Transcript Sleep disordered breathing in women

Sleep Disordered Breathing
in Pregnant Women
By
Prof. Suzan Salama
Professor of Pulmonology and Sleep Medicine
Assiut University
Physiology of pregnancy
Adaptation of the circulation:
(1) Heart pressure
Increases
(2) Blood pressure
Decreases
(3) Cardiac output
Increases
(4) Stroke volume
Increases
(5) System vascular resistance
Decreases
(6) Pulmonary vascular resistance
Decreases
15-20 beats/min
30-50%
20-30%
Adaptation of the
respiratory system
Parameters
(1) VO2
(2) RR
(3) VT
(4) TLC
(5) FRC
(6) FEV1
Direction
Increases
Unchanged
Increases
Unchanged
Decreased
Unchanged
(20-35%)
(30-35%)
(10-25%)
Typical arterial blood
gases values
PaO2
PaCO2
pH
A-a gradient
(1) Non-pregnant
98
40
7.40
2
(2) Tearm pregnancy, seated
101
28
7.45
14
(3) Tearm pregnancy, supine
95
28
7.45
20
(A) Sleep disordered breathing in
non-pregnant women
1- OSA 2- Upper airway resistance 3- Central apnea
The OSA is a frequent but often unrecognized condition,
especially in younger women.
Wisconsin sleep cohort study recorded.
Ninety three (93%) of women with moderate to
severe OSA were not clinically diagnosed in the
Wisconsin study.
Under-diagnosis was most frequently encountered
among women, younger, poorer, less educated and
who had not yet developed hypertension or
atherosclerotic disorder.
Burden of OSA
Burden of the disease: In comparison to persons
without OSA
The presence of moderate to severe OSA was
associated with:
(1) Hypertension with an (odd ratio of 2.9) at 4 years
follow up especially at age (40-59 years).
(2) The presence of mild OSA (AHI >5) was an
independent risk factor for prevalent coronary
disease (odds ratio 4.1).
(4)
OSA is an independent risk factor for incident
strokes.
(5)
OSA is an independent risk factor for incident
atrial fibrillation.
(6)
OSA is associated with prevalent congestive heart
failure.
(7)
OSA is associated with prevalent
intolerance and insulin resistance.
(8)
Oxygen desaturation index (>4%) is a better
predictor of insulin resistance than BMI.
glucose
Clinical presentations of OSA in women
The classic OSA presentation that is:
Older obese men, with loud and habitual snoring.
Witnessed apneas and EDS.
Women with OSA were differ with men matched as regards
age, AHI, BMI and Epworth sleepiness score complaining with:
Frequent insomnia.
Nocturnal palpitation.
Depression
Hypothyrodism.
Asthma and allergies.
Migraine.
Weakness, drowsiness, lack of energy.
Irritable bowel syndrome.
Don’t focused
Risk factors of OSA in women
(1) Age:
The prevalence among women 30-39 years (10.9%).
6.5% mild OSA (AHI >5).
4.4% moderate severe (AHI >15).
The prevalence among pre-menopausal (40-55)
years old (14.4%).
10.8% mild OSA.
3.6% moderate to severe OSA.
(2) Obesity:
A well-demonstrated risk factor of OSA.
World health organization (WHO) defines obesity
among Indian women as:
BMI >25kg/m2.
Waist-hip ratio > 0.8.
Neck circumference >43cm.
Waist circumferences > 88cm.
Skin hold thickens.
Obesity a risk factor for 41% of the mild OSA
58% of moderate to severe OSA.
World wide obesity epidemic in 25% of men
in 36% of women.
(3) Craniofacial features:
Associated with narrowed upper airway
(long-narrow face, large tonsils) among far
east Asians odds ratio 2.51.
(4) Chronic rhinitis, asthma:
A strong marker for OSA (odds ratio 3.2).
(5) Polycystic ovarian syndrome:
The prevelance of OSA among women with
polycystic ovarian syndrome as high as 70%.
(6) Menopause:
Is associated with 2.6 odds ratio of having
OSA (AHI >5), adjusted for age, BMI,
smoking, exercise, alcohol, cardiovascular
disease.
(7) Pregnancy:
Is a risk factor for snoring and OSA in
obese women.
Sleep disordered breathing
during pregnancy
(1) Alterations of sleep in normal pregnancy
1- Changes in the sleep pattern and architecture.
During the first trimester:
Increased:
– Sleep duration, daytime sleepiness,
– Insomnia, sleep disturbances.
PSG:
– Increased total sleep time.
