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Table of Contents
CASE REPORT  
Year : 2014  |  Volume : 17  |  Issue : 1  |  Page : 46-51
Cardiac surgery during pregnancy: Continuous fetal monitoring using umbilical artery Doppler flow velocity indices


1 Department of Cardiaothoracic and Vascular Anesthesiology, Medanta The Medicity, Gurgaon, Haryana, India
2 Department of Cardiaothoracic and Vascular Surgery, Medanta The Medicity, Gurgaon, Haryana, India

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Date of Submission27-Apr-2013
Date of Acceptance08-Oct-2013
Date of Web Publication2-Jan-2014
 

   Abstract 

The fetal death rate associated with cardiac surgery with cardiopulmonary bypass (CPB) is as high as 9.5-29%. We report continuous monitoring of fetal heart rate and umbilical artery flow-velocity waveforms by transvaginal ultrasonography and their analyses in relation to events of the CPB in two cases in second trimester of pregnancy undergoing mitral valve replacement. Our findings suggest that the transition of circulation from corporeal to extracorporeal is the most important event during surgery; the associated decrease in mean arterial pressure (MAP) at this stage potentially has deleterious effects on the fetus, which get aggravated with the use of vasopressors. We suggest careful management of CPB at this stage, which include partial controlled CPB at initiation and gradual transition to full CPB; this strategy maintains high MAP and avoids the use of vasopressors. Maternal and fetal monitoring can timely recognize the potential problems and provide window for the required treatment.

Keywords: Cardiac surgery; Cardiopulmonary bypass; Fetal monitoring; Mitral valve disease; Pregnancy

How to cite this article:
Mishra M, Sawhney R, Kumar A, Bapna KR, Kohli V, Wasir H, Trehan N. Cardiac surgery during pregnancy: Continuous fetal monitoring using umbilical artery Doppler flow velocity indices. Ann Card Anaesth 2014;17:46-51

How to cite this URL:
Mishra M, Sawhney R, Kumar A, Bapna KR, Kohli V, Wasir H, Trehan N. Cardiac surgery during pregnancy: Continuous fetal monitoring using umbilical artery Doppler flow velocity indices. Ann Card Anaesth [serial online] 2014 [cited 2019 May 27];17:46-51. Available from: http://www.annals.in/text.asp?2014/17/1/46/124141



   Introduction Top


The incidence of heart disease in pregnant women ranges from 1% to 4%, accounting for 10-15% of maternal deaths, which is similar to the non-pregnant women undergoing similar cardiac procedures on cardiopulmonary bypass (CPB). [1] The fetal mortality in such patients has remained unchanged at 9.5-29%, with an average of 19% over the past 25 years. [1],[2],[3] Arguably, perioperative management of pregnant women undergoing cardiac surgery with CPB should take the well-being of both mother and fetus into consideration; fetal and maternal monitoring during cardiac surgery with CPB can allow the greatest control of risk in the pregnant patient. Although, successful valve repair and replacements during pregnancy have been reported. [4],[5],[6] Most of these studies are case reports, at times organized as literature review. [4] This report documents the procedure details and outcome of cardiac surgery in two pregnant women in second trimester of pregnancy with rheumatic mitral valve disease at our tertiary care referral hospital.


   Case Reports Top


Case 1

A 33-year-old gravida III, para II was admitted to our hospital at 16-week gestation with palpitation and acute shortness of breath (NYHA Class IV). Her medical history revealed history of balloon mitral valvulotomy (BMV) at the age of 21 years for rheumatic mitral valve stenosis (MS). The MS was diagnosed during first pregnancy when she became symptomatic at 20 weeks gestation. On examination, she was found to be in atrial fibrillation with fast ventricular rate of 146 beats/min. Transthoracic echocardiography revealed a thickened, heavily calcified stenosed mitral valve with an area of 0.6 cm 2 , moderately severe eccentric jet of mitral regurgitation and a clot in left atrial (LA) appendage, which ruled out BMV as a treatment option. Hence, mitral valve repair/replacement was the treatment of choice. Obstetrical examination revealed positive fetal viability and an ultrasound demonstrated normal development consistent with the gestational age of 16 weeks.

