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LETTER TO EDITOR
Year : 2012  |  Volume : 56  |  Issue : 3  |  Page : 310-311  

Management of hypertrophic obstructive cardiomyopathy in prone position


Department of Anaesthesia and Critical Care, Grant Medical College and Sir. J. J. Groups of Hospitals, Mumbai, India

Date of Web Publication20-Jul-2012

Correspondence Address:
Surbhi D Mundada
51 Rohini Bldg., NOFRA, Colaba (Navy Nagar), Mumbai 400 005
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5049.98796

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How to cite this article:
Gosavi KS, Mundada SD. Management of hypertrophic obstructive cardiomyopathy in prone position. Indian J Anaesth 2012;56:310-1

How to cite this URL:
Gosavi KS, Mundada SD. Management of hypertrophic obstructive cardiomyopathy in prone position. Indian J Anaesth [serial online] 2012 [cited 2019 Nov 20];56:310-1. Available from: http://www.ijaweb.org/text.asp?2012/56/3/310/98796

Sir,

Hypertrophic obstructive cardiomyopathy (HOCM), a genetic disorder characterised by asymmetrical septal and left ventricular hypertrophy with an incidence of approximately 0.2% in the adults, is the most common cause of sudden cardiac death. [1] Obstruction of the left ventricular outflow tract (LVOT) in HOCM cases is of dynamic nature and is affected by preload, afterload and heart rate. [2] (HR). Position of the patient under anaesthesia can affect one or more of these parameters and hence the cardiac output. [3] We managed this 32-year-old male, a known case of HOCM, with atrial fibrillation posted for spine surgery at the L3-L4 level.

He had a history of syncope, irregular pulse with ventricular rate of 80-130/ min and blood pressure (BP) 118/74 mmHg and systolic murmur but no signs of congestive cardiac failure.

On 2-D echo, asymmetrical septal hypertrophy was seen with 50% ejection fraction, mild diastolic dysfunction and mild mitral regurgitation. Left atrial diameter was 50 mm, with no clots, and left ventricular wall thickness was 23 mm.

The patient was receiving Propranolol, aspirin and warfarin, which were replaced by low-molecular weight heparin. With standard monitoring, crystalloid preloading and opioid premedication, we induced the patient with Thiopentone and vecuronium. Measures to prevent tachycardia were taken, including EMLA for i.v. cannulation, lignocaine i.v. and spray to reduce intubation response. Internal jugular vein and radial artery were cannulated for haemodynamic monitoring.

While turning the patient prone, a sudden drop in BP from 126/76 to 80/56 mmHg (CVP 12 cm, HR 68) was noted, which did not respond to inj. Mephentermine. BP returned to 108/76 mmHg after turning him supine (CVP 9-10 cm). We loaded 200 mL crystalloid (CVP 12 cm, BP above 110/70 mmHg, and observed him for 10 min) and turned him prone, which again resulted in hypotension to 76/60 mmHg (CVP 15 cm, HR 68) and ventricular premature complexes (VPCs) (8-10/min) started appearing. We turned him supine immediately and the BP jumped to 106/68 mmHg and the VPCs reduced dramatically to an occasional one. We did not attempt to reposition the patient prone for almost 10 mins. As vitals remained stable thereafter, we assumed that these fluctuations were position related. [3],[4] To prevent hypotension and VPCs, we injected 100 mcg of phenylephrine and prophylactic amiodarone 150 mcg i.v. bolus followed by infusion of 1 mg/min. With BP 130/80 and CVP 12 cm, we turned the patient prone. This time, the BP dropped only to 92/70 mmHg. We initiated infusion of phenylephrine 30 mcg/min and continued infusion amiodarone throughout the surgery, which helped to keep the systolic BP above 100 mmHg. Surgery was carried out using nitrous oxide-oxygen, sevoflurane and fentanyl. Fluids were given according to CVP, blood pressure and urine output. Extubation and the post-operative period was uneventful. Phenylephrine infusion was stopped 4 h after extubation and amiodarone after 24 h in the intensive care unit.

In HOCM, conductance of left ventricular outflow tract (LVOT) is the most important factor in determining cardiac output. We took all precautions to prevent its spasm and tachycardia, including beta blockers, preloading, opioids, local anaesthetics and vasopressors, but hypotension still occurred. This was probably due to approximation of the hypertrophied septum and left anterior free wall in the prone position along with systolic anterior motion of the mitral valve that aggravates the obstruction in LVOT. [4] This mechanical obstruction would have been relieved in the supine position as the ventricular walls fall apart. Unfortunately we did not have echocardiography to confirm this. Phenylephrine, being a strong venoconstrictor, helps to maintain turgidity of LVOT by sustained increase in preload while amiodarone suppressed the arrhythmogenisity.

It can be concluded that positioning can affect factors determining cardiac output in an HOCM patient, and should be done cautiously in the operation theatre.

 
   References Top

1.Maron BJ. Hypertrophic cardiomyopathy: An important global disease (editorial). Am J Med 2004;116:63-5.  Back to cited text no. 1
[PUBMED]    
2.Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ, Seidman CE, et al. ACC/ESC clinical expert consensus document on hypertrophic cardiomyopathy: A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol 2003;42:1687-713.  Back to cited text no. 2
[PUBMED]    
3.Yokoyama N, Nishikawa K, Takazawa T, Saito S, Goto F. Ventricular tachycardia induced by the change of position for epidural catheter insertion in a patient with hypertrophic obstructive cardiomyopathy. Masui 2004;53:910-3.  Back to cited text no. 3
[PUBMED]    
4.Poliac LC, Barron ME, Maron BJ. Hypertrophic cardiomyopathy. Anesthesiology 2006;104:183-92.  Back to cited text no. 4
[PUBMED]    




 

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