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Review Article
Hypertrophic cardiomyopathy part II Anesthetic and surgical considerations Praveen Kerala Varma, Suneel Puthuvassery Raman1, Praveen Kumar Neema2 Departments of Cardiac Surgery and 1Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, 2Department of Anaesthesiology, All India Institute of Medical Sciences Raipur, Chhattisgarh, India
ABSTRACT
Received: 18-04-14 Accepted: 27-05-14
Hypertrophic cardiomyopathy (HCM) poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation, heart rate, and increased afterload are required to decrease the left ventricular outflow tract obstruction. Comprehensive intraoperative transesophageal echocardiography (TEE) examination confirms the diagnosis, elucidates the pathophysiology, and identifies the various anomalies of mitral valve apparatus and allows assessment of the adequacy of surgery. In this review, we focus on the preoperative assessment, conduct of anesthesia and comprehensive TEE examination of patients presenting for surgery with HCM. The various surgical options are extended myectomy and resection, plication and release. Key words: Anesthesia; Hypertrophic cardiomyopathy; Myectomy; Transesophageal echocardiography
INTRODUCTION
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Cleland[1] in Hammersmith Hospital, London performed the first surgery for hypertrophic cardiomyopathy (HCM). It consisted of a simple incision in the prominent muscular ridge in the septum (myotomy). Morrow et al.[2,3] pioneered the surgical therapy for HCM. His procedure: Surgical myectomy became the gold standard for treatment of HCM patients with left ventricular outflow tract obstruction (LVOTO). Other surgical procedures were also described and include left atrial approach for septal myectomy; right ventricular approach with thinning of the ventricular septum, mitral valve replacement, modified Konno’s procedure, and left ventricular (LV) apicoaortic conduit. Recently, minimally invasive left atrial approach for septal myectomy was described by Mohr et al.[4] Earlier, we had reviewed the pathology and pathophysiology of HCM and indications for surgery.[5] Preoperative workup The aim of preoperative evaluation is to identify patients with obstructive physiology
and patients likely to develop obstruction on provocation, optimize cardiac function and prepare an appropriate intraoperative and postoperative plan for monitoring and management. [6] Dyspnea due to diastolic dysfunction, and syncope and presyncope due to LVOTO occur in symptomatic patients. Angina may occur in the absence of coronary artery disease and is due to myocardial oxygen supply-demand imbalance, diastolic abnormalities, and abnormal coronary vasodilation. [7] History should include previous episodes of arrhythmia, requiring treatment. Characteristic murmur of HCM is heard on the left sternal border and does not radiate to carotids and is worsened by conditions that decrease preload.[8] The chest X-ray may be normal, or the heart shadow may be slightly enlarged. Features of left atrial enlargement may be present. The electrocardiography (ECG) abnormalities include increased QRS voltages, left axis deviation, left ventricular hypertrophy (LVH), and ST-T abnormalities. There is poor correlation between the ECG voltages and the extent of LVH seen on echocardiography.[9] Transthoracic echocardiography (TTE) is the
Address for correspondence: Dr. Praveen Kerala Varma, Department of Cardiac Surgery, Division of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala, India. E-mail: [email protected]
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primary modality for screening and diagnosis of HCM. [9] Comprehensive TTE should document the points shown in Table 1. [10] Cardiac magnetic resonance imaging (MRI) [Figure 1] is recommended when TTE findings are equivocal and is very useful for quantification of myocardial fibrosis seen as late gadolinium enhancement.[10,11] Nuclear studies and positron emission tomography are currently used only as experimental tools.[10,11] Patients identified for corrective procedure undergo hemodynamic assessment [Table 2]. Left ventricular end-diastolic pressure (LVEDP) provides an idea of the coronary perfusion pressure that must be maintained in these patients in the perioperative period. Coronary angiogram is indicated in patients with angina and intermediate and high-risk for coronary artery disease.[9] ANESTHESIA CONSIDERATIONS Patients with HCM are treated with β-blockers, calcium channel blockers, amiodarone, disopyramide; these drugs should be continued through the perioperative period. It may be prudent to start metoprolol in patients not receiving any cardiac medications. Metoprolol is titrated to a heart rate of 60-65 beats/min, which is considered a marker of adequate dosing.[6,9] β-blockers reduce the heart rate and LV contractility, both of which are beneficial Table 1: Transthoracic echocardiography assessment[10] Presence of hypertrophy and its distribution LV dimensions and wall thickness (septal, posterior, and maximum) LV ejection fraction
for reducing the LVOTO. The preoperative anxiety is controlled with benzodiazepines and/or opioids. Premedication with glycopyrrolate and atropine is avoided because of tachycardia. In patients with atrial fibrillation, oral anticoagulant should be converted to heparin in the perioperative period. Prolonged perioperative fasting and dehydration should be avoided; the reduction in preload, which is exacerbated with anesthesia induction, will worsen the LVOTO. The hypertrophic noncompliant myocardium is very sensitive to ischemia; hence, adequate coronary perfusion pressure should be maintained. A controlled heart rate and sinus rhythm are very much desirable because the hypertrophied and poorly complaint LV requires timed atrial “kick” for effective filling. Consequently, preservation of preload and afterload, controlled heart rate, sinus rhythm, mild suppression of myocardial contractility, and maintenance of myocardial perfusion pressure are the goals of anesthetic management. Intraoperative monitoring Invasive arterial blood pressure must be continuously monitored as hypotension is poorly tolerated by these patients. The central venous pressure poorly reflects the left sided filling pressures due to reduced LV compliance. Pulmonary capillary wedge pressure is usually less than the measured LVEDP due to diastolic dysfunction associated with LV hypertrophy. The peak “a” wave pressure of the pulmonary capillary wedge pressure trace represents the best estimate of LVEDP in the presence of diastolic dysfunction.[11] Pulmonary artery catheter placement has been associated with
RV hypertrophy and RV dynamic obstruction Left atrial volume indexed to body surface area LV diastolic function Pulmonary artery systolic pressure Dynamic obstruction at rest and with Valsalva maneuver Identify the site of obstruction and the gradient Mitral valve and papillary muscle evaluation Direction, mechanism, and severity of mitral regurgitation HCM: Hypertrophic cardiomyopathy, RV: Right ventricular, LV: Left ventricular
