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| Year : 2010
| Volume
: 13 | Issue : 3 | Page
: 253-256 |
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| Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: A case series |
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Rajendra K Sahoo, Sananta K Dash, Pradeep S Raut, Usha R Badole, Chitra B Upasani
Department of Anesthesia and Critical Care, Grant Medical College and Sir J.J. Group of Hospital, Byculla, Mumbai - 400 008, Maharashtra, India
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| Date of Submission | 11-Dec-2009 |
| Date of Acceptance | 27-May-2010 |
| Date of Web Publication | 6-Sep-2010 |
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 Abstract | | |
Hypertrophic cardiomyopathy with or without left ventricular outflow tract obstruction is characterized by asymmetric hypertrophy of the interventricular septum causing intermittent obstruction of the left ventricular outflow tract. Because Hypertrophic cardiomyopathy is the most common genetic cardiovascular disease, it may present to the anesthesiologist more often than anticipated, sometimes in undiagnosed form during routine preoperative visit. Surgery and anesthesia often complicate the perioperative outcome if adequate monitoring and proper care are not taken. Therefore, a complete understanding of the pathophysiology, hemodynamic changes and anesthetic implications is needed for successful perioperative outcome. We hereby describe the perioperative management of three patients with Hypertrophic cardiomyopathy for different surgical procedures. Keywords: Anesthesia, hypertrophic cardiomyopathy, left ventricular outflow tract obstruction
How to cite this article:
Sahoo RK, Dash SK, Raut PS, Badole UR, Upasani CB. Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: A case series. Ann Card Anaesth 2010;13:253-6 |
How to cite this URL:
Sahoo RK, Dash SK, Raut PS, Badole UR, Upasani CB. Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: A case series. Ann Card Anaesth [serial online] 2010 [cited 2022 Nov 29];13:253-6. Available from: https://www.annals.in/text.asp?2010/13/3/253/69049 |
| Introduction | |  |
Hypertrophic cardiomyopathy (HCM) with or without left ventricular outflow tract (LVOT) obstruction is characterized by asymmetric hypertrophy of the interventricular septum (IVS) causing intermittent obstruction of the LVOT. Sudden unexpected death, presumably caused by acute LVOT obstruction or a fatal cardiac dysrrhythmia, is possible in an asymptomatic patient. [1] .Patients with HCM pose considerable anesthetic challenge as the outflow tract obstruction can be worsened by decrease in the preload or afterload or by sympathetic stimulation (a common occurrence during anesthesia and surgery) leading to an increase in myocardial contractility. In addition, the higher incidence of ischemic heart disease in patients with HCM may further increase the risk of anesthesia and surgery. [2]
| Case Reports | | |
Case 1
A 55-year-old male, weighing 64 kg, diagnosed as left-sided pelvi-ureteric junction calculus, was scheduled to undergo percutaneous nephrolithotomy. His past history revealed chest pain with breathlessness 4 years back. He was diagnosed then as HCM and was on regular medication (aspirin 150 mg once daily and metoprolol 25 mg twice daily).
Examination revealed a pulse rate (PR) of 72/min and blood pressure (BP) of 144/82 mmHg. Electrocardiogram (ECG) showed "Q" waves in the chest leads and features of left ventricular hypertrophy (LVH). The transthoracic echocardiogram (TTE) showed LVH, asymmetric IVS hypertrophy, left ventricular ejection fraction (LVEF) 55%, gradient across the LVOT 40 mmHg, IVS/posterior wall (PW) thickness ratio 1.4 and moderate diastolic dysfunction.
Case 2
A 55-year-old male weighing 54 kg, diagnosed as carcinoma right tonsil with neck metastasis, was scheduled to undergo right radical neck dissection. He was a known smoker and hypertensive on oral metoprolol 25 mg, amlodipine 5 mg once daily. On examination, the PR was 56/min and the BP was 130/80 mmHg. The ECG revealed features suggestive of anterolateral ischemia. TTE revealed concentric LVH with asymmetric septal hypertrophy, with LVEF of 60%, and IVS/PW thickness ratio of 1.4.
Case 3
A 25year-old female, second gravida, with one living issue at 36 weeks of gestation, presented for safe confinement. She was a known case of HCM with mild mitral regurgitation. She had a ventricular septal myectomy carried out under cardiopulmonary bypass. TTE revealed severe concentric LVH, presence of systolic anterior motion (SAM) of anterior mitral leaflet, LVEF - 75%, IVS/PW thickness ratio of 1.2 and LVOT gradient of 80 mmHg. She was on oral verapamil 40 mg thrice daily. Examination revealed PR - 70/min and BP - 110/70 mmHg. Oral metoprolol 25 mg was added in view of significant LVOT obstruction.
