Considerations for the Anesthetic Management of the Parturient with Mitral Valve Stenosis
The following discussion falls under the "I hope dont ever get a patient like that" category. Over the years Ive been adding certain medical situations or events to this category and joining this list is the pregnant patient who has rheumatic mitral stenosis. The chances of of actually having to provide anesthesia to someone with this problem is a rarity since the estimated prevalence of mitral stenosis is only 1% in the pregnat population. But there is a truism in the medical community that states that the longer one stays involved in the profession the greater the chances of coming face to face with our fears.
Although nothing can really prepare the clinician to handle patients with this disease (other than experience, of course), it is my intent to present some of the salient features of this disease and then list some of the equipment and supplies you may need in the anesthetic management of the pregnant patient with mitral stenosis.
I think it should be made clear from the onset that most patients with mitral stenosis can undergo vaginal delivery. Now thats a good thing because truly I would hate to manage this pateint on the operating room table. However, patients with symptoms of congestive heart failure or moderate to severe mitral stenosis should undergo hemodynamic monitoring with a Swan Ganz catheter during labor, delivery, and for several hours into the post-partum period. And I submit that in these patients, epidural anesthesia is probbly better tolerated hemodynamically than general anesthesia during labor and delivery. But Im "jumping the gun" here.
Lets first turn our attention to the physiological changes brought on by mitral stenosis. Mitral stenosis can prevent normal emptying of the left atrium and filling of the left ventricle, which results in a reduced stroke volume, a fixed cardiac output,elevated left atrium and PA pressures, and eventually pulmonary edema. In severe cases, the right ventricle can develop compensatory hypertrophy that leads to an increased PVR, pulmonary hypertension, and right heart failure. The specific cardiovascular alterations that occur during labor that can worsen symptoms in patients with MS include an increase in heart rate, an increase in blood volume, acute changes in CO, and venous return that can lead to an increase in left atrial irritability. All of these can lead to an elevated transmitral gradient and left atrium pressure and result in acute pulmonary edema. The time of maximum risk for these patients is during late pregnancy, labor, and immediately postpartum. What this means in practical terms is that this would be an ideal time for you to be out of town.
But if you cant escape then It seems to me that our goal in managing this patient is five fold:
1. Provide good maternal analgesia which is intrinsic to:
2. Minimizing the release of maternal endogenous catecholamines which,in turn helps:
3. Prevent tachycardia.
4. Maintain an optimal preload while:
5. Avoiding a rapid decrease in afterload
I am of the opinion that there is no better way to control the pain of labor than with a labor epidural or with combined spinal epidural analgesia. I am joined in this opinion by others in the anesthesia community who have reported successful management of these patients when epidural local anesthetics are titrated incrementallyin conjunction with intrathecal or epidural opioids. A word of caution needs to be inserted here. Be careful with your intravenous preload, because excessive hydration can lead to pulmonary edema in patients with mitral stenosis.
I know many of us who provide labor analgesia often preload our patients with crystalloids at a rate 15-20 cc/kg prior to to the initiation of labor analgesia. I have long been critical of this approach even in healthy parturients. And why is that? Well, consider that it takes only 500 ml of Ringers solution to expand what Hahn (1) refers to as an adult females expandable target volume which is about 40% or 5 liters of her 12 liter extracellular volume. Using various infusion rates of 25 ml/kg over 15 minutes to 80 minutes or 12.5 ml/kg over 30 minutes, Hahn and his coworkers have demonstrated that Ringers acetate will expand the target volume by a maximum of 550 ml; greater volumes given acutely were either renally eliminated or sequestered into a less compliant extracellular space (1).
And Im not so sure we do the fetus much good if we overhydrate our patient. Consider the findings of Carvalho et al (2) in which 30% of their patients who received a 20 ml/kg preload developed hypotension while those who received only 10 ml/kg preload had no episodes of hypotension. Moreover, (and heres the kicker!)in the 20 ml/kg group umbilical artery pH was lower (7.30±0.04) than the 10 ml/kg group (7.34±0.02). Perhaps the fall in umbilical artery pH may have been a consequence of a reduction in cyclic guanosine monophosphate (cGMP) and an increase in atrial natriuretic peptide (ANP) which occurs with fluid preloads as little as 15/ml kg (6). You have to remember that in normal pregnancies, the role of cGMP and ANP is to maintain uteroplacental perfusion by producing vascular smooth muscle relaxation and by reducing sympathetic vascular stimulation. So, it just could be that acute hydration exceeding 10 ml/kg prior to the initiation of spinal conductive anesthesia may actually have an adverse effect of uteroplacental blood flow by reducing the concentration of cGMP while coterminously increasing ANP. Anyway, based on these findings it seems reasonable me to limit fluid preload to 10 ml/kg, which in many situations may be equivalent to giving only 500 ml of a balanced salt solution; and I find it not so not surprising that Pan and DAngelo(3) had no problem managing their patient with mitral stenosis with only 250cc fluid preload.