Table 2: Hemodynamic data in HCM LVOT gradient at rest and provocation Spike and dome appearance in aortic pressure tracings Raised LVEDP and LA pressure due to diastolic dysfunction Raised Pulmonary artery pressure (1/3rd of patients) 15% patients show evidence of RVOT obstruction Labile and variable outflow gradient LVOT: Left ventricular outflow tract, LVEDP: Left ventricular end diastolic pressure, LA: Left atrium, RVOT: Right ventricular outflow tract, HCM: Hypertrophic cardiomyopathy
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a
b
Figure 1: (a) Four-chamber end-diastolic cardiac magnetic resonance (CMR) image of a 27-year-old asymptomatic patient with hypertrophic cardiomyopathy (HCM) with predominately ventricular septal hypertrophy (maximal wall thickness, 24 mm). (b) Four-chamber end-diastolic CMR image in a 16-year-old patient demonstrates increased left ventricular wall thickness confined to the apex (asterisks), consistent with a diagnosis of apical HCM. CMR is increasingly used to delineate all the phenotypic expressions of HCM. LA: Left atrium; RV: Right ventricle; VS: Interventricular septum; CMR: Cardiac MRI” Reprinted from Nagueh et al.[10] with permission from Elsevier Inc
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arrhythmias that may adversely affect hemodynamics.[6] Its routine use is not necessary in view of the risks associated with its placement and its limited diagnostic utility.[6,8] Conduct of anesthesia In patients of HCM, increased myocardial contractility, decreased preload and afterload, exacerbate the degree of LVOTO. Anesthetic induction should be performed carefully by titration of induction agents to avoid hypotension as well as sympathetic activation. Either propofol or thiopentone sodium can be used; both have myocardial depressant properties and can lower the afterload. Etomidate has little untoward effect on the cardiovascular system and is an attractive option provided sympathetic ablation is provided by adequate doses of opioids. [12] Any decrease in blood pressure should be treated by judicious preloading and by increasing the afterload. Use of α1-adrenergic agonists such as phenylephrine increases the systemic vascular resistance (SVR) and decreases the LVOTO.[6,10,13] β-adrenergic agents, dopamine, dobutamine, epinephrine or isoproterenol, worsen LVOTO due to their positive inotropic and chronotropic effects.[6,13] It is important not to inactivate an implanted DDD pacemaker during anesthesia when it has been placed for timed atrial contraction and gradient reduction.[14] Tachycardia associated with direct laryngoscopy and intubation can be prevented by pretreatment with intravenous metoprolol or esmolol. This practice is recommended, especially in patients with history of heart failure symptoms, angina, or HCM-related syncope or high resting gradients.[6] It is important to choose a muscle relaxant without histamine releasing (atracurium) and vagolytic (pancuronium) properties. Vecuronium is well-suited for this purpose as it produces a desirable decrease in heart rate when combined with opioids; however, one should consider basal heart rate before selecting a muscle relaxant. Cardiac arrest has been reported with vecuronium in patients receiving β-blocker and opioids. Sevoflurane is better suited for the maintenance of anesthesia than isoflurane or desflurane as it has minimal effect on heart-rate and SVR.[6,13] Volatile agents may cause atrioventricular block and depress myocardial function in patients who are on verapamil.[15] Although nitrous oxide use is reported in HCM patients,[16] it is not preferred because of sympathetic stimulation and possibility of increase in the pulmonary vascular resistance.[13] Dexmedetomidine is useful as it reduces the heart rate and blocks the sympathetic stimulation, [15] Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
however boluses can lead to hypotension. Mechanical ventilation with high tidal volume and positive end expiratory pressure are unsuited due to the reduction in the preload, which provokes LVOTO. [13] The anticipated sympathetic stimulation during surgical incision, sternotomy, etc., should be controlled by opioids and volatile agents. In case of development of atrial fibrillation, early synchronized cardioversion is the treatment of choice.[13] Pharmacologic correction of atrial fibrillation with amiodarone is inappropriate as its action takes time and its bolus is associated with hypotension. [17,18] These patients can also develop other arrhythmia such as brady-arrhythmia, supraventricular tachycardia, ventricular tachycardia or ventricular fibrillation[13] for which appropriate pharmacologic agent and/or defibrillation should be kept ready. ANESTHESIA FOR NONCARDIAC SURGERY In general, all considerations mentioned above apply. However, the management of a parturient patient with HCM presents several unique challenges. Several hemodynamic changes occur during various trimesters and stages of delivery. The major hemodynamic changes during pregnancy are decreased SVR, an increase in blood volume, and aortocaval compression during later stages of pregnancy. Increased blood volume can offset aggravating LVOTO effect of decreased SVR. The effect of aortocaval compression is variable depending on their effects on preload and afterload. Uterine contraction of labor increases preload and afterload, increased preload and afterload are beneficial for LVOTO, but has potential to precipitate pulmonary edema by increasing the LVEDP. Patients with obstructive physiology poorly tolerate the Valsalva maneuvers associated with the second stage of labor.[19] Major blood loss during labor can aggravate LVOTO by decreasing preload and reflex tachycardia. In the immediate post-delivery period, there is auto-transfusion of uterine blood and a rapid increase in peripheral vascular resistance due to involution of the uterus. Overzealous fluid resuscitation to replace blood loss of labor can lead to pulmonary edema during this phase.[6,19] Both ergometrine and oxytocin induce uterine contraction. The uterine contraction-induced by oxytocin can increase the central blood volume by 10-25%.[20] The actions of ergometrine and oxytocin on SVR are different. Oxytocin reduces the SVR and increases the heart rate, whereas ergometrine increases the SVR and appears beneficial for these patients. The risk of death during pregnancy is increased in patients with HCM and LVOT obstruction. Therefore, the patients 213