Monitoring
Pulse oximetry, ECG with automated ST segment analysis, noninvasive BP, invasive BP, central venous pressure (CVP), end-tidal carbon dioxide (EtCO 2 ), temperature and urine output in all the three patients.
Anesthetic management
All the cardiac medications were continued till the day of surgery. Aspirin was stopped 5 days before surgery. All the patients were preloaded with 500 ml Ringer's lactate (RL) and premedicated with injection midazolam (1.5 mg total, given slow, intravenous).
General anesthesia was induced with fentanyl 100 μg, midazolam 1 mg and propofol 30 mg. Vecuronium 6 mg was used to facilitate endotracheal intubation. Esmolol 30 mg was given slowly over 3 min before intubation. Anesthesia was maintained with 66% nitrous oxide in oxygen and halothane 0.4-1%, with intermittent positive pressure ventilation. Anesthesia was deepened with halothane and fentanyl 50 μg before skin incision. Intraoperatively, one episode of hypotension in patient (systolic BP 70-74 mmHg) was managed with administration of 200 ml RL and injection phenylephrine 60 μg. CVP was maintained within 10-12 cm of water. The hemodynamic parameters remained stable, with heart rate from 64 to 80/min and systolic BP from 100 to 120 mmHg throughout the procedure.
At the end of the surgery, neuromuscular blockade was reversed with standard doses of neostigmine and glycopyrrolate. Injection esmolol 30 mg IV was again repeated before extubation. Injection tramadol 50 mg IV was given for pain relief. The patient was monitored overnight in the intensive care unit (ICU).
The second patient suddenly developed a narrow complex tachycardia with a ventricular rate of 180-200/min, suggestive of atrial fibrillation (AF) intraoperatively. The BP was 110-120/70-80 mmHg. Halothane and nitrous oxide were discontinued and the patient was administered 100% oxygen. CVP and EtCO 2 were within normal limits. Injection fentanyl 60 μg IV was administered. 3 mg of metoprolol was administered slowly intravenously, while hemodynamic monitoring was carried out continuously. A 12-lead ECG was obtained and AF was confirmed. When no response was observed to the administration of metoprolol, dilatiazem 10 mg was administered intravenously. The ventricular rate decreased to 150-160/min. Arterial blood gas values and serum electrolytes were within normal limits. Fifteen minutes later, diltiazem 15 mg was repeated. The ventricular rate decreased to 110/min. The patient was transferred to the ICU and put on assist control mode of ventilation with midazolam (4 mg/h) sedation. Bedsides, echocardiography did not show any dynamic LVOT obstruction. Injection metoprolol 5 mg IV thrice daily was continued for the heart rate control. With the above therapy, the heart rate gradually decreased to 80-90/min, with sinus rhythm over the next 18 h. The patient was extubated the following day. His stay over the next 12 h in the ICU was uneventful and he was transferred to the ward with oral metoprolol (25 mg twice daily).
The parturient (case 3) was taken for emergency cesarean section. Management was similar to that of the first case, aside from taking a few precautions for a cesarean delivery, such as left uterine displacement, aspiration prophylaxis, rapid sequence intubation with thiopentone and succinylcholine and avoiding fentanyl till delivery of the baby.
| Discussion | | |
HCM is a complex cardiac disease with unique pathophysiologic characteristics. [3] It affects patients of all ages. The prevalence may approach 1 in 500. [4] It is often hereditary and is transmitted as an autosomal-dominant character. It is most common of the genetic cardiovascular diseases caused by a multitude of mutations in genes encoding proteins of the cardiac sarcomere. [5] The clinical course varies widely, with most patients remaining asymptomatic throughout life.
Massive LVH is characteristic of HCM, which can be diagnozed by echocardiography. Hypertrophy is more common in the upper IVS, below the aortic valve leading to LVOT obstruction. This is accentuated by the anterior motion of the septal leaflet of the mitral valve, known as SAM. [5],[6] There may also be diastolic dysfunction due to prolongation of isovolumetric relaxation time and decreased left ventricular volume. Almost all the above features were present in all the three patients.