Not only does epidural analgesia most effectively eliminate the pain of labor and of course the attending increase in catecholamines and resulting elevation in blood pressure and heart rate, but because of the sympathectomy that usually ensues from its use, preload is constrained during labor and delivery and in the immediate postpartum period. This is a good thing because, as you may recall, during labor and delivery, hemodynamic fluctuations can be profound. Each uterine contraction results in the displacement of 300 to 500 ml of blood into the general circulation. And under normal conditions this would cause an increase in stroke volume and consequently cardiac. But the patient with mitral stenosis does not have a compliant heart and so such an increase in intravascular volume only puts her at risk for developing pulmonary edema.
And the benefits of using epidural analgesia is extended into the immediate postpartum period in which a relative state of hypervolemia and increased venous return ensues. Consequently, at least in the normal parturient, central venous pressure rises and stroke volume and cardiac output increase as much as 75% above predelivery values. All this occurs ,of course, from the relief of caval compression, reduced lower extremity venous pressure (which enhances transcapillary refill) and a reduction of maternal vascular capacitance (i.e. elimination of the intervillous space) by a volume that often exceeds normal blood loss (i.e.autotransfusion)(4). Thus by increasing venous capacitance, the epidural helps prevent the fluid onslaught with which the already comprised heart must contend.
Now lets suppose that our patient would require a general anethetic. This would be an ideal time to leave town, but barring this approach what are our primary considerations? I think we need to remember that the potential hazards of general anesthesia include acute increases in PVR and heart rate during laryngoscopy and intubation,decreased venous return during positive pressure ventilation, and negative inotropic effects of certain inhalation anesthetic agents. Thus a balanced anesthetic with a relatively high dose of narcotic and the judiciuos use of a beta blocker would be called for. In this latter situation maternally administered esmolol would be ideal dispite the fact it has been associated with fetal bradycardia and hypoxemia. In this particular case the benefits of reducing the sympathetic responses and controlling heart rate during laryngoscopy and intubation outweigh the risk to the fetus. Addtional, calcium channel blockers and digoxin can be used to control heart rate, whereas procainamide and quinidine are recommended if suppressive antiarrhythmic therapy is required during pregnancy because they have the longest history of safety in parturients.5-7
A carefully and gradually titrated lumbar epidural analgesia or CSEA, with consideration to optimize preload, afterload, heart rate, and rhythm, can be used for analgesia and anesthesia in nearly all patients withmitral stenosis. However, when contraindications to regional anesthesia are present, general anesthetic can be safely administered for cesarean delivery, but care should be used to avoid the significant increases in
heart rate, SVR, and PVR commonly associated with induction and emergence. With either regional or general anesthesia techniques, invasive monitoring should be reserved for patients with severe disease...in which case, Im definitely leaving town.
1. Hahn RG, Drobin D, Stehle L. Volume kinetics of ringers solution in female volunteers. Br. J. Anaesth, 1997; 78: 144-148
2. Carvalho JCA, Mathias RS, Senra WG, Torres MCA, et al. Maternal, fetal and neonatal consequence of acute hydration during epidural anesthesia for C-section. Regional Anesthesia, 1993, Vol 18/2s, Mar-Apr, Suppl, 19.
3. Pan PH and DAngelo. Management of Mitral Stenosis During Pregnancy.Regional Anesthesia and Pain Medicine, Vol 29, No 6 (November-December), 2004: pp 610-615
4. Obstetric Anesthesia, Principles and Practice. David H Chestnut(ed), Mosby-Year Book Inc, St Louis, Mo, 1994 pp17-37.
5. Chow T, Galvin J, McGovern B. Antiarrhythmic drug therapy in pregnancy and lactation. Am J Cardiol 1998;82:58-68.
6. Slavik RS, Zed PJ. Intravenous amiodarone for conversion of atrial fibrillation: Misled by meta-analysis? Pharmacotherapy 2004;24:792-798.
7. Joglar JA, Page RL. Treatment of cardiac arrhythmias during pregnancy. Practical Drug Safety 1999;20:85-94.