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with obstructive physiology should be identified, and their risk of sudden cardiac death should be evaluated. Asymptomatic HCM patients can be reassured about their pregnancy.[21] Patients with HCM benefit from labor analgesia and active intervention during labor. For the hypotensive patient, resuscitation should be done with fluids and phenylephrine. Left lateral decubitus position mitigates the inferior vena-caval compression from the gravid uterus. Inotropes and vasodilators are avoided. The second stage of labor should be preferably cut short by a planned instrumental delivery under labor analgesia.[6,19] Patients undergoing cesarean section need careful anesthetic evaluation. Because of the vasodilatation associated with sympathetic blockade, regional anesthesia may lead to critical reduction of preload and afterload and precipitate LVOTO in these patients. However, the safety of neuraxial blockade has been documented in two large case series of pregnant patients with HCM some of whom required anesthesia for labor.[21,22] Epidurals have been employed in patients with significant LVOT gradient (“florid disease”). There was no maternal or fetal morbidity from neuraxial blockade.[23] When local anesthetics are employed, dilute solutions are better and boluses should be administered in fractional doses.[22] Isobaric bupivacaine has been used intrathecally for cesarean[24] and epidural boluses of 0.25% bupivacaine have been administered without event.[25] Ropivacaine should be considered the local anesthetic of choice because it is more cardio-stable than bupivacaine and has longer onset time than lignocaine. The longer the onset time, gentler the onset of sympathetic blockade from neuraxial blockade.[22] There is no risk of adverse hemodynamic changes from administration of intrathecal or epidural opioid and hence can be safely employed for non-cardiac surgery. The use of pneumo-peritoneum for laparoscopic surgery requires special mention. The cardiovascular effects of pneumo-peritoneum are due to the effects of hypercarbia and elevated intraabdominal pressure. The combined effect is to produce sympathetic stimulation and an acute decrease in venous return, which is poorly tolerated by patients with HCM. Intraabdominal pressure should be carefully monitored and maintained below 15 mm Hg, and the duration of pneumo-peritoneum should be kept short. [26] Transesophageal echocardiography (TEE) during non-cardiac surgery is an evolving area and appears useful in symptomatic patients with diagnosed HCM and in those patients in whom hemodynamic status deterioration is not corrected with the usual resuscitative measures.[27] 214
Intraoperative Transesophageal Echocardiography [Table 1] Two-dimensional TEE assessment Confirmation of diagnosis Hypertrophic cardiomyopathy is usually diagnosed when the LV wall thickness exceed >15 mm in any myocardial segment without any other apparent cause.[5] The symptomatic patients have septal wall thickness exceeding 20 mm. The typical pattern of ventricular thickening is asymmetric hypertrophy rather than uniform concentric hypertrophy and usually involves the basal and mid anterior wall. [5] The involvement of basal septum can be appreciated in the mid-esophageal (ME) 5-chamber view or ME long-axis view (MELAX). The LVH and the wall thickness can also be assessed in the trans-gastric (TG) short axis views;[28] the LV walls are greatly hypertrophied and there is near obliteration of the ventricular cavity during systole. The inferolateral wall (formerly called the posterior wall) thickness is also measured in this view. A ratio of the septal wall to the inferolateral wall thickness >1.3 is suggestive of asymmetric septal hypertrophy in nonhypertensive individuals. In hypertensive individuals this ratio must be >1.5 for the diagnosis of asymmetric hypertrophy.[29] The various patterns of LVH in HCM and differentiation from sigmoid septal bulge seen in elderly patients are described in part 1 of the review.[5] Tissue Doppler imaging (TDI) will identify reduced systolic (S) and diastolic (e’) velocity; this reduction in velocities may occur even before the onset of significant hypertrophy.[10,30] The reduced systolic velocity in the presence of a normal or elevated ejection fraction is suggestive of HCM. Mitral annular systolic velocity 33 mm are likely candidates for horizontal AML plication. Leaflet calcification should be excluded as it contraindicates this type of repair. Patients with AML length >40 mm may require resection of the terminal portion of the AML or may require an Alfieri type of repair.[33,40] The mismatch between the AML and PML can be quantified by measuring the coaptation zone between the two leaflets.[10] The coaptation zone between the leaflets is best seen in the DTGLAX view.
Assessment of mitral valve Understanding the mechanics of the mitral-septal contact is important in individualizing the repair for each patient. There are a number of structural abnormalities of the mitral valve in HCM that contribute to the overlap of the inflow and outflow portions of the LV.[5] These factors lead to a coaptation between the bodies of the two leaflets rather than the leaflet tips.[33,38] Mostly, it is the AML that makes contact with the septum. Rarely, it is the posterior mitral leaflet (PML) that extends beyond the coaptation point and obstructs the LVOT.[39] The slack mitral valve is swept into the LVOT towards the hypertrophied basal septum because of the “drag force” developed 216
The papillary muscles are usually hypertrophied; additionally, 13% patients with HCM have abnormal insertion of papillary muscles. Anomalous insertion of papillary muscles occurs when one or both heads of papillary muscles insert into the ventricular aspect of the tip, mid or base of the AML or rarely into the sub-aortic septum. These attachments occur without intervening chordae tendinae. In addition, there may be chordal attachments that connect the AML to the lateral LV wall. The net effect of these abnormal attachments is to draw the mitral valve into the LVOT and contribute to the LVOTO. Failure to detect and Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
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address this issue during surgery leads to unrelieved gradients after surgery.[33,40] The TG two-chamber view is ideal for studying the papillary muscle thickness and insertion. These findings should be supplemented with the information from the ME 5-chamber and the MELAX views. Particular care must be taken to exclude antero-apical displacement of anterolateral papillary muscle, shorter inter-papillary distance, double bifid papillary muscle, direct papillary muscle attachment to mitral valve without chordae, aberrant papillary muscle and hypermobile anterolateral papillary muscles. Anomalous insertion of papillary muscles should be carefully looked for especially when the gradients are high and septal wall thickness is 20 mmHg, the E/e’ ratio is markedly elevated [Figures 7a and b].[10] The flow propagation velocity measured from a color M mode of the mitral inflow shows a reduced slope.[33] Another clue to diastolic function is the left atrial size. If the left atrial size is normal, then the left atrial pressure and the LVEDP are likely normal.[43] Left atrial volume indexed to body surface area should be assessed to get a true estimate of the left atrial size.[10] Patients with HCM who have a normal left atrial volume of ≤28 cm3/m2 have normal LV filling pressures.[43] Post cardiopulmonary bypass assessment Transesophageal echocardiography is used to assess the adequacy of repair and detect postoperative complications. With adequate repair, the LVOT is widened, the SAM, MR and outflow gradient are greatly improved. Color flow Doppler of the LVOT should
Figure 7a: Assessment of left ventricle (LV) diastolic function in a patient with hypertrophic cardiomyopathy with elevated LV end-diastolic pressure but normal left atrium (LA) pressure. Mitral inflow shows a short mitral A duration at the level of the mitral annulus, whereas the Ar velocity in pulmonary venous flow is increased in amplitude and duration. Lateral annular e’ velocity is normal, and the ratio of peak E velocity (at the level of mitral tips) to e’ velocity is 20 mm Hg. Arrow points to L velocity seen in impaired relaxation (reprinted with permission from Nagueh et al.[10] from Elsevier Inc.)
