mise à jour du
23 décembre 2004
American J Physiology
1944; 142; 721-726
Influence of dying gasps, yawns and sighs on blood pressure and blood flow
R Woodbury, B Abretj
Department of Pharmacology, University of Georgia School of Medicine, Augusta
Remarques sur la signification physiologique du bâillement Lepp FH


Earlier studies have demonstrated that interesting and important circulatory changes accompany excessively prolonged or severe expiratory activities such as crying, coughing and straining. Circulatory changes would also be expected to accompany excessively prolonged or severe inspiratory acts such as dying gasps, yawns and sighs. Yet, none are described in the current literature and textbooks. It is interesting that Stephen Hales in 1733 observed that deep sighing and respiratory efforts of dying mares increased systematic arterial pressure. He believed the greater motion of the lungs caused the blood to pass more freely and in greater quantity to the left heart.
The observations reported in the present study are limited principally to the effects of normal respiration, deep breathing and dying gasps, since yawns and sighs could not be induced experimentally in dogs. However, the data have allowed appreciation of the hemodynamic changes induced by sighs and yawns.
METHODS. Morphine sulfate, 5 mg per kg, was administered subcutaneously 30 minutes prior to the experiments. All operative procedures were accomplished with the aid of local infiltrations of 1 per cent procaine hydrochloride. In those experiments where it was necessary to enter the chest, the appropriate intercostal nerves were blocked.
Changes in the pressure relationships between the thoracic and abdominal cavities were measured since they modify venous return from the abdominal reservoirs to the right heart. Balloons fastened to leaden tubes and inserted into the abdominal and thoracic cavities were connected to a differential manometer so that the intrathoracic pressure was subtracted from the abdominal pressure. This differential pressure has been called the abdominal thoracic pressure gradient. Changes in this gradient modify venous return to the right heart and can result from unequal increases or decreases in the intrathoracic or intra-abdominal pressures. When it was unnecessary to enter the chest, the balloons were inserted through the mouth and into the esophagus or stomach. Long balloons only partially filled were used since they tend to dissipate pressure changes from the activity of the alimentary canal but register the changes transmitted to them from the intrapleural space and abdominal cavity. These esophageal and gastric pressures were considered to change in parallel with thoracic and abdominal pressures.
Hollow sounds constructed from stainless steel tubing G 12 to 16 and adapted to the size of the animal were connected to other optical manometers and were inserted 1, down the left carotid and into the left ventricle, and 2, down the right external jugular and into the right ventricle. Saline infused through these sounds at the rate of about 1 cc. per minute reduced the danger of obstruction by coagulation. This made it possible to obtain continuous simultaneous pressure records from the left and right ventricles in the closed chest. Both gross and net ventricular pressures were obtained. The gross pressures were obtained with simple manometers (1), as commonly measured from the ventricular cavities and show both active and passive changes. The net ventricular pressures are the gross pressures minus the intrathoracic pressure and were obtained with differential manometers (4) where the ventricular pressures were led to the rear chambers and the intrathoracic pressure was led to the front chambers of the manometers in the usual manner. These net ventricular pressures show only active changes and are the pressures actually distending the heart cavities. They are the effective blood pressures to the blood vessels and organs within the thorax. The net left ventricular systolic pressure can be considered equivalent to the net coronary systolic pressure. The net right ventricular systolic pressure be can considered equivalent to the net pulmonary arterial systolic pressure. In addition to the net coronary systolic and the net pulmonary arterial systolic pressures, when necessary to determine net pulmonary venous and net inferior vena cava pressures, they can be obtained from such records by considering thefollowing as equivalents: the net right ventricular diastolic pressure is equivalent to the net inferior vena cava pressure; the net left ventricular diastolic pressure is equivalent to the net pulmonary venous pressure.
Similar methods supplied measurements of the gross and net systemic arterial pressure to the central nervous system. The gross systemic arterial pressure acts to push blood to organs including the brain and spinal cord. The pressure within the craniospinal cavity acts to hinder blood inflow. Therefore, the effective arterial pressure to the central nervous system is the arterial pressure minus the cerebrospinal fluid pressure. This effective pressure has been called the net arterial pressure to the brain and spinal cord and has been calculated from simultaneous measurements of the arterial pressures and cerebrospinal fluid pressures. The cerebrospinal fluid pressure was recorded from no. 18 or no. 20 G needles inserted in three animals into the subarachnoid space in the region of the first or second lumbar vertebra.
Acute cardiac arrest was produced by electrically induced ventricular fibrillation. In four dogs the electrodes were placed upon the ventricles while inserting the thoracic balloons. The chest was then closed and the pneumpthorax was reduced. In two other animals where the chest was not opened an insulated sound with the end serving as the stimulating electrode was introduced down the external jugular into the right ventricle. An indifferent electrode was placed upon the skin over the heart. The various gross and net pressures were then recorded while stimuli were applied to the ventricle using two batteries and a Harvard Inductorium at full strength. (...)
yawn blood pressure
RESULTS AND DISCUSSION. First the effects of normal respiration will be described. As shown in figure 2A, normal inspiration (arrow) lowers the thoracic pressure and increases the abdominal thoracic pressure gradient which increases venous return td the heart from the portal system and the inferior vena cava. During inspiration the net right ventricular pressure pulses show a higher pulse pressure and a peak with a wider plateau, see second and third NR pressure pulses of figure 2A. These changes indicate a larger and more prolonged effective ejection period without any appreciable change in the duration of systole. These changes are interpreted as characteristic of an increased right cardiac output secondary to an increased filling with inspiration.
