Transcript The Lungs in Pregnancy

Dr. khaled wagih
Assistant professor of pulmonary medicine
Ain shams university
Objectives
 I. ANATOMIC
CHANGES OF
NORMAL PREGNANCY
- Airways
- Respiratory Muscles and the Thoracic Cage
 II.
PHYSIOLOGICAL CHANGES OF
NORMAL PREGNANCY
- Respiratory Physiology
- Cardiovascular Physiology
- Sleep Disturbances
- Dyspnea of Pregnancy
 III. ACUTE
RESPIRATORY
DISTRESS IN PREGNANCY

IV. RESPIRATORY DISEASES IN
PREGNANCY
- Asthma
- Venous Thromboembolism
- Pulmonary Hypertension
- Sleep-Disordered Breathing
- Cystic Fibrosis
PULMONARY COMPLICATIONS IN
PREGNANCY
Pulmonary Complications Obstetric Causes:
 Dyspnea of pregnancy Mechanical
 Hormonal (biochemical)
 Hemodynamic changes
 Pulmonary diseases
 Pneumothorax and pneumomediastinum
Valsalva maneuver (second stage of labor)
 Pulmonary edema Aspiration
 Eclampsia
 Tocolytic therapy

Pulmonary embolism
 Amniotic fluid embolism
 Disseminated intravascular coagulation
 Trophoblastic embolism
 Transfusion reactions
 Sepsis (septic abortion)
 Pleural effusion Postpartum
 Pulmonary hypertension
 Sarcoidosis, rhinitis, asthma, tuberculosis,
and cystic fibrosis

 The
respiratory system is affected by the
normal anatomic and physiologic alterations
that take place throughout pregnancy,
parturition, and early postpartum.
 A healthy pregnant woman experiences
minimal or tolerably mild respiratory
symptoms.
 A pre-existing pulmonary problem, however,
can be exacerbated by pregnancy. On the
other hand, the normal course of the
pregnancy can be adversely affected by preexisting respiratory disorders to the point of
threatening the pregnancy itself
ANATOMIC CHANGES OF NORMAL
PREGNANCY:
 Basic
structural changes occur in the
upper and lower airways, thoracic cage,
and the respiratory muscles, most
notably the diaphragm.
Airways :
upper airways
 Hyperemia,
friability, mucosal edema,
and hypersecretion of the airway mucosa
 May
be aggravated by preeclampsia, upper
respiratory tract infection, or allergic rhinitis.
Nasal obstruction, epistaxis, sneezing
episodes, and vocal changes.

Nasal and sinusoidal polyposis is often seen
and tends to recur in women with each
pregnancy.
 Nasal
obstruction may contribute to upper
airway obstruction during sleep, leading to
snoring and even obstructive sleep apnea.
 Lower
airways :
 The
anatomic changes not characterized, but
some of the mucosal changes that affect the
upper airways may also occur in the central
portion of the airway, such as the larynx and
trachea.

Nonspecific complaints of airway irritation,
such as irritant cough or sputum production,
may be intensified during pregnancy, often in
association with functional changes in airway
reactivity and/or coexistent pulmonary
conditions.
 The
physiological causes of nasal mucosal
changes appear to be predominantly
mediated by estrogens
Respiratory Muscles and the Thoracic Cage:
The enlarging uterus produces upward
displacement of the diaphragm.
 Although the diaphragm may be elevated up to
4 cm cephalic, diaphragmatic function is not
impaired
 increase in the antero posterior and transverse
diameters of the thoracic cage. Diminished tone
and activity of the abdominal muscles

Progressive relaxation of the ligamentous
attachments of the ribs broadens the subcostal
angle by approximately 50percent. ,
 There is a 5 to 7 cm increase in chest
circumference.
 upward and lateral displacement of the cardiac
apex on chest radiography.

PHYSIOLOGICAL CHANGES OF NORMAL
PREGNANCY:
Both respiratory and cardiovascular changes
ensure the delivery of necessary oxygenated blood
and other nutrients required for this process.