reveal laminar flow.[44] Outflow tract gradient and MR are assessed only after the postcardiopulmonary bypass (CPB) hemodynamics has been optimized. Two important causes of persisting LV outflow gradient are missing a concomitant mid-cavity obstruction and failure to correct mitral valve/papillary muscle abnormalities.[40] Detection of mid-cavity HCM should be carefully assessed especially in the ME views. It may be associated with an akinetic chamber in the apex. Akinetic chamber results in a paradoxical color flow Doppler. Blood is trapped within the apex during systole due to the mid-cavity HCM and flows into the body of the LV during early diastole.[44] Residual gradient also should prompt for careful assessment of abnormalities of the papillary muscle and mitral valve that shift the mitral apparatus and coaptation point anteriorly. Residual MR jets must be assessed qualitatively and quantitatively. Any regurgitant jet that is more than trivial should be studied for direction, size, systolic duration, location and mechanism. Early systolic jets or closing jets are due to irregularities along the coaptation surface and are considered benign, whereas pan-systolic jets represent unaddressed structural defects.[45] The zone of coaptation of the mitral valve leaflets must be studied in the DTGLAX view. A coaptation zone of at least 5 mm is required for adequate mitral valve closure. [45] Another area of concern is excluding ventricular septal defect. Ventricular septal defect can occur in the immediate postoperative period or can occur within days or months after myectomy. It follows excessive septal resection, especially when the septal thickness is 50 years), female gender, concomitant Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
coronary artery bypass grafting, preoperative atrial fibrillation, and transverse left atrial dimension of >46 mm.[61] Immediate perioperative complications reported include new onset of atrial fibrillation, ventricular septal defect and aortic insufficiency. SUMMARY Hypertrophic cardiomyopathy poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation and heart rate and increased afterload are required to decrease the LVOTO. The team taking care of HCM patients should be aware of the pathophysiology of this disease[5] as well as it’s anesthetic and surgical considerations. TEE is useful in determining the extent of the required resection, evaluating structural abnormalities of the mitral valve, evaluation of residual postmyectomy obstruction, and assessment of post-pump run MR.[6] REFERENCES 1.
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strain rate imaging by tissue Doppler ultrasonography. Circulation 2004;110:3808-14. Sherrid MV, Arabadjian M. Echocardiography to individualize treatment for hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2012;54:461-76. Rehfeldt KH, Mauermann WJ, Nuttall GA, Oliver WC Jr. Cardiomyopathies. In: Perioperative Transesophageal Echocardiography. A Companion to Kaplan’s Cardiac Anesthesia. Philadelphia: Saunders; 2013. p. 171-9. Sherrid MV, Gunsburg DZ, Pearle G. Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy: The lobster claw abnormality. J Am Soc Echocardiogr 1997;10:707-12. Sherrid MV, Wever-Pinzon O, Shah A, Chaudhry FA. Reflections of inflections in hypertrophic cardiomyopathy. J Am Coll Cardiol 2009;54:212-9. Aurigemma G, Battista S, Orsinelli D, Sweeney A, Pape L, Cuénoud H. Abnormal left ventricular intracavitary flow acceleration in patients undergoing aortic valve replacement for aortic stenosis. A marker for high postoperative morbidity and mortality. Circulation 1992;86:926-36. Cavalcante JL, Barboza JS, Lever HM. Diversity of mitral valve abnormalities in obstructive hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2012;54:517-22. Maron BJ, Harding AM, Spirito P, Roberts WC, Waller BF. Systolic anterior motion of the posterior mitral leaflet: A previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation 1983;68:282-93. Swistel DG, Balaram SK. Surgical myectomy for hypertrophic cardiomyopathy in the 21st century, the evolution of the “RPR” repair: Resection, plication, and release. Prog Cardiovasc Dis 2012;54:498-502. Yu EH, Omran AS, Wigle ED, Williams WG, Siu SC, Rakowski H. Mitral regurgitation in hypertrophic obstructive cardiomyopathy: Relationship to obstruction and relief with myectomy. J Am Coll Cardiol 2000;36:2219-25. Nagueh SF, Lakkis NM, Middleton KJ, Spencer WH 3rd, Zoghbi WA, Quiñones MA. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation 1999;99:254-61. Geske JB, Sorajja P, Nishimura RA, Ommen SR. The relationship of left atrial volume and left atrial pressure in patients with hypertrophic cardiomyopathy: An echocardiographic and cardiac catheterization study. J Am Soc Echocardiogr 2009;22:961-6. Nakamura T, Matsubara K, Furukawa K, Azuma A, Sugihara H, Katsume H, et al. Diastolic paradoxic jet flow in patients with hypertrophic cardiomyopathy: Evidence of concealed apical asynergy with cavity obliteration. J Am Coll Cardiol 1992;19:516-24. Fischer GW, Anyanwu AC, Adams DH. Intraoperative classification of mitral valve dysfunction: The role of the anesthesiologist in mitral valve reconstruction. J Cardiothorac Vasc Anesth 2009;23:531-43. Bartels K, Daneshmand MA, Mathew JP, Glower DD, Swaminathan M, Nicoara A. Delayed postmyectomy ventricular septal defect. J Cardiothorac Vasc Anesth 2013;27:381-4. Siegman IL, Maron BJ, Permut LC, McIntosh CL, Clark RE. Results of operation for coexistent obstructive hypertrophic cardiomyopathy and coronary artery disease. J Am Coll Cardiol 1989;13:1527-33. Awasthi A, Wormer D, Heggunje PS, Obeid A. Long-term follow-up of acquired coronary artery fistula after septal myectomy for hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2002;15:1104-7. Swaminathan M, Debruijn NP, Glower DD, Mathew JP. Unexpected transesophageal echocardiographic finding after septal myectomy. J Cardiothorac Vasc Anesth 2002;16:384-5. Ommen SR, Park SH, Click RL, Freeman WK, Schaff HV, Tajik AJ. Impact of intraoperative transesophageal echocardiography in the surgical management of hypertrophic cardiomyopathy. Am J Cardiol 2002;90:1022-4. Sadat K, Diddi HP, Klas B, Asaad AH, Çekirdekçi EI, Sungur A, et al. Live/real time three-dimensional transesophageal echocardiographic assessment of ventricular septal volume and mass before and after myectomy in hypertrophic cardiomyopathy. Echocardiography 2013;30:1227-31. Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
