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    Abstract
   Introduction
   Case Report
   Discussion
   Summary
    References

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Table of Contents
CASE REPORT  
Year : 2014  |  Volume : 17  |  Issue : 1  |  Page : 52-55
Emergency mitral valve replacement for acute severe mitral regurgitation following balloon mitral valvotomy: Pathophysiology of hemodynamic collapse and peri-operative management issues


1 Department of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
3 Department of Anesthesiology, All India Institute of Medical Sciences, Raipur, (CG), India

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Date of Submission04-Jul-2013
Date of Acceptance15-Nov-2013
Date of Web Publication2-Jan-2014
 

   Abstract 

Severe mitral regurgitation (MR) following balloon mitral valvotomy (BMV) needing emergent mitral valve replacement is a rare complication. The unrelieved mitral stenosis is compounded by severe MR leading to acute rise in pulmonary hypertension and right ventricular afterload, decreased coronary perfusion, ischemia and right ventricular failure. Associated septal shift and falling left ventricular preload leads to a vicious cycle of myocardial ischemia and hemodynamic collapse and needs to be addressed emergently before the onset of end organ damage. In this report, we describe the pathophysiology of hemodynamic collapse and peri-operative management issues in a case of mitral valve replacement for acute severe MR following BMV.

Keywords: Atrial fibrillation; Balloon mitral valvotomy; Mitral regurgitation; Mitral stenosis; Right ventricular dysfunction

How to cite this article:
Bayya PR, Varma PK, Raman SP, Neema PK. Emergency mitral valve replacement for acute severe mitral regurgitation following balloon mitral valvotomy: Pathophysiology of hemodynamic collapse and peri-operative management issues. Ann Card Anaesth 2014;17:52-5

How to cite this URL:
Bayya PR, Varma PK, Raman SP, Neema PK. Emergency mitral valve replacement for acute severe mitral regurgitation following balloon mitral valvotomy: Pathophysiology of hemodynamic collapse and peri-operative management issues. Ann Card Anaesth [serial online] 2014 [cited 2019 Jun 17];17:52-5. Available from: http://www.annals.in/text.asp?2014/17/1/52/124143



   Introduction Top


Mitral regurgitation (MR) occurs in up to 50% patients after percutaneous balloon mitral valvotomy (BMV) for rheumatic mitral stenosis (MS). [1],[2] In most cases, the MR is mild and only minimally detracts from the clinical improvement provided by the relief of MS. [3] Severe MR, defined as an increase in MR by ≥ 2 grades, may occur in up to 15% patients after BMV. [3],[4] Most of these patients underwent non-emergency mitral valve replacement (MVR) and the MR did not result in severe adverse hemodynamics. The patients with severe MR as defined by a Doppler color flow mapping of regurgitant jet-to-left atrial (LA) area ratio of 76-100% usually require emergency MVR. [5] Acute severe MR can lead to hemodynamic collapse. We describe the pathophysiology of hemodynamic collapse and the peri-operative management issues in a patient developing acute severe MR following BMV who underwent emergent MVR.


   Case Report Top


A 39-year-old woman suffering from rheumatic heart disease and severe MS underwent BMV. She had undergone surgical closed mitral valvotomy 15 years ago. She presented with New York Heart Association (NYHA) class II dyspnea on exertion. Her heart rate (HR) was 78/min and she was in atrial fibrillation (AF). Transthoracic and transesophageal echocardiography (TEE) showed severe MS (gradient 24/13 mmHg), MV area of 0.6 cm 2 , mild MR, large LA with no clots, mild tricuspid regurgitation (TR), moderate pulmonary arterial hypertension (PAH), right ventricular (RV) internal diameter (ID) 12 mm and left ventricular (LV) ejection fraction (EF) 52%. The MV lateral commissure was fused and the patient was taken up for BMV. The MV was dilated to 23 mm using a 26 mm Accura balloon (Vascular Concepts Limited, India). The patient developed severe MR (MR jet-to-LA area ratio >76%) with increase in mean LA pressures, prominent 'v' waves and severe PAH. The patients' vital parameters showed HR - 140/min, blood pressure (BP) - 80/50 mmHg, respiratory rate - 26/min and SpO 2 95% on 6 L/min O 2 administered by Venturi mask. The extremities of the patient were cold and clammy. The patient was taken up for urgent MVR.

