Irregular Breathing Patterns and Body Oxygenation
Clinical manifestations and symptoms
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Early signs and symptoms
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Healthy lifestyle factors- Exercise with strictly nasal
breathing |
Lifestyle risk factors- Sleeping with mouth
open |
Breathing irregularities are symptoms of the chronic hyperventilation syndrome which is typical for people with clinical pathologies (see Table for minute ventilation in the sick based on 34 research papers and medical science articles related to heart disease, cancer, diabetes, asthma, COPD, sleep apnea, and many other disorders). Chronic hyperventilation cannot increase normal oxygenation of the arterial blood (98%), but does cause hypocapnia (CO2 deficiency in the alveoli, and, if there is no perfusion-ventilation mismatch, in arterial blood and body cells). Clinical observation of patients with irregular breathing patterns and periodic breathing suggests that their body oxygenation, measured using the DIY Control Pause test (stress-free breath-holding time) is less than 20 s during daytime and less than 15 s immediately after waking up in the morning. These numbers are 2-3 times below normal.
Medical research and science articles have shown that low level of CO2 disrupts and overexcites the nerve cells of the breathing center located in the medulla oblangata of the brain. For research abstracts and clinical studies, see the references below.
Correction of lifestyle risk factors and breathing normalization are necessary. Positive changes and even elimination of existing symptoms is expected with the application of following breathing therapies: the Buteyko breathing method, Frolov breathing device and Amazing DIY breathing device. Significant improvements are possible with Strelnikova paradoxical breathing gymnastic.
Relevant and useful web pages:
Module 12.
How to develop diaphragmatic breathing 24/7 (with 2 breathing
exercises, tips, and causes of chest breathing or costal breathing)
Article - Why most modern people do not have diaphragmatic breathing
Why normal breathing
is shallow (or light and easy) (i.e., small in tidal volume)
Normal
breathing pattern (in healthy people) What is the type of
breathing pattern of healthy people?
Ineffective breath pattern (in the sick) What is the usual
respiratory pattern in mildly sick people?
Breath Pattern in the
severely sick Breathing pattern type in the severely sick
people
Ideal breathing
pattern Is there an "ideal breathing" pattern for super
health?
Types of breathing patterns
Summary (List of 4 types of regular respiratory breathing patterns and
corresponding body oxygenation)
References and abstracts about healing powers of CO2
J Appl Physiol. 1997 Mar;82(3):918-26.
Effects of inhaled CO2 and added dead space on idiopathic central sleep
apnea.
Xie A, Rankin F, Rutherford R, Bradley TD.
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario,
Canada.
Abstract
We hypothesized that reductions in arterial PCO2 (PaCO2) below the
apnea threshold play a key role in the pathogenesis of idiopathic
central sleep apnea syndrome (ICSAS). If so, we reasoned that raising
PaCO2 would abolish apneas in these patients. Accordingly, patients
with ICSAS were studied overnight on four occasions during which the
fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during
room air breathing (N1), alternating room air and CO2 breathing (N2),
CO2 breathing all night (N3), and addition of dead space via a face
mask all night (N4). Central apneas were invariably preceded by
reductions in fraction of end-tidal CO2. Both administration of a
CO2-enriched gas mixture and addition of dead space induced 1- to
3-Torr increases in transcutaneous PCO2, which virtually eliminated
apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and
hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P
< 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room
air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2
inhalation during N2 (P < 0.01), and to 11.6% of the room air
level while the patients were breathing through added dead space during
N4 (P < 0.005). Because raising PaCO2 through two different
means virtually eliminated central sleep apneas, we conclude
that central apneas during sleep in ICSA are due to reductions in PaCO2
below the apnea threshold.
J Physiol. 1991;440:17-33.
The influence of induced hypocapnia and sleep on the endogenous
respiratory rhythm in humans.
Datta AK, Shea SA, Horner RL, Guz A.
Department of Medicine, Charing Cross and Westminster Medical School,
London.