[Downloaded free from http://www.annals.in on Saturday, July 05, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Varma, et al.: Hypertrophic cardiomyopathy 52. Bicudo LS, Tsutsui JM, Shiozaki A, Rochitte CE, Arteaga E, Mady C, et al. Value of real time three-dimensional echocardiography in patients with hypertrophic cardiomyopathy: Comparison with two-dimensional echocardiography and magnetic resonance imaging. Echocardiography 2008;25:717-26. 53. Jungwirth B, Adams DB, Mathew JP, Swaminathan M, Glower DD, Mackensen GB. Mitral valve prolapse and systolic anterior motion illustrated by real time three-dimensional transesophageal echocardiography. Anesth Analg 2008;107:1822-4. 54. Willert JL, Shook D, D’Ambra MN. 3D transesophageal echocardiography: Systolic anterior motion with hypertrophic obstructive cardiomyopathy. Anesth Analg 2006;102:1361-2. 55. Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 1994;58:575-7. 56. Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. Circulation 1995;92 9 Suppl: II122-7. 57. Minakata K, Dearani JA, Nishimura RA, Maron BJ, Danielson GK. Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg 2004;127:481-9. 58. Balaram SK, Sherrid MV, Derose JJ Jr, Hillel Z, Winson G, Swistel DG. Beyond extended myectomy for hypertrophic cardiomyopathy: The resection-plication-release (RPR) repair. Ann Thorac Surg 2005;80:217-23.
59. Sherrid MV, Chaudhry FA, Swistel DG. Obstructive hypertrophic cardiomyopathy: Echocardiography, pathophysiology, and the continuing evolution of surgery for obstruction. Ann Thorac Surg 2003;75:620-32. 60. Maron BJ, Merrill WH, Freier PA, Kent KM, Epstein SE, Morrow AG. Long-term clinical course and symptomatic status of patients after operation for hypertrophic subaortic stenosis. Circulation 1978;57:1205-13. 61. Woo A, Williams WG, Choi R, Wigle ED, Rozenblyum E, Fedwick K, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy. Circulation 2005;111:2033-41. 62. ten Berg JM, Suttorp MJ, Knaepen PJ, Ernst SM, Vermeulen FE, Jaarsma W. Hypertrophic obstructive cardiomyopathy. Initial results and long-term follow-up after Morrow septal myectomy. Circulation 1994;90:1781-5. 63. Maron BJ. Surgical myectomy remains the primary treatment option for severely symptomatic patients with obstructive hypertrophic cardiomyopathy. Circulation 2007;116:196-206.
Cite this article as: Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - Anesthetic and surgical considerations. Ann Card Anaesth 2014;17:211-21. Source of Support: Nil, Conflict of Interest: None declared.
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Review Article
Hypertrophic cardiomyopathy part II Anesthetic and surgical considerations Praveen Kerala Varma, Suneel Puthuvassery Raman1, Praveen Kumar Neema2 Departments of Cardiac Surgery and 1Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, 2Department of Anaesthesiology, All India Institute of Medical Sciences Raipur, Chhattisgarh, India
ABSTRACT
Received: 18-04-14 Accepted: 27-05-14
Hypertrophic cardiomyopathy (HCM) poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation, heart rate, and increased afterload are required to decrease the left ventricular outflow tract obstruction. Comprehensive intraoperative transesophageal echocardiography (TEE) examination confirms the diagnosis, elucidates the pathophysiology, and identifies the various anomalies of mitral valve apparatus and allows assessment of the adequacy of surgery. In this review, we focus on the preoperative assessment, conduct of anesthesia and comprehensive TEE examination of patients presenting for surgery with HCM. The various surgical options are extended myectomy and resection, plication and release. Key words: Anesthesia; Hypertrophic cardiomyopathy; Myectomy; Transesophageal echocardiography
INTRODUCTION
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Website: www.annals.in PMID: *** DOI: 10.4103/0971-9784.135852 Quick Response Code:
Cleland[1] in Hammersmith Hospital, London performed the first surgery for hypertrophic cardiomyopathy (HCM). It consisted of a simple incision in the prominent muscular ridge in the septum (myotomy). Morrow et al.[2,3] pioneered the surgical therapy for HCM. His procedure: Surgical myectomy became the gold standard for treatment of HCM patients with left ventricular outflow tract obstruction (LVOTO). Other surgical procedures were also described and include left atrial approach for septal myectomy; right ventricular approach with thinning of the ventricular septum, mitral valve replacement, modified Konno’s procedure, and left ventricular (LV) apicoaortic conduit. Recently, minimally invasive left atrial approach for septal myectomy was described by Mohr et al.[4] Earlier, we had reviewed the pathology and pathophysiology of HCM and indications for surgery.[5] Preoperative workup The aim of preoperative evaluation is to identify patients with obstructive physiology
and patients likely to develop obstruction on provocation, optimize cardiac function and prepare an appropriate intraoperative and postoperative plan for monitoring and management. [6] Dyspnea due to diastolic dysfunction, and syncope and presyncope due to LVOTO occur in symptomatic patients. Angina may occur in the absence of coronary artery disease and is due to myocardial oxygen supply-demand imbalance, diastolic abnormalities, and abnormal coronary vasodilation. [7] History should include previous episodes of arrhythmia, requiring treatment. Characteristic murmur of HCM is heard on the left sternal border and does not radiate to carotids and is worsened by conditions that decrease preload.[8] The chest X-ray may be normal, or the heart shadow may be slightly enlarged. Features of left atrial enlargement may be present. The electrocardiography (ECG) abnormalities include increased QRS voltages, left axis deviation, left ventricular hypertrophy (LVH), and ST-T abnormalities. There is poor correlation between the ECG voltages and the extent of LVH seen on echocardiography.[9] Transthoracic echocardiography (TTE) is the
Address for correspondence: Dr. Praveen Kerala Varma, Department of Cardiac Surgery, Division of Cardiac Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala, India. E-mail: [email protected]
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primary modality for screening and diagnosis of HCM. [9] Comprehensive TTE should document the points shown in Table 1. [10] Cardiac magnetic resonance imaging (MRI) [Figure 1] is recommended when TTE findings are equivocal and is very useful for quantification of myocardial fibrosis seen as late gadolinium enhancement.[10,11] Nuclear studies and positron emission tomography are currently used only as experimental tools.[10,11] Patients identified for corrective procedure undergo hemodynamic assessment [Table 2]. Left ventricular end-diastolic pressure (LVEDP) provides an idea of the coronary perfusion pressure that must be maintained in these patients in the perioperative period. Coronary angiogram is indicated in patients with angina and intermediate and high-risk for coronary artery disease.[9] ANESTHESIA CONSIDERATIONS Patients with HCM are treated with β-blockers, calcium channel blockers, amiodarone, disopyramide; these drugs should be continued through the perioperative period. It may be prudent to start metoprolol in patients not receiving any cardiac medications. Metoprolol is titrated to a heart rate of 60-65 beats/min, which is considered a marker of adequate dosing.[6,9] β-blockers reduce the heart rate and LV contractility, both of which are beneficial Table 1: Transthoracic echocardiography assessment[10] Presence of hypertrophy and its distribution LV dimensions and wall thickness (septal, posterior, and maximum) LV ejection fraction