Anesthesia was induced with fentanyl 400 μg, midazolam 4 mg and vecuronium 8 mg. During anesthesia induction, the HR increased to 200/min, and systolic BP decreased to 50 mmHg; the central venous pressure (CVP) was 20 mmHg. Intravenous metoprolol 2.5 mg was given and epinephrine infusion was started at 0.05 μg/kg/min. HR decreased to 140/min and systolic BP improved marginally. Anesthesia was maintained with fentanyl 10 μg/Kg and sevoflurane 2%. Intraoperative TEE showed poor RV contractility. Tricuspid annular plane excursion (TAPSE) was 8 mm. The right atrium (RA) and RV were dilated and the interventricular septum (IVS) was shifted toward the LV. The MV was fish mouthed and stenotic with thickened leaflets and fused commissures with short and thickened chordae. A large tear in the anterior mitral leaflet created severe MR with no relief of the severe MS. Tear in the interatrial septum (IAS) of 0.8 cm × 0.3 cm was noted with left to right shunt. Cardiopulmonary bypass (CPB) was instituted with aorto-bicaval cannulation. The MV was replaced with 23 mm St-Jude Masters mechanical valve prosthesis (St. Jude Medical Inc., USA) and the tear in IAS was repaired. The CPB and aortic cross clamp times were 94 and 48 min respectively. She was weaned off CPB at BP of 78/40 mmHg, CVP of 14 mmHg and on infusions of epinephrine and nor-epinephrine at 0.1 μg/kg/min and dobutamine 10 μg/kg/min. She had frequent runs of fast AF. TEE showed good LV function, moderately depressed RV function (TAPSE score 12 mm) and good prosthetic valve function. Her BP improved over the next few hours to 115/60 mmHg, CVP dropped to 8 mmHg and she was extubated after 15 h of surgery. Epinephrine was weaned off on the first post-operative day. Norepinephrine and dobutamine were weaned off on the 2 nd and the 3 rd post-operative day. During the weaning of inotropes, the mean BP was maintained at 70 mmHg and CVP below 10 mmHg. Post-operatively her renal and liver function tests were normal. Her intensive care unit (ICU) stay was 4 days and hospital stay 10 days. Echocardiography at discharge showed normal septal motion, LV EF 58%, mild PAH, trivial TR with normal RV and prosthetic valve function.


   Discussion Top


The most common mechanism of severe MR following BMV for MS is a non-commissural tear in relatively thin leaflet areas. [3],[4],[5],[6] The extensively fused and thickened subvalvar structures and calcium in the commissures are unyielding sites of greater resistance leading to persistent MS. The PAH of the unrelieved MS is acutely worsened by severe MR. The LV unloads partly into the LA resulting in elevated LA pressure. The patient's pulmonary congestion rapidly worsens leading to tachypnea and dyspnea. The acute rise of LA pressure leads to severe pulmonary venous hypertension, acute rise of PAH and increased RV afterload. In a similar pathological model of massive pulmonary embolism, the RV progressively dilates in response to increase in pulmonary artery pressures with a concurrent increase in RV systolic pressure and later, as the RV fails, by a pronounced increase in the end-diastolic pressure and dimensions. The rise is more acute if the patient does not already have TR, which serves as a protective mechanism in these situations [7],[8],[9]

Under normal loading conditions, in normal individuals, the RV is thin-walled and ejects blood at approximately 25% of LV afterload. Such RV poorly tolerates acute rise of afterload. However, in patients with chronic MS, the RV adapts to PAH by developing compensatory hypertrophy. Acute rise of afterload can cause RV failure by decreasing the myocardial oxygen supply. [10] In normal individuals, the RV has short isovolumic contraction and relaxation periods, allowing for sustained low-pressure ejection. In this low-pressure circuit, right coronary artery perfusion occurs during diastole as well as systole. In right ventricles subjected to chronically elevated afterload, the pressure-volume relationship resembles LV. In such models, the myocardial perfusion predominantly occurs during diastole [11],[12] and further rise of afterload acutely increases the RV end diastolic pressure leading to decrease in coronary perfusion pressure, myocardial ischemia and RV failure. Canine experiments have shown that the resulting rise in RA pressures opposes venous return to the heart and the diminishing cardiac output (CO) eventually leads to coronary ischemia which in turn diminishes the force of RV contraction. [8],[9] All these pathophysiological changes result in a dilated RA and RV and grossly increased RA filling pressures. After BMV, the left to right shunt across the IAS defect contributes to the rise in RA pressures. Increased RV ID coupled with LV unloading leads to a reversal of the left to right diastolic pressure gradient leading to end-diastolic and systolic septal flattening [10] and leftward shift. This septal shift leads to reduced LV volume, compliance and increased ventricular interdependence in a patient with already decreased LV preload, causing decreased CO, decreased BP, further worsening the myocardial O 2 supply and thus initiating a vicious cycle leading to hemodynamic collapse.

