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CASE REPORT
Year : 2021  |  Volume : 22  |  Issue : 2  |  Page : 180-182
 

Overcoming the obstruction, anesthetic management of hypertrophic obstructive cardiomyopathy: The prudent paradox of less is more!


Division of Neuroanesthesia, Department of Anesthesia, PD Hinduja Hospital and Medical Research Centre, Mumbai, Maharashtra, India

Date of Submission18-Mar-2021
Date of Acceptance16-Jul-2021
Date of Web Publication29-Sep-2021

Correspondence Address:
Dr. Joseph Nascimento Monteiro
PD Hinduja Hospital and Medical Research Centre, Mumbai - 400 016, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/TheIAForum.TheIAForum_42_21

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  Abstract 


Hypertrophic obstructive cardiomyopathy (HOCM) is a genetically mediated disease causing left ventricular outflow tract obstruction (LVOTO) predisposing the patient to systolic and diastolic dysfunction leading to arrhythmias and sudden cardiac deaths in the perioperative period. This case report describes the anesthetic management of a 76-year-old female posted for a semi-emergent three level lumbar canal decompression with severe HOCM with dynamic LVOTO with an initial resting gradient >70 mmHg, noninsulin-dependent diabetes mellitus, bronchial asthma, deep-vein thrombosis, and hypothyroidism as comorbidities. Preoperative evaluation of the risks, cardiac optimization, interdisciplinary shared decision making, preoperative invasive monitoring, preanesthetic placement of defibrillator pads, careful titration of anesthetic agents, with meticulous perioperative monitoring, and perioperative intensive care collaboration contributed to a successful outcome.


Keywords: Hypertrophic obstructive cardiomyopathy, neuroanesthesia, spine surgery


How to cite this article:
Monteiro JN, Bedekar UP, Ponde C, Sankhe M. Overcoming the obstruction, anesthetic management of hypertrophic obstructive cardiomyopathy: The prudent paradox of less is more!. Indian Anaesth Forum 2021;22:180-2

How to cite this URL:
Monteiro JN, Bedekar UP, Ponde C, Sankhe M. Overcoming the obstruction, anesthetic management of hypertrophic obstructive cardiomyopathy: The prudent paradox of less is more!. Indian Anaesth Forum [serial online] 2021 [cited 2021 Dec 7];22:180-2. Available from: http://www.theiaforum.org/text.asp?2021/22/2/180/326977





  Introduction Top


Hypertrophic obstructive cardiomyopathy (HOCM) once considered obscure is a relatively common disorder, and patients undergoing noncardiac surgery have increased rates of both MI and death; therefore, comprehending their physiologic goals is essential.


  Case Report Top


A 76-year-old woman presented with severe back pain and weakness (grade 4/5 power) in both lower extremities. She was posted for semi-emergent three level lumbar canal decompression with comorbidities of HOCM with left ventricular outflow tract obstruction (LVOTO), deep-vein thrombosis, type 2 diabetes mellitus, bronchial asthma, and hypothyroidism.

Two-dimensional ECHO was suggestive of severe symmetric HOCM with mid-cavity obstruction, left ventricular ejection fraction 55%, right ventricular ejection fraction 50%, Grade 1 TR, trace MR, and sclerotic aortic valve with type 1 diastolic dysfunction. LA volume was 30 ml/cm2. There was moderate concentric LVH with significantly high dynamic LVOT gradient of 70 mmHg. PAP was 35 mmHg.

Preoperative optimization with oral ß-blockers reduced the LVOT gradient to 30 mmHg. In the operation theater, the patient was positioned on a tilt capable trolley for induction and preoxygenated. Real-time 5-lead electrocardiogram, noninvasive blood pressure, pulse oximetry monitoring was commenced, peripheral nerve train of four (TOF), and Bispectral Index (BIS) probes were attached.

Peripheral venous access was secured with 2 18G cannula and invasive arterial blood pressure monitoring through the right radial artery under local anesthesia. Single-use defibrillator pads (Phillips Heartstart M3716A) [Figure 1] were applied in view of the risk of perioperative arrhythmias.
Figure 1: Preinduction, preemptive, application of disposable defibrillator pads to the patient prior to proning

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General anesthesia was induced with the aim of hemodynamic stability and to avoid tachycardia, with intravenous Fentanyl 1.5 μg/kg, titrated etomidate (0.2 mg/kg) neuromuscular blockade with vecuronium (0.1 mg/kg) and intravenous 2% lignocaine to attenuate the hemodynamic responses to laryngoscopy and intubation. Following a smooth and quick laryngoscopy airway secured with a 7.5 cuffed flexo-metallic tube. A co-ordinated proning of the patient was done, and the patient was positioned on the MaquetR frame with adequate padding and pressure point coverage and care of the eyes was taken. Anesthesia was maintained on air: Oxygen mixture (FiO2 0.5), Sevoflurane and Vecuronium boluses guided by TOF and BIS (maintained in the range 40–60) monitoring ensured adequate depth of anaesthesia. Injection enoxaparin (0.6 ml) was given subcutaneously in view of the preoperative presence of lower limb thrombus was decided to avoid pneumatic compression stockings intraoperatively.

Titrated aliquots of balanced crystalloid PlasmalyteR was used to maintain the preload, we aimed and achieved a target heart rate <80/min and afterload reductions were avoided.