– Decrease of:
- Sleep efficiency.
- Stages 3 and 4 and REM sleep.
In the second trimester:
- Normal nocturnal sleep times.
- Increase sleep complaints (nocturia, fetal mov.).
PSG: - Reduced (stages 3 and 4).
- Reduced (REM).
In the third trimester
- Decreased total sleep time.
PSG
- Increase stage 1 and 2.
- Decrease stage 3, 4 and REM stages.
Sleep disorder breathing in pregnancy
Although during pregnancy in normal women oxygen
desaturation is reduced in the supine position.
Mild respiratory disturbances during sleep in late
pregnancy may result in significant reduction of
maternal and fetal oxygenation.
After delivery nocturnal oxygenation return to
normal.
Severe OSA, that was significantly improved 12
weeks postpartum.
Promoting mechanisms of SDB
Physical changes:
A- The elevation of the diaphragm results in:
Reduction of functional residual capacity
Maternal oxygenation reserve is reduced because of
increased alveolar-arterial oxygen gradient.
Ventilation-perfusion mismatch, due to closure of
airway above FRV during tidal ventilation.
(Prominent in late pregnancy and in the supine position).
B- The increase of blood volume during
pregnancy resulting in hyperemia and edema
of nasal mucosa.
C- High estrogen level, may cause vasomotor
rhinitis in 20%-42% in the third trimester and
reduced nasopharyngeal patency.
(2) Hormonal changes:
A- High circulating levels of progesterone and estrogen:
Enhance respiratory drive resulting in hyperventilation.
Leads to a reduction of arterial carbon dioxide pressure
PaCO2 28-32.
Respiratory alkalosis pH= 7.47.
Increased the frequency of central apneas.
The enhanced respiratory drive, lead to more negative
inspiratory pressures, increased suction pressure on (UA)
upper airway structures, and a tendency for collapse of
(UA) during sleep.
Protective mechanisms of SDB
1- Physical changes:
Supine sleep posture increase the frequency of OSA
events compared with lateral or prone positions.
Lateral position preserves cardiac output and
oxygenation.
The observed reduction of REM sleep during late
pregnancy may protect pregnant women from SDB.
2- Hormonal changes:
Increase minute ventilation, may serve as an adaptation
to the increased oxygen consumption demands of
pregnancy.
Progesterone stimulates respiratory drive, resulting in
increased tidal volume and hyperventilation.
The higher respiratory drive, enhances responsiveness
of upper airway dilator ms to chemical stimuli.
Progesterone increases the electromyographic activity
of pharyngeal dilating muscles, to protect against SDB.
Risk factors for OSA during pregnancy
(1) Snoring
There is evidence that snoring is increased during
pregnancy and is common in the third trimester in
27%.
Self reported snoring recorded 14% of 350 pregnant
women of the second trimester.
There is reduction of snoring at 5% at 3 months after
delivery.
Not only snoring but also gasping, choking and
witnessed apneas were increased significantly during
pregnancy.
(2) Obesity
Obesity is a major risk factor for sleep apnea
generally.
During pregnancy, increased initial body mass index
and greater changes in neck circumference have been
associated with higher prevalence of SDB.
Habitual snoring associated with weight gain.
Neck circumference is a predictor of sleep apnea,
independent of weight, which reflect the changes in
the upper airway anatomy.
During pregnancy
Maternal Complications Due to SDB
Maternal complications due to SDB
(1)Preeclampsia: is condition that may
complicate 5% to 6% of pregnancies
characterized by PIH (pregnancy included
hypertension) and proteinurea (>300mg/d) that
may result in maternal morbidity and mortality,
premature delivery and fetal growth retardation.
Known risk factors for preeclampsia include:
Family history primiparity.
Advanced maternal age – obesity.
Pre-existing hypertension – renal disease.
Mechanism of link (preeclampsia and OSA):
The pathogenesis of preeclampsia is not
known but, recently it has been associated with
oxidative stress and endothelial dysfunction.
OSA is common in the general population ad
has been linked with the development of
arterial hypertension even in cases of mild
severity.
Moreover, it has been hypothesized that OSA and
nocturnal hypoxemia activate the sympathetic
nervous system, impaired endothelial function,
elevate the levels of vasoconstriction substances, and
cause the development of oxidative stress leading to
inflammatory changes and vascular damage.
Hypoxemia and increased body weight during
pregnancy may occur without the presence of
significant SDB, however, and may predispose to the
development of PIH.
