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* From Institut de Médecine Navale du Service de Santé des Armées (Dr. Boussuges), Toulon Armées; and Université de la Méditerranée (Drs. Blanc and Carturan), Laboratoire de Physiopathologie et Action Thérapeutique des Gaz sous Pression, Faculté de Médecine Nord, Marseille, France.
Correspondence to: Alain Boussuges, MD, PhD, IMNSSA, B.P.610, 83800 Toulon; Toulon Armées, France; e-mail: alainboussuges{at}libertysurf.fr
Abstract
Objective: Cardiac changes induced by scuba diving were investigated using Doppler echocardiography.
Material and methods: Ten healthy scuba divers dove to a mean depth of 34.3 ± 2.7 m of sea water (113 ± 9 feet) and a mean duration of 25.3 ± 3.5 min.
Results: One hour after the dive, microbubbles could be detected in the right-heart chambers of all subjects. Left atrial and left ventricular (LV) diameters significantly decreased after the dive. Cardiac output, assessed by aortic blood flow, remained unchanged. Heart rate increased and stroke volume (SV) decreased after the dive. LV filling was assessed on transmitral profile. An increase of the contribution of the atrial contraction to LV filling was observed. Right cavity diameters were unchanged, but an increase of the right ventricular/right atrial gradient pressure was found.
Conclusion: The diving profile studied promotes a rather important bubble grade in all volunteers. A significantly reduced cardiac diameters and SV was found by our hemodynamic study 1 h after diving. Two factors can explain these results: low volemia secondary to immersion, and venous gas embolism induced by nitrogen desaturation. Consequently, restoration of the water balance of the body should be considered in the recovery process after diving.
Key Words: cardiac function • decompression • diving • Doppler • immersion • ultrasonography
During a scuba dive, subjects undergo environmental constraints such as immersion, exposure to cold, and increased ambient pressure. All of these constraints may be responsible for hemodynamic modifications, which have been well studied in healthy volunteers. Immersion in water induces a cephalad shift of peripheral venous blood that augments central blood volume.12 Atrial natriuretic peptid and diuresis are markedly increased.3 Ventilation against resistance induces modifications of intrathoracic pressure and consequently modifications of cardiac preload and afterload.4
During the scuba dive, increased ambient pressure generates an increase in PO2 and nitrogen partial pressure. A decrease in cardiac output (CO) related to the simultaneous decrease of the heart rate (HR) and the stroke volume (SV) is found at high PO2.5 Beginning from the partial pressure of 1 atmosphere absolute, an increase in systemic vascular resistance is also observed.6
Henry’s law states a proportional relationship between the solubility of a gas in a liquid and the partial pressure of that gas above the liquid. Thus, body tissues saturate with nitrogen during the dive. As the diver returns to the surface, the sum of the gas tensions in the tissues may exceed the absolute ambient pressure, and a state of supersaturation is created.
If the decompression is sufficiently rapid and extensive, the exceeding nitrogen may create circulating venous bubbles from preexisting gas nuclei.7 Intravascular gas bubbles are carried from the venous circulation to the pulmonary vessel, where they are eliminated through the lungs. The formation of bubbles is recognized as the basis for decompression illness, but such bubbles are also commonly detected in venous circulation of asymptomatic divers.8 Experimental studies910 have proved that right cardiac function and pulmonary arterial pressure may be disturbed by pulmonary gas embolism.
If all these parameters are known to influence cardiovascular function, few studies have investigated the modifications of cardiac function, including left ventricular (LV) systolic and diastolic function, after scuba diving. If there are hemodynamic changes, this could have an importance for the recovery after a dive. Furthermore, these findings could be important for intensivists in the management of decompression sickness.
To our knowledge, in only one study11 have the cardiac function modifications induced by scuba diving been investigated. But in this study, important hemodynamic parameters such as SV and CO have not been recorded. Consequently, the present study was conducted to assess changes in the hemodynamic status of healthy volunteers after an open-sea scuba dive, using Doppler echocardiography.