Case 2

A 26-year-old gravida II, para I was admitted with complaints of breathlessness on exertion (NYHA Class III) at 17 weeks of gestation. She had undergone BMV 3 years ago during her first pregnancy when she went into congestive cardiac failure at 24 weeks gestation. At present, she was in normal sinus rhythm with a heart rate of 112 beats/min. Echocardiography demonstrated severe MS with an area of 0.8 cm 2 , moderate tricuspid valve regurgitation and moderate pulmonary artery hypertension. Surgery was the only option at this stage of gestation.

Both families were counseled about the risks of the procedure. Progesterone 100 mg intramuscular was started a day prior to surgery. Services of a dedicated obstetrician and a ultrasonologist were ensured inside the operating room to monitor fetal heart rate (FHR) and interpret umbilical artery flow-velocity waveform throughout the procedure. As both cases are similar in their clinical profile and surgery was performed within an interval of 2 months following similar technique, hence the anesthetic and CPB management are being discussed together. Baseline FHR and rhythm were recorded before induction of anesthesia. Anesthesia was induced with etomidate and fentanyl; vecuronium 0.1 mg/kg was administered to facilitate endotracheal intubation. Anesthesia was maintained with O 2 : Air mixture (50:50), isoflurane 1-1.5%, fentanyl 5 μg/kg, and incremental doses of vecuronium. During surgery, the patients were monitored with radial artery pressure, a pulmonary artery catheter placed through the right internal jugular vein, and transesophageal echocardiography. Additionally, FHR and umbilical artery flow-velocity waveforms were continuously monitored by transvaginal ultrasonography (Siemens, ACUSON X300™ ultrasound system and transvaginal ultrasound probe 9-14 MHz) and analyzed in relation to events of the CPB. Heparin, 4 mg/kg was given for anticoagulation and activated clotting time was maintained at >550 s. [4] CPB management was standard and included aortic and two separate vena cava cannulation, crystalloid prime, Capiox sx 18R hollow fiber membrane oxygenator (Terumo cardiovascular systems Inc., Elkton, MD 21921) and 38 μ arterial filter (AFFINITY® , Medtronic, Inc. MN 55432). Initially, to avoid precipitous decrease in mean arterial pressure (MAP), partial CPB with a single venous cannula was established then gradually, after ensuring hemodynamic stability, full CPB was established. Thereafter, aorta was clamped, during clamping myocardium was protected by topical cooling with ice slush and hyperkalemic, cold (4°C) blood cardioplegia infused into the aortic root at 10 ml/kg body weight at 20 min interval. Systemic normothermia at 35-36°C was maintained. The MAP during CPB was aimed to be maintained at 70-80 mmHg and the CPB flow was kept between 2 and 2.5 L/m 2 /min. If MAP was lower than 70 mmHg; initially, the CPB flow was increased, vasoconstrictors were used sparingly. Hematocrit was maintained between 25-30% and PaO 2 at 400 mmHg. Pulsatile flow was maintained throughout CPB, using Terumo Sarns™ Modular Perfusion System 8000 (Terumo CVS-Ann Arbor MI 48103). Case 1 underwent mitral valve replacement with 27 mm (Epic™ St. Jude Medical Minnesota 55117 USA) bioprosthesis along with removal of LA clot and ligation of LA appendage. Case 2 underwent mitral valve replacement with similar 25 mm bioprosthesis along with tricuspid valve repair. Aortic cross clamp time was 30 min in Case 1 and 48 min in Case 2. After unclamping of the aorta, cardiac activity resumed after a single defibrillation with 10 joules in Case 1, whereas it returned spontaneously in Case 2. Both the patients were weaned from CPB without any inotropic support; the CPB times were 38 min and 55 min, respectively [Table 1]. After the patients were weaned off CPB, protamine was administered and hemostasis completed. In both the cases after bypass, the FHR gradually increased (over 15 min) to 135-150 beats/min. Patients were shifted to intensive care unit and continuous maternal and fetal monitoring was continued. Patients were extubated 6 h and 8 h after surgery. Post-operative course was uneventful.
Table 1: Summary of cardiac procedures done on both pregnant patients