for reducing the LVOTO. The preoperative anxiety is controlled with benzodiazepines and/or opioids. Premedication with glycopyrrolate and atropine is avoided because of tachycardia. In patients with atrial fibrillation, oral anticoagulant should be converted to heparin in the perioperative period. Prolonged perioperative fasting and dehydration should be avoided; the reduction in preload, which is exacerbated with anesthesia induction, will worsen the LVOTO. The hypertrophic noncompliant myocardium is very sensitive to ischemia; hence, adequate coronary perfusion pressure should be maintained. A controlled heart rate and sinus rhythm are very much desirable because the hypertrophied and poorly complaint LV requires timed atrial “kick” for effective filling. Consequently, preservation of preload and afterload, controlled heart rate, sinus rhythm, mild suppression of myocardial contractility, and maintenance of myocardial perfusion pressure are the goals of anesthetic management. Intraoperative monitoring Invasive arterial blood pressure must be continuously monitored as hypotension is poorly tolerated by these patients. The central venous pressure poorly reflects the left sided filling pressures due to reduced LV compliance. Pulmonary capillary wedge pressure is usually less than the measured LVEDP due to diastolic dysfunction associated with LV hypertrophy. The peak “a” wave pressure of the pulmonary capillary wedge pressure trace represents the best estimate of LVEDP in the presence of diastolic dysfunction.[11] Pulmonary artery catheter placement has been associated with
RV hypertrophy and RV dynamic obstruction Left atrial volume indexed to body surface area LV diastolic function Pulmonary artery systolic pressure Dynamic obstruction at rest and with Valsalva maneuver Identify the site of obstruction and the gradient Mitral valve and papillary muscle evaluation Direction, mechanism, and severity of mitral regurgitation HCM: Hypertrophic cardiomyopathy, RV: Right ventricular, LV: Left ventricular
Table 2: Hemodynamic data in HCM LVOT gradient at rest and provocation Spike and dome appearance in aortic pressure tracings Raised LVEDP and LA pressure due to diastolic dysfunction Raised Pulmonary artery pressure (1/3rd of patients) 15% patients show evidence of RVOT obstruction Labile and variable outflow gradient LVOT: Left ventricular outflow tract, LVEDP: Left ventricular end diastolic pressure, LA: Left atrium, RVOT: Right ventricular outflow tract, HCM: Hypertrophic cardiomyopathy
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a
b
Figure 1: (a) Four-chamber end-diastolic cardiac magnetic resonance (CMR) image of a 27-year-old asymptomatic patient with hypertrophic cardiomyopathy (HCM) with predominately ventricular septal hypertrophy (maximal wall thickness, 24 mm). (b) Four-chamber end-diastolic CMR image in a 16-year-old patient demonstrates increased left ventricular wall thickness confined to the apex (asterisks), consistent with a diagnosis of apical HCM. CMR is increasingly used to delineate all the phenotypic expressions of HCM. LA: Left atrium; RV: Right ventricle; VS: Interventricular septum; CMR: Cardiac MRI” Reprinted from Nagueh et al.[10] with permission from Elsevier Inc
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arrhythmias that may adversely affect hemodynamics.[6] Its routine use is not necessary in view of the risks associated with its placement and its limited diagnostic utility.[6,8] Conduct of anesthesia In patients of HCM, increased myocardial contractility, decreased preload and afterload, exacerbate the degree of LVOTO. Anesthetic induction should be performed carefully by titration of induction agents to avoid hypotension as well as sympathetic activation. Either propofol or thiopentone sodium can be used; both have myocardial depressant properties and can lower the afterload. Etomidate has little untoward effect on the cardiovascular system and is an attractive option provided sympathetic ablation is provided by adequate doses of opioids. [12] Any decrease in blood pressure should be treated by judicious preloading and by increasing the afterload. Use of α1-adrenergic agonists such as phenylephrine increases the systemic vascular resistance (SVR) and decreases the LVOTO.[6,10,13] β-adrenergic agents, dopamine, dobutamine, epinephrine or isoproterenol, worsen LVOTO due to their positive inotropic and chronotropic effects.[6,13] It is important not to inactivate an implanted DDD pacemaker during anesthesia when it has been placed for timed atrial contraction and gradient reduction.[14] Tachycardia associated with direct laryngoscopy and intubation can be prevented by pretreatment with intravenous metoprolol or esmolol. This practice is recommended, especially in patients with history of heart failure symptoms, angina, or HCM-related syncope or high resting gradients.[6] It is important to choose a muscle relaxant without histamine releasing (atracurium) and vagolytic (pancuronium) properties. Vecuronium is well-suited for this purpose as it produces a desirable decrease in heart rate when combined with opioids; however, one should consider basal heart rate before selecting a muscle relaxant. Cardiac arrest has been reported with vecuronium in patients receiving β-blocker and opioids. Sevoflurane is better suited for the maintenance of anesthesia than isoflurane or desflurane as it has minimal effect on heart-rate and SVR.[6,13] Volatile agents may cause atrioventricular block and depress myocardial function in patients who are on verapamil.[15] Although nitrous oxide use is reported in HCM patients,[16] it is not preferred because of sympathetic stimulation and possibility of increase in the pulmonary vascular resistance.[13] Dexmedetomidine is useful as it reduces the heart rate and blocks the sympathetic stimulation, [15] Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