Abstract
1. Ventilation has been studied during hypocapnia produced by passive
mechanical ventilation in ten normal human subjects. 2. During
wakefulness, disconnection of the ventilator led to inconsistent apnoea
of only brief duration. During sleep, at a similar degree of
hypocapnia, disconnection of the ventilator led more consistently to
apnoea which was also of much longer duration; the deeper the sleep
stage, the longer the apnoea. 3. The resumption of breathing during
sleep could precede or follow arousal or be unaccompanied by arousal;
in the absence of prior arousal, the evidence suggests that a
starting end-tidal CO2 pressure (PET, CO2) less than 41 mmHg could
result in an apnoea during sleep stages I and II. 4. Subjects
did not report any common sensation which led them to breathe following
an apnoea whilst awake. 5. Prior hyperoxia in one subject prolonged the
apnoea duration in both slow-wave sleep and rapid eye movement sleep.
6. The results are interpreted as showing that even during light sleep,
the maintenance of the respiratory rhythm is critically dependent on
the arterial CO2 and O2 tensions. During wakefulness, other behavioural
drives, which may not reach consciousness, supervene.
J Physiol. 2004 Oct 1;560(Pt 1):1-11. Epub 2004 Jul 29.
The ventilatory responsiveness to CO(2) below eupnoea as a determinant
of ventilatory stability in sleep.
Dempsey JA, Smith CA, Przybylowski T, Chenuel B, Xie A, Nakayama H,
Skatrud JB.
The John Rankin Laboratory of Pulmonary Medicine, Department of
Population Health Sciences, University of Wisconsin-Madison, Madison,
WI, 53726-2368, USA. jdempsey@wisc.edu.
Abstract
Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold,
whereby apnoea is initiated by small transient reductions in arterial
CO(2) pressure (P(aCO(2))) below eupnoea and respiratory rhythm is not
restored until P(aCO(2)) has risen significantly above eupnoeic levels.
We propose that the 'CO(2) reserve' (i.e. the difference in P(aCO(2))
between eupnoea and the apnoeic threshold (AT)), when combined with
'plant gain' (or the ventilatory increase required for a given
reduction in P(aCO(2))) and 'controller gain' (ventilatory
responsiveness to CO(2) above eupnoea) are the key determinants of
breathing instability in sleep. The CO(2) reserve varies inversely with
both plant gain and the slope of the ventilatory response to reduced
CO(2) below eupnoea; it is highly labile in non-random eye movement
(NREM) sleep. With many types of increases or decreases in background
ventilatory drive and P(aCO(2)), the slope of the ventilatory response
to reduced P(aCO(2)) below eupnoea remains unchanged from control. Thus,
the CO(2) reserve varies inversely with plant gain, i.e. it is widened
with hyperventilation and narrowed with hypoventilation, regardless of
the stimulus and whether it acts primarily at the peripheral or central
chemoreceptors. However, there are notable exceptions, such
as hypoxia, heart failure, or increased pulmonary vascular pressures,
which all increase the slope of the CO(2) response below eupnoea and
narrow the CO(2) reserve despite an accompanying hyperventilation and
reduced plant gain. Finally, we review growing evidence that
chemoreceptor-induced instability in respiratory motor output during
sleep contributes significantly to the major clinical problem of
cyclical obstructive sleep apnoea.
J Appl Physiol. 1983 Sep;55(3):813-22.
Interaction of sleep state and chemical stimuli in sustaining rhythmic
ventilation.
Skatrud JB, Dempsey JA.
Abstract
The effect of sleep state on ventilatory rhythmicity following graded
hypocapnia was determined in two normal subjects and one patient with a
chronic tracheostomy. Passive positive-pressure hyperventilation (PHV)
was performed for 3 min awake and during nonrapid-eye-movement (NREM)
sleep with hyperoxia [fractional inspired O2 concentration (FIO2) =
0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no
immediate posthyperventilation apnea was noted following abrupt
cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal
CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During
spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr
awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep
caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep
levels and 1-2 Torr below the waking level. In hypoxia, PETCO2
increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM
sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr
below NREM sleep levels and 1-2 Torr above awake levels. Apnea
duration (5-45 s) was significantly correlated to the magnitude of
hypocapnia (range 27-41 Torr). PHV caused no apnea when
isocapnia was maintained via increased inspired CO2. Prolonged hypoxia
caused periodic breathing, and the abrupt transition from short-term
hypoxic-induced hyperventilation to acute hyperoxia caused apnea during
NREM sleep when PETCO2 was lowered to or below the subject's apneic
threshold as predetermined (passively) by PHV. We concluded that
effective ventilatory rhythmogenesis in the absence of stimuli
associated with wakefulness is critically dependent on chemoreceptor
stimulation secondary to PCO2-[H+].