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MAP, FHR and umbilical artery Doppler flow-velocity indices at the initiation of CPB and during CPB

Progressive deceleration of FHR was noted with the onset of CPB in both the cases [Figure 1]. In Case 1, the initiation of CPB was accompanied by fetal bradycardia, the FHR decreased to 80 beats/min; the CPB flow was increased to 3.5 L/m 2 /min, which led to an increase in FHR to > 100/min. The FHR recovered completely within 15 min of separation from CPB. In Case 2, the FHR decreased to 40 beats/min after initiation of CPB; this decrease in FHR was accompanied by a fall in MAP to 46 mmHg and responded transiently to an increase in pump flow rates. The MAP increased in a few minutes to 65 mmHg after the administration of ephedrine 5 mg, yet the FHR did not increase above 60 beats/min on CPB. Hydrocortisone 100 mg was administered and infusion of nitroglycerin was started empirically in the hope of avoiding a further decrease in FHR due to placental vasoconstriction leading to fetal hypoxia. The FHR recovered gradually until completion of operation.
Figure 1: Graphic depiction of fetal and maternal vital signs during surgery

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The FHR and Doppler flow velocitymetry indices of umbilical artery flow were analyzed in order to diagnose fetal hypoxia and/or acidosis, which are presumed to be associated with elevated placental vascular resistance. A thorough analysis of the [Figure 2]a-d. substantiates the above presumption. In Case 2, At the initiation of CPB when the MAP decreased to 46 mmHg, the Doppler flow velocity profile showed absence of diastolic flow and fetal bradycardia [Figure 2]a, the diastolic flow gradually appeared over 5 min as the MAP increased, though with vasopressors, but fetal bradycardia persisted [Figure 2]b. The umbilical artery flow, both systolic and diastolic improved further after nitroglycerin infusion [Figure 2]c. At 30 min on CPB, the FHR again decreased to 40 beats/min and once again, the diastolic flow disappeared, despite a MAP of 70 mmHg [Figure 2]d. The flow-velocity indices went up, the resistive index (RI) increased to 1.96 and the pulsatility index (PI) was 6.2 [Figure 3], which indicates an increased utero-placental resistance. Interestingly, the arterial blood gases remained normal throughout the CPB and did not indicate any problem with the fetal circulation.
Figure 2

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Figure 3: Graphic demonstration of changes in resistive index and pulsatility index of umbilical artery flow during surgery

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Outcome of pregnancy

Case 1 recovered uneventfully and was discharged from the hospital on the 6 th post-operative day. Serial fetal ultrasounds revealed a normal fetus. She underwent a full term normal vaginal delivery at 38 weeks gestation and delivered a healthy normal baby. The Case 2 had normal FHR and fetal movements for the first four post-operative days. On the 5 th post-operative day, FHR could not be located and fetal demise was detected, which was followed by spontaneous expulsion of fetus.


