|Year : 2021 | Volume
| Issue : 2 | Page : 199-201
Anesthesia management in patient with nonobstructive hypertrophic cardiomyopathy with severe mitral valvular regurgitation with severe pulmonary artery hypertension for mitral valve replacement: Its “walk a tight rope”
Nikhil N Mudgalkar
Department of Anesthesiology, Prathima Institute of Medical Sciences, Karimnagar, Telangana, India
|Date of Submission||09-Dec-2020|
|Date of Decision||08-Feb-2021|
|Date of Acceptance||09-Feb-2021|
|Date of Web Publication||24-Aug-2021|
Dr. Nikhil N Mudgalkar
D 101, Prathima Institute of Medical Sciences, Nugnur Road, Karimnagar - 505 001, Telangana
Source of Support: None, Conflict of Interest: None
Hypertrophic cardiomyopathy (HCM) is a genetic disorder that is characterized by left ventricular hypertrophy unexplained by secondary causes and a nondilated left ventricle with preserved or increased ejection fraction. Mitral regurgitation is common in HCM secondary to distortion of mitral valve apparatus leading to systolic anterior motion. We report a case of HCM with rheumatic involvement of mitral valve with severe pulmonary artery hypertension and atrial fibrillation. With regard to hemodynamic management in patients with postcardiac surgery status, anesthetic management seems to be a “walk a tight rope.”
Keywords: Hypertrophic cardiomyopathy, mitral regurgitation, mitral valve replacement
|How to cite this article:|
Mudgalkar NN. Anesthesia management in patient with nonobstructive hypertrophic cardiomyopathy with severe mitral valvular regurgitation with severe pulmonary artery hypertension for mitral valve replacement: Its “walk a tight rope”. BLDE Univ J Health Sci 2021;6:199-201
|How to cite this URL:|
Mudgalkar NN. Anesthesia management in patient with nonobstructive hypertrophic cardiomyopathy with severe mitral valvular regurgitation with severe pulmonary artery hypertension for mitral valve replacement: Its “walk a tight rope”. BLDE Univ J Health Sci [serial online] 2021 [cited 2022 Jan 26];6:199-201. Available from: https://www.bldeujournalhs.in/text.asp?2021/6/2/199/324518
Hypertrophic cardiomyopathy (HCM) is associated with left-sided gradients across left ventricular outflow tract (LVOT). Mitral regurgitation is common in HCM secondary to distortion of mitral valve apparatus, leading to systolic anterior motion. The management line is very clear in scenarios where gradients across LVOT are higher, but difficulty arises when gradients are mild (<20), mitral regurgitation is severe with rheumatic etiology and dilated left atrium and elevated pulmonary artery pressures. Obvious plan of management is mitral valve replacement with prosthetic valve. Since few such cases are reported, there are no established guidelines in this scenario, making anesthetic management even more challenging.
| Case Report|| |
A 38-year-young male presented with increasing shortness of breath. On evaluation, he had severe mitral valve regurgitation, dilated left atrium (6.1 cm), and right atrium [Figure 1]. The patient was in atrial fibrillation and had severe pulmonary artery hypertension (right ventricular systolic pressures of 50). The HCM was asymmetric with septal thickness at base of 1.9 cm. There was systolic anterior motion of mitral valve [Figure 2]. The gradients across LVOT were 20. The cause of mitral valve disease was mitral involvement in rheumatic heart disease. The plan of surgery decided was to have mitral valve replacement and to check gradients across LVOT. If gradients were deemed to be higher, intraoperative myomectomy was planned.
A normal anesthetic induction was planned. 16G peripheral cannula, 20G left radial, 5 French femoral catheter, and 7 French triple lumen internal jugular cannulation were done under ultrasound guidance in local anesthesia. Monitoring included 5-lead electrocardiogram, invasive blood pressure, and central venous pressure, and transesophageal echo. Baseline pressures recorded to be 80 systolic; rhythm was atrial fibrillation with heart rate of 120. Central venous pressure was 20 which got slightly reduced after a diuretic dose. Midline sternotomy was done, and the patient went on pump after adequate dose of heparin. Mitral valve was replaced with saint jude mechanical valve 27 mm. Bypass was weaned slowly with systolic pressures of 70. Slight fluid bolus (200 ml) raised pulmonary artery pressure with slowing down of heart which was managed by unloading of heart from perfusion side, while slight inotrope (0.04 mcg/kg/min phenylephrine) led heart to fibrillate by virtue of closure of LVOT. The decision was taken to accept blood pressures of 70 systolic with mean pressures of 55 in view of closure of LVOT related to ionotrope use. Pressures slowly improved in next 6 h and ranged between 80 and 90. The peculiar scenario we faced in early postoperative period was a slight fluid bolus lead to increase in pulmonary artery pressures and slowing of heart rate while we could not give inotropes in view of LVOT obstruction related to ionotrope infusion. Weaning attempts after 24 h failed in view of generalized tonic–clonic seizures. Computed tomography brain was normal, but patient developed hemiparesis on the left side and weaned off ventilator with tracheotomy tube in next 96 h according to standard protocols. The patient was discharged without residual neurologic damage on 7th postoperative day. He is on follow up at 3rd month.
| Discussion|| |
In patients of HCM, increased myocardial contractility, decreased preload, and after load exacerbate the degree of LVOTO. Anesthetic induction needs to focus on blunting intubation response as well avoiding hypotension related to cardiodepressant medications. Phenylephrine is a good choice for hypotension while ionotropes and chronotropes need to be avoided. Lower heart rate and sinus rhythm are very much important to maintain coronary perfusion pressure as the left ventricle is very less compliant. The goals of anesthesia stated are preservation of preload and after load, controlled heart rate, sinus rhythm, mild suppression of myocardial contractility, and maintenance of myocardial perfusion pressure.,
In our case, there are many negative factors which we could not control. The first is atrial fibrillation, which stopped the atrial kick and increased pressure on already noncomplaint left ventricle. The very high pulmonary artery pressure and tendency toward bradycardia related to slight increase in preload was another obstacle in management., Tendency toward fibrillation with slightest dose of phenylephrine was another obstacle. Hence, we accepted lower physiological goals of blood pressure. Although the patient developed stroke, patient recovered after a long postoperative stay in intensive care unit with fully preserved neurologic function.
| Conclusion|| |
To conclude, there is a very thin line between avoiding LVOT obstruction in view of nonavailability of many choices of ionotropes and slight fluid overload, leading to increase in pulmonary artery pressures in such scenarios. Accepting lower targets of blood pressure might be a reasonable strategy in such cases.
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
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]