Beta blockers and calcium channel blockers have been used to treat HCM. The beneficial role of beta blockers is due to the decreased heart rate with consequent prolongation of diastole, increased passive ventricular filling and decrease in myocardial oxygen requirement. Verapamil imparts benefits due to ventricular relaxation and filling. AF is the most common dysrrhythmia in patients with HCM and is associated with increased risk of thromboembolism and sudden death. Paroxysmal AF may cause rapid clinical deterioration by decreasing diastolic filling and cardiac output. [3]th
Few factors during anesthesia and surgery are inevitable, such as sympathetic stimulation arising out of laryngoscopy and intubation, incision, surgical stress and blood loss. Inappropriate monitoring may worsen dynamic outflow tract obstruction. Thus, management in these patients is directed toward minimizing LVOT obstruction. These patients may deteriorate perioperatively due to arrhythmia, dynamic LVOT obstruction and diastolic dysfunction. Hence, preventive measures include (1) aggressive maintenance of sinus rhythm with defibrillation or pharmacological therapy, (2) prevention or treatment of LVOT obstruction by maintaining preload and maintaining afterload with phenylephrine and (3) administration of beta blockers or verapamil and suppression of sympathetic stimulation. [2],[7]th
Preloading before induction helps maintain stroke volume and minimizes adverse events of positive pressure ventilation. Premedication with midazolam helps in alleviating anxiety thus avoiding unnecessary sympathetic stimulation. Halothane was preferred over other inhalational anesthetic agents because it decreases heart rate and myocardial contractility and has minimal decrease in systemic vascular resistance (SVR). Selective alpha-1 agonist, like phenylephrine is preferred over ephedrine and dopamine for treating intraoperative hypotension along with RL as it increases SVR without any significant effect on the myocardial contractility and heart rate. [2]
In the second patient who developed AF intraoperatively with fast ventricular rate, rate control was successfully performed with beta-blocker and diltiazem. As the patient was hemodynamically stable, pharmacological therapy was preferred over cardioversion. [8] Poliac et al recommend early cardioversion in the event of any intraoperative AF. The authors agree that cardioversion would have been a better way to control the heart rate. [2]
Pregnancy and delivery are usually well tolerated in patients with HCM despite decrease in SVR and the risk of impaired venous return owing to uterine compression of the inferior vena cava. They present a major anesthetic challenge at term, as bearing down (valsalva maneuver) may increase LVOT obstruction. Although general anesthesia is preferred in these patients, there are case reports where epidural anesthesia has been successfully used with CVP monitoring. [9] Oxytocin must be administered carefully because of its vasodilating properties and compensatory tachycardia. Pulmonary edema has been observed in parturients with HCM after delivery, emphasizing the delicate fluid management in these patients. [10]
| Conclusion | | |
Three patients with HCM undergoing different surgical procedures are presented. It may be worth emphasizing that successful anesthetic management of a patient with HCM requires thorough understanding of the hemodynamic changes, proper intraoperative vigilance, avoiding factors that may increase LVOT obstruction with proper medication and intravascular fluid therapy.
| References | | |
| 1. | Nicod P, Polikas R, Peterson KL. Hypertrophic cardiomyopathy and sudden cardiac death. N Engl J Med 1988;318:1255-7.  |
| 2. | Poliac LC, Barron ME, Maron BJ. Hypertrophic Cardiomyopathy. Anesthesiology 2006;104:183-92. [PUBMED] [FULLTEXT] |
| 3. | Spirito P, Seidman CE, McKenna WJ, Maron BJ. The management of hypertrophic cardiomyopathy. N Engl J Med 1997;336:775-85. [PUBMED] [FULLTEXT] |
| 4. | Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults: Echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation 1995;92:785-9. [PUBMED] [FULLTEXT] |
| 5. | Maron BJ. Hypertrophic cardiomyopathy: A systematic review. JAMA 2002;287:1308. [PUBMED] [FULLTEXT] |
| 6. | Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003;348:295-303. [PUBMED] [FULLTEXT] |
| 7. | Haering JM, Comunale ME, Parker RA, Lowenstein E, Douglas PS, Krumholz HM, et al. Cardiac risk of noncardiac surgery in patients with asymmetric septal hypertrophy. Anesthesiology 1996;85:254-9. [PUBMED] [FULLTEXT] |
| 8. | Field JM, Gonzales L, Hazinski MF, Rupie J, Talley R, Elling B et al. Advanced cardiovascular life support. American Heart Association, 2006;98-9. |
| 9. | Autore C, Brauneis S, Apponi F, Commisso C, Pinto G, Fedele F. Epidural anesthesia for cesarean section in patients with hypertrophic cardiomyopathy: A report of three cases. Anesthesiology 1999;90:1205-7. [PUBMED] [FULLTEXT] |
| 10. | Tessler MJ, Hudson R, Naugler-Colville M, Biehl DR. Pulmonary oedema in two parturients with hypertrophic obstructive cardiomyopathy (HOCM). Can J Anaesth 1990;37:469-73. [PUBMED] [FULLTEXT] |
Correspondence Address:
Sananta K Dash
Room No-117, 300 Resident Doctor Hostel, Grant Medical College and Sir J.J. Group of Hospital, Byculla, Mumbai - 400 008, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0971-9784.69049
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