J Appl Physiol 101: 866 – 872, 2006.
First published May 25, 2006; doi:10.1152/japplphysiol.00759.2005.
Increased pulmonary vascular resistance and reduced stroke volume in
association with CO2 retention and inferior vena cava dilatation
Darija Baković, Davor Eterović, Zoran Valic, Žana Saratlija-Novaković,
Ivan Palada, Ante Obad, and Željko Dujić
Department of Physiology, University of Split School of Medicine, Split, Croatia
Submitted 27 June 2005; accepted in final form 18 May 2006
diving response; ultrasound scanning; Doppler; arterial pressure;
human
BREATH-HOLD DIVING IN HUMANS is associated with a diving reflex
characterized by bradycardia, peripheral vasoconstriction, increased arterial blood pressure, and decreased cardiac output
(CO) (16). These physiological responses are caused by simultaneous activation of the sympathetic and parasympathetic
nervous systems (9, 11), achieving temporary reduction of O2
uptake from air trapped in the lungs, which increases dive
duration (8). Although these intra-apneic effects are well documented, the impact of consecutive breath holds on central
hemodynamics in the postapneic period is unknown. Yet, these
effects may be substantial and last over an hour after the last
apnea, as indicated by our laboratory’s earlier studies on
peripheral hemodynamics, spleen size (1), and plasma volume
(2), using the model of cold water-face immersion apneas. The
Address for reprint requests and other correspondence: Ž. Dujić, Dept. of
Physiology, Univ. of Split School of Medicine, Soltanska 2, 21000 Split,
Croatia (e-mail: [email protected]).
866
sustained effects of repetitive episodes of hypoxia and hypercapnia on central hemodynamics may partly be due to substantial slowing of tissue O2 and CO2 store dynamics after breathhold diving (17, 20). On the other hand, consecutive breath
holds may serve as a human model of sleep apnea caused by
either intermittent obstruction of upper airways (OSA) or
reduced drive to breathe. Although intermittent hypoxic training improves exercise performance in athletes, the chronic
cyclic episodes of hypoxia and hypercapnia in OSA are associated with the number of adverse changes, including increased
systemic and pulmonary vascular resistance (PVR), right ventricular hypertrophy, and cardiac arrhythmias (19). In animal
models, hypercapnia has been shown to produce negative
inotropic and chronotropic effects and to dilate peripheral
arterioles (5, 21), whereas in humans Kiely et al. (15) provided
echocardiographic evidences that hypercapnia increases the
PVR and pulmonary pressure without affecting the heart contractility. The use of animal models or nonphysiological levels
of respiratory gases and the absence of breath hold limit the
extrapolation of these results to what happens in patients with
sleep apnea. Therefore, the purpose of this study was to
investigate the influences of five maximal breath holds on
peripheral and central hemodynamics in the postdive period,
up to 60 min. This would augment our knowledge on breathhold diving and suggest what may be happening in sleep apnea
syndrome. The use of both trained apnea divers and subjects
without diving experience would account for potentially different response to intermittent breath holds of persons with
chronic episodes of hypoxia and hypercapnia compared with
persons without sleep apnea. We hypothesized that the series
of apneas will be followed by CO2 retention, an increase in
PVR, reduction of venous return and decrease in CO for
relatively long period after the cessation of apneas.
METHODS
Participants. All experimental procedures were conducted in accordance with the American Physiological Society’s Guiding Principles for
Research Involving Animals and Human Beings and were approved by
Research Ethics Committee of the University of Split School of Medicine. Each method and potential risks were explained to the participants
in detail, and they gave written, informed consent before the experiment.
Sixteen men participated in the study. There were eight trained breathhold divers (BHD) and eight untrained (UT) subjects. There were only
two smokers in the study, and they both belonged to untrained group. The
groups were anthropometrically matched (Table 1).
Experimental protocols. All experiments were carried out in an
acclimatized environment during afternoon hours. One participant
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
8750-7587/06 $8.00 Copyright © 2006 the American Physiological Society
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Baković, Darija, Davor Eterović, Zoran Valic, Žana SaratlijaNovaković, Ivan Palada, Ante Obad, and Željko Dujić. Increased
pulmonary vascular resistance and reduced stroke volume in association with CO2 retention and inferior vena cava dilatation. J Appl
Physiol 101: 866 – 872, 2006. First published May 25, 2006;
doi:10.1152/japplphysiol.00759.2005.—Changes in cardiovascular
parameters elicited during a maximal breath hold are well described.