Am J Respir Crit Care Med. 2002 May 1;165(9):1251-60.
Effect of ventilatory drive on carbon dioxide sensitivity below eupnea
during sleep.
Nakayama H, Smith CA, Rodman JR, Skatrud JB, Dempsey JA.
The John Rankin Laboratory of Pulmonary Medicine, Department of
Population Health Sciences, University of Wisconsin School of Medicine,
Madison 53705, USA.
Abstract
We determined the effects of changing ventilatory stimuli on the
hypocapnia-induced apneic and hypopneic thresholds in sleeping dogs.
End-tidal carbon dioxide pressure (PET(CO2)) was gradually reduced
during non-rapid eye movement sleep by increasing tidal volume with
pressure support mechanical ventilation, causing a reduction in
diaphragm electromyogram amplitude until apnea/periodic breathing
occurred. We used the reduction in PET(CO2) below spontaneous
breathing required to produce apnea (DeltaPET(CO2)) as an index of the
susceptibility to apnea. DeltaPET(CO2) was -5 mm Hg in
control animals and changed in proportion to background ventilatory
drive, increasing with metabolic acidosis (-6.7 mm Hg) and nonhypoxic
peripheral chemoreceptor stimulation (almitrine; -5.9 mm Hg) and
decreasing with metabolic alkalosis (-3.7 mm Hg). Hypoxia was the
exception; DeltaPET(CO2) narrowed (-4.1 mm Hg) despite the accompanying
hyperventilation. Thus, hyperventilation and hypocapnia, per se,
widened the DeltaPET(CO2) thereby protecting against apnea and
hypopnea, whereas reduced ventilatory drive and hypoventilation
narrowed the DeltaPET(CO2) and increased the susceptibility to apnea.
Hypoxia sensitized the ventilatory responsiveness to CO2 below eupnea
and narrowed the DeltaPET(CO2); this effect of hypoxia was not
attributable to an imbalance between peripheral and central
chemoreceptor stimulation, per se. We conclude that the DeltaPET(CO2)
and the ventilatory sensitivity to CO2 between eupnea and the apneic
threshold are changeable in the face of variations in the magnitude,
direction, and/or type of ventilatory stimulus, thereby altering the
susceptibility for apnea, hypopnea, and periodic breathing in sleep.
Sleep apnea references
Am J Respir Crit Care Med. 1995 Dec;152(6 Pt 1):1950-5.
Hypocapnia and increased ventilatory responsiveness in patients with
idiopathic central sleep apnea.
Xie A, Rutherford R, Rankin F, Wong B, Bradley TD.
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario,
Canada.
Abstract
We previously demonstrated that central apneas during sleep in
patients with idiopathic central sleep apnea (ICSA) are triggered by
abrupt hyperventilation.
In addition, baseline PCO2 at the time of augmented breaths
which triggered central apneas was lower than for augmented breaths
which did not trigger apneas. These observations led us to
hypothesize that patients with ICSA chronically hyperventilate
maintaining their PCO2 close to the threshold for apnea during sleep
owing to increased chemical respiratory drive. To test these
hypotheses, we recorded transcutaneous PCO2 (PtcCO2) during overnight
sleep studies on nine consecutive patients with ICSA and nine sex-,
age-, and body-mass-index-matched control subjects. Daytime PaCO2 as
well as rebreathing and single breath ventilatory responses to CO2 were
also measured. Compared with the control subjects, the
patients had significantly lower mean PtcCO2 during sleep (37.8 +/- 1.2
versus 42.7 +/- 10.9 mm Hg, p < 0.01) and lower PaCO2 while
awake (35.1 +/- 1.3 versus 38.8 +/- 0.9 mm Hg, p < 0.05).
Furthermore, patients with ICSA had significantly higher ventilatory
responses to CO2 for both the rebreathing (3.14 +/- 0.34 versus 1.60
+/- 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51
+/- 0.10 versus 0.25 +/- 0.04 L/min/mm Hg, p < 0.05). We
conclude that: (1) patients with ICSA chronically hyperventilate awake
and asleep and (2) chronic hyperventilation is probably related to
augmented central and peripheral respiratory drive which predisposes to
respiratory control system instability.