A single episode of bradycardia (rate 38/min) probably a vasovagal reflex during the surgical dissection was treated with intravenous, glycopyrollate 0.2 mg. The rest of the procedure was uneventful [Figure 2]. Following the procedure, the patient was made supine, and the neuromuscular blockade was reversed, after ensuring a TOF of 4 and BIS >90, with intravenous neostigmine 0.05 mg/kg and glycopyrollate 0.4 mg, and extubated. The patient was electively shifted to the intensive care unit and discharged from the hospital following an uneventful stay.
Figure 2: Intra-operative monitoring of the patient

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  Discussion Top


HOCM is a relatively common inherited disorder, with a prevalence of 1:500.[1] Our patient presented for an elective surgery. The anesthetic perioperative management is dictated by the presenting pathophysiology.[2] It is reported that approximately, 60% of patients with HOCM experience perioperative cardiac arrhythmias, cardiac arrest, myocardial infarction,[4] and congestive heart failure.[3] HOCM is further classified into hypertrophic nonobstructive cardiomyopathy, apical HOCM, mid-ventricular HOCM, and dilated-phase HOCM.[5] The dynamic LVOTO further increases the risks of perioperative adverse events [Table 1].[7] Our patient had an obstruction at rest with hypertrophied interventricular septum and a gradient of more than 70 mmHg reduced to 30 mmHg with ß-blockers.
Table 1: Echocardiographic Red Flags for HOCM Patients Undergoing Non-cardiac Surgery due to Increased Risk of Perioperative Complications[6]

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The dynamic nature of HOCM and associated multifactorial and dynamic LVOTO increases the unpredictability of the risk. Increases in heart rate, rhythm disturbances, increases in contractility, and decreases in preload and decreases in afterload will exacerbate LVOTO and may cause hemodynamic deterioration. The maintenance of cardiac output by an adequate preload including increasing preload in the Trendelenburg position, drugs that increase afterload (systemic vascular resistance), without increasing heart rate or contractility (e.g., phenylephrine and vasopressin), we preferred phenylephrine if required in our patient. Increased chronotropy and increased contractility and secondary to several intraoperative stimuli can accentuate LVOTO can precipitate hemodynamic collapse, we planned to mitigate these effects with an infusion of esmolol hydrochloride if required. It is also imperative to maintain sinus rhythm because LVH and decreased compliance in HOCM dictate increased dependence on atrial kick for maintaining the cardiac output. Direct current cardioversion maybe necessary in the case of sudden onset of atrial fibrillation that is hemodynamically unstable,[7] we had electively placed defibrillator pads on the patient prior to induction and in the perioperative period.

In case the patient had suffered a cardiac arrest in the prone position requiring chest compressions; a sandbag and a 500 ml saline bottle were kept ready to increase the efficacy of compressions.[8] Making the patient supine would have required a minimum of 4 people and a time of 3 min wasting the golden period of starting early effective chest compressions as well being a cumbersome relatively impractical solution. Indirect pressure from the back transmits to the sternum to achieve sufficient cardiac output. Performing cardiopulmonary resuscitation in the prone position is more tiring which is to be noted.

Although our patient was 76 years, age, per se, does not predict the outcome of lumbar spine surgeries, and therefore, should not be used as the sole criterion in the surgical decision-making process.[9] Preoperative risk assessment, medical optimisation, interdisciplinary shared decision-making,[10] perioperative vigilant monitoring, preanesthetic placement of defibrillator pads, careful titration of anesthetic agents, with meticulous perioperative monitoring, and postoperative intensive care are key to a safe outcome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Towbin JA. Hypertrophic cardiomyopathy. Pacing Clin Electrophysiol 2009;32 Suppl 2:S23-31.  Back to cited text no. 1
    
2.
Davies MR, Cousins J. Cardiomyopathy and anaesthesia. Contin Educ Anaesth Crit Care Pain 2009;9:189-93. [doi.org/10.1093/bjaceaccp/mkp032].  Back to cited text no. 2
    
3.
Cheng TO. Cardiac risk of non-cardiac surgery in patients with hypertrophic cardiomyopathy. Int J Cardiology 2008;129:307-8.  Back to cited text no. 3
    
4.
Hreybe H, Zahid M, Sonel A, Good CB, Shaver J, Saba S. Noncardiac surgery and the risk of death and other cardiovascular events in patients with hypertrophic cardiomyopathy. Clin Cardiol 2006;29:65-8.  Back to cited text no. 4
    
5.
Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011;124:e783-831.  Back to cited text no. 5
    
6.
Hensley N, Dietrich J, Nyhan D, Mitter N, Yee MS, Brady M. Hypertrophic cardiomyopathy: a review. Anesth Analg. 2015 Mar;120(3):554-69. doi: 10.1213/ANE.0000000000000538. PMID: 25695573.  Back to cited text no. 6
    
7.
Poliac LC, Barron ME, Maron BJ. Hypertrophic cardiomyopathy. Anesthesiology 2006;104:183-92.  Back to cited text no. 7
    
8.
Atkinson MC. The efficacy of cardiopulmonary resuscitation in the prone position department of anaesthesia, royal infirmary of Edinburgh, Edinburgh, Scotland. Crit Care Resusc 2000;2:188-90.  Back to cited text no. 8
    
9.
Palliyil NS, Shah S,Rai RR, Dalvie S,Monteiro JN.Age - Does it really count? A study of the Perioperative Morbidity and Long-Term Outcome in Patients Above 70 Years of Age Undergoing Spine surgery for Lumbar Degenerative Disorders.December 2019 Revista Brasileira de Ortopedia 55(3) DOI: 10.1055/s-0039-1700833  Back to cited text no. 9
    
10.
Supriya S, Ommen SR, Mital S, Burke MA, Day SM, Deswal A, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: A report of the American College of Cardiology/American Heart Association Joint Committee on clinical practice guidelines. J Am Coll Cardiology 2020;142:e558-631.  Back to cited text no. 10
    


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