Materials and Methods
Divers
The subjects included in the study were 10 medically fit, male, recreational divers (mean age, 44 ± 7 years; range, 33 to 54 years; mean weight, 79 ± 11 kg; range, 58 to 96 kg; mean height, 177 ± 5 cm; range, 170 to 186 cm; mean body mass index, 25 ± 3; range, 19.8 to 31.7). In accordance with French law concerning biomedical research, the divers gave informed consent and protocol was approved by the institutional ethical committee. Each subject passed a screening examination, including physical examination and medical history. All volunteers denied taking any medication at the time of the study. Diving was the only physical activity performed by eight of the subjects. Diving took place in sea water at a mean depth of 34.3 ± 2.7 m of sea water (113 ± 9 feet) and a mean duration of 25 ± 4 min.
The breathing mixture was air (N2O2), and the decompression procedures were conducted in accordance with the 1992 French Labor Ministry decompression table. The descent time was included in the dive time, the ascent was linear, and the ascent rate up to the decompression stop was 9 m of sea water per minute (29.52 feet/min). The control was made by using a chronometer, a depth meter, and a dive computer equipped with a bar graph of ascent (Maestro Pro; Beuchat; Marsailles, France).
This dive profile is usually performed by recreational divers in the Mediterranean Sea, and it has been studied by our team in previous work.1213 It induced a rather important bubble grade in most divers. The maximum bubble count was reached 60 min after surfacing.
The divers were equipped with neoprene diving suits; the thickness of the suits was in accordance with the temperature of the water. None of the divers reported suffering from the cold. The divers had to reduce exertion as much as possible before and after diving. After diving, the subjects were undressed and were taken to the laboratory. The divers did not have a warm shower before the end of the Doppler echography, so the results were not biased.
Doppler Echographic Study
Divers underwent two Doppler echographic examinations with a 1-week interval: the first examination in basal conditions, and the second examination 1 h after the investigational scuba dive. The ultrasonographic examinations were carried out by an experienced investigator (A.B.) using a commercially available Doppler echocardiograph (Diasonics Vingmed CFM 750 A; GE Medical Systems; Milwaukee, WI) connected to a transducer array of 2.5 to 3.5 MHz. Investigations were performed in a quiet room with a stable environmental temperature (25°C). Subjects stayed at rest for 10 min before the ultrasonographic examination. HR was recorded by echocardiogram, and the rate was averaged over 60 s. Sphygmomanometric BP measurements on the right arm were obtained after each echographic examination. Two-dimensional (2D) echography and Doppler studies were used to detect circulating bubbles after diving and to assess cardiac function.
Circulating Bubble Screening
Circulating bubbles were screened using 2D echography and pulsed Doppler. Bubble detection was performed 1 h after diving and before cardiac function assessment. Images were obtained from the parasternal view (long axis and short axis) and from the apical four-chamber view (Fig 1
). Gas bubbles appear as high intensity "blobs" in the images. A quantitative evaluation of circulating bubbles was performed using 2D images. Each view was recorded for 30 s on videotape.
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Cardiac Function Assessment
Examinations were made using 2D and M-mode echocardiography associated with pulsed and continuous-wave Doppler. Echocardiography allows the measurements of cardiac diameters and LV systolic function; Doppler permits the measurements of CO as well as an assessment of LV filling pattern.
Images were obtained via a transthoracic approach from the parasternal views (long axis and short axis) and from an apical four-chamber view. The subjects were placed in a left lateral position for the parasternal views and in a supine position for the apical four-chamber view. Second harmonic imaging was used to improve the image quality.
Doppler recordings were performed at the end of normal expiration in order to eliminate the effects of respiration on the parameters studied. Measurements were averaged from at least three consecutive beats. Tape recordings were obtained at a paper speed of 100 mm/s with simultaneous tracing of the ECG. Examinations were recorded on standard videotape for later review.