However, the impact of consecutive maximal breath holds on central
hemodynamics in the postapneic period is unknown. Eight trained
apnea divers and eight control subjects performed five successive
maximal apneas, separated by a 2-min resting interval, with face
immersion in cold water. Ultrasound examinations of inferior vena
cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and
60 min after the last apnea. The arterial oxygen saturation level and
blood pressure, heart rate, and transcutaneous partial pressures of CO2
and O2 were monitored continuously. At 20 min after breath holds,
IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and
21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke
volumes in the presence of reduced end-diastolic ventricular volumes.
Transcutaneous partial pressure of CO2 increased in all participants
during breath holding, returned to baseline between apneas, but
remained slightly elevated during the postdive observation period
(⬃4.5%). Thus increased right ventricular afterload and decreased
cardiac output were associated with CO2 retention and signs of
peripheralization of blood volume. These results indicate that repeated
apneas may cause prolonged hemodynamic changes after resumption
of normal breathing, which may suggest what happens in sleep apnea
syndrome.
VENODILATION AFTER MAXIMAL APNEAS
Table 1. Anthropometric data
Age, yr
Height, cm
Weight, kg
Years diving
FVC, % of normal predicted
FEV1, % of normal predicted
Trained Apnea Divers
(n ⫽ 8)
Untrained Persons
(n ⫽ 8)
29.9⫾0.9
183.6⫾1.4
89.2⫾2.7
9.5⫾2.2
111.3⫾4.1
109.2⫾3.6
30.4⫾1.4
181.9⫾1.4
77.3⫾3.0
103.8⫾3.3
99.5⫾3.8
Values are means ⫾ SE; n, no. of subjects. FVC, forced vital capacity;
FEV1, forced expiratory volume in 1 s.
J Appl Physiol • VOL
gulating the transducer in a clockwise rotation, the five-chamber
apical view allowed us to see the aortic valve and the measure aortic
diameter and aortic flow velocity curve. After collection of data for
cardiac evaluation, subjects switched to the supine posture for IVC
recording on the abdominal echograms. Evaluation of the diameter
and volume flow of the IVC was done from a subcostal window.
Measurement of an IVC diameter was performed with the IVC in its
retrohepatic position and always cranial to the crossing of portal vein
to record the same site. The site of the sampling was guided by
color-flow mapping to position the sample volume at the center of the
color flow signal and to create the smallest angle of insonation
between the direction of blood flow and the Doppler beam. The
images were stored on a personal computer. At a later date, by using
scanner software, all images were analyzed by the same author (Ante
Obad). The accuracy, reliability, and validity of measuring IVC
diameter by abdominal echograms were reported in an earlier study
(14).
Cardiopulmonary measurements. Arterial pressure was measured
continuously using photoplethysmometer [mean arterial pressure
(MAP); Finometer, Finapres Medical Systems, Arnhem, The Netherlands] with the cuff on the middle finger of the nondominant hand.
SaO2 was monitored continuously by pulse oximetry (Dash 2000, GE,
Marquette, WI) with the probe placed on the middle finger of the
dominant hand. HR was continuously recorded on a personal computer by the use of Polar belts positioned around the subject’s chest.
PtcCO2 and PtcO2 were measured continuously by placing the sensor
electrode of the analyzer (model TCM3, Radiometer, Copenhagen,
Denmark) over the subscapular muscle. Piezo respiratory belt transducer (AD Instruments, Castle Hill, Australia) was located around the
chest of 10 subjects (5 apnea divers and 5 controls) for analysis of the
voluntary phase in total breath-hold time. Analog signals of arterial
pressure, HR, SaO2, and respiratory movement were continuously
recorded and stored on a personal computer (Apple eMac PC) using
a PowerLab 16S data-acquisition system (ADInstruments) at a sampling rate of 100 Hz.
Data analysis. MAP was calculated offline from recorded arterial
pressure analog signal. Average values for HR, MAP, SaO2, PtcO2, and
PtcCO2 were calculated as control values during the period 30 –90 s
before each apnea. For HR and MAP, an average value was calculated
during each 5 s period during the apnea and also for the last 10 s. For
SaO2, an average value was calculated for each 5-s period from the
beginning of apnea until 30 s after apnea and also for the 10 s period
ending with the nadir SaO2.