however boluses can lead to hypotension. Mechanical ventilation with high tidal volume and positive end expiratory pressure are unsuited due to the reduction in the preload, which provokes LVOTO. [13] The anticipated sympathetic stimulation during surgical incision, sternotomy, etc., should be controlled by opioids and volatile agents. In case of development of atrial fibrillation, early synchronized cardioversion is the treatment of choice.[13] Pharmacologic correction of atrial fibrillation with amiodarone is inappropriate as its action takes time and its bolus is associated with hypotension. [17,18] These patients can also develop other arrhythmia such as brady-arrhythmia, supraventricular tachycardia, ventricular tachycardia or ventricular fibrillation[13] for which appropriate pharmacologic agent and/or defibrillation should be kept ready. ANESTHESIA FOR NONCARDIAC SURGERY In general, all considerations mentioned above apply. However, the management of a parturient patient with HCM presents several unique challenges. Several hemodynamic changes occur during various trimesters and stages of delivery. The major hemodynamic changes during pregnancy are decreased SVR, an increase in blood volume, and aortocaval compression during later stages of pregnancy. Increased blood volume can offset aggravating LVOTO effect of decreased SVR. The effect of aortocaval compression is variable depending on their effects on preload and afterload. Uterine contraction of labor increases preload and afterload, increased preload and afterload are beneficial for LVOTO, but has potential to precipitate pulmonary edema by increasing the LVEDP. Patients with obstructive physiology poorly tolerate the Valsalva maneuvers associated with the second stage of labor.[19] Major blood loss during labor can aggravate LVOTO by decreasing preload and reflex tachycardia. In the immediate post-delivery period, there is auto-transfusion of uterine blood and a rapid increase in peripheral vascular resistance due to involution of the uterus. Overzealous fluid resuscitation to replace blood loss of labor can lead to pulmonary edema during this phase.[6,19] Both ergometrine and oxytocin induce uterine contraction. The uterine contraction-induced by oxytocin can increase the central blood volume by 10-25%.[20] The actions of ergometrine and oxytocin on SVR are different. Oxytocin reduces the SVR and increases the heart rate, whereas ergometrine increases the SVR and appears beneficial for these patients. The risk of death during pregnancy is increased in patients with HCM and LVOT obstruction. Therefore, the patients 213
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with obstructive physiology should be identified, and their risk of sudden cardiac death should be evaluated. Asymptomatic HCM patients can be reassured about their pregnancy.[21] Patients with HCM benefit from labor analgesia and active intervention during labor. For the hypotensive patient, resuscitation should be done with fluids and phenylephrine. Left lateral decubitus position mitigates the inferior vena-caval compression from the gravid uterus. Inotropes and vasodilators are avoided. The second stage of labor should be preferably cut short by a planned instrumental delivery under labor analgesia.[6,19] Patients undergoing cesarean section need careful anesthetic evaluation. Because of the vasodilatation associated with sympathetic blockade, regional anesthesia may lead to critical reduction of preload and afterload and precipitate LVOTO in these patients. However, the safety of neuraxial blockade has been documented in two large case series of pregnant patients with HCM some of whom required anesthesia for labor.[21,22] Epidurals have been employed in patients with significant LVOT gradient (“florid disease”). There was no maternal or fetal morbidity from neuraxial blockade.[23] When local anesthetics are employed, dilute solutions are better and boluses should be administered in fractional doses.[22] Isobaric bupivacaine has been used intrathecally for cesarean[24] and epidural boluses of 0.25% bupivacaine have been administered without event.[25] Ropivacaine should be considered the local anesthetic of choice because it is more cardio-stable than bupivacaine and has longer onset time than lignocaine. The longer the onset time, gentler the onset of sympathetic blockade from neuraxial blockade.[22] There is no risk of adverse hemodynamic changes from administration of intrathecal or epidural opioid and hence can be safely employed for non-cardiac surgery. The use of pneumo-peritoneum for laparoscopic surgery requires special mention. The cardiovascular effects of pneumo-peritoneum are due to the effects of hypercarbia and elevated intraabdominal pressure. The combined effect is to produce sympathetic stimulation and an acute decrease in venous return, which is poorly tolerated by patients with HCM. Intraabdominal pressure should be carefully monitored and maintained below 15 mm Hg, and the duration of pneumo-peritoneum should be kept short. [26] Transesophageal echocardiography (TEE) during non-cardiac surgery is an evolving area and appears useful in symptomatic patients with diagnosed HCM and in those patients in whom hemodynamic status deterioration is not corrected with the usual resuscitative measures.[27] 214
Intraoperative Transesophageal Echocardiography [Table 1] Two-dimensional TEE assessment Confirmation of diagnosis Hypertrophic cardiomyopathy is usually diagnosed when the LV wall thickness exceed >15 mm in any myocardial segment without any other apparent cause.[5] The symptomatic patients have septal wall thickness exceeding 20 mm. The typical pattern of ventricular thickening is asymmetric hypertrophy rather than uniform concentric hypertrophy and usually involves the basal and mid anterior wall. [5] The involvement of basal septum can be appreciated in the mid-esophageal (ME) 5-chamber view or ME long-axis view (MELAX). The LVH and the wall thickness can also be assessed in the trans-gastric (TG) short axis views;[28] the LV walls are greatly hypertrophied and there is near obliteration of the ventricular cavity during systole. The inferolateral wall (formerly called the posterior wall) thickness is also measured in this view. A ratio of the septal wall to the inferolateral wall thickness >1.3 is suggestive of asymmetric septal hypertrophy in nonhypertensive individuals. In hypertensive individuals this ratio must be >1.5 for the diagnosis of asymmetric hypertrophy.[29] The various patterns of LVH in HCM and differentiation from sigmoid septal bulge seen in elderly patients are described in part 1 of the review.[5] Tissue Doppler imaging (TDI) will identify reduced systolic (S) and diastolic (e’) velocity; this reduction in velocities may occur even before the onset of significant hypertrophy.[10,30] The reduced systolic velocity in the presence of a normal or elevated ejection fraction is suggestive of HCM. Mitral annular systolic velocity 33 mm are likely candidates for horizontal AML plication. Leaflet calcification should be excluded as it contraindicates this type of repair. Patients with AML length >40 mm may require resection of the terminal portion of the AML or may require an Alfieri type of repair.[33,40] The mismatch between the AML and PML can be quantified by measuring the coaptation zone between the two leaflets.[10] The coaptation zone between the leaflets is best seen in the DTGLAX view.