Am Rev Respir Dis. 1993 Aug;148(2):330-8.
Role of hyperventilation in the pathogenesis of central sleep
apneas in patients with congestive heart failure.
Naughton M, Benard D, Tam A, Rutherford R, Bradley TD.
Sleep Research Laboratory, Queen Elizabeth Hospital, Ontario, Canada.
Comment in:
Am J Respir Crit Care Med. 1994 Apr;149(4 Pt 1):1053; author reply
1053-4.
Am J Respir Crit Care Med. 1994 Apr;149(4 Pt 1):1053; author reply
1053-4.
Abstract
Periodic breathing with central apneas during sleep is typically
triggered by hypocapnia resulting from hyperventilation. We therefore
hypothesized that hypocapnia would be an important determinant of
Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in
patients with congestive heart failure (CHF). To test this hypothesis,
24 male patients with CHF underwent overnight polysomnography during
which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear
circulation time (LECT), derived from an ear oximeter as an estimate of
circulatory delay, and CSR-CSA cycle length were determined. Patients
were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3
central apneas and hypopneas per h sleep) and a control group without
CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep).
There were no significant differences in left ventricular ejection
fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two
groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were
significantly lower in the CSR-CSA group than in the control group
(33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/-
1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively).
Neither group had significant awake or sleep-related hypoxemia. In
addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p
< 0.001). We conclude that (1) hypocapnia is an
important determinant of CSR-CSA in CHF and (2) circulatory delay plays
an important role in determining CSR-CSA cycle length.
Am J Respir Crit Care Med. 1994 Aug;150(2):489-95.
Interaction of hyperventilation and arousal in the pathogenesis of
idiopathic central sleep apnea.
Xie A, Wong B, Phillipson EA, Slutsky AS, Bradley TD.
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario,
Canada.
Abstract
Central apneas during sleep may arise as a result of reduction
in PaCO2 below the apnea threshold. We therefore hypothesized that
hyperventilation and arousals from sleep interact to cause hypocapnia
and subsequent central apneas in patients with idiopathic central sleep
apnea (ICSA). Accordingly, the relationships among preapneic
ventilation, arousal from sleep, and the onset and duration of
subsequent central apneas were examined during Stage 2 non-REM sleep in
eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and
hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic
breathing with central apneas were triggered by hyperventilation. Minute
ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p
< 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8
+/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic
breathing than during stable breathing. VI during the
ventilatory phase of the periodic breathing cycle increased
progressively with increasing grades of associated arousals from Grade
0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/-
1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p
< 0.01). There was a corresponding progressive increase in
central apnea length following the ventilatory period from no arousal
(14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1
+/- 2.0 s, p < 0.01). We conclude that arousals and
hyperventilation interact to trigger hypocapnia and central apneas in
ICSA.
J Appl Physiol. 1996 Jun;80(6):2102-7.
Effects of inspired gas on sleep-related apnea in the rat.
Christon J, Carley DW, Monti D, Radulovacki M.
Department of Medicine, University of Illinois, Chicago 60612, USA.
Abstract
Central apneas have been reported to occur in the rat during all stages
of sleep. Two types of apnea have been described: spontaneous and
postsigh, which are immediately preceded by an augmented breath. We
studied the effect of inspired gas on the number and type of apneas in
nine adult male Sprague-Dawley rats that were surgically prepared with
cortical electroencephalogram and nuchal electromyogram electrodes. In
addition to the electroencephalogram and electromyogram, we recorded
respiration by the barometric method by using a single-chamber
plethysmograph. Each rat was recorded from 1000 until 1600 on 4
separate days by using different inspired gases: room air, 100% O2, 15%
O2, and 5% CO2. We found that the sleep-related apnea index
was significantly higher during 100% O2 compared with room air (P
< 0.05) and was significantly lower during 15% O2 and 5% CO2
compared with room air (P < 0.05). Postsigh apneas
occurred more frequently than did spontaneous apneas (P <
0.0001). The coupling between sighs and apneas was strengthened by
hyperoxia and weakened by hypoxia and hypercapnia (P < 0.05 for
each). We conclude that stimulation of chemoreceptors acts to oppose
apnea in the rat.
J Appl Physiol. 2006 Jan;100(1):171-7. Epub 2005 Sep 22.
Influence of arterial O2 on the susceptibility to posthyperventilation
apnea during sleep.