Respiratory Physiology :






changes in lung volumes .
The expiratory reserve volume ( ERV) decreases by 8 to
40 percent and the residual volume ( RV ) by 7 to 22
percent.
10 to 25 percent decrease in functional residual capacity
( FRC ) after the fifth or sixth month of pregnancy.
Inspiratory capacity ( IC ) increases.
Vital capacity ( VC ) and total lung capacity (TLC)
are not substantially changed in normal healthy gravidas,
Although total lung capacity does minimally decrease in
the third trimester. Residual volume to total lung capacity
ratio is low in the third trimester.
Tidal volume increases considerably, 30 to 35%,
as a result of increased ventilatory drive.
 Maximum voluntary ventilation does not change
greatly during pregnancy.
 Values of FEV1 throughout pregnancy are not
significantly different from the non pregnant
condition.
 Increased gastric and esophageal pressure
occurring in late pregnancy has been considered
major factors that produce a decrease in trans
pulmonary pressure leading to peripheral airway
collapse.
 An increase in lung water, resulting in a change in
the elastic properties of the lungs.

Progressive increases of airway conductance
have been reported to occur between 6 months
of pregnancy and term along with a decrease
in airway resistance.
 Total pulmonary resistance, consisting of both
airway and tissue resistance, is reduced by
approximately 50 percent in pregnancy.
 Lung compliance does not change.
 Compliance of the thoracic cage decreases, as
the anatomic changes in chest wall and the
decrease in tone and activity of the abdominal
musculature

In early pregnancy, the diffusing capacity is either
unchanged or slightly increased.
 Throughout the rest of pregnancy, the diffusing
capacity decreases, returning to normal or slightly
lower than normal values.
 The relative contributions of the specific factors
that affect diffusion, such as membrane diffusing
capacity and pulmonary capillary blood volume,
are not known.
 Minute ventilation increases 20 to 50 percent
before the end of the first trimester due
to the effect of increased serum progesterone

Carbon dioxide production and oxygen
consumption increase as a result of the
increase in basal metabolic rate.
 Progesterone levels increase gradually during
pregnancy from 25 ng/ml at 6 weeks to 150
ng/ml at 37 weeks.
 Mouth occlusion pressures increase
progressively during pregnancy in keeping with
increasing progesterone levels.
 Estrogen may have an additional effect by
causing an increased responsivity of the
respiratory center.

Arterial PCO2 falls to levels of 32 to 28 mmHg.
 plasma bicarbonate decreases to 21 to 18
mEq/L.
 Arterial pH is maintained in the range of 7.40 to
7.45.
 Values for arterial PO2 are generally greater
than 100 mmHg during pregnancy.
 With the supine position, the alveolar-arterial
oxygen gradient may widen, and mild arterial
hypoxemia may develop.
 Respiratory responses during parturition are
greatly affected by stage of labor and the
response to pain and anxiety






During labor, tidal volumes ranging from 350 to
2250 ml and minute ventilations from 7 to 90
L/min have been recorded.
The higher values were close to the maximum
voluntary ventilation and were associated with the
second stage of labor
The lower values were obtained in the first stage
of labor while the patient was sedated.
Along with the alveolar hyperventilation, oxygen
consumption during labor doubles and can even
triple (e.g., to 750 ml/min) during uterine
contractions.
The possibility of relative hypoventilation between
contractions coupled with the grave implications
of fetal hypoxemia makes it reasonable to be
liberal in the use of oxygen
Sleep Disturbances:
 Sleep
quality is often poor.
 Sleep disruption can be due to leg cramps,
low back pain, urinary frequency, or
responsibilities relating to child care.
 Total sleep time and daytime sleepiness
increase during the first trimester, whereas
sleep time decreases and complaints of an
increase in the number of nocturnal arousals
increase in the third trimester.
Sleep Disturbances:
 Polysomnographic
studies have shown
an increase in sleep latency, an increase in
the amount of stage I sleep and a decrease
in rapid eye movement (REM) sleep and
delta sleep, as well as an increase in the
number of awakenings.
 The
incidence of sleep-disordered breathing
during pregnancy is unknown.
Cardiovascular Physiology:
Beginning around the fifth week of pregnancy and
continuing into the postpartum period.
 Cardiac output increases and peaks near term at 30
to 50 percent above normal.
 Increases in heart rate, stroke volume (10 to 30%)
above prepartum values by week 12 and a decrease
(20 to 30%) in pulmonary and peripheral vascular
resistances.
 This response is principally a result of an increase in
endogenous catecholamines and an increase in
venous return of up to 300 to 500 ml of blood that
occurs during uterine contractions.


