Polyuria in Paroxysmal Tachycardia and Paroxysmal Atrial Flutter and Fibrillation

Abstract

When Paul Wood spoke about this to the British Cardiac Society in 1961, we were impressed by the originality of his work on a subject that so many had noticed but failed to investigate. A few months before his death in July 1962, when I asked him if his paper was ready for thejournal, he said that he had not yet been able to get all the evidence he hoped for to establish the full explanation. Unfortunately, he had not the time to complete this. I have, therefore, tried to set out as clearly as possible the stage that he had reached. MAURICE CAMPBELL For some nine years (since 1952) I have observed that a remarkable polyuria may accompany paroxysmal tachycardia. The phenomenon seems little known. Thus Paul White (1951) says "An occasional symptom during or following paroxysmal tachycardia is increased frequency or increased amount of urination, doubtless a nervous reflex." Friedberg in his first edition (1949) states that "there may be polyuria at the termination of the paroxysm," but changes this in his second edition (1956) to "during or at the termination of the paroxysm." Katz and Pick (1956) in a book devoted to the arrhythmias say " Frequency of urination is an unusual symptom in short attacks, but polyuria is often seen after the termination of long ones." I could find no other mention of polyuria relating to paroxysmal tachycardia in any textbook of cardiology written in the English language-except in the second edition of my own book (1956) where it says "If the heart is normal, there is usually a remarkable degree of polyuria during the attack." At that time the mechanism of the diuresis was obscure. In 1955 in a letter to Dr. Carter about a woman of 46 with paroxysmal tachycardia associated with the Wolff-Parkinson-White syndrome, I wrote " She has had the attacks off and on for six months and is now getting them very frequently, even several a week, and sometimes they last up to 24 hours. The palpitations are fast, regular, and of abrupt onset: the offset does not seem to her abrupt, but she is aware when the attack ends. Twenty minutes after the onset polyuria begins and she passes large quantities of water every 20 minutes throughout the attack. This state of functional transient diabetes insipidus is characteristic of paroxysmal tachycardia with a good cardiac output, but we have no idea whether the effect is related to the renal blood flow or whether it is due to suppression of the anti-diuretic hormone of the pituitary for reasons that are not understood." I decided to let the matter rest until I had collected sufficient clinical data to be worth analysing, in the hope that natural experiments would point the way to the solution of the problem. These data are now available and I would like to present them to you. In the first place three statements may be made with confidence. (1) Polyuria may occur with any form of paroxysmal arrhythmia with rapid heart rate (but so far not with paroxysmal heart block or with paroxysmal nodal rhythm). (2) Polyuria does not usually occur in short attacks lasting ...

Atrial natriuretic peptide: what is the excitement all about?

“…Grossly increased plasma ANP concentrations would not appear to be a distinguishing feature of human essential hypertension. It has long been known that the onset of tachycardia can be associated with a profound natriuresis and diuresis of uncertain cause (Wood, 1963). Preliminary results showed that the onset of tachycardia was associated with very large (up to 140 pmol/1) rises of the plasma ANP concentration in patients who had normal levels (less than 15 pmol/1) immediately before onset, and that these returned rapidly to normal after reversion to sinus rhythm (Anderson et al 19866).…”

Biologically active atrial peptides.

“…Expansion of the extracellular fluid volume fails to elicit an increase in urine flow when atrial stretch is prevented (2). Conversely, inflation of a balloon within the right atrium, even in the absence of extracellular fluid volume expansion, results in enhanced urine flow and salt excretion (3), and natriuresis and diuresis frequently accompany paroxysmal atrial tachyarrhythmias (4,5). The renal response provoked by atrial distension or atrial tachycardias has usually been ascribed to reflex stimulation of neural stretch receptors located in the subendocardium (6) but a humoral mediator has also been considered (1).…”

Plasma Atrial Natriuretic Peptide Is Increased During Atrial Pacing in Conscious Rabbits

“…(1986) demonstrated in anaesthetized rabbits that plasma ANP concentration rose with cardiac pacing even after vagal or sympathetic blockade. It has been suggested that atrial distension is the main stimulus for release of ANP in these patients (Schiffrin et al 1985) as pressure in the right atrium increases during paroxysmal supraventricular tachycardia (Wood 1963). Furthermore studies in rats recently suggested that plasma ANP most closely correlates with right atrial pressure (Katsube et al 1985).…”