|Year : 2017 | Volume
| Issue : 2 | Page : 103-105
Anaesthetic management of a patient with hypertrophic obstructive cardiomyopathy posted for emergency lower segment caesarean section
Pradnya M Bhalerao, Pritam B Adsule, Radhika M Marathe
Department of Anaesthesiology, Government Medical College Miraj and Sangli Civil Hospital, Sangli, Maharashtra, India
|Date of Web Publication||7-Nov-2017|
Pradnya M Bhalerao
Department of Anaesthesiology, Government Medical College Miraj and Sangli Civil Hospital, Sangli, Maharashtra
Source of Support: None, Conflict of Interest: None
Hypertrophic cardiomyopathy is characterised by asymmetric hypertrophy of the interventricular septum causing intermittent obstruction of the left ventricular outflow tract. This disease may present to the anaesthesiologist in an undiagnosed form during routine pre-operative visit. Surgery and anaesthesia often complicate the peri-operative outcome in this group of patients. A 22-year-old patient was brought in for emergency lower segment caesarean section. She was a diagnosed case of hypertrophic obstructive cardiomyopathy (HOCM) with severe left ventricular outflow tract obstruction and moderate subaortic stenosis. Factors such as tachycardia, hypovolemia, vasodilatation, and increased cardiac contractility leads to exacerbation of this obstruction. We managed this case successfully considering the pathological issues caused by the disease and pregnancy.
Keywords: Caesarean section, general anaesthesia, HOCM
|How to cite this article:|
Bhalerao PM, Adsule PB, Marathe RM. Anaesthetic management of a patient with hypertrophic obstructive cardiomyopathy posted for emergency lower segment caesarean section. J Obstet Anaesth Crit Care 2017;7:103-5
|How to cite this URL:|
Bhalerao PM, Adsule PB, Marathe RM. Anaesthetic management of a patient with hypertrophic obstructive cardiomyopathy posted for emergency lower segment caesarean section. J Obstet Anaesth Crit Care [serial online] 2017 [cited 2021 May 8];7:103-5. Available from: https://www.joacc.com/text.asp?2017/7/2/103/217769
| Introduction|| |
Hypertrophic cardiomyopathy is an autosomal dominant genetic cardiac disorder caused by a mutation in 1 of at least 10 genes that encode the proteins of the cardiac sarcomere. It occurs in 1 in every 500 adults in the general population, with a male: female ratio of 2:1. The prevalence is approximately 0.2% in the general population, and the incidence in pregnant females is approximately 0.1–0.5%. It includes massive hypertrophy primarily involving the ventricular septum.,, Although majority of the patients are asymptomatic throughout life, some present with severe limiting symptoms of dyspnoea, angina, and syncope and a few may even die suddenly because of ventricular arrhythmias. Left ventricle outflow tract obstruction (LVOT) can be precipitated by sympathetic stimulation and decrease in pre-load and afterload to the left ventricle. In pregnant patients with HOCM, the gravid uterus causes aortocaval compression and hence decreased pre-load. Labour pains lead to tachycardia. Hence, these patients pose higher risk for peri-operative events.
| Case Report|| |
A 22-year-old patient was posted for emergency lower segment caesarean section, indication being foetal bradycardia. Her previous documents revealed that she was a diagnosed case of hypertrophic obstructive cardiomyopathy during her last pregnancy 3 years ago. Presently asymptomatic she was on tablet metoprolol 20 mg once daily since. On examination, her pulse rate was 96 beats per minute and blood pressure was 140/60 mmHg. She had systolic murmur over all the chest fields. Routine laboratory investigations were within normal limits. Electrocardiogram (ECG) showed left ventricular hypertrophy. Her old echocardiography report revealed features of hypertrophic obstructive cardiomyopathy with severe LVOT obstruction. Left ventricular ejection fraction (LVEF) was 40%.