Stoke volume (SV) is equal to the product of the cross-sectional
area (CSA) of the aorta and aortic flow velocity integral: SV ⫽
CSA ⫻ VTI. Because flow velocity varies during a flow ejection
period, individual velocities of Doppler spectrum are summed (i.e.,
integrated) to measure total flow during a given ejection period. The
sum of velocities is called time velocity integral (VTI). CSA is
calculated from measured aortic diameter as CSA ⫽ ␲(D/2)2, where
D is aortic diameter. CO was calculated from a product of SV and HR.
The total peripheral resistance (TPR) was calculated as MAP/CO
(mmHg ⫻ min ⫻ l⫺1). Ascending aortic diameter and the flow
velocity curve are recorded from an apical window. The diameter and
velocity measurements are made at the same anatomic site. By using
pulsed Doppler, the pulmonary artery flow was recorded from the
parasternal short axis. Next, the sample volume was placed in the
region of the pulmonary valve annulus. Pulmonary artery acceleration
time (PAT) in milliseconds was determined as the time interval
between beginning of flow and its peak velocity. The mean of three
consistent waveforms at each time point was used for the purpose of
analysis. Mean pulmonary artery pressure (MPAP) in mmHg was
calculated as MPAP ⫽ 73 ⫺ (0.42 ⫻ PAT) (6). Total PVR was
calculated as PVR ⫽ MPAP/CO ⫻ 80 dyn 䡠 s 䡠 cm⫺5. The left ventricular global ejection fraction (EF) was calculated as EF ⫽ [(EDV ⫺
ESV)/EDV] ⫻ 100%. The IVC diameter was measured from the B
images at the same location as the Doppler interrogation (1–2 cm
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was tested each day. Participants were instructed not to eat for at least
4 h and to abstain from smoking for at least 12 h before the arrival to
the laboratory. They were directed to arrive at the laboratory 30 min
before the start of the testing for acclimatization and detailed explanation of the experimental procedures. Each participant had body
mass and height measured, from which we calculated body mass
index. We carried out dynamic spirometry (Quark b2, Cosmed, Rome,
Italy) in all subjects, who then resumed a prone position for the rest
of the experiment. The participants were instructed to rest for 15 min
in a prone position on a bed with the head placed on the cover of a
container filled with cold water (12°C). The participants were instructed not to hyperventilate before diving. They wore nose clips and
were not allowed to exhale into the water during simulated diving.
Apnea times were recorded by the use of a stopwatch. After collection
of baseline parameters, each participant performed five maximal
breath holds with the face immersed in cold water. The subjects were
instructed to expire to residual volume and take a deep but not
maximal breath before the apneas and to expire completely after the
apneas. Successive apneas were separated by 2-min intervals, allowing for data collection. This was the same diving protocol used
previously (1, 2, 22).
Initially, Doppler and two-dimensional echocardiographic evaluation of the left and right sides of the heart were performed, followed
by inferior vena cava (IVC) diameter and flow velocity measurements.
This lasted ⬃2 min. Simultaneously, arterial blood pressure and oxygen
saturation (SaO2), heart rate [HR, respiratory movement, and transcutaneous partial pressures of oxygen (PtcO2) and carbon dioxide (PtcCO2)]
were continuously measured and stored on a personal computer. After
the last breath hold, the participants were observed for 1 h, with
measurements performed at 0, 10, 20, 40, and 60 min.
Ultrasound evaluations. The same experienced cardiologist took all
ultrasonographic measurements with a 1.5- to 3.3-MHz phase array
probe (Vivid 3, GE, Milwaukee, WI). The subjects rested supine for
15 min before baseline measurements. In between apneas, the participants switched from the prone to the lateral decubitus and supine
positions for ultrasound evaluation. First, the subjects switched to the
lateral decubitus position where heart images were obtained in three
views: parasternal long and short axis, and apical. The parasternal
long-axis view was obtained by placing the transducer at the left
parasternal area in the second or third intercostal space, whereas the
parasternal short-axis view was obtained by rotating the transducer
90° clockwise from the longitudinal position. The parasternal shortaxis view at the aortic valve level was used for visualization and
Doppler measurement of volume flow in the pulmonary artery. The
apical four-chamber view was identified initially by palpation of the
left ventricular apex with the patient in the left lateral decubitus
position. Transducer position was then adjusted as needed to obtain
optimal images. The four-chamber view displays all four cardiac
chambers, as well as the ventricular and atrial septa. This view was
used for left ventricular end-systolic (ESV) and end-diastolic volume
(EDV) calculations using Simpson’s method. Because both enddiastolic and end-systolic measurements are needed for volume calculations, the electrocardiogram was continuously recorded. By an-
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VENODILATION AFTER MAXIMAL APNEAS
distal to the junction with the hepatic vein) for VTI. Measurements
were done in B mode because of deep localization of the IVC. By
using technical skills of the ultrasound (cine loop), we managed the
similar effect as we were using M mode for measuring excursions of
the IVC diameter. Direct timing was not done, but by using always the
same method (cine loop) enabled us to measure IVC diameter in the
same moment of maximal dilatation.