Absence of nocturnal dipping (10-20mmHg) in
systolic blood pressure is seen in both
preeclampsia and OSA, suggesting a common
link between the two.
In a study showed that preeclampstic women
had significantly higher RDI (18.4vs 8.3;
P<0.05). And lower endothelial function index
(1.5 vs 1.8; P<0.05); compared with the
control group.
Results in:
Reduced oxygen placental delivery to the fetus.
These mechanisms suggest a relationship of
sleep apnea with intrauterine growth retardation
and small birth weight.
Several studies report the presence of OSA
syndrome in pregnant women associated with:
- PIH and preeclampisa.
Or
Or
- Pulmonary hypertension.
- Gestational diabetes.
Evaluation and screening of OSA
during pregnancy
1- There are no specific guidelines for screening pregnant
women for OSA.
2- Pien and Schwab (2004), have proposed that pregnant
women with.
-
ED sleepiness.
- Loud snoring.
Witnessed apnea.
- Preexisting obesity.
Large neck size with PLM.
Preeclampsia should be evaluated for OSA with
overnight PSG.
3- Santiago et al., (2001) argued that until the incidence
of SDB in normal and complicated pregnancy is
defined, the indications of PSG should be expended
to include those with:
Hypertension.
Previous babies with unexplained intrauterine growth
restriction.
Persistant sleep-related symptoms (hypersomnia or
insomnia).
Associated with snoring or obesity
Strength of recommendation, C.
There are multiple studies that have
successfully performed nocturnal PSG without
difficulty.
However, the preference of pregnant women to
sleep in the lateral position, it is possible that
AHI may be under estimated.
Fetal Complications
Fetal complications:
Intermittent hypoxia during pregnancy
observed with OSA, leads to placental
ischemia, causes fetal heart rate decelerations,
decreased fetal breathing and movements and
fetal growth restriction.
Franklin et al., (2000), found that pregnant
women with self reported snoring delivered
infants with lower APGAR scores and lower
weight (7.1vs 2.6) than non snorers.
SDB had been proposed as a risk factor for
adverse fetal outcomes:
Fetal heart rate abnormalities.
Fetal growth retardation.
Fetal death.
On the other hand, a study on 325 pregnant
women did not find relationship between
snoring and infant birth weight.
Treatment of OSA during pregnancy
(1) Conservative measures:
Control of body weight gain.
Avoidance of sleep in the supine position.
Elevation of the head during sleep.
Restriction of alcohol and sedatives consumption.
These measures are useful even in non-OSA pregnant
women (strength recommendation, C).
(2) Nasal CPAP:
CPAP is the therapy of choice for OSA.
CPAP during pregnancy has been shown to be safe, effective and
well tolerated.
CPAP is not recommended in preeclampsia without objective
documentation of OSA (strength recommended, A).
CPAP recommended in pregnant women with (mild apnea
AHI>5-30 events/h), and severe apnea (AHI >30 events/hour) or
recurrent SaO2 <90%.
CPAP therapy also has been shown to improve cardiac output
while reducing total peripheral resistance in patients with
preeclampsia.
(3) Oral appliances:
Have not been investigated
and impractical.
(4) Surgical therapies:
(uvulopalatopharynegeoplasty).
Are not recommended during pregnancy,
because they are less effective.
(5) Oxygen therapy:
For pregnant women who refuse to use or are
unable to tolerate CPAP, to improve minimal
oxyhemoglobin saturation.
No recommendation for chronic use of oxygen
as a therapy for OSA as a primary treatment.
Moreover, there are potential dangers like
prolongation of apnea duration, increased
hypercarbia, and ventricular irritability
associated with oxygen therapy.
Post partum management of OSA
OSA precipitated by
improves after delivery.
pregnancy
usually
Significant spontaneous improvement of AHI
values, SaO2, arousal indices occurred by 3 to
6 months postpartum.
Nasal CPAP was discontinued within 2 weeks
of delivery in all the patients.
Based on expert opinion (2004):
1- Postpartum withdrawal of CPAP therapy with
follow up in mild to moderate OSA
pregnancy associated for symptoms recur, a
repeat PSG to assess baseline AHI is indicated.
2- For severe pregnancy-associated sleep
apnea, therapy should be continued and, when
weight returns to 10% to 15% of baseline,
repeat PSG to establish baseline, of AHI and
any need for continued therapy.
patients with pre-existing OSA can safely,
when their weight returns to 10% to 15% of
baseline, repeat PSG to determine new AIH.
All women with gestational sleep apnea should
monitored closely for symptoms recurrence in
subsequent pregnancies.