Doppler Echocardiographic Parameters
Cardiac Size and LV Systolic Function:
Left atrial (LA) diameter, LV end-systolic diameter (LVESD), LV end-diastolic diameter (LVEDD), LV end-systolic and end-diastolic interventricular septal thickness, and LV end-systolic and end-diastolic posterior wall thickness were measured by M-mode echocardiography from the left short- and long-axis views.15 LV mass (LVM) was assessed by M-mode echocardiography and the application of the Devereux formula16: LVM = 1.04 x ([LVEDD + LV end-diastolic interventricular septal thickness + LV end-diastolic posterior wall thickness]3 – LVEDD3) – 13.6. Standard index of global LV systolic performance was LV percentage of fractional shortening (%FS). %FS was taken as the ratio of (LVEDD – LVESD)/LVEDD.
Determination of CO Across the Aortic Valve:
CO was derived from aortic blood flow. Aortic cross-section diameter was measured by 2D echocardiography from the left parasternal short-axis view at the level of the aortic root. The aortic cross-section area (ACSA) was calculated as follows: ACSA = 3.14 x (diameter/2)2. The aortic systolic flow velocity time integral (VTI) was measured by computer-assisted determination using the pulsed-wave Doppler profile of aortic blood flow from the apical four-chamber view allowing to calculate LV SV [LV SV = aortic systolic flow VTI x ACSA] and CO (LV CO = LV SV x HR).
LV Filling:
LV filling was studied using transmitral blood velocities recorded by pulsed Doppler.17 Doppler measurements were averaged from at least three consecutive beats. Transmitral blood velocities were obtained from the apical four-chamber view, positioning the sample volume at the mitral valve leaflet tips. Doppler velocity curves were recorded at 100mm/s. Peak velocity and VTI of the initial flow (E wave), representing the early filling phase, and of the late flow (A wave), representing the atrial contraction, were measured. The peak velocities ratio (E/A) and the ratio of the A wave VTI to the total VTI (relative contribution of atrial contraction to the total LV filling) were calculated. Other following variables were measured: the deceleration pressure half time of early diastolic transmitral flow (pressure half-time) and isovolumetric relaxation time (IVRT). The IVRT was the interval from the aortic valve closure signal to the mitral valve opening signal.
RV Diameters:
RV end-systolic diameter and RV end-diastolic diameter (RVEDD) were measured by M-mode echocardiography from the left parasternal long-axis views.
RV-Right Atrial Pressure Gradient:
As we did not measure the right atrial (RA) pressure, we expressed our results as instantaneous systolic pressure gradient from RV to RA, without any calculation of systolic pulmonary artery pressure. Tricuspid regurgitant flow was identified in continuous Doppler mode from the apical four-chamber view. Instantaneous systolic pressure gradient from RV to RA (RV/RAg) was calculated with the modified Bernoulli equation from the peak velocity of the tricuspid regurgitant signal: RV/Rag = 4V2, where V is the maximal regurgitant velocity in meters per second.
Statistical Analysis
Continuous variables were expressed as mean ± SD. Statistical tests were run on statistical software (Sigma Stat; SPSS; Chicago, IL). Each subject has served as his/her own control. Two series of measurements were obtained: the first as control, and the second after scuba diving. Data distribution was studied using a Kolmogorov-Smirnov test. When data distribution reflected a normal distribution, we used a t test for paired data. In the case of cohorts of variables not having a normal distribution, comparisons were done with the Wilcoxon matched-pair signed-ranks test; p values < 0.05 were considered as significant.
Results
Baseline Echocardiographic Variables
Baseline echocardiographic examinations were normal in all volunteers. Mean indexed LVM was 101 ± 21 g/m2. Mean aortic cross-section surface was 4.2 ± 0.54 cm2. A tricuspid regurgitant flow was identified in 7 of 10 divers, and instantaneous systolic pressure gradient from the RV to RA could be assessed in these subjects.
After Diving
None of the divers presented any disorders suggesting a diving accident.