Xie A, Skatrud JB, Puleo DS, Dempsey JA.
Department of Medicine, University of Wisconsin, Madison, USA.
axie@facstaff.wisc.edu
Abstract
To investigate the contribution of the peripheral chemoreceptors to the
susceptibility to posthyperventilation apnea, we evaluated the time
course and magnitude of hypocapnia required to produce apnea at
different levels of peripheral chemoreceptor activation produced by
exposure to three levels of inspired P(O2). We measured the apneic
threshold and the apnea latency in nine normal sleeping subjects in
response to augmented breaths during normoxia (room air), hypoxia
(arterial O2 saturation = 78-80%), and hyperoxia (inspired O2 fraction
= 50-52%). Pressure support mechanical ventilation in the assist mode
was employed to introduce a single or multiple numbers of consecutive,
sigh-like breaths to cause apnea. The apnea latency was measured from
the end inspiration of the first augmented breath to the onset of
apnea. It was 12.2 +/- 1.1 s during normoxia, which was similar to the
lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia
shortened the apnea latency (6.3 +/- 0.8 s; P < 0.05), whereas
hyperoxia prolonged it (71.5 +/- 13.8 s; P < 0.01). The apneic
threshold end-tidal P(CO2) (Pet(CO2)) was defined as the Pet(CO2)) at
the onset of apnea. During hypoxia, the apneic threshold Pet(CO2) was
higher (38.9 +/- 1.7 Torr; P < 0.01) compared with normoxia
(35.8 +/- 1.1; Torr); during hyperoxia, it was lower (33.0 +/- 0.8
Torr; P < 0.05). Furthermore, the difference between the eupneic
Pet(CO2) and apneic threshold Pet(CO2) was smaller during hypoxia (3.0
+/- 1.0 Torr P < 001) and greater during hyperoxia (10.6 +/- 0.8
Torr; P < 0.05) compared with normoxia (8.0 +/- 0.6 Torr). Correspondingly,
the hypocapnic ventilatory response to CO2 below the eupneic Pet(CO2) was
increased by hypoxia (3.44 +/- 0.63 l.min(-1).Torr(-1); P <
0.05) and decreased by hyperoxia (0.63 +/- 0.04 l.min(-1).Torr(-1); P
< 0.05) compared with normoxia (0.79 +/- 0.05
l.min(-1).Torr(-1)). These findings indicate that posthyperventilation
apnea is initiated by the peripheral chemoreceptors and that the
varying susceptibility to apnea during hypoxia vs. hyperoxia is
influenced by the relative activity of these receptors.
J Appl Physiol. 2010 Feb;108(2):369-77. Epub 2009 Nov 25.
Effect of episodic hypoxia on the susceptibility to hypocapnic
central apnea during NREM sleep.
Chowdhuri S, Shanidze I, Pierchala L, Belen D, Mateika JH, Badr MS.
Medical Service, John D. Dingell Veterans Affairs Medical Center,
Detroit, MI 48201, USA. schowdh@med.wayne.edu
Abstract
We hypothesized that episodic hypoxia (EH) leads to alterations in
chemoreflex characteristics that might promote the development of
central apnea in sleeping humans. We used nasal noninvasive positive
pressure mechanical ventilation to induce hypocapnic central apnea in
11 healthy participants during stable nonrapid eye movement sleep
before and after an exposure to EH, which consisted of fifteen 1-min
episodes of isocapnic hypoxia (mean O(2) saturation/episode: 87.0 +/-
0.5%). The apneic threshold (AT) was defined as the absolute measured
end-tidal PCO(2) (Pet(CO(2))) demarcating the central apnea. The
difference between the AT and baseline Pet(CO(2)) measured immediately
before the onset of mechanical ventilation was defined as the CO(2)
reserve. The change in minute ventilation (V(I)) for a change in
Pet(CO(2)) (DeltaV(I)/ DeltaPet(CO(2))) was defined as the hypocapnic
ventilatory response. We studied the eupneic Pet(CO(2)), AT Pet(CO(2)),
CO(2) reserve, and hypocapnic ventilatory response before and after the
exposure to EH. We also measured the hypoxic ventilatory response,
defined as the change in V(I) for a corresponding change in arterial
O(2) saturation (DeltaV(I)/DeltaSa(O(2))) during the EH trials. V(I)
increased from 6.2 +/- 0.4 l/min during the pre-EH control to 7.9 +/-
0.5 l/min during EH and remained elevated at 6.7 +/- 0.4 l/min the
during post-EH recovery period (P < 0.05), indicative of
long-term facilitation. The AT was unchanged after EH, but the CO(2)
reserve declined significantly from -3.1 +/- 0.5 mmHg pre-EH to -2.3
+/- 0.4 mmHg post-EH (P < 0.001). In the post-EH recovery
period, DeltaV(I)/DeltaPet(CO(2)) was higher compared with the baseline
(3.3 +/- 0.6 vs. 1.8 +/- 0.3 l x min(-1) x mmHg(-1), P < 0.001),
indicative of an increased hypocapnic ventilatory response. However,
there was no significant change in the hypoxic ventilatory response
(DeltaV(I)/DeltaSa(O(2))) during the EH period itself. In conclusion,
despite the presence of ventilatory long-term facilitation, the
increase in the hypocapnic ventilatory response after the exposure to
EH induced a significant decrease in the CO(2) reserve. This form of
respiratory plasticity may destabilize breathing and promote central
apneas.
