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Yetkin E 1. Affiliations 1 author 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract It is important not to overlook supraventricular tachycardia SVT in patients complaining of palpitation or tachycardia-related symptoms but with normal ECG and heart rate in emergency department or outpatient clinics.
Free full text. Cardiovasc Endocrinol Metab. Published online May PMID: Ertan Yetkin. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Received Oct 5; Accepted Dec All rights reserved. This article has been cited by other articles in PMC.
Go to:. Keywords: atrial natriuretic peptide, brain natriuretic peptide, C-type natriuretic peptide, natriuretic peptides, supraventricular tachycardia. Table 1 Diagnostic challenges in supraventricular tachycardia. Open in a separate window. Conflicts of interest There are no conflicts of interest. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol ; 31 — Circulation ; :e—e Supraventricular tachycardia.
N Engl J Med ; — Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder.
Arch Intern Med ; — Panic attacks and supraventricular tachycardias: the chicken or the egg? Neth Heart J ; 21 — Yetkin E. An extremely rare presentation of supraventricular tachycardia: burping. Int J Cardiol ; — Yetkin E, Kaleagzi FC. Recovery of absence seizure-like symptoms in a patient after slow pathway radiofrequency ablation.
Yetkin E, Tandogan I. Tinnitus preceding tachycardia and syncope. Asthma-like attacks terminated by slow pathway ablation. Ann Thorac Med ; 12 — Symptoms in supraventricular tachycardia: is it simply a manifestation of increased heart rate? Med Hypotheses ; 91 — Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Can J Cardiol ; 27 — Documented but non-induced supraventricular tachycardia and vice versa.
A cost-effectiveness analysis of a randomized trial of external loop recordersversus Holter monitoring. Am Heart J ; Electrophysiological studies in patients with paroxysmal supraventricular tachycardias but no electrocardiogram documentation: findings from a prospective registry. Europace ; 17 — Supraventricular tachycardia and the struggle to be believed. Eur J Cardiovasc Nurs ; 6 — Wood P.
Polyuria in paroxysmal tachycardia and paroxysmal atria1 flutter and fibrillation. Br Heart J ; 25 — Paroxysmal tachycardia with polyuria.
Ann Intern Med ; 65 — Plasma levels of immunoreactive atrial natriuretic factor increase during supraventricular tachycardia. Am Heart J ; — Renal response to paroxysmal tachycardia. Br Heart J ; 27 Endothelial production of C-type natriuretic peptide and its marked augmentation by transforming growth factor-beta.
J Clin Invest ; 90 — Effects of synthetic atria1 natriuretic factor on renal function and renin release. Am J Physiol ; :F—F A rapid and potent natriuretic response to intravenous injection of atrial myocardial extracts in rats.
Life Sci ; 28 — Plasma atrial natriuretic polypeptide concentrations during and after reversion of paroxysmal supraventricular tachycardias. Br Heart J ; 59 — Time course of changes in plasma vasopressin during atria1 distention.
Can J Physiol Pharmacol ; 60 — Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man.
Clin Sci Lond ; 82 — Atrial natriuretic peptide during supraventricular tachycardia and relation to hemodynamic changes and renal function. Am J Cardiol ; 16 — Physiologic changes during supraventricular tachycardia and release of atrial natriuretic peptide. Am J Cardiol ; 62 — Effects of auriculin atria1 natriuretic factor on blood pressure, renal function and the renin—aldosterone system in dogs. Am J Med ; 77 — Inhibition of aldosterone production by an atria1 extracts. Science ; — Renal hemodynamic and hormonal effects of human alpha atrial natriuretic peptide in healthy volunteers.
Lancet ; 1 — Plasma atrial natriuretic peptide in cardiac disease and during infusion in healthy volunteers. Natriuretic peptide system and the heart. Front Horm Res ; 43 — Potter LR. Natriuretic peptide metabolism, clearance and degradation. FEBS J ; — Abstract Introduction Hypothesis Diagnostic challenges in supraventricular tachycardia Natriuretic peptides and supraventricular tachycardia Conclusion Acknowledgements References.
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Multiple case reports of polyuria in patients with paroxysmal supraventricular tachycardia have been published [ 1 - 3 ]. A reduction of antidiuretic hormone ADH and secretion of atrial natriuretic peptide ANP are known to be involved in this phenomenon [ 4 , 5 ].
This phenomenon more commonly affects patients with paroxysmal atrial fibrillation a-fib than it does those with a valvular disease or chronic heart failure [ 1 , 3 , 6 ]. Here, we report a case of a-fib during insertion of a swan-ganz catheter, followed by polyuria during living-donor liver transplantation surgery. A year-old male, diagnosed with hepatocellular carcinoma, was admitted for a living-donor liver transplant.