Circulating Bubbles Detection:
Circulating bubbles were detected in all divers. Bubbles were observed in right cavities of the heart using 2D echocardiography in seven divers. Pulsed Doppler confirmed the existence of venous gas emboli in these cases and detected circulating bubbles that were not seen in 2D echography in three other divers. Discrepancies were observed in subjects with poor image quality. Circulating bubbles were graded according to the 2D echocardiographic and pulsed Doppler grade. A grade 3 was observed in seven divers, grade 2 in one diver, and grade 1 in two divers. No circulating bubbles were detected in left heart cavities.
Cardiac Function Assessment After Diving:
Hemodynamic variables after diving in comparison to baseline mean values are shown in Table 2
. Systolic and diastolic arterial pressures did not vary significantly after diving. HR significantly increased, whereas a significant decrease of the SV was observed after diving. CO, assessed by aortic blood flow, remained unchanged.
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We emphasize that our study was conducted in actual diving conditions because more bubbling has been reported when the dives were performed in the open sea rather than when they were performed in hyperbaric chambers.18 Furthermore, during water immersion several modifications including hemodynamic, neuroendocrine, and autonomic activities changes have been demonstrated.123 Consequently, hemodynamic modifications should be very different after scuba diving when compared with dry hyperbaric exposures.
The diving profile studied is commonly performed by recreational divers but generates a rather important bubble grade in all volunteers. Indeed, a grade 3 was found in 7 of 10 divers 1 h after surfacing.
The population studied is representative of the population of recreational divers. Experienced divers with an average age of 44 years and a mean body mass index of 25 ± 3 were studied. Eight of 10 subjects did not practice any sport activities if not scuba diving. The incidence of individual factors as age, adiposity, and physical fitness on bubble formation is recognized.13 Thus, characteristics of the population studied may be responsible for the important bubble production.
A significantly reduced SV was found by our hemodynamic study 1 h after diving. A decrease in cardiac preload, a decrease in myocardial contractility, or an increase in cardiac afterload could explain this change.
Cardiac contractility remained normal after diving with preservation of LV %FS. Mean values for systolic and diastolic BP remained unchanged, and ventricular diameters were not enlarged. So, the hypothesis of an increase in LV afterload was low. However, a reduction in LV preload was evidenced by the reduction in LA diameter, LVEDD, and LVESD. This reduction in cardiac preload may be attributed to a contraction in plasma volume. Indeed, in previous studies,1920 the loss of the plasma volume and resulting hemoconcentration have been demonstrated either in subjects after a single dive, repeated dives, or periods of daily diving. The plasma volume loss could be induced by environmental constraints.
Water immersion promotes a redistribution of blood volume with a relative increase in central blood volume.12 The relative hypervolemia lead to the release of atrial natriuretic peptide and the lowering of noradrenaline, arginine vasopressin, aldosterone, and plasma rennin activity.212223 The changes in neuroendocrine activities produce a marked diuresis.24 Body fluid loss is increased by exercise (swimming) during scuba diving. Consequently, dehydration is frequently observed after cessation of immersion.
Furthermore, experimental studies252627 have demonstrated that during the decompression, circulating bubbles activate leukocytes and platelets, adversely affect blood rheology, and induce an activation of the complement system and a release of kinines. Endothelial transformations seem to be due to the mechanical effects of the circulating bubbles as well as the activation of leukocytes.282930
An increased hematocrit and a loss of plasma volume have been observed in both animals and male victims of decompression sickness.3132 Furthermore, venous gas emboli may damage the pulmonary vascular endothelium, causing permeability pulmonary edema in man.33 Consequently, the extravasation of plasma through injured endothelium might play a part in the hemoconcentration observed after the dive.
In our population, a significantly increase in HR was found after diving. Reduction in cardiac preload and pulmonary gas emboli could be responsible for the tachycardia.31 The decrease in SV was offset by the increase in HR such that CO remained unchanged.
LV filling profile was also modified after diving. A decrease in E/A ratio with a decrease in early transmitral velocity were observed. This filling pattern demonstrated a contribution of the atrial contraction to LV filling that became more important after diving. This LV filling profile modification has been previously observed by Marabotti et al.11 Several factors as variations of cardiac loading, ventricular interdependence, or LV relaxation alteration may be responsible for this modification.