Tachycardia and inotropic stimulation are the only means of maintaining CO at a vital level when LV filling is mechanically restrained. [10] However extreme tachycardia decreases diastolic filling time and CO. Young individuals have fast AV nodal conduction velocities that can lead to fast ventricular rate further worsening the hemodynamics. For rate control, beta-blockers and calcium channel blockers are indicated; however, they should be used with extreme caution because of their negative inotropic response. Amiodarone although appears safe takes time for its rhythm control action to set in. Intravenous digoxin is not useful in acute setting as it takes 2 h for its action to set in. The ideal agent for heart rate control in this scenario is not well established. Electrical DC version is not useful in chronic AF.

Rapid rise in PAH leads to pulmonary congestion and edema. This can result in hypoxemia and hypercarbia leading to further rise in PA pressure worsening the RV failure. Anesthesia in this setting is very challenging. The goal of anesthesia would be to induce the patient avoiding hypoxia and systemic hypotension. Although there are no ideal agents, opioids and etomidate are least harmful. Inhalation anesthetic agents should be used very carefully in view of hypotension. However, they can be used during CPB. Ideally, the diastolic BP should be maintained at > 70 mmHg; however, how to manage if the BP decreases during pre-bypass period is a tricky issue. Phenylephrine and vasopressin can worsen acute MR, epinephrine in modest doses appears logical as by improving forward flow it can break the worsening cycle of hemodynamic collapse. In desperate situation, small boluses of phenylephrine or vasopressin may be the only choice but should be used carefully. Phenylephrine may cause increase in PAH, hence vasopressin may be a better choice. [13] Urgent sternotomy and opening of the pericardium improves RV function by allowing the RV free wall to bulge out reducing the ventricular interdependence. Rapid institution of CPB prevents irreversible RV sub-endocardial ischemia but RV dysfunction is usually inevitable after discontinuation of CPB. It is due to myocardial stunning and responds to inotropes. [13] The management of post-operative RV dysfunction should aim to optimize the preload, improve RV contractility, maintain systemic perfusion pressure and reduce the RV afterload. [14] However, unmonitored fluid challenges are not advised in the setting of RV dysfunction. RV volume overload can be identified by rising V wave on CVP or by increasing TR during echocardiography. Serial echocardiograms should be done in the ICU especially when the CVP shows a rising trend. Hypervolemia can be addressed by diuretics or by hemofiltration. Inotropes are often used in the setting of RV failure and here the treatment goal is to increase the aortic root pressure and maintain it above the pulmonary artery pressures thereby maintaining the right coronary blood flow. The phosphodiesterase III inhibitor milrinone is preferred over dobutamine, norepinephrine and levosimendan. [14] The use of dopamine may be inadvisable in the background of cardiogenic shock of RV origin. The use of vasopressin may be required in cases of vasodilatory shock and pulmonary vascular dysfunction. RV afterload reduction by means of pulmonary vasodilators after cardiac surgery is supported by moderate quality evidence and there is a strong recommendation for their use. Inhaled agents that reduce the PVR have reduced adverse effects compared to systemic agents. Inhaled nitric oxide and prostacyclin are particularly suited for use in refractory RV failure [13],[14] Atrial septostomy to improve the CO has been tried; however, it is rarely helpful in these cases because of severe hypoxemia and elevated LA pressures due to massive right to left shunt. [15] Mechanical assist devices like temporary right ventricular assist devices (RVAD) may not be indicated as the PAH of MS take time to resolve and RVAD performs poorly in cases of increased afterload and pulsatile devices may cause pulmonary microcirculatory damage in PAH. [14] Extra corporeal membrane oxygenation is the treatment of choice in such settings.

Elective ventilation is recommended with every effort to avoid intrinsic positive end-expiratory pressures (PEEP), high plateau and inspiratory pressures as they increase the RV afterload. [13] High levels of PEEP and pulmonary hyperinflation can worsen the ventilation-perfusion mismatch by narrowing the capillaries in the well-ventilated areas and diverting the blood flow to less ventilated areas and should be avoided. [12] Variables that decrease pulmonary blood flow such as hypoxia, acidosis, hypercarbia and increased lung volumes (high tidal volume) should also be avoided. [14]


   Summary Top


Severe MR can occur after BMV. Pulmonary hypertension of the unrelieved MS is acutely worsened by severe regurgitation causing increased RV afterload, decreased coronary perfusion, RV failure, interventricular septal shift and falling LV preload and a vicious cycle of myocardial ischemia and hemodynamic collapse. Fast ventricular rate of AF further exacerbate hemodynamic collapse. In the present patient, metoprolol in a small dose was found useful to control the ventricular rate. Vasopressors may be required to maintain the aortic root pressure and thus increase the coronary perfusion pressure. Early institution of CPB decompresses and protects the RV and limit the end organ damage.