The patient The patient had no notable medical history other than hypertension. No notable findings were obtained from the chest X-ray, electrocardiogram ECG , transthoracic echocardiography, coronary artery computed tomography, brain magnetic resonance image MRI , lung function test, blood tests, and arterial blood gas analysis performed at the time of admission. We placed a catheter in the right radial artery, two catheters in the right internal jugular vein, and a catheter in the right subclavian vein to secure access to a central vein.
We administered a beta blocker esmolol , which did not markedly change the ECG. The arrhythmia lasted for about 9 min, and a normal heart rhythm was spontaneously achieved. To avoid further a-fib, we retracted the swan-ganz catheter to a depth of 15 cm and attempted to fully reinsert it after 20 min; however, a-fib with a RVR occurred again Fig. The patient was immediately given a beta blocker esmolol , but the arrhythmia persisted; thus, an anti-arrhythmic agent amiodarone was continuously infused.
Hence, we decided to continue the surgery while carefully monitoring the patient. The results indicated natriuresis sodium clearance, The surgery proceeded without notable problems, after which the patient was transferred to the intensive care unit ICU.
According to Wood [ 1 ] and Luria et al. ADH and ANP are known to be potentially involved in the mechanism underlying tachycardia-polyuria syndrome [ 2 , 4 , 5 , 7 , 8 ]. In addition to receiving blood into the heart and releasing it into the ventricles, the atria also serve the function of detecting and regulating the intravenous volume.
This process, which begins with the atrial receptors, is known to involve neuronal and hormonal networks such as ADH and ANP [ 4 ].
An elevation of venous return in the body leads to atrial distention, which stimulates the atrial receptors [ 9 ]. These receptors depolarize the afferent vagal nerve to decrease the efferent sympathetic and vasomotor tones of the renal nerve, and to reduce ADH activity, thereby inducing diuresis [ 6 ].
Polyuria refers to an abnormally high output of diluted urine i. It can be caused by a variety of factors, and these conditions are collectively referred to as polyuria-polydipsia syndrome. The causes can be broadly classified into three factors: central diabetes insipidus CDI , nephrogenic diabetes insipidus NDI , and primary polydipsia. Because the causes and treatments for each of these factors differ, differential diagnosis is crucial [ 10 ]. The patient in this case had no abnormal preoperative brain MRI findings and had no history of endocrine diseases such as diabetes mellitus or renal diseases.
Further, the patient had a normal electrolyte balance during surgery, and none of the medications administered intraoperatively were known to induce polyuria. The patient developed polyuria during induction of anesthesia, allowing us to eliminate volume overload. It has been reported that paroxysmal a-fib induces atrial pressure and atrial volume expansion in canines under anesthesia [ 11 ]. Similarly, the a-fib observed in our patient is believed to have induced atrial volume expansion and, consequently, atrial wall distention, which would have led to a suppression of ADH and, thereby, caused diuresis.
However, contrary to the mechanism of tachycardia-polyuria syndrome as it is currently understood, our patient had a higher-than-normal plasma ADH concentration. ADH is known to regulate water absorption through the expression of aquaporin-2 on the V2 receptors of the collecting duct, and its production increases in response to increased plasma osmolality, reduced atrial pressure, and reduced intravascular volume [ 12 ].
Fuji et al. Thus, the elevated ADH in our case seems to be a compensation mechanism to counteract the reduction of intravascular volume caused by polyuria, as opposed to being the cause of polyuria.
ANP, which serves an essential role in tachycardia-polyuria syndrome, is a cardiac hormone secreted as a result of stretching of the atrial cardiocytes [ 13 ], and elevated atrial pressure is an important factor involved in its production [ 5 ].
ANP regulates the intravascular volume by blocking renin, angiotensin, and aldosterone secretion to induce natriuresis and diuresis [ 14 ].
Kinney et al. This suggests that sodium excretion was the cause of the observed diuresis [ 2 ]. One hour after achieving a normal rhythm, test results confirmed that natriuresis was reduced and, consequently, ANP levels would have been lowered [ 4 , 5 ]. Taken together, increased ANP seems to be the main mechanism of tachycardia and polyuria accompanied with natriuresis.
However, the fact that we did not measure ANP concentration is a limitation to our report. If the patient is hemodynamically unstable, they should be treated with electrical or chemical e. However, when unresponsive tachycardia occurs, as in the present case, DC cardioversion may be necessary to achieve a normal sinus rhythm.
The present case highlighted the possibility that iatrogenic a-fib occurring during insertion of a swan-ganz catheter may cause polyuria. Polyuria during surgery has a great influence on the patient's volume management. Therefore, an anesthesiologist must be familiar with the discrimination and treatment about perioperative polyuria.
Notably, if atrial fibrillation is the cause of polyuria, DC cardioversion could be a way to stop polyuria if the drug does not respond. This is atrial fibrillation occurred when swan-ganz catheter was inserted. This is atrial fibrillation occurred when swan-ganz catheter was re-inserted.
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