During the dive, subjects undergo respiratory constraints such as increased ambient pressure and ventilation through the scuba gear. An increase in PO2 can induce an impairment in cardiac relaxation.34 However, the duration of the myocardial effect after the end of hyperoxia exposure and inhalation of room air is unknown. The time course of vascular changes during systemic hyperoxic stress has been well studied on retinal vasculature. The latency for recovery from vasoconstriction was approximately 5 min after a normobaric hyperoxic exposure and 10 min after an hyperbaric oxygen exposure.3536
In our study, ultrasonographic investigations were performed 1 h after diving; consequently, the probability of an hyperoxia-induced cardiac relaxation impairment was low. Physiologically, the RV and LV are two distinct chambers that are anatomically and functionally bound: both share the interventricular septum and both are enclosed in the pericardium. As a consequence, alterations in RV size and function influence LV filling.37 In the present study, RV diameters were unchanged after the dive and no LV septal shift was observed. Consequently, the decrease of the cardiac preload demonstrated by cardiac diameters and SV decrease seemed to be the principal factor of the LV filling modification.
IVRT measurement confirms our hypothesis. The decreased LV preload, as seen previously, by reducing the pressure gradient from the LA to the LV may explain the increase in IVRT observed after diving (Table 4). An increase in maximal velocity of tricuspid regurgitation flow, suggesting an increase in the RV/RA gradient, was also observed.
A decrease in LV preload was demonstrated by LV study. Consequently, a decrease in RA pressure was very likely; however, an increase in pulmonary arterial pressure could be induced by pulmonary gas embolism.1031 These two factors could explain an increase in RV/RA gradient.
RV diameters were unchanged after the dive. The association of an elevation in RV afterload and a reduction in RV preload may explain the lack of modification in RVEDD in our work.
In individuals with patent foramen ovale, circulating bubbles might cross over from the right side of the heart to the left side.38 An increase in right-sided cardiac pressures during decompression could promote the right-to-left shunt. Unfortunately, as we did not measure RA pressure, we could not estimate right cardiac pressures. Previous studies3940 have proved that the measurement of the inferior vena cava diameters provide a noninvasive estimation of the RA pressure. This method could be used in further studies to assess right-sided cardiac pressures during the decompression after a scuba dive.
Conclusion
Numerous hemodynamic changes were observed 1 h after an open-sea scuba dive. LA and LV diameters significantly decreased after the dive. CO remained unchanged but was the result of two opposite modifications: an increase in HR and a decrease in SV. Transmitral profile was modified with an increase of the contribution of the atrial contraction to LV filling. Right cavities diameters were unchanged, but an increase of the RV/RA pressure gradient was found.
Two factors can explain these results: low volemia secondary to immersion, and venous gas embolism induced by nitrogen desaturation. Lowering of plasma volume takes part in microcirculatory perfusion alterations observed during experimental decompression sickness.2641 For recreational divers, hemoconcentration and reduction in plasma volume could interact with biological changes due to circulating bubbles and induce decompression sickness.42 Consequently, the restoration of the water balance of the body is an important part of the recovery process after diving. Oral hydration should be particularly important in case of repeated dives or during periods of daily diving. Further studies are needed to develop appropriate fluid-replacement strategies according to the diving procedure.
Acknowledgements
The authors thank Mme Denise Hamou for assistance during the preparation of the manuscript.
Footnotes
Abbreviations: ACSA = aortic cross-section area; CO = cardiac output; 2D = two dimensional; HR = heart rate; IVRT = isovolumetric relaxation time; LA = left atrium; LV = left ventricle/ventricular; LVEDD = left ventricular end-diastolic diameter; LVESD = left ventricular end-systolic diameter; LVM = left ventricular mass; %FS = left ventricular percentage of fractional shortening; RA = right atrium; RV = right ventricle/ventricular; RVEDD = right ventricular end-diastolic diameter; RV/Rag = pressure gradient between right ventricle and right atrium; SV = stroke volume; VTI = velocity time integral
Received for publication April 1, 2005. Accepted for publication October 25, 2005.
References
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