J Appl Physiol. 2000 Jul;89(1):192-9.
Effect of gender on the development of hypocapnic apnea/hypopnea
during NREM sleep.
Zhou XS, Shahabuddin S, Zahn BR, Babcock MA, Badr MS.
John D. Dingell Veterans Affairs Medical Center, and Division of
Pulmonary and Critical Care Medicine, Wayne State University School of
Medicine, Detroit, Michigan 48201, USA.
Abstract
We hypothesized that a decreased susceptibility to the development of
hypocapnic central apnea during non-rapid eye movement (NREM) sleep in
women compared with men could be an explanation for the gender
difference in the sleep apnea/hypopnea syndrome. We studied eight men
(age 25-35 yr) and eight women in the midluteal phase of the menstrual
cycle (age 21-43 yr); we repeated studies in six women during the
midfollicular phase. Hypocapnia was induced via nasal mechanical
ventilation for 3 min, with respiratory frequency matched to eupneic
frequency. Tidal volume (VT) was increased between 110 and 200% of
eupneic control. Cessation of mechanical ventilation resulted in
hypocapnic central apnea or hypopnea, depending on the magnitude of
hypocapnia. Nadir minute ventilation in the recovery period was plotted
against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute
ventilation was given a value of 0 during central apnea. The apneic
threshold was defined as the x-intercept of the linear regression line.
In women, induction of a central apnea required an increase in VT to
155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/-
0.57 Torr. In men, induction of a central apnea required an increase in
VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr
(P = 0.002). There was no difference in the apneic threshold between
the follicular and the luteal phase in women. Premenopausal women are
less susceptible to hypocapnic disfacilitation during NREM sleep than
men. This effect was not explained by progesterone. Preservation of
ventilatory motor output during hypocapnia may explain the gender
difference in sleep apnea.
Can J Physiol Pharmacol. 2003 Aug;81(8):774-9.
The essential role of carotid body chemoreceptors in sleep apnea.
Smith CA, Nakayama H, Dempsey JA.
The John Rankin Laboratory of Pulmonary Medicine, Department of
Population Health Sciences, University of Wisconsin School of Medicine,
504 North Walnut Street, Madison, WI 53726-2368. USA. casmith4@wisc.edu
Abstract
Sleep apnea is attributable, in part, to an unstable
ventilatory control system and specifically to a narrowed "CO2 reserve"
(i.e., the difference in P(a)CO2 between eupnea and the apneic
threshold). Findings from sleeping animal preparations with denervated
carotid chemoreceptors or vascularly isolated, perfused carotid
chemoreceptors demonstrate the critical importance of peripheral
chemoreceptors to the ventilatory responses to dynamic changes in
P(a)CO2. Specifically, (i) carotid body denervation prevented the apnea
and periodic breathing that normally follow transient ventilatory
overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was
about one half that for brain chemoreceptors; and (iii) hypocapnia
isolated to the carotid chemoreceptors caused hypoventilation that
persisted over time despite a concomitant, progressive brain
respiratory acidosis. Observations in both humans and animals are cited
to demonstrate the marked plasticity of the CO2 reserve and, therefore,
the propensity for apneas and periodic breathing, in response to
changing background ventilatory stimuli.