When ventricular fibrillation was induced with strong tetanizing electrical stimuli applied directly to the heart in the closed chest, respiratory activity continued for several minutes after effective cardiac action had ceased. The deep foreeful natural breathing (see fig. 2B) produced significant changes in the blood pressure and circulated blood. During inspirations (arrows) the abdominal thoracic pressure gradient is increased; the gross right ventricular pressures returned toward zero; but the effective net right ventricular pressure (NR) increased. As shown in figure 2B, it reached values between 25 and 30 mmHg which were approximately equal to those produced by the right ventricle when it was contracting (fig. 2A). Simultaneously these deep respiratory efforts produced only small changes in the effective net left ventricular pressures (NL). It can be concluded from these data that repeated deep forceful breathing, even in the presence of complete cardiac arrest, repeatedly increased venous return to the right ventricle and to the pulmonary vessels while moving a smaller quantity of blood from the pulmonary vessels on into the left ventricle. This also means that deep forceful breathing in the presence of cardiac failure can contribute to pulmonary engorgement by transferring blood from the abdominal venous reservoirs to the pulmonary vessels.
Since sighs and yawns are modified deep breaths they also should increase venous return to the right heart. It has been observed by one of the authors that small children when asleep will usually yawn if they are lifted into an upright position. Sometimes the yawn would occur repeatedly each time they were changed to an upright position. This yawn could be physiologically required to increase air exchange or to increase venous return. There is no reason to expect any real need of increased air exchange. However, it is conceivable that a sudden change to an upright position in an individual whose muscles are relaxed would retard venous return sufficiently so that a mechanism to increase venous return operates.
A yawn to be truly satisfying frequently is accompanied by a stretch. When present the stretch not only contributes to venous return but also, like the dying gasp, tends to divert blood to the heart and central nervous system.
Circulatory changes are pronounced during dying gasps. The effective net
right ventricular pressure is elevated to values as high as 50 mmHg (see fig. 2C). The pulmonary vessels become so engorged that blood is pushed through to the left ventricle and elevates the effective net pressure in that chamber to 30 to 50 mmHg.
These dying gasps not only increase venous return but they cause significant coronary blood flow. Blood is pushed or diverted into the coronary vessels as a result of the extensive skeletal muscle activity and the elevated abdominal pressure, both of which squeeze blood vessels and increase peripheral resistance. Simultaneously the intrathoracic pressure is reduced so that peripheral resistance in the coronary vessels is lowered while the effective net coronary arterial pressure is elevated.
In similar experiments net cerebrospinal arterial pressures of 20 to 40 mmHg were produced by dying gasps. Therefore blood flow to the central nervous system is also accomplished by dying gasps. The mechanisms responsible for blood flow to the central nervous system were only slightly less effective than those described above which produced coronary flow, since dying gasps lower the cerebrospinal fluid pressure only slightly less than they lower the intrathoracic pressure. This is due to the fact that the cerebrospinal fluid pressure is influenced by the algebraic sum of the intrathoracic and abdominal pressure, though unpublished data indicate that it follows the intrathoracic pressure more closely than it follows the abdominal pressure.
These gasps produce air exchange and move blood to the vital areas, whereas mechanical resuscitators provide air exchange but do not cause any significant blood flow to the vital areas.
Cases have been encountered where patients apparently dead and without any evidence of heart action have again developed palpable pulse and audible heart contractions immediately after making dying gasps. Similar observations have probably been passed off with the remark "I must have been wrong when I failed to observe any pulse the first time." it is conceivable however that the blood pumping action of the dying gasps contributed to the return of effective cardiac contractions.
Gross and net, left and right ventricular pressures are recorded from dogs without operative entrance into the chest by means of hollow sounds inserted down the left carotid into the left ventricle and down the right jugular into the right ventricle.
Normal inspiration increases venous return to the right heart and produces contour changes characteristic of larger and more prolonged effective ejection without significantly changing the duration of systole.
Dying gasps, deep breathing, yawns and sighs which are generally considered as respiratory acts, markedly increase venous return. In the presence of cardiac arrest, dying gasps pump blood through the lungs and temporarily provide blood flow to the vital areas, the central nervous system and heart. Effective net pressure as great as 50 mmHg in the pulmonary artery, 50 mmHg in the coronary arteries and 40 mmHg in the central nervous system arteries were created by dying gasps in dogs where cardiac action had ceased.
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-Woodbury R, B Abretj Influence of dying gasps, yawns and sighs on blood pressure and blood flow Am J Physiol 1944; 142; 721-726