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Pulmonary Disorders

Dr. Manal Shafik Swelem


Lecturer of Obstetrics &
Gynecology
PULMONARY PHYSIOLOGY
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decreases 20 % from
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Increase 20%
PULMONARY PHYSIOLOGY
The expanding uterus & increased
abdominal pressure cause chest
wall compliance to be reduced by a
third.
Minute ventilation increases about
30 to 40 % due to increased tidal
volume.
Arterial pO2 also increases from
100 to 105 mm Hg
Carbon dioxide production
increases approximately 30 %, but
diffusion capacity also increases,
and with alveolar hyperventilation,
the pCO2 decreases from 40 to 32
mm Hg.
ASTHMA
Asthma is common in young women and therefore
is seen frequently during pregnancy.
Asthma prevalence increased steadily in many
countries beginning in the mid-1970s but may
have plateaued during the past decade.
Estimated asthma prevalence during pregnancy to
range between 4 and 8 %.
Moreover, some reported that the prevalence in pregnant women appears to be
increasing.??
Pathophysiology
Asthma is a chronic inflammatory airway disorder with a
major hereditary component.
Increased airway responsiveness & persistent subacute
inflammation.
a) have been associated with genes on chromosomes 5, 11, &
12 that include cytokine gene clusters, -adrenergic &
glucocorticoid receptor genes, and the T-cell antigen
receptor gene.
b) There inevitably is an environmental allergic stimulant
such as influenza or cigarette smoke, irritants, viral
infections, aspirin, cold air, and exercise in susceptible
individuals.
The hallmarks of asthma are reversible airway obstruction from
bronchial smooth muscle contraction, vascular congestion, tenacious
mucus, and mucosal edema.
Pathphysiology

Inflammation is caused by response


of mast cells, eosinophils,
lymphocytes & bronchial epithelium.
A number of inflammatory mediators
by these & other cells include
histamine, leukotrienes, PG,
cytokines & many others.
IgE also plays a central role in
pathophysiology.
Because F-series prostaglandins
and ergonovine exacerbate asthma,
these commonly used obstetrical
drugs should be avoided if possible.
Clinical Course
Asthma represents a broad
spectrum of clinical illness
ranging from mild wheezing to
severe bronchoconstriction.
The functional result of acute
bronchospasm is airway
obstruction and decreased
airflow.
The work of breathing
progressively increases, and
patients present with chest
tightness, wheezing, or
breathlessness.
The variations of asthma manifestations have led to a
simple classification that considers severity as well as
onset and duration of symptoms
Pathophysiology
Hypoxia initially
is well
compensated
by hyperventilation Normal for pregnancy
Difference from non-pregnant?
Although these changes are generally reversible
& well tolerated by the healthy non-pregnant
individual, even early stages of asthma may be
dangerous for the pregnant woman & her fetus.

This is because smaller functional residual


capacity render the woman more susceptible to
hypoxia & hypoxemia.
Effects of Pregnancy on Asthma
Effects of Pregnancy on Asthma
Baseline severity is correlated with asthma morbidity
during pregnancy. Women with severe disease are more
likely to have an exacerbation during pregnancy.
Approximately 20 % of women with mild or moderate
asthma have been reported to have an intrapartum
exacerbation.
Conversely, others reported exacerbations at the time of
delivery in only 1% of women.
Some reported an 18-fold increased risk of exacerbation
following cesarean versus vaginal delivery.
Effects of Pregnancy on Asthma
Life-threatening complications from status
asthmaticus include muscle fatigue with
respiratory arrest, pneumothorax,
pneumomediastinum, acute cor pulmonale, &
cardiac arrhythmias.

Maternal & perinatal mortality rates are


substantively increased when mechanical
ventilation is required.
Pregnancy Outcome
Pregnancy outcomes in asthmatics have improved during
the past 20 years.
Unless there is severe disease, pregnancy outcomes are
generally excellent.
In some studies, there is a slightly increased incidence of
preeclampsia, preterm labor, accidental hemorrhage,
preterm rupture of membranes, low-birthweight infants, &
perinatal mortality.
But, in a recent European report, 37,585 pregnancies of
women with asthma were compared with pregnant
nonasthmatics. Risks of most obstetrical complications
were not higher in asthmatic women, except depression,
miscarriages, and cesarean delivery.
Fetal Effects
With reasonable control of
asthma, perinatal outcomes
are generally good.