Med Clin North Am. 1985 Nov;69(6):1205-19.
Central sleep apnea.
White DP.
Abstract
Central sleep apnea is a disorder characterized by apneic episodes
during sleep with no associated ventilatory effort. More commonly than
not these apneas are seen in patients who also have obstructive and
mixed events. Although patients with this disorder frequently complain
of insomnia and depression, frank hypersomnolence is rarely
encountered. As these complaints are common ones seen in numerous
clinical situations, and since sleep studies are rarely conducted to
investigate their etiology, the true incidence of central sleep apnea
has not been determined. The etiology of central apnea remains unknown,
although the association between these breathing events and a number of
other disease processes has increased our understanding of the
disorder. Central apneas during sleep commonly occur after
hyperventilation with the associated hypocapnic alkalosis. This occurs
at high altitude when hyperventilation is induced by hypoxia and at sea
level when spontaneous nocturnal hyperventilation occurs. This
suggests that PCO2 is the primary stimulus to ventilation during sleep
and that loss of this drive, as occurs with hypocapnia, may produce
dysrhythmic breathing. Patients with complete absence of
ventilatory chemosensitivity such as occurs with Ondine's curse
(central alveolar hypoventilation) or the obesity-hypoventilation
syndrome may also have central apneas. For reasons that remain
unexplained, central sleep apnea is commonly seen in patients with
congestive heart failure, nasal obstruction, and certain neurologic
disorders. However, in most patients with central sleep apnea no
obvious cause or association can be found. The treatment of this
disorder is not entirely satisfactory. If it is severe, mechanical
ventilation during sleep can be provided by any one of a number of
techniques. However, for the patient who simply complains of insomnia
and is found to have a moderate number of central apneas, the treatment
choices are limited. Acetazolamide has been shown to decrease central
apneas during short-term use, but results have been variable with
prolonged administration. Other ventilatory stimulants seem to have
little efficacy. Interestingly, oxygen administration has been shown to
reduce central apneas considerably in a number of studies, although the
explanation for its success is unknown. Central sleep apnea therefore
remains a relatively rare disorder whose etiology is not fully
understood and whose treatment is not completely satisfactory.
Am J Otolaryngol. 2010 May 11. [Epub ahead of print]
End-tidal carbon dioxide concentration monitoring in obstructive sleep
apnea patients.
Weihu C, Jingying Y, Demin H, Yuhuan Z, Jiangyong W.
Department of Otorhinolaryngology-Head and Neck Surgery, Beijing
Tongren Hospital, Capital Medical University, Key Laboratory of
Otorhinolaryngology Head and Neck Surgery, Ministry of Education,
Beijing, China.
Abstract
PURPOSE: The objective of this study was to investigate the end-tidal
carbon dioxide concentration (ETco(2)) monitoring in obstructive sleep
apnea (OSA) patients during sleep and to explore whether the ETco(2)
value may explain a significant portion of the relationship between
ETco(2) value and apnea/hypopnea index (AHI) and nocturnal oxygenation
indices. MATERIALS AND METHODS: Thirty-eight consecutive patients
underwent overnight polysomnography and were synchronously monitored
for ETco(2) using an microstream capnometer. Mean and maximum values
during wake time and different sleep stages were recorded. We grouped
38 OSA patients into 2 subgroups on the basis of their difference of
mean total sleep time and wake time ETco(2) [(T - W) ETco(2)]; one
group, 20 patients with (T - W) ETco(2) less than 0, and the other
group,18 patients with (T - W) ETco(2) greater than 0. RESULTS: Group
with (T - W) ETco(2) less than 0 patients exhibited higher AHI (mean
+/- SD, 68.58 +/- 22.78 vs. 27.61 +/- 19.44 events/h) and lower
nocturnal oxygenation indices (minimum Sao(2), 67.85 +/- 10.08 vs.
82.61% +/- 6.07%; mean Sao(2), 91.29 +/- 3.31 vs. 95.15% +/- 1.88%)
compared with the other group. CONCLUSIONS: In summary, the
study provides preliminary data showing that ETco(2) potentially can be
used in continuous monitoring of OSA patients. And, (T - W) ETco(2) can
indicate the severity of OSA. Copyright © 2010 Elsevier Inc.
All rights reserved.