patient is hemodynamically unstable and this has been safely performed in pregnancy [35] . Cardioversion , if needed, should be undertaken in the operating room with simultaneous preparation for cesar- ean section. Recommendations for cardioversion are described in Table 45.14 and Figure 45.1 . Anticoagulation t herapy in a p arturient Mechanical heart valves, new - onset atrial fi brillation, dilated cardiomyopathy, and cardiopulmonary bypass surgery are Table 45.14 Cardioversion in Pregnancy. • Recommendations ᭺ Prepare for Emergency C - section ᭺ Monitoring – FHR monitoring ᭺ MAC Low energy levels biphasic ᭺ Anterior Posterior Gel Pad Placement ᭺ GETA for High energy levels MAC, monitored anesthesia care; GETA, general endotracheal anesthesia; FHR, fetal heart rate. Table 45.15 Recommendations based on American Society of Regional Anesthesia Guidelines for neuraxial block placement in parturients receiving anticoagulation. Anticoagulant Timing of needle insertion Timing of epidural catheter removal NSAIDs/aspirin No specifi c concerns No specifi c timing Warfarin (Coumadin) Stop drug for at least 48 hours PT/INR checked subsequently should be within normal limits before neuraxial attempts PT/INR checked and confi rmed to be within normal limits before removal Low molecular weight heparin Stop LMWH 12 hours before placing epidural catheter If larger doses of LMWH have been used (e.g. enoxaparin 1 mg/kg), a 24 - hour interval is needed before attempting neuraxial technique At least 2 hours should elapse after removal of catheter before redosing LMWH to reinstitute anticoagulation Monitoring anti - Xa levels is not recommended for LMWH activity. Thromboelastogram is used in some centers to determine coagulation status but cannot be recommended. NSAID, non - steroidal anti - infl ammatory drugs; PT, prothrombin time; INR, International Normalized Ratio (normal value is 1.2); LMWH, low molecular weight heparin. . 639 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 45 Anesthesia Considerations for the Critically. Intracranial hemorrhage Fetal loss Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease 641 bidity in these parturients are the presence of congestive heart failure and. absence of risk factors [5] . Labor analgesic techniques and anesthetic management in the critically ill parturient are determined largely by the nature of the presenting illness. Issues dictating