   Discussion Top


Cardiovascular changes during pregnancy are usually well tolerated in healthy women. However, 1-4% of women of childbearing age have some degree of concomitant heart disease and they may present with compromised cardiac function. [1] The CPB induces a non-physiologic hemodynamic state that can adversely affect the mother and the fetus during cardiac surgery. [3],[7] The CPB is accompanied by alterations in the cellular and protein components of the blood. Apart from hemodilution and coagulation protein changes, activation of immune responses, particulate and air embolism and hypotension during CPB further add to the deleterious effects of CPB. [3],[4] These changes are relatively well tolerated by the mother, to the extent that the maternal mortality rate associated with CPB in pregnant women is similar to that in non-pregnant women who undergo similar cardiac procedures on CPB. [7] Cardiovascular maternal morbidity and mortality during pregnancy correlate strongly with maternal functional status. [8],[9] Four major risk factors predict adverse maternal outcomes: (1) History of transient ischemic attack, stroke, or arrhythmia. (2) NYHA heart failure classification of three or four before onset of pregnancy (3) left-heart obstruction-mitral valve area <2 cm 2 , aortic valve area <1.5 cm 2 (4) left ventricular ejection fraction <40%. [5] However, the fetal mortality rate during cardiac surgery with CPB still remains high, the maternal mortality rate range from 1.5% to 5% and the fetal mortality rate range from 9.5% to 29%. [1],[2] Most adverse maternal and fetal outcomes from cardiac surgery during pregnancy are a result of CPB and the underlying cardiac status of the mother, not the anesthetic agent used [10] in spite of the fact that all the inhaled anesthetics and most of the intravenous anesthetics are highly lipid soluble and freely cross the placenta. Volatile anesthetics are also potent uterine relaxants and decrease uterine blood flow (UBF). All opioids may cause fetal respiratory depression, bradycardia and loss of beat-to-beat variability as they readily cross the placental barrier. Etomidate is likely to have minimal impact on the fetus or UBF. Therefore, in addition to providing hemodynamic stability, etomidate is an excellent choice for anesthetic induction in the parturient with cardiac disease. [5]

An important event during CPB is the initial hypotension that occurs when the circulation goes from corporeal to extracorporeal. Maternal hypotension shortly after the commencement of CPB is caused by a decrease in the systemic vascular resistance affected by reduced flow rate, hemodilution and release of vasoactive substances, which can result in significant reduction in placental perfusion. [9],[11] Although fetal bradycardia is known to develop frequently during the initiation of CPB and to normalize after CPB, it is likely to be caused by fetal hypoxia or acidosis, maternal hypothermia, maternal hypoglycemia or administration of drugs that are transferable through the placenta. Fetal hypoxia can be caused by reduced oxygen content of the maternal blood, reduced uterine perfusion pressure, or increased uterine arterial resistance. Like fetal bradycardia, compensatory tachycardia that frequently follows fetal distress is also reported to indicate fetal hypoxia. Fetal bradycardia has been described as a response to the decrease in utero-placental perfusion and the resultant uterine contractions and can be corrected by increased maternal blood flow by increasing CPB flow rates, which is expected to increase placental perfusion. During pregnancy, the placental blood vessels are maximally dilated, the UBF is not autoregulated and is directly proportional to the maternal MAP and inversely proportional to the uterine vascular resistance. [1],[4] Sustained uterine contractions during cardiac surgery and CPB are accepted as the most important cause of fetal death. [3],[4] The excitability of uterine muscle is probably enhanced by hormonal dilution, mainly by the dilution of progesterone. The post-operative administration of progesterone has successfully eliminated premature labor. [3],[11] In both our patients, progesterone therapy was instituted in the peri-operative period, which proved beneficial in preventing uterine contractions during surgery and also in the post-operative period.

Pulsatile flow preserves endothelial nitric oxide synthesis and decreases activation of the fetal renin-angiotensin pathway, resulting in improved blood flow to the feto-placental unit. [3],[12] In both the cases pulsatile flow was used during CPB. In Case 2, the MAP decreased to 46 mmHg at the commencement of CPB and responded transiently to increase in pump flow rates, and ephedrine had to be used to maintain MAP. This patient had prolonged bradycardia with increases in umbilical artery flow-velocity indices RI and PI [Figure 2] and [Figure 3], which indicate increased utero-placental resistance. Many reports document abnormal FHR on CPB, which did not return to normal value for several hours post-operatively. [1],[5],[7] There is only one report of return of FHR after surgical intervention despite its complete disappearance during CPB and not resulting in fetal mortality. [1]

