Introduction
Sinus tachycardia, atrial premature beats and, in some cases, atrial fibrillation are frequent complications of overt hyperthyroidism.1 We report a rare case of a patient with subclinical hypothyroidism where supraventricular tachycardia was the presenting feature.
Case Reports
A 24 year old, 80 kg male, case of post traumatic stricture urethra was posted for urethroplasty. Following a road traffic accident, he underwent suprapubic catheterization under local anaesthesia and later visual internal urethrotomy under spinal anaesthesia. Anaesthesia course for these procedures was uneventful. He was a chronic gutkha chewer and had restricted mouth opening with an interincisor distance measuring 2 finger breadths. Rest of the history was unremarkable. Laboratory investigations including complete haemogram, blood sugar, renal and liver function tests and S. electrolyes were within normal range. Chest radiograph was normal.
His preoperative vitals were as follows: Pulse: 82/minute, regular, Blood pressure: 110/84 mmHg, SpO2: 99% on room air. We planned an awake fibreoptic nasotracheal intubation. Procedure was explained to patient and informed consent was obtained. IV Glycopyrrolate 0.2 mg and IV Metoclopramide 10 mg was administered. Topical analgesia for the procedure was achieved by nebulisation of 160 mg of Lignocaine in saline for 15 minutes. Xylometazoline drops were then instilled into both the nostrils. IV Midazolam 1 mg and IV Fentanyl 100 µg was administered. After re-explaining the procedure to the patient, the fibrescope was introduced via the right nostril. As soon as the tip of the fibrescope touched the nasal mucosa, patient’s heart rate increased to 190/minute with narrow complex tachycardia on cardioscope. Blood pressure measured 75/46.The scope was immediately removed and patient was administered 100% oxygen. Rate of IV fluid administration was increased. The blood pressure rose to 90/60 mmHg in 2 minutes and then 105/70 in another 2 minutes. The heart rate and rhythm however, persisted. Carotid sinus massage was given which failed to revert the tachyarrhythmia. Additional IV Midazolam 1 mg was given. 500 ml of IV Ringer’s lactate was administered over a period of 20 minutes. Patient was deeply sedated but heart rate persisted in the range of 180-210/minute. Blood pressure remained stable thereafter. 12 lead ECG was done which showed narrow complex tachycardia. Cardiology opinion was sought and patient was observed in the OR keeping all anticipated emergency drugs and defibrillator ready. After a total duration of 1 hour and 15 minutes, the rhythm suddenly reverted to normal, from a heart rate of 182/minute to 82/minute. Blood pressure measured 116/76 mmHg. A decision to defer surgery was taken and the patient was shifted to the PACU for continued observation. A detailed cardiac evaluation and thyroid profile was advised.
Further evaluation revealed him to be a case of Hashimoto’s thyroiditis. T3 and T4 were on the lower side of normal and TSH was very high (64.8 µIU/ml against a reference range of 0.27-4.20 µIU/ml) Serum antimitochondrial antibodies were positive in high titres.He was started on Tab. Levothyroxine 125 µg OD. Echocardiogram was normal with an ejection fraction of 60%. He was started on Tab. Diltiazem for 1 month after the tachyarrhythmia episode. Thyroid function tests reverted to normal and the patient was posted for urethroplasty 4 months later. Repeat laboratory investigations were within normal limits. Patient was administered Tab. Diazepam 10 mg on the night prior to surgery and Tab. Levothyroxine in his usual dose on the day of surgery. We performed the surgery using combined spinal epidural anaesthesia. Surgery lasted 4˝ hours. Vital parameters remained stable throughout and the patient had an uneventful perioperative course. He was discharged on the 4th postoperative day with advice to be on regular endocrine follow up.
Discussion
Supraventricular tachycardia is any tachyarrhythmia that requires atrial or atrioventricular junctional tissue for its initiation and maintenance. The term “paroxysmal atrial tachycardia” was coined to describe supraventricular tachycardia that began and ended abruptly.
