CARDIOVASCULAR EFFECTS OF
"BUCCAL PUMPING" IN BREATH-HOLD DIVERS

Originally published in: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 103-106.


INTRODUCTION

"Buccal pumping" is a technique by which some breath-hold divers voluntarily can increase their lung volume above their normal total lung capacity (TLC). After a completed maximum inspiration, the diver "gasps" air into the mouth while the glottis is closed. After the mouth has been closed, a positive oral pressure is created by a swallowing manoeuvre, while at the same time the glottis is opened. Thus, the air is pumped into the lungs. Thereafter the cycle is repeated until as much as 1.5 litres has been added to the TLC (7). Buccal pumping is used by these breath-hold divers to increase pre-dive lung volume and thereby supposedly also the theoretical diving depth.

Due to the elastic recoil of the chest wall, the intrathoracic pressure is increased during breath-holding at TLC with relaxed respiratory muscles. This reduces the venous return and thus cardiac output (4), which causes a transient reduction in arterial blood pressure (BP) during the first 20 s of breath-holding (1, 3). This reduction in BP would be expected to be accentuated by buccal pumping. Fainting has been reported to occur in association with buccal pumping by individual divers (personal communications).

This study was designed to elucidate the circulatory effects of this manoeuvre and to verify the hypothesis that fainting could be caused by a fall in BP due to the excessive intrathoracic pressure after buccal pumping.


METHODS

Subjects
This study was approved by the Research Ethics Committees at the Universities of Göteborg and Lund. Three subjects (Table 1), capable of buccal pumping at least 0.5 liters above TLC, volunteered for the study after being informed about the procedures. They all had significant experience from breath-hold diving.


Table 1. Subject characteristics.

Subject No.	Age [yr]	Height [cm]	Weight [kg]	TLC [L]	TLC + Bucc [L]
1	25	184.0	72.5	5.50	6.00
2	25	189.0	70.4	5.54	6.54
3	17	190.5	74.0	6.45	8.13

Procedures
Each subject was sitting in a chair during all measurements. In order to obtain a standardised cardiopulmonary situation before each measurement, the subject stood up and bended knees after which he made a VC-manoeuvre in the sitting position. One minute of rest and spontaneous breathing then preceded each measurement. First a series of measurements at normal TLC was made. A mouthpiece with a computer regulated on/off valve was connected to a spirometer (Vicatest 5, Mijnhardts, The Netherlands). At TLC the subject took the mouthpiece in his mouth and relaxed his lungs against the closed valve for measurement of airway pressure. The valve was opened and 0.5 litres of air was allowed to passively pass out of the lungs, after which the valve was closed and relaxation pressure was measured again. The "apnoea" lasted for about 1 minute during which the lung volume was gradually lowered by passive exhalation to the subject's functional residual capacity and then actively to his residual volume through the valve controlled mouthpiece. This simulated to some extent a breath-hold dive with compression of pulmonary gas and elimination of the high intrathoracic pressure. In each subject 7-8 recordings were made both at TLC and TLC with additional buccal pumping (TLC + Bucc).

Cardiovascular and pulmonary parameters were continuously recorded and stored in a computer. Systolic and diastolic blood pressures were recorded with a photoplethysmograph (Finapres 2300, Ohmeda, Madison, Wisconsin), while heart rate was derived from an EKG-monitor (Micromon 7142, Kontron Instruments, Watford, U.K.). Arterial haemoglobin oxygen saturation (SaO2) was recorded with a pulse oximeter (Biox 3700, Ohmeda, Madison, Wisconsin). Heart rate and blood pressure values before the manoeuvres during quiet breathing (control) and at peak inspiration were compared both at TLC and at TLC+Bucc with a paired t test.


RESULTS

High intrathoracic pressures were produced by the buccal pumping. At TLC, the average relaxation airway pressure was 3.1 kPa. After buccal pumping at TLC, the relaxation airway pressure was increased to 6.1 kPa. For other pulmonary results, please see Örnhagen et al (7).

Systolic and diastolic blood pressures (BP) were reduced at both TLC and TLC+Bucc compared to values before the inspiration (Fig. 1). At TLC, average systolic and diastolic BP were reduced by 27% and 26%, respectively, while at TLC+Bucc they were reduced by 49% and 36%, respectively (Table 2). The lowest BP recorded at TLC+Bucc in subjects 2 and 3 were 26/24 mmHg and 49/44 mmHg, respectively, while in subject 1 it did not fall below the value at TLC.

After inspiration to TLC, heart rate increased by 8%. After buccal pumping heart rate increased by 24% compared to the control values (Table 2). The SaO2 never fell below 96% in any subject.