Sympathomimetic agents such as ephedrine and phenylephrine can be used to maintain perfusion pressure and are considered to be safe during pregnancy, this impression is largely due to the studies suggesting improved fetal acid-base status with both these drugs in patients undergoing cesarean section under spinal anesthesia. [13] Nitroglycerine is reported to be an effective tocolytic with the minimal complications and its use during obstetric procedures has been described; [14] however, in spite of its use in the second case, a stillbirth occurred after surgery on the 5 th post-operative day. Based on published reports, fetal hypoxia or acidosis is likely to show elevated placental vascular resistance or low cerebral vascular resistance, a phenomenon that is most apparent in fetal growth retardation cases. With the use of Doppler velocitymetry, a relationship between cardiotocography findings, which reflect fetal hypoxia or acidosis and flow velocity waveform changes has been established. [12],[15] Various strategies to improve fetal survival have been advocated. Use of the intra-aortic balloon pump in pregnancy has also been reported, specifically in an attempt to improve uterine perfusion and to relieve profound fetal bradycardia. [16] Monitoring of FHR and the uterus has been reported to reduce fetal mortality rate to 9.5% by enabling early recognition of potential problems during CPB and timely provision of the required treatment. [3],[8],[11],[17]

Chandrasekhar et al., [5] suggested the following strategies during CPB for fetal protection: A high pump flow rate (2.5 L/min/m 2 ) and perfusion pressure >70 mmHg to maintain UBF; The maternal hematocrit be maintained >28% to optimize oxygen-carrying capacity; [9] Pulsatile flow that prevents the drop in placental perfusion and limits the rise in placental vascular resistance that is observed with non-pulsatile flow; [12] In one series, the fetal mortality was 0% with normothermic perfusion during CPB, [4] whereas it was 24% when hypothermic CPB was used. Finally, alpha stat pH management may be advantageous for maintenance of CO 2 homeostasis and UBF. [5],[12] The changes in CO 2 tension can affect UBF; specifically, hypocapnia causes utero-placental vasoconstriction, whereas hypercapnia increases UBF. All the above-mentioned strategies were followed while managing these two cases, yet there was fetal demise in second case. This could be attributed to maternal hypotension, which occurred at the commencement of CPB, possibly leading to sustained fetal hypoxia. The deceleration of fetal heart and the changes in the Doppler flow-velocity indices of umbilical artery also give an indication of fetal hypoxia, which probably got aggravated with the use of vasopressors.

In summary, the chief concerns in the optimal management of pregnant patients undergoing CPB are maintaining high pump flow rates, normothermic CPB, pulsatile perfusion and keeping the CPB time as short as possible. The most important event during surgery is the transition of corporeal circulation to extracorporeal; the decrease in MAP at this stage may have potential deleterious effects on the fetus and should be avoided. It is advisable to establish gradually full CPB, maintaining high MAP and avoiding the use of vasoconstrictors, which may have a profound effect on the placental unit. Maternal and fetal monitoring can enable early recognition of potential problems during CPB and timely initiation of the required treatment thereby ameliorating fetal hypoperfusion and hypoxia and minimizing the risks to the mother and the fetus.