But when respiratory


alkalosis develops, both
animal & human studies
suggest that fetal hypoxemia
develops well before the
alkalosis compromises
maternal oxygenation.
Fetal Effects
It is hypothesized that the fetus is
jeopardized from decreased uterine blood
flow, decreased maternal venous return, &
an alkaline induced leftward shift of the
oxyhemoglobin dissociation curve.
The fetal response to maternal hypoxemia is
decreased umbilical blood flow, increased systemic
and pulmonary vascular resistance & decreased
cardiac output.
Fetal Effects
Observations confirm that the incidence
of fetal-growth restriction increases with
asthma severity. This realization
underscores the need for aggressive
management.

Monitoring the fetal response is, in


effect, an indicator of maternal status.
Fetal Effects
Possible teratogenic or adverse fetal effects of
drugs given to control asthma have been a
concern.
Fortunately, considerable data have showed no
evidence that commonly used anti-asthmatic
drugs are harmful.
Despite this, some reported a 13-54 % patient-
generated decrease in -agonist & corticosteroid
use between 5 to 13 weeks of pregnancy.
Clinical Evaluation
The subjective severity of asthma
frequently does not correlate with
objective measures of airway
function or ventilation.
Clinical examination also is
inaccurate as a predictor of
severity.
Useful clinical signs include
dyspnea, tachycardia, pulsus
paradoxus, prolonged expiration,
& use of accessory muscles.
Signs of a potentially fatal attack
include central cyanosis & altered
consciousness.
Arterial blood gas
Arterial blood gas analysis
provides objective assessment of
maternal oxygenation, ventilation,
and acidbase status, helping to
assess the severity of an acute
attack.
If used, the results must be
interpreted in relation to normal
values for pregnancy.
For example, a pCO2 35 mm Hg
with a pH 7.35 is consistent with
hyperventilation and CO2
retention in a pregnant woman.
Pulmonary function testing
Pulmonary function testing should be
routine in the management of chronic
and acute asthma.
Sequential measurement of the FEV1 or
the peak expiratory flow ratePEFR
are the best measures of severity.
Each woman determines her own
baseline when asymptomatic personal
bestto compare with values when
symptomatic.
An FEV1 1 L, or 20 % of predicted
value, correlates with severe disease
defined by hypoxia, poor response to
therapy& a high relapse rate.
Pulmonary function testing
Pulmonary function testing
The PEFR correlates well
with the FEV1, and it can
be measured reliably with
inexpensive portable
meters.

Some researchers showed


that the PEFR did not
change during the course
of pregnancy in normal
women.
MANAGEMENT
The general principles of asthma management during
pregnancy do not differ substantially from the management
of non-pregnant asthmatics.
The ultimate goal for the pregnant asthmatic is to have no
limitation of activity, minimal chronic symptoms, no
exacerbations, normal pulmonary function, and minimal
adverse effects of medications.
It is the clinicians job to provide optimal therapy to
maintain asthma control that improves maternal quality of
life and allows for normal fetal maturation.
Management of Chronic Asthma
The most recent management guidelines of the Working
Group on Asthma and Pregnancy include:
1. Patient educationgeneral asthma management and its
effect on pregnancy.
2. Environmental precipitating factorsavoidance or control.
3. Objective assessment of pulmonary function and fetal
wellbeing monitor with PEFR or FEV1.
4. Pharmacological therapyin appropriate combinations
and doses to provide baseline control and treat
exacerbations.
Pulmonary function testing
In general, women with moderate
to severe asthma should measure
& record either their FEV1 or
PEFR twice daily.
The FEV1 ideally is 80 % of
predicted. For PEFR, predicted
values range from 380 - 550
L/min.
Each woman has her own
baseline value & and therapeutic
adjustments can be made using
this
Treatment
Treatment depends on
the severity of disease.
For mild asthma,
inhaled -agonists as
needed are usually
sufficient.
For persistent asthma,
inhaled corticosteroids
are administered every
3 to 4 hours.
Treatment
Although - agonists help to abate bronchospasm,
corticosteroids treat the inflammatory component.
The goal is to reduce the use of -agonists for
symptomatic relief.
Inhaled corticosteroids reduce hospitalizations by 80
%.
It was found that about 55% reduction in re-
admissions for severe exacerbations in pregnant
asthmatics can be achieved by giving maintenance
inhaled corticosteroids along with -agonist therapy.
(salbutamol = ventolin/ terbutaline=bricanyl)

(bronchodilator)

