A sigh, defined as a breath larger than 3 times the average breath volume, is a normal phenomenon occurring in healthy adults, when they are relaxed in a semi-recumbent position, at an average rate of 9–10 per hour. There are two types of sigh, according to the exact point at which they interrupt the regular breathing cycle. Fifty per cent of sighs ‘take off’ from the early expiratory phase following a normal intake of breath (Type I), while the rest ‘take off’ from the end of the expiratory phase (Type II). The new-born human infant, asleep, typically has Type II sighs (2 × average breath volume) at a frequency of 18–70 per hour in the first 24 hours of life; by 5 days the frequency is down to 6–36 per hour. Studies in anaesthetized cats and rabbits, who also sigh, have demonstrated the presence of an inspiratory-augmenting reflex, mediated by vagus nerve receptors within the lung airway, and this mechanism may be responsible, in part, for the sighing. The reflex is particularly sensitive to excitation after short periods of airway occlusion resulting in patchy lung collapse with increasing lung stiffness and hypoxia. With a sigh, collapsed areas of lung open up, removing the stimulus to sigh and at the same time restoring lung stiffness to its normal range. Moreover, we now know that a large breath will stimulate production, by some cells in the lung airspaces, of a surface-active material that minimizes the surface tension in the fluid lining the airspaces. This surface tension would otherwise tend to close the airspaces, particularly when they are small. Quiet breathing, whether spontaneous or on a ventilator, in adult humans at rest is associated over time with an increase in lung stiffness; this is completely reversed by 1–2 sighs, which may explain the sense of satisfaction and well-being produced by the sigh.
During the 1930s, sighing became a symptom of a ‘respiratory neurosis’. It was a particular feature of soldiers who had served in the 1914–18 War and developed ‘effort syndrome’. This was first thought to be a ‘cardiac neurosis’, particularly because of the frequency of left submammary pain and the complaints of ‘breathlessness at rest’ together with ‘inability to get enough air into the lungs’. Objectively, all that was found was an irregularity of respiratory depth and rate together with frequent (Type I) sighing; the heart and lungs were normal. Breathing became abnormal with the slightest emotional stimuli. Extreme yawning often accompanied the sighing, and this commonly caused temporary relief of the sense of respiratory oppression. Nowadays, we would consider these patients as having a chronic anxiety state, with or without panic, with a predisposition to overbreathe in response to stress. Sighing (Type I) may occur at rates of up to 25/min! We have no clear-cut neurophysiogical basis for this breathing behaviour, now called a ‘hyperventilation disorder’. However, we do know that breathing can be ‘driven’ by activation of the amygdaloid nucleus within the limbic system — a complex brain area concerned with feeling and emotions. Common experience confirms the reality of this link, no better documented than by W. Shakespeare in Jacques' soliloquy in As You Like It, Act II, Scene 5 — ‘All the world's a stage … And then the lover, Sighing like a furnace, with a woeful ballad, Made to his mistress' eyebrow.’
Baker, D. M. (1934). Sighing respiration as a symptom. The Lancet, Jan 27th, 174–6.
Bendixen, H. H.,, Smith, G. M.,, and and Mead, J. (1964). Pattern of ventilation in young adults. Journal of Applied Physiology, 19(2), 195–8.
Thach, B. T. and and Taeusch, H. W. Jr. (1976). Sighing in newborn human infants: role of inflation-augmenting reflex. Journal of Applied Physiology, 41(4), 502–7.
See also hyperventilation; lungs; surfactant.