 
   References Top

1.Mahli A, Izdes S, Coskun D. Cardiac operations during pregnancy: Review of factors influencing fetal outcome. Ann Thorac Surg 2000;69:1622-6.  Back to cited text no. 1
[PUBMED]    
2.Davies GA, Herbert WN. Congenital heart disease in pregnancy. J Obstet Gynaecol Can 2007;29:409-14.  Back to cited text no. 2
[PUBMED]    
3.Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascular system. Int J Cardiol 2005;98:179-89.  Back to cited text no. 3
[PUBMED]    
4.John AS, Gurley F, Schaff HV, Warnes CA, Phillips SD, Arendt KW, et al. Cardiopulmonary bypass during pregnancy. Ann Thorac Surg 2011;91:1191-6.  Back to cited text no. 4
[PUBMED]    
5.Chandrasekhar S, Cook CR, Collard CD. Cardiac surgery in the parturient. Anesth Analg 2009;108:777-85.  Back to cited text no. 5
[PUBMED]    
6.de Souza JA, Martinez EE Jr, Ambrose JA, Alves CM, Born D, Buffolo E, et al. Percutaneous balloon mitral valvuloplasty in comparison with open mitral valve commissurotomy for mitral stenosis during pregnancy. J Am Coll Cardiol 2001;37:900-3.  Back to cited text no. 6
[PUBMED]    
7.Patel A, Asopa S, Tang AT, Ohri SK. Cardiac surgery during pregnancy. Tex Heart Inst J 2008;35:307-12.  Back to cited text no. 7
[PUBMED]    
8.Drenthen W, Pieper PG, Roos-Hesselink JW, van Lottum WA, Voors AA, Mulder BJ, et al. Outcome of pregnancy in women with congenital heart disease: A literature review. J Am Coll Cardiol 2007;49:2303-11.  Back to cited text no. 8
[PUBMED]    
9.Arnoni RT, Arnoni AS, Bonini RC, de Almeida AF, Neto CA, Dinkhuysen JJ, et al. Risk factors associated with cardiac surgery during pregnancy. Ann Thorac Surg 2003;76:1605-8.  Back to cited text no. 9
[PUBMED]    
10.Arendt K, Abel M. The pregnant patient and cardiopulmonary bypass. In: Cohen NH, editor. Medically Challenging Patients Undergoing Cardiothoracic Surgery: A Society of Cardiovascular Anesthesiologists Monograph. Philadelphia, PA: Lippincott Wiliams and Wilkins; 2009. p. 215-44.  Back to cited text no. 10
    
11.Iscan ZH, Mavioglu L, Vural KM, Kucuker S, Birincioglu L. Cardiac surgery during pregnancy. J Heart Valve Dis 2006;15:686-90.  Back to cited text no. 11
[PUBMED]    
12.Vedrinne C, Tronc F, Martinot S, Robin J, Allevard AM, Vincent M, et al. Better preservation of endothelial function and decreased activation of the fetal renin-angiotensin pathway with the use of pulsatile flow during experimental fetal bypass. J Thorac Cardiovasc Surg 2000;120:770-7.  Back to cited text no. 12
[PUBMED]    
13.Habib AS. A review of the impact of phenylephrine administration on maternal hemodynamics and maternal and neonatal outcomes in women undergoing cesarean delivery under spinal anesthesia. Anesth Analg 2012;114:377-90.  Back to cited text no. 13
[PUBMED]    
14.O'Grady JP, Parker RK, Patel SS. Nitroglycerin for rapid tocolysis: Development of a protocol and a literature review. J Perinatol 2000;20:27-33.  Back to cited text no. 14
[PUBMED]    
15.Jahangiri M, Clarke J, Prefumo F, Pumphrey C, Ward D. Cardiac surgery during pregnancy: Pulsatile or nonpulsatile perfusion? J Thorac Cardiovasc Surg 2003;126:894-5.  Back to cited text no. 15
    
16.Willcox TW, Stone P, Milsom FP, Connell H. Cardiopulmonary bypass in pregnancy: Possible new role for the intra-aortic balloon pump. J Extra Corpor Technol 2005;37:189-91.  Back to cited text no. 16
[PUBMED]    
17.Karahan N, Oztürk T, Yetkin U, Yilik L, Baloglu A, Gürbüz A. Managing severe heart failure in a pregnant patient undergoing cardiopulmonary bypass: Case report and review of the literature. J Cardiothorac Vasc Anesth 2004;18:339-43.  Back to cited text no. 17
    

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DOI: 10.4103/0971-9784.124141

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