Assessment of mitral valve Understanding the mechanics of the mitral-septal contact is important in individualizing the repair for each patient. There are a number of structural abnormalities of the mitral valve in HCM that contribute to the overlap of the inflow and outflow portions of the LV.[5] These factors lead to a coaptation between the bodies of the two leaflets rather than the leaflet tips.[33,38] Mostly, it is the AML that makes contact with the septum. Rarely, it is the posterior mitral leaflet (PML) that extends beyond the coaptation point and obstructs the LVOT.[39] The slack mitral valve is swept into the LVOT towards the hypertrophied basal septum because of the “drag force” developed 216
The papillary muscles are usually hypertrophied; additionally, 13% patients with HCM have abnormal insertion of papillary muscles. Anomalous insertion of papillary muscles occurs when one or both heads of papillary muscles insert into the ventricular aspect of the tip, mid or base of the AML or rarely into the sub-aortic septum. These attachments occur without intervening chordae tendinae. In addition, there may be chordal attachments that connect the AML to the lateral LV wall. The net effect of these abnormal attachments is to draw the mitral valve into the LVOT and contribute to the LVOTO. Failure to detect and Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
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address this issue during surgery leads to unrelieved gradients after surgery.[33,40] The TG two-chamber view is ideal for studying the papillary muscle thickness and insertion. These findings should be supplemented with the information from the ME 5-chamber and the MELAX views. Particular care must be taken to exclude antero-apical displacement of anterolateral papillary muscle, shorter inter-papillary distance, double bifid papillary muscle, direct papillary muscle attachment to mitral valve without chordae, aberrant papillary muscle and hypermobile anterolateral papillary muscles. Anomalous insertion of papillary muscles should be carefully looked for especially when the gradients are high and septal wall thickness is 20 mmHg, the E/e’ ratio is markedly elevated [Figures 7a and b].[10] The flow propagation velocity measured from a color M mode of the mitral inflow shows a reduced slope.[33] Another clue to diastolic function is the left atrial size. If the left atrial size is normal, then the left atrial pressure and the LVEDP are likely normal.[43] Left atrial volume indexed to body surface area should be assessed to get a true estimate of the left atrial size.[10] Patients with HCM who have a normal left atrial volume of ≤28 cm3/m2 have normal LV filling pressures.[43] Post cardiopulmonary bypass assessment Transesophageal echocardiography is used to assess the adequacy of repair and detect postoperative complications. With adequate repair, the LVOT is widened, the SAM, MR and outflow gradient are greatly improved. Color flow Doppler of the LVOT should
Figure 7a: Assessment of left ventricle (LV) diastolic function in a patient with hypertrophic cardiomyopathy with elevated LV end-diastolic pressure but normal left atrium (LA) pressure. Mitral inflow shows a short mitral A duration at the level of the mitral annulus, whereas the Ar velocity in pulmonary venous flow is increased in amplitude and duration. Lateral annular e’ velocity is normal, and the ratio of peak E velocity (at the level of mitral tips) to e’ velocity is 20 mm Hg. Arrow points to L velocity seen in impaired relaxation (reprinted with permission from Nagueh et al.[10] from Elsevier Inc.)
reveal laminar flow.[44] Outflow tract gradient and MR are assessed only after the postcardiopulmonary bypass (CPB) hemodynamics has been optimized. Two important causes of persisting LV outflow gradient are missing a concomitant mid-cavity obstruction and failure to correct mitral valve/papillary muscle abnormalities.[40] Detection of mid-cavity HCM should be carefully assessed especially in the ME views. It may be associated with an akinetic chamber in the apex. Akinetic chamber results in a paradoxical color flow Doppler. Blood is trapped within the apex during systole due to the mid-cavity HCM and flows into the body of the LV during early diastole.[44] Residual gradient also should prompt for careful assessment of abnormalities of the papillary muscle and mitral valve that shift the mitral apparatus and coaptation point anteriorly. Residual MR jets must be assessed qualitatively and quantitatively. Any regurgitant jet that is more than trivial should be studied for direction, size, systolic duration, location and mechanism. Early systolic jets or closing jets are due to irregularities along the coaptation surface and are considered benign, whereas pan-systolic jets represent unaddressed structural defects.[45] The zone of coaptation of the mitral valve leaflets must be studied in the DTGLAX view. A coaptation zone of at least 5 mm is required for adequate mitral valve closure. [45] Another area of concern is excluding ventricular septal defect. Ventricular septal defect can occur in the immediate postoperative period or can occur within days or months after myectomy. It follows excessive septal resection, especially when the septal thickness is 50 years), female gender, concomitant Annals of Cardiac Anaesthesia z Vol. 17:3 z Jul-Sep-2014
coronary artery bypass grafting, preoperative atrial fibrillation, and transverse left atrial dimension of >46 mm.[61] Immediate perioperative complications reported include new onset of atrial fibrillation, ventricular septal defect and aortic insufficiency. SUMMARY Hypertrophic cardiomyopathy poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation and heart rate and increased afterload are required to decrease the LVOTO. The team taking care of HCM patients should be aware of the pathophysiology of this disease[5] as well as it’s anesthetic and surgical considerations. TEE is useful in determining the extent of the required resection, evaluating structural abnormalities of the mitral valve, evaluation of residual postmyectomy obstruction, and assessment of post-pump run MR.[6] REFERENCES 1.
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Cite this article as: Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - Anesthetic and surgical considerations. Ann Card Anaesth 2014;17:211-21. Source of Support: Nil, Conflict of Interest: None declared.
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