Table 2. Sitting mean heart rate and blood pressure during control (quiet breathing) and during apnoea at TLC and TLC+Bucc.

	Heart rate [bpm]		Blood pressure [mmHg]
	Control	During	Control	During
TLC	79	85**	154/92	112/67
TLC + Bucc	78	97***	170/98	86/63***

Values are means from 3 subjects. Differences compared to control values are indicated with ** (P<0.01) and *** (P<0.001), respectively.





Figure 1.  Click to enlarge the figure in a separate window. Arterial blood pressure during TLC (top) and TLC+Bucc (bottom) in subject 3. Arrows indicate start of inspiration and beginning of expiration. A.c. in top figure indicates autocalibration period of the Finapres.



CONCLUSIONS

During normal breath-holding after an inspiration to TLC, a brief transient tachycardia and fall in arterial BP develops (1). However, during continued breath-holding at TLC this initial drop develops into a rise in BP within the first 15 sec of apnoea (1, 3). A similar BP response was observed in this study after inspiration of TLC. During TLC the pulse pressure is still 45 mmHg which indicates that venous return was not completely impeded (Table 2). During buccal pumping the pulse pressure is dramatically reduced and the systolic pressure is gradually falling (Table 2, Fig. 1) indicating that venous return was impeded to a great extent by the high intrathoracic pressure. If the high intrathoracic pressure had been kept longer than 15 s as if a person had practised breath-holding after buccal pumping on land it is most likely that syncope had been the result. The very rapid gain in BP when intrathoracic pressure is relieved (Fig. 1) indicate that syncope from buccal pumping is a risk if the diver remains at the surface and not when diving, because already at 2 m depth the pulmonary "over-inflation" is eliminated due to compression of pulmonary gas.

Inspired and held lung volume during apnoea has been shown to affect the human diving response (i.e., bradycardia and vasoconstriction) by both mechanical and pulmonary stretch receptor effects (1). The mechanical effects are most pronounced in the beginning of breath-holding and similar to the effects observed in this study. The stretch receptor effects are probably effective during the entire apnoea if the lung volume is kept constant. It is not clear how these considerably high intrathoracic pressures affect the high pressure sensitive pulmonary J-receptors (2). Neither is it certain that the pulmonary J-receptors, if stimulated, affect the circulation in the normal way (i.e., reflex cardiac slowing and vasodilatation) upon stimulation during TLC+Bucc (5). Also, in our experiments the influence from pulmonary stretch receptors was most likely reduced towards the end of the apnoea when the lung volume and pressure were small.

The BP recorded during quiet breathing in the sitting young subjects were somewhat high and probably reflects the normal cardiovascular response to a new and demanding situation for the subjects. Digital artery blood pressure values recorded with the Finapres have also been reported to be slightly higher than brachial artery measurements (6).

Our results support the suggestion that reported cases of fainting among breath-hold divers performing buccal pumping, could have been caused by the excessive increase in intrathoracic pressure. The most dramatic reductions in BP observed at peak buccal pumping indicate that loss of consciousness must be considered as a risk, especially if the diver remains at the surface. One should also bear in mind that the levels of buccal pumping performed by the subjects in this study were not maximal since avoidance of syncope was pursued and it was a demanding protocol with several repetitions. In an authentic diving situation were buccal pumping is performed to a maximal or near maximal level, the cardiovascular effects are probably even more pronounced.


REFERENCES

1. Andersson, J. and E. Schagatay (1998). Effects of lung volume and involuntary breathing movements on the human diving response. Eur. J. Appl. Physiol. 77:19-24.
2. Kaufman, M.P., G.A. Iwamoto, J.H. Ashton and S.S. Cassidy (1982). Responses to inflation of vagal afferents with endings in the lung of dogs. Circ. Res. 51:525-531.
3. Kawakami, Y., B.H. Natelson and A.B. DuBois (1967). Cardiovascular effects of face immersion and factors affecting diving reflex in man. J. Appl. Physiol. 23:964-970.
4. Linér, M.H. (1994). Cardiovascular and pulmonary responses to breath-hold diving in humans. Acta Physiol. Scand. 151(Suppl 620):1-32.
5. Shepherd, J.T. (1981). The lungs as receptor sites for cardiovascular regulation. Circulation 63:1-10.
6. Stroud, M.A., D.P. James, D. Railton and P.J. Sowood (1994). Digital and brachial artery blood pressure measurements during peripheral, cold-induced vasoconstriction. Eur. J. Appl. Physiol. 68:134-138.
7. Örnhagen, H., E. Schagatay, J. Andersson, E. Bergsten, P. Gustafsson and S. Sandström (1998) Mechanisms of "buccal pumping" and its pulmonary effects. This volume.



Published by courtesy of "European Underwater and Baromedical Society".

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