Statistical analysis. Data are expressed as means ⫾ SE. The effect
of apnea diving on studied variables in different postdive times was
evaluated by Friedman analysis of variance, whereas post hoc comparisons were done by Wilcoxon signed-rank test. Nonparametric
tests were used because of the small sample size (n ⫽ 8). To minimize
the effect of intersubject variability, the postdive changes from baseline values were used in these analyses, instead of the raw data.
Associations between metric variables were evaluated by Pearson’s
coefficient of correlation. A P value ⬍0.05 was considered significant.
All analyses were done using Statistica 6.0 software (Statsoft, Tulsa,
OK).
RESULTS
Fig. 1. Duration of 5 maximal apneas and response in mean arterial pressure (MAP), arterial oxygen saturation (SaO2), heart rate (HR), total peripheral resistance
(TPR) (A), and transcutaneous partial pressure of carbon dioxide (Ptc CO2) (B). Values are means ⫾ SE. Graphs represent values obtained after 5 successive
maximal apneas (A1–A5) separated by 2-min recovery period, and the values during the 1-h postapnea period (10 – 60), in all subjects. Values are statistically
significant (P ⬍ 0.05) compared with baseline (B) values: *for breath-hold divers (BHD); †for untrained subjects (UT).
J Appl Physiol • VOL
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Descriptive data. Anthropometric data for all subjects, BHD
(n ⫽ 8) and UT (n ⫽ 8), are shown in Table 1. The two groups
were anthropometrically comparable, except that BHD were
heavier than the UT persons. Spirometry in the two body
postures did not differ significantly between groups.
MAP, HR, SaO2, TPR, and transcutaneous blood gases.
Durations of the five maximal apneas and the responses of
MAP, SaO2, HR, and PtcCO2 are summarized in Fig. 1A. Apneic
time increased over the series of five apneas significantly by
49.8 s (48%; P ⫽ 0.0005) in BHD, whereas UT subjects did
not show significant increases (9 s). Overall, BHD performed
longer apneas than UT persons (P ⫽ 0.0001). MAP increases
were approximately equal after all five apneas and quickly
normalized after the cessation of apneas. Significantly greater
bradycardia was found in the BHD group (P ⫽ 0.03). Anticipatory HR increased before the onset of the first apnea and
subsequently decreased below baseline values equally after all
apneas. HR was quickly restored to baseline values in the
2-min periods between apneas in all participants (data not
shown). There was no distinction in baseline SaO2 between
BHD and UT subjects (98.0 ⫾ 0.3 and 98 ⫾ 0.3%, respectively). SaO2 decreased significantly below baseline values after
VENODILATION AFTER MAXIMAL APNEAS
all apneas in both groups (P ⫽ 0.00000). Oxygen desaturation
was less apparent in UT persons (P ⫽ 0.005, compared with
BHD). SaO2 was restored in the period between apneas in both
groups and in all apnea attempts (data not shown). TPR
increased significantly after the last apnea in both groups (P ⫽
0.02) and remained at elevated levels even 1 h after cessation
of breath holds. Preapneic PtcCO2 in tissue remained unchanged
over all five apneas in all groups, indicating constant baseline
conditions in blood gases for each apnea attempt (Fig. 1B).
After the series of apneas, PtcCO2 remained significantly elevated in trained and untrained persons (P ⫽ 0.01).
Central hemodynamic variables. CO decreased significantly
after the cessation of apneas in both groups (P ⫽ 0.01)
predominantly due to SV reduction (Fig. 2), because HR was
unchanged. EDV decreased by 13.5% in BHD and by 7.95% in
UT persons 10 min after cessation of apneas and was followed
Fig. 3. Ultrasonographically assessed end diastolic volume (EDV) in the 1-h
postapnea period for all subjects. Values are means ⫾ SE. Values are
statistically significant (P ⬍ 0.05) compared with baseline values: *for BHD;
†for UT. EDV decreased significantly in both groups in the postapnea period
and remained at decreased values throughout the 1-h period after cessation of
breath holds.