Maternal blood volume increases progressively
throughout pregnancy, beginning as early as 4 to 6
weeks of gestation and plateauing at approximately
32 to 34 weeks of gestation .Total blood volume
increases up to 35 to 50 percent above baseline
(approximately 1.6 L), peaking by the third trimester.

Plasma volume increases to a greater degree than
red blood cell mass, which increases less, and more
gradually, to an average increase of about 25%.

These changes result in a decrease of hemoglobin
concentration and hematocrit, producing the
“physiological anemia of pregnancy.”

The increase in blood volume is probably
determined by multiple, primarily endocrine factors,
such as estrogen stimulation of aldosterone, nonrenal renin, and atrial natriuretic factor. Chorionic
somatomammotropin, progesterone, and possibly
prolactin probably stimulate the increase in red
blood cell mass.

Extracellular water increases by 1 to 2 L, results in
the peripheral edema that occurs in 50 to 80 %of
normal pregnancies.

Left ventricular wall thickness increases by 28 %
and left ventricular mass by 52 % above baseline,
resulting in a decrease in left ventricular
compliance.
 Central
venous pressure, pulmonary
capillary wedge pressure, and left ventricular
stroke work do not change significantly

Systemic blood pressure, especially the
diastolic component, is slightly lower during
pregnancy.
 Diastolic
blood pressure reaches its nadir in
the middle of the third trimester, falling by 10 to
20% of prepregnancy values. Subsequently,
blood pressure increases to near prepregnancy
levels.
Dyspnea of Pregnancy
 60
to 70 %.
 commonly occur during the first and
second trimester and remain stable or
improve near term .
 increased ventilatory drive and
increased mechanical load.
 Excessive chemoreceptor sensitivity to
carbon dioxide or hypoxemia.
ACUTE RESPIRATORY DISTRESS IN
PREGNANCY

As a rule, causes of respiratory distress due to
conditions specific to pregnancy (e.g., amniotic
fluid embolism, or pulmonary edema secondary to
preeclampsia or tocolytic therapy) pose little
problem in clinical diagnosis.

invasive hemodynamic monitoring to differentiate
between cardiogenic and noncardiogenic
pulmonary edema. Pulmonary thromboembolism
should always be strongly considered
RESPIRATORY DISEASES IN
PREGNANCY

Bronchial Asthma:
The risks of poorly controlled asthma to the mother
and fetus are greater than those posed by most
medications (including oral corticosteroids)
 Approximately 4 to 8 % of pregnant women in the
United States are asthmatic
 No association between asthma and preterm
delivery or adverse perinatal outcomes
 Neonatal sepsis and an increased maternal
cesarean section rate in women with moderate or
severe asthma.

Pharmacologic management is quite similar
utilizing inhaled short acting beta2-agonists,
inhaled corticosteroids, inhaled long acting beta2agonists, and systemic corticosteroids.
 leukotriene receptor antagonists and Theophylline
are safe
 Oral corticosteroid use in the first trimester is
associated with a small increased risk of isolated
cleft lip with or without cleft palate (0.1 to 0.3
percent), and may be associated with increased
risks of pregnancy-induced hypertension,
preeclampsia, preterm delivery, and low birth
weight.


Class A: Controlled human studies have demonstrated no
risks to the fetus.

Class B: Presumed safe, based on animal studies; no wellcontrolled human studies are available.

Class C: Safety is uncertain; data from human studies do not
exist, and animal studies have shown some question of risk to
the fetus. Pregnant women may take these medicines if they
clearly need them.

Class D: Evidence suggests the possibility of the medication
causing birth defects or other problems, but a pregnant woman
still might need to take it for her own medical needs.