(foradil/serevent diskus)
Theophylline
Theophylline is a methylxanthine, and its various
salts are bronchodilators & possibly anti-
inflammatory agents.
They have been used less frequently since inhaled
corticosteroids became available.
Some theophylline derivatives are considered useful
for oral maintenance therapy if the initial response
is not optimal to inhaled corticosteroids and
-agonists.
When oral theophylline was compared with inhaled
beclomethasone for maintenance, both had about
20% exacerbations. Women taking theophylline had
a significantly higher discontinuation rate because
of side effects. Pregnancy outcomes were similar in
the two groups.
Leukotriene modifiers
Leukotriene modifiers (singulair) inhibit their synthesis &
include zileuton, zafirinkast, and montelukast.
These drugs are given orally or by inhalation for
prevention, but they are NOT effective for acute disease.
For maintenance, they are used in conjunction with inhaled
corticosteroids to allow minimal dosing.
About half of asthmatics will improve with these drugs.
They are not as effective as inhaled corticosteroids.
Finally, there is little experience with their use in
pregnancy.
Mast cell stabilizers / Monoclonal IgE
Cromolyn (intal aerosol) and nedocromil inhibit mast cell
degranulation.
They are ineffective for acute asthma & are taken
chronically for prevention.
They likely are not as effective as inhaled corticosteroids
& have generally been replaced by leukotriene modifiers.
There is no experience in pregnant women with
omalizumab (Xolair), a recombinant humanized
monoclonal anti-IgE antibody.
It binds circulating IgE to deactivate it.
Management of Acute Asthma
Treatment of acute asthma during pregnancy is similar to
that for the non-pregnant asthmatic. An exception is a
significantly lowered threshold for hospitalization.
IV hydration may help clear pulmonary secretions, and
supplemental oxygen is given by mask.
The therapeutic aim is to maintain the pO2 greater than 60
mm Hg, along with 95 % oxygen saturation.
Baseline pulmonary function testing includes FEV1 or
PEFR.
Continuous pulse oximetry & electronic fetal monitoring
may provide useful information.
Management of Acute Asthma
First-line therapy for acute asthma includes a
adrenergic agonist, such as terbutaline (bricanyl),
which is given subcutaneously, taken orally, or
inhaled.
These drugs bind to specific cell-surface receptors
& activate adenylyl cyclase to increase
intracellular cyclic AMP & modulate bronchial
smooth muscle relaxation.
Long-acting preparations are used for outpatient
therapy.
Corticosteroids
If not previously given for maintenance, inhaled corticosteroids
are commenced along with intensive -agonist therapy.
Corticosteroids should be given early to all patients with severe
acute asthma.
Unless there is a timely response to treatment, oral or parenteral
preparations are given. Intravenous methylprednisolone, 40 to
60 mg, every 6 hours is commonly used.
Equipotent doses of hydrocortisone by infusion or prednisone
orally can be given instead.
Because their onset of action is several hours, corticosteroids
are given initially along with -agonists for acute asthma.
Management & Follow up
Further management depends on the response to therapy.
If initial therapy with -agonists is associated with
improvement of FEV1 or PEFR to above 70 % of baseline,
then discharge can be considered.
Alternatively, for the woman with obvious respiratory
distress, or if the FEV1 or PEFR is less than 70 % of
predicted after 3 doses of -agonist, admission is advisable.
Intensive therapy includes inhaled -agonists, intravenous
corticosteroids, and close observation for worsening
respiratory distress or fatigue in breathing.
The woman is cared for in the delivery unit or an
intermediate or intensive care unit
Status Asthmaticus &
Respiratory Failure
Status asthmaticus is severe asthma
of any type not responding to
intensive therapy for 30 - 60 minutes.
Management in an intensive care
setting results in a good outcome in
most cases.
Consideration should be given to
early intubation when maternal
respiratory status worsens despite
aggressive treatment.
Fatigue, carbon dioxide retention, &
hypoxemia are indications for
mechanical ventilation.
Labor and Delivery
Maintenance medications are
continued through delivery.
Stress-dose corticosteroids are
administered to any woman given
systemic steroid therapy within the
preceding 4 weeks.
The usual dose is 100 mg of
hydrocortisone given IV / 8 hours
during labor & for 24 hours after
delivery.
The PEFR or FEV1 should be determined on admission, & serial
measurements are taken if symptoms develop.
Labor and Delivery
Oxytocin or PG E1 or E2 are used
for cervical ripening & induction.
A non-histamine releasing
narcotic as fentanyl may be used
for labor, & epidural analgesia is
ideal.
For surgical delivery, conduction
analgesia is preferred because
tracheal intubation can trigger
severe bronchospasm.
Labor and Delivery
Postpartum hemorrhage is
treated with oxytocin or
prostaglandin E2.

Prostaglandin F2 or
ergotamine derivatives
are contraindicated
because they may cause
significant
bronchospasm.
Thank
you

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