J Appl Physiol • VOL
Fig. 4. Left ventricle ejection fraction (EF), calculated from left ventricular
volumes, in the 1-h postapnea period for all subjects. Values are means ⫾ SE.
by a gradual return to baseline values in the 60-min postapnea
period (Fig. 3). EF decreased nonsignificantly after apneas
(Fig. 4). MPAP and PVR increased significantly after the
cessation of breath holds (P ⬍ 0.05; Fig. 5, A and B). There
was no difference in increase between groups.
Fig. 5. Mean pulmonary artery pressure (MPAP; A) and pulmonary vascular
resistance (PVR; B), calculated from the pulmonary acceleration time, in the 1-h
postapnea period for all subjects. Values are means ⫾ SE. Values are statistically
significant (P ⬍ 0.05) compared with baseline values: *for BHD; †for UT. MPAP
and PVR increased significantly after the cessation of breath holds.
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Fig. 2. Ultrasonographically assessed stroke volume (SV) in the 1-h postapnea
period for all subjects. Values are means ⫾ SE. Values are statistically
significant (P ⬍ 0.05) compared with baseline values: *for BHD; †for UT. SV
decreased significantly in both groups in the postapnea period and remained at
decreased values throughout the 1-h period after cessation of breath holds.
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IVC hemodynamics. Figure 5 shows the IVC diameter
changes during the period after the series of apnea in BHD and
UT persons. The greatest increase in IVC diameter occurred 10
min after the cessation of apneas (16.2% in BHD and 10.4% in
UT persons). It was still elevated after at the 1-h period
following cessation of diving in both groups (P ⫽ 0.01; Fig.
6A). Maximal IVC dilatation occurred 40 min after the last
apnea, most notably in BHD subjects. VTI through IVC decreased significantly in the BHD group (P ⫽ 0.01) in the
10-min postdiving period, and was followed by a gradual
return to baseline values in the 60-min postapnea period. In the
UT persons, nonsignificant decreases were found (Fig. 6B).
Figure 7 shows the IVC diameter changes in subject 5 before
and after a series of five maximal apneas.
DISCUSSION
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This study shows that substantial hemodynamic effects of a
series of maximal apneas, interrupted by short interapneic
intervals, last at least 1 h after the last apnea. During that
postapneic time, the CO2 retention occurred in association with
dilatation of IVC. This fact, substantiated with reduction of
ventricular volume and EDV, suggests that hypercapnia-re-
Fig. 7. Echocardiographic subcostal view of the IVC in diver 5. Images
represent IVC diameter before the start of repetitive apneas in the resting
supine position (A) and at 20 min (B) and 60 min (C) after cessation of apneas.
It is clearly visible that performing repetitive apneas causes IVC dilatation.
Fig. 6. Ultrasonographically assessed inferior vein cava (IVC) diameter (A)
and velocity time integral (VTI; B) in the 1-h postapnea period for all subjects.
Values are means ⫾ SE. Values are statistically significant (P ⬍ 0.05)
compared with baseline values: *for BHD; †for UT group. Diameter increased
significantly in both groups. VTI decreased significantly by 22% in BHD,
whereas in UT it decreased by 12% (nonstatistical significance) in postapnea
period.
J Appl Physiol • VOL
lated venodilation decreased venous return, causing the observed decrease in SV and CO. Elevated levels of CO2 or
prolonged effects of previous hypoxic/hypercapnic episodes
may also explain rather large, persistent elevations in PAP and
PVR after the apnea series. These data suggest that hemodynamic effects of a series of hypoxic/hypercapnic episodes may
be well extended after resumption of normal breathing. Although the signs of blood volume peripheralization were more
pronounced in trained apnea divers, overall the effects were not
found to depend significantly on chronic exposure to hypoxic/
hypercapnic episodes.
PtcCO2 increased in all participants during breath holding,
returned to baseline in between apneas, but remained slightly
elevated during the postdiving observation (4.5%). This is in
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VENODILATION AFTER MAXIMAL APNEAS
J Appl Physiol • VOL
the prolonged increase in the PVR after apneic episodes may
contribute to the observed association of obstructive sleep
apnea and pulmonary hypertension (19).
There are several study limitations. Although we did measure both IVC diameter and its VTI, IVC irregular shape
precluded calculating IVC flow by combining these data.