A written, informed high-risk consent was taken. General anaesthesia was planned for lower segment caesarean section as indication was foetal bradycardia. Intravenous line was secured and ringer lactate was started. Pulse oximeter and ECG were attached. The patient was pre-medicated with injection ranitidine 50 mg intravenously (iv), injection ondansetron 4 mg, and injection fentanyl 50 μg iv. After left uterine displacement, rapid sequence induction was performed with injection thiopentone 250 mg iv and suxamethonium 75 mg iv was given to facilitate endotracheal intubation with portex cuffed tube. Anaesthesia was maintained on sevoflurane 0.8 to 1%, and vecuronium 3 mg iv. as a muscle relaxant. Injection oxytocin 10 units was given as a slow infusion. Haemodynamic stability was maintained throughout the procedure. At the end of the surgery, the patient was reversed with intravenous glycopyrrolate 0.04 mg and neostigmine 2 mg.
| Discussion|| |
Pathophysiology of hypertrophic obstructive cardiomyopathy includes “dynamic” obstruction of LVOT, as this obstruction is variable and depends on the volume of blood in ventricle immediately before ventricular systole. The dynamic obstruction is caused by systolic anterior motion of anterior mitral valve leaflet causing mitral regurgitation, diastolic dysfunction, and dysarrhythmias. The additional volume load of pregnancy causes enlargement of the ventricular cavity, which theoretically might reduce the LVOT obstruction; however, the increased cardiac output counteracts this effect and the LVOT gradient increases with advancing gestation. The same volume loading increases distension of the left atrium and thereby the risk of atrial fibrillation. In the context of diastolic disease, the volume changes and increased heart rate are not well tolerated, aggravating the symptoms of dyspnoea and lowering the threshold for developing left heart failure. Severity of obstruction is increased by the factors which reduce ventricular size. Pregnancy further complicates the disease due to decrease in systemic vascular resistance and risk of impaired venous return due to compression of inferior venacava by gravid uterus. However, women with HOCM generally tolerate pregnancy well. The risk is higher in women who are symptomatic before pregnancy and when severe LVOT obstruction exists.
Factors such as anxiety, stress, and labour pain increase heart rate and contractility.
We preferred to give general anaesthesia to our patient as it was an emergency foetal distress. Our patient was on tab. metoprolol. Metoprolol has an added advantage of reduced heart rate, improved ventricular filling, and myocardial oxygen demand, however, the use of beta blockers in pregnancy is controversial as they may lead to fetal acidosis. Further, it reduces the hemodynamic response to intubation. Injection fentanyl was given as it alleviates sympathetic activity with added analgesia. Use of intravenous induction agents such as thiopental is acceptable to induce anaesthesia but sudden decrease in systemic vascular resistance should be avoided. Sevoflurane, for maintenance, was used in our case as it is cardiostable. Non-depolarising muscle relaxants have only minimal effect on haemodynamics. We preferred using vecuronium as it is cardiostable. Hypotension may occur in response to decrease in pre-load and after load, and should be treated with α-agonists such as phenylepherine. Drugs with beta agonistic activity such as dopamine, ephedrine, and dobutamine may be avoided as they tend to increase myocardial contractility and heart rate, thus precipitating LVOT obstruction. Slow and continuous administration of oxytocin is safer as hypotension and tachycardia are known side effects. Pulmonary edema has been observed in patients after delivery, thus delicate fluid management is necessary. Severe hypertrophic cardiomyopathy can be monitored with transthoracic echocardiography to guide management of fluids and vasopressors during elective caesarean section.
Epidural anaesthesia with precise drug titration is a safer and better alternative, and is well tolerated by the parturient. Epidurals must be administrated cautiously in patients with severe LVOT obstruction. There is a reduced risk of mortality, myocardial infarction, and supraventricular arrhythmia. The benefits of pain reduction and reduced sympathetic stimulation may overweigh the disadvantage of vasodilatation and hypotension in epidural analgesia. The epidural technique has an additional advantage of post-operative analgesia as epidural top-ups can be given post-operatively. Spinal anaesthesia should be avoided in patients with HOCM as it leads to sudden hypotension and decreased venous return, and decrease in pre-load and after-load aggravates LVOT obstruction. Good analgesia should be given to keep the patient pain free post-operatively. Monitoring of HOCM patients should be continued post-operatively as cardiac failure has been noted even 48 hours post-operatively.
| Conclusion|| |
Successful anaesthetic management in patients with HOCM requires understanding of hemodynamic changes, proper intraoperative monitoring and preventing factors which cause LVOT obstruction.
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Conflicts of interest
There are no conflicts of interest.
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