Class X: Proven risks to the fetus outweigh any possible
benefits to the mother
 Venous
Thromboembolism:
0.5 to 3.0 per 1000 pregnancies in those without a
history of thromboembolism.
 Prior thromboembolic disease, smoking, prior
venous thrombosis, and thrombo-philias are risk
factors for deep venous thrombosis or pulmonary
embolism (PE) during pregnancy.
 The risk of venous thromboembolism is greatest in
the postpartum period.
 Evaluation… venous ultrasound LLS. If negative, a
ventilation-perfusion (V-P) scan or helical computed
tomography (CT) scan should be performed next

Confirmed cases of venous thromboembolism
during pregnancy should be managed with
unfractionated or low molecular weight heparins.
 Coumarin should be avoided due to the risk of
embryopathy.

 Pulmonary

Hypertension:
The cardiovascular and hemodynamic changes
associated with pregnancy, anesthesia, and
delivery pose a severe risk to women with primary
pulmonary hypertension, Eisenmenger’s
syndrome, and secondary pulmonary
hypertension.

Studies have documented maternal mortalities
in these groups from 30 to 56 percent, although
most of these studies evaluated patients who
did not receive current vasodilator therapy.

Recent case reports have documented
successful use of intravenous or inhaled
epoprostenol, and sildenafil in pregnant women
with pulmonary hypertension; however, their
long-term effect on overall pregnancy related
mortality is unknown.
 Pulmonary
Edema:
Obstetric causes of pulmonary edema include
aspiration pneumonia, sepsis, transfusion
reactions, allergic reactions, disseminated
intravascular coagulation, amniotic fluid
embolism, toxemia of pregnancy, tocolytic
therapy, and eclampsia, the latter being the most
common cause of pulmonary.
- Bromocriptine therapy to suppress lactation
can also cause postpartum pulmonary edema
- Decreased venous tone and venous resistance
lead to iatrogenic pulmonary edema.
 Pleural
Effusion
 Pleural
effusions occur with toxemia of
pregnancy, preeclampsia, pulmonary
edema, pulmonary embolism,
choriocarcinoma, and amniotic fluid
embolism .
 Small
pleural effusions are common in the
postpartum period in normal pregnancy.
 Sleep-Disordered
Breathing:
Hormonal changes of increased estrogen
resulting in hyperemia and upper airway
narrowing.
 increased progesterone resulting in increased
respiratory drive.
 Other physiologic changes of sleep (decreased
FRC and respiratory system compliance)
predispose to alterations in sleep during
pregnancy.
 While snoring is increased in pregnancy, and
sleep-disordered breathing may worsen during
pregnancy, the incidence and prevalence of
sleep-disordered breathing during pregnancy are
unknown

 Symptoms
of sleep-disordered breathing
should be reviewed with women who
develop pregnancy-induced hypertension or
preeclampsia, and all pregnant women with
symptoms of sleep-disordered breathing
should be evaluated with a polysomnogram
and treated with nasal continuous positive
airway pressure as indicated.
 Cystic
 As
Fibrosis:
survival of individuals with cystic
fibrosis continues to improve, Maternal
and fetal outcomes are satisfactory for
women with good lung function and
nutritional status. Pregnancy appears to
have no deleterious effect on long-term
survival in women with cystic fibrosis.
 Barotrauma:
 Spontaneous pneumothorax and pneumo
mediastinum may appear during pregnancy,
but these are more likely to occur during the
second stage of labor.
 Repeated
Valsalva maneuvers are the most
frequent cause of these problems. Pneumo
mediastinum is a rare complication of
pregnancy, and symptoms usually are not
noted until after delivery
 Kyphoscoliosis
 Most
common abnormality of the thoracic
cage affecting pregnancy.
 Kyphoscoliosis is known to result in
ventilatory failure by interfering with the
respiratory mechanics.
 Severe kyphoscoliosis is associated with
increased perinatal and maternal mortality.
 Regular lung function tests, arterial blood
gases measured, and be given oxygen if
hypoxaemic
Smoking and Pregnancy
 spontaneous
pregnancy loss.
 placental abruption.
 preterm premature rupture of
membranes.
 placenta previa.
 preterm labor and delivery.
 stillbirth, and low birth weight .
 postnatal morbidities
Smoking and Pregnancy