Therefore, we were not able to measure directly this significant
portion (⬃2/3) of the venous return. As for the ultrasound
cardiopulmonary assessments, the reliability of the methods
vary from accepted standards (aortic CO) to less well-evaluated methods (assessment of MPAP). Also the transcutaneous
estimates of arterial respiratory gases depend on stable cutaneous blood flow; the methods work best in neonates (25) and
worst in hemodynamically unstable patients (24). In healthy
individuals, the methods reliably monitor trends due to respiratory changes (4, 7, 23, 26); the O2 absolute readings are
systematically below the corresponding arterial values,
whereas temperature-corrected CO2 readings deviate much less
(26). Theoretically, in this study, the observed decrease in
cardiac output could have influenced the cutaneous blood flow
and thus the transcutaneous estimates of blood gases. However,
this effect would be more pronounced in case of O2, contrary
to what was observed: only PtcCO2 remained elevated in the
postapneic period.
In conclusion, we have found that hemodynamic effects of a
series of maximal face-immersion apneas with short interapneic intervals last over an hour after, both in trained apnea
divers and in controls. These effects include the reduced filling
and increased afterload to the right heart, reduced SV and
cardiac output in the presence of CO2 retention, and signs of
blood volume peripheralization.
ACKNOWLEDGMENTS
The authors thank Dr. JoAnn A. Giaconi for editing of the manuscript.
GRANTS
This study was supported by Croatian Ministry of Science Grants 0216006
and 0216007.
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6. Dabestani A, Mahan G, Gardin JM, Takenaka K, Burn C, Allfie A,
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accordance with previous findings of large tissue CO2 retention
and prolonged recovery of CO2 elimination after repetitive
breath holds with short interapneic resting intervals (20). Muscle tissue is the largest CO2 reservoir, holding 10 liters of CO2,
or 60% of the total labile CO2 store. Muscle’s time constant for
CO2 mobilization is 30 min, whereas other soft tissues have
both smaller CO2 stores and faster CO2 mobilization, with time
constants between 1.6 and 2.5 min (10). If apnea duration is
long enough with a short interapneic period, as in the present
study, a substantial CO2 retention in slow-equilibrating tissues
can occur. A CO2 retention after apneas in BHD may be
potentiated by chronically blunted ventilatory response to hypercapnia. This effect was found in assisted-diving Ama (18)
and in Royal Navy divers (12) as an effect of training. An acute
resetting of chemoreceptors by a series of maximal breath
holds should also be considered as a cause. Unfortunately, in
this study the ventilation was not measured. However, a significant CO2 retention occurred even 1 h after a series of
maximal breath holds, which could have contributed to
changes in peripheral and central hemodynamics.
Trained BHD had an augmented diving reflex (bradycardia and apparently increased MAP), as was previously
shown by Lin (16). Postdiving ultrasound measurements
showed IVC dilatation with subsequent decreases in CO in
both groups, due to decreased SV, in the presence of
decreased ventricular EDV and increased right ventricular
afterload. HR was unchanged, whereas TPR increased in
both groups. Possible factors affecting SV are preload,
afterload and myocardial contractility. Reduced EDV suggests decreased preload to the right ventricle, which, in
conjunction with its significantly increased afterload, explains the diminution of the right ventricular SV. Given
unchanged/slightly decreased left ventricular afterload (assessed by peripheral systolic pressure), the left ventricular
performance was likely only the reflection of the conditions
on the right side. However, a small contribution from the
reduction in left ventricular contractility, suggested by apparent decrease in its ejection fraction, cannot be excluded.
Reduced ventricular EDV and increased IVC diameter
suggest the redistribution of blood volume from central
blood pools to peripheral veins, after the reduction in
venous return. The venous return is expected to decrease if
either the peripheral blood volume or vessels capacitance
decreases (as the determinants of the mean circulatory
filling pressure). The blood volume was not measured in this
study, but in our laboratory’s previous study, using the same
apnea diving protocol, the plasma volume increased after
apneas, likely due to CO2 retention (2). This, in conjunction
with signs of peripheralization of blood, suggests an increase rather than decrease in peripheral blood pools after
apnea series, reducing the possible causes of reduced venous
return to decreased capacitance of peripheral blood vessels.
If real, decreased peripheral vessels capacitance can also be
explained by hypercapnia, which directly relaxes the vascular smooth muscle (3, 13).
The series of voluntary apneas is a unique human model of
sleep apnea, with presence and realistic intensities of all three
factors: cyclic hypoxemia, hypercapnia, and absent ventilation.
This study shows that the aggravating hemodynamic effects of
consecutive apneas are long lasting and primarily affect the
right heart. If these results can be extrapolated to sleep apnea,
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