 
   References Top

1.Herrmann HC, Kleaveland JP, Hill JA, Cowley MJ, Margolis JR, Nocero MA, et al. The M-Heart percutaneous balloon mitral Valvuloplasty registry: Initial results and early follow-up. The M-Heart Group. J Am Coll Cardiol 1990;15:1221-6.  Back to cited text no. 1
[PUBMED]    
2.Roth RB, Block PC, Palacios IF. Predictors of increased mitral regurgitation after percutaneous mitral balloon valvotomy. Cathet Cardiovasc Diagn 1990;20:17-21.  Back to cited text no. 2
[PUBMED]    
3.Herrmann HC, Lima JA, Feldman T, Chisholm R, Isner J, O'Neill W, et al. Mechanisms and outcome of severe mitral regurgitation after Inoue balloon valvuloplasty. North American Inoue Balloon Investigators. J Am Coll Cardiol 1993;22:783-9.  Back to cited text no. 3
[PUBMED]    
4.Essop MR, Wisenbaugh T, Skoularigis J, Middlemost S, Sareli P. Mitral regurgitation following mitral balloon valvotomy. Differing mechanisms for severe versus mild-to-moderate lesions. Circulation 1991;84:1669-79.  Back to cited text no. 4
[PUBMED]    
5.Varma PK, Theodore S, Neema PK, Ramachandran P, Sivadasanpillai H, Nair KK, et al. Emergency surgery after percutaneous transmitral commissurotomy: Operative versus echocardiographic findings, mechanisms of complications, and outcomes. J Thorac Cardiovasc Surg 2005;130:772-6.  Back to cited text no. 5
[PUBMED]    
6.Hernandez R, Macaya C, Bañuelos C, Alfonso F, Goicolea J, Iñiguez A, et al. Predictors, mechanisms and outcome of severe mitral regurgitation complicating percutaneous mitral valvotomy with the Inoue balloon. Am J Cardiol 1992;70:1169-74.  Back to cited text no. 6
    
7.Guyton AC, Lindsey AW, Gilluly JJ. The limits of right ventricular compensation following acute increase in pulmonary circulatory resistance. Circ Res 1954;2:326-32.  Back to cited text no. 7
[PUBMED]    
8.Brooks H, Kirk ES, Vokonas PS, Urschel CW, Sonnenblick EH. Performance of the right ventricle under stress: Relation to right coronary flow. J Clin Invest 1971;50:2176-83.  Back to cited text no. 8
[PUBMED]    
9.Jardin F, Dubourg O, Guéret P, Delorme G, Bourdarias JP. Quantitative two-dimensional echocardiography in massive pulmonary embolism: Emphasis on ventricular interdependence and leftward septal displacement. J Am Coll Cardiol 1987;10:1201-6.  Back to cited text no. 9
    
10.Goldstein JA, Vlahakes GJ, Verrier ED, Schiller NB, Tyberg JV, Ports TA, et al. The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction. Circulation 1982;65:513-22.  Back to cited text no. 10
[PUBMED]    
11.Bristow MR, Zisman LS, Lowes BD, Abraham WT, Badesch DB, Groves BM, et al. The pressure-overloaded right ventricle in pulmonary hypertension. Chest 1998;114:101S-6.  Back to cited text no. 11
[PUBMED]    
12.Haddad F, Couture P, Tousignant C, Denault AY. The right ventricle in cardiac surgery, a perioperative perspective: II. Pathophysiology, clinical importance, and management. Anesth Analg 2009;108:422-33.  Back to cited text no. 12
[PUBMED]    
13.Forrest P. Anaesthesia and right ventricular failure. Anaesth Intensive Care 2009;37:370-85.  Back to cited text no. 13
[PUBMED]    
14.Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: Current and emerging options for management: A systematic literature review. Crit Care 2010;14:R169.  Back to cited text no. 14
[PUBMED]    
15.Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: A detailed review of the pathophysiology, diagnosis, and management. Curr Cardiol Rev 2008;4:49-59.  Back to cited text no. 15
    

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Correspondence Address:
Praveen Kerala Varma
Division of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.124143

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