Maternal smoking during pregnancy
may impair in utero airway development
or alter lung elastic properties, and
these effects may be important factors
predisposing infants to the occurrence of
wheezing illness later in childhood.
 Tuberculosis
Hippocratic view
young woman with tuberculosis should
become pregnant to improve her outcome!!
1850 - 1920s
tuberculosis was harmful during
pregnancy, and termination of
pregnancy - recommended

Tuberculosis during pregnancy -rarely
an indication for a therapeutic abortion
But

pregnant woman with MDRTB, should be
offered abortion counseling medications used
are known to cause fetal abnormalities
 Diagnosing tuberculosis in pregnancy
 Symptoms like malaise & fatigue may be
ignored in pregnancy late diagnosis
 sputum examination and culture -same as for
non-pregnant
 Maternal
outcome
Depends on site & timing of diagnosis
Late diagnosis – morbidity increase 4 fold
Early diagnosis – outcome similar to non
pregnant women
Perinatal outcome
Late diagnosis increase incidence of
prematurity and LBW
Early diagnosis outcome similar to non
pregnant woman
 Anti-tuberculous
therapy
 No increase in congenital malformations or
fetal damage when rifampicin, isoniazid and
ethambutol are used in combination
 pyrazinamide is also considered to be a
safe drug in pregnancy
 Congenital tuberculosis
Cantewell Criteria
1. Lesion in the first week
2. Primary hepatic complex or caseating
granuloma
3. Documented TB of placenta or endometrium
4. Exclusion of TB infection by carrrier
 Breast
feeding
Appears to be safe when the mother is
taking standard anti-tuberculous medication.
If the mother is taking isoniazid, pyridoxine
supplementation should be given to the child
as a small amount of isoniazid is present in
breast milk
It is usually unnecessary for the child to
receive treatment unless the mother is
diagnosed with open (infectious) at the time
of delivery
Mother with open Tuberculosis
Breast feeding can be done with:
INAH prophylaxis
mother can use a mask
 Neonate….
 INAH
prophylaxis is given for 3 months
 Check Mantoux
 Mantoux Negative need BCG vaccination
 Contraception
 Oral
contracepitves: effectiveness is reduced
 HIV,TB
 If
and pregnancy
a pregnant women is diagnosed to have
active TB should we screen for HIV?
 Sarcoidosis
 Sarcoidosis
does not seem to have any
adverse effects on the course of pregnancy .
Pregnancy, on the other hand, is reported to
lead to improvement of sarcoidosis in some
patients.
 Patients with active sarcoidosis usually
experience partial or complete resolution of
chest roentgenographic abnormalities during
pregnancy ,although many in this group will
experience exacerbation of sarcoid within 3
to 6 months after delivery
 Amniotic
 It’s
Fluid Embolism
estimated that between 5-18 % of all
maternal deaths are due to AFE
 Reported mortality rates range from 26% to
as high 86%
 AFE constitutes the leading cause of
mortality during labor and the first few
postpartum hours
 Maternal death occurs in one of three ways:
1) sudden cardiac arrest, 2) hemorrhage
due to coagulopathy, 3) or initial survival w/
death due to ARDS and multiple organ
failure
Risk Factors for AFE
1.
2.
3.
4.
5.
6.
7.
Advanced age
Multiparity
Tumultuous labor
Rupture of membranes
Fetal death
Trauma
Uterine overdistention (multiple
gestation, fetal macrosomia)
Pathophysiology of AFE
The anaphylactoid reaction to AFE breaks down
to 3 phases:
 Immediate Phase: occurs when initially
exposed and can present as 1) resp distress
2) cyanosis
3)hemodynamic instability
4) cerebral hypoperfusion w/ seizures,
confusion or coma
 Second Phase: characterized by coagulopathy
and hemorrhage ; this may be the first and only
presentation of AFE
Pathophysiology
Phase Three: the period after the acute
insult is over and the tissue injury is
established
 These patients may die from the severe
lung or brain injury, multi-organ failure, or
because of an infection acquired during the
stay at the ICU