It is well known that thyroid hormones have electrophysiological actions that are important in triggering supraventricular arrhythmias.Thyroid hormones have direct positive chronotropic effect because of a reduced time of repolarization phase of the action potential, which results in shortening of the effective refractory period.2
In most cases, supraventricular tachyarr-hythmias have been associated with hyperthyroidism. Several reports cite thyrotoxicosis and thyroid storm manifesting as supraventricular tachycardia.3-5
In a study of thyroid function in patients with paroxysmal supraventricular tachycardia who presented to a cardiology clinic, Vanin et al6 report that 6 out of 29 patients were found to have latent thyroid disorders, with 4 diagnosed as having hypothyroidism. They suggest that thyroid dysfunction may be just a triggering factor of arrhythmia since thyrostatic and replacement therapy eliminate paroxysms of tachycardia, while organic pathology of the heart and its conductive network remains unaffected.
Inama et al7 report that 3.8% of their patients visiting the cardiology clinic had evidence of dysthyroidism. The control of the thyroid pattern, especially as regards atrial fibrillation and paroxysmal supraventricular reciprocating tachycardia resulted in absence of arrhythmic episodes even without treatment in 40% of cases, and in an easier drug control in the other cases.
In patients with sustained supraventricular tachycardia who do not have serious haemodynamic compromise, an attempt to determine the mechanism of the tachycardia should be made before initiating treatment. Immediate measures to terminate the arrhythmia include vagal manoeuvres and Adenosine, an a1-receptor agonist with a rapid onset and brief duration of action. The calcium-channel blockers verapamil and diltiazem, when given intravenously, are also useful. Electrical cardioversion may also be used when necessary. Long term therapy includes use of calcium channel blockers and radiofrequency ablation in selected cases.8
In conclusion, supraventricular tachycardia may rarely be a feature of undiagnosed hypothyroidism. It is necessary to carry out systematic research of a thyroid dysfunction in all patients with cardiac arrhythmias.
References
- Olshausen KV, Bischoff S, Kahaly G, et al. 1998 Cardiac arrhythmias and heart rate in hyperthyroidism. Am J Cardiol 63 : 930-3.
- Biondi B, Fazio S, Coltorti F, et al. Reentrant atrioventricular nodal tachycardia induced by levothyroxine. J Clin Endocrinol Metab 1998 Aug; 83(8) : 2643-5.
- Wald DA, Silver A. Cardiovascular manifestations of thyroid storm: a case report. J Emerg Med 2003 Jul; 25(1) : 23-8.
- Yu YH, Bilezikian JP. Tachycardia-induced cardiomyopathy secondary to thyrotoxicosis: a young man with previously unrecognized Graves’ disease. Thyroid 2000 Oct; 10(10) : 923-7.
- Hadidy S, Issa F, Hourani N. Supraventricular arrhythmias and the relation to thyroid dysfunction in a group of Syrian patients. Trop Geogr Med 1986 Jun; 38(2) : 158-61.
- Vanin LN, Smetnev AS, Sokolov SF, et al. Study of thyroid function in patients with paroxysmal supraventricular tachycardia. Kardiologiia 1989 Jan; 29(1) : 71-4.
- Inama G, Furlanello F, Fiorentini F, et al. Arrhythmogenic implications of non-iatrogenic thyroid dysfunction. G Ital Cardiol 1989 Apr; 19(4) : 303-10.
- Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332(3) : 162-72.
STROKE - PREVENTION IS BETTER THAN CURE
Unfortunately, despite years of research, alteplase is still the only approved treatment for ischaemic stroke. Alteplase is efficacious in some patients if given within 3 h of stroke onset. Ideally, a stroke centre will have access to MRI, which according to Julio Chalela and colleagues, is better than computed tomography for detection of acute ischaemia, and is also able to detect acute and chronic haemorrhage.
Combination therapies - e.g., combining alteplase with antiplatelet agents - might prove to be of benefit, as could sonothrombolysis - the use of ultrasound waves to break up clots. New thrombolytics are also in development: desmotoplase tenectoplase seem to be most promising.
A third of all stroke deaths are in people younger than 70 years of age, with 94% of those deaths taking place in low-income or middle-income countries. Implementation of intervention that reduce hypertension, poor diet, and tobacco use will save more lives than all the thrombolytics, antiplatelets, and neuroprotectants combined.
The Lancet 2007; 369 : 247.
*Associate Professor; **Registrar; Department of Anaesthesiology, T N Medical College and BYL Nair Hospital, Mumbai - 8.
|