Clinical Manifestations
 Signs
and symptoms tend to be
nonspecific and common to other forms of
embolism
 Resp distress, cyanosis, cardiovascular
collapse, coma, and hemorrhage tend to
be the five cardinal signs of AFE
 Hemorrhage and fetal distress may be the
initial symptoms
Diagnosis of AFE
 In
the past, the definitive diagnosis was
made only at autopsy by finding fetal
squamous cells in the maternal pulmonary
circulation
 However, cells of fetal origin were only
found in 73% of patients who expired and
underwent autopsy
 Conversely , some Obstetricians have
found fetal squamous cells in maternal
circulation w/o any evidence of AFE
Diagnosis of AFE
 CXR
may be completely normal and the
EKG may show signs of acute right
ventricular strain in the early stages
 Echocardiography at the bedside usually
confirm severe left ventricular failure
 Most patients are hemodynamically
unstable so it is often difficult to do any
specific testing in time to alter
management
Management of AFE
Treatment of AFE is supportive and
directed toward:
 Maintaining oxygenation
 Maintaining cardiac output, SBP>90 mmHg
 Acceptable peripheral organ perfusion
(urine output >25 ml/hr)
 Correcting coagulation abnormalities
 RE-establishing uterine tone
Management of AFE
Pharmacological treatment may include:
• Crystalloids, vasopressors, and inotropic agents
(fluids should be restricted once the initial
hypotensive episode has resolved to prevent
pulmonary edema w/ subsequent ARDS)
• Corticosteroids (Hydrocortisone 500mg Q6 hr)
• Therapeutic heparinization to limit intravascular
coagulation is controversial
• In rare instances, cardiopulmonary bypass and
pulmonary thromboembolectomy have been
successfully used
Venous Air Embolism (VAE)
 VAE
is possibly the most common embolic
event during the intraoperative period and
air can be demonstrated by precordial
Doppler auscultation in up to 50% of C/S’s
 Even
so, VAE is responsible for only about
1% of maternal deaths for a rate of
approximately one death per 100,000 live
births
Risk Factors for VAE
A gradient of -5 cm H2O between the periphery
and the heart would allow significant entry of air
into venous circulation
 Trendelenburg position and exteriorizing the
uterus during C/S increase this gradient
 Uterine exteriorization is thought to predispose to
VAE by: 1) increasing the hydrostatic gradient by
raising the incisional area above the level of the
heart ; 2) by the simultaneous enlargement of the
uterine sinuses providing more exposure to air

Pathophysiology
The major cause of death from VAE is circulatory
arrest from air entrapped in the right ventricular
outflow tract
 5 ml/ kg of air may be lethal by formation of an “air
lock” in the right ventricle or in the pulmonary
arterial circulation ; this can result in cardiogenic
shock
 In combination w/ PA vasoconstriction , this
phenomenon can result in acute cor pulmonale
 Increased capillary permeability, platelet activation,
and coagulopathy may result from the effect of air
on endothelial surfaces

Clinical Manifestations
 Massive
VAE can present as a sudden and
devastating event w/ hypotension,
hypoxemia, and even cardiac arrest
 Typically, the clinical picture is much less
dramatic
 Significant hemodynamic compromise at
delivery is only seen about 0.7% to 2% of
the time
 Signs of air embolism include tachycardia,
tachypnea, cyanosis, mottled skin, and
occasionally, a wheel-mill murmur heard by
stethoscope
Resuscitation of Massive VAE
1. Discontinue
nitrous oxide and give 100% O2
2. Prevent further air entrapment ( flood surgical field,
change position)
3. Support ventilation as needed
4. Support circulation
5. If hemodynamic instability persists, consider
placement of central line to attempt aspiration of air
6. Expedite delivery
7. If there is delayed emergence from GA, consider
neurodiagnostic imaging to r/o intracerebral air
( arterial gas embolism) ; these patients may benefit
from hyperbaric therapy, esp. if done w/in 5 hrs
Thank You