2. Pulmonary Disorders
• m/c in pregnancy: asthma (4%)
• No evidence that pulmonary function is impaired
because of pregnancy but, advanced pregnancy may
intensify the pathophysiological effects of some lung
diseases.
- The disparate number of maternal deaths during
the influenza pandemics of 1918 and 1957.
- The poor tolerance for pregnancy of women with
severe chronic lung disease.
3. Pulmonary Physiology
• Vital capacity and inspiratory capacity
- increase by 20 percent by late pregnancy
• Expiratory reserve volume
- decreases from 1300 mL to 1100 mL
• Tidal volume
- increases 40 percent
- respiratory stimulant properties of progesterone
4. Pulmonary Physiology
• Minute ventilation
- increases about 30 to 40 percent(d/t tidal volume ↑)
• Arterial pO2
- increases from 100 to 105 mm Hg
• Carbon dioxide production: increases 30 percent
• Diffusion capacity : increases
• pCO2 : decreases from 40 to 32 mm Hg
5. Pulmonary Physiology
• Residual volume
- decreases 20 percent from 1500 mL to 1200 mL
• The expanding uterus and increased abdominal pr.
-> chest wall compliance to be reduced by a third.
-> the functional residual capacity
(the sum of expiratory reserve and residual
volumes) : decreases.
6. Pulmonary Physiology
• The sum of these changes
-> substantively increased ventilation
due to deeper but not more frequent breathing.
-> induced by basal oxygen consumption, which
increases incrementally by 20 to 40 mL/min in the
second half of pregnancy.
7. Asthma
• Prevalence
- increased steadily in many countries beginning
in the mid-1970s
- plateaued in the United States during the past
decade
• almost 8 percent of the general population has
asthma.
• prevalence during pregnancy to range between 4 and
8 percent (Kwon and associates,2006)
9. Pathophysiology of asthma
• Chronic inflammatory airway disorder
• Associated with hereditary component
- increased airway responsiveness and persistent
subacute inflammation have been genes on
chromosomes 5, 11, and 12
(cytokine gene clusters, -adrenergic and
glucocorticoid receptor genes, and the T-cell antigen
receptor gene)
• environmental allergic stimulant
- influenza or cigarette smoke etc.
10. Pathophysiology of asthma
Reversible airway obstruction from bronchial smooth
muscle contraction, vascular congestion, tenacious mucus,
and mucosal edema.
12. Pathophysiology of asthma
• Inflammation : caused by response of mast cells,
eosinophils, lymphocytes, and bronchial epithelium.
• inflammatory mediators : histamine, leukotrienes,
prostaglandins, cytokines, and many others.
• IgE also plays a central role in pathophysiology
(Strunk and Bloomberg, 2006)
• F-series prostaglandins and ergonovine exacerbate
asthma -> should be avoided if possible.
13. Clinical Course
• Mild wheezing to severe bronchoconstriction.
• Acute bronchospasm
-> airway obstruction and decreased airflow.
-> work of breathing progressively increases
-> chest tightness, wheezing, or breathlessness.
14.
15.
16. Clinical Course
• generally reversible and well tolerated by the healthy
nonpregnant individual.
• But even early stages of asthma may be dangerous
for the pregnant woman and her fetus.
- smaller functional residual capacity
- more susceptible to hypoxia and hypoxemia.
17. Effects of Pregnancy on Asthma
• No evidence that pregnancy has a predictable effect
on underlying asthma.
• Approximately 20 percent of women with mild or
moderate asthma have been reported to have an
intrapartum exacerbation
(Schatz and associates, 2003)
• Conversely, reported exacerbations at the time of
delivery in only 1 percent of women.
(Wendel and associates,1996)
19. Pregnancy Outcome
• Significantly increased morbidity
- associated with progressively more severe disease,
poor control, or both.
(Källén and Otterblad Olausson, 2007)
• Life-threatening complications from status
asthmaticus include muscle fatigue with respiratory
arrest, pneumothorax, pneumomediastinum, acute cor
pulmonale, and cardiac arrhythmias.
• Maternal and perinatal mortality rates are
substantively increased when mechanical ventilation is
required.
20. Fetal Effects
• With reasonable control of asthma
-> perinatal outcomes are generally good.
• when respiratory alkalosis develops
-> both animal and human studies suggest that fetal
hypoxemia develops well before the alkalosis
compromises maternal oxygenation
(Rolston and associates, 1974)
21. Fetal Effects
• The fetal response to maternal hypoxemia
-> decreased umbilical blood flow,
-> increased systemic and pulmonary vascular resistance
-> decreased cardiac output.
• Incidence of fetal-growth restriction increases with
asthma severity. (Bracken and colleagues ,2003)
• Monitoring the fetal response
-> an indicator of maternal status.
22. Fetal Effects
• No evidence that commonly used anti-asthmatic drugs
are harmful
(Blais and colleagues, 2007; Källén, 2007; Namazy and Schatz, 2006).
• Despite this, a 13- to 54-percent patient-generated
decrease in -agonist and corticosteroid use between
5 to 13 weeks of pregnancy
(Enriquez and co-workers ,2006)
23. Clinical Evaluation
• The subjective severity of asthma
-> frequently does not correlate with objective
measures of airway function or ventilation.
• Useful clinical signs
-> labored breathing, tachycardia, pulsus paradoxus,
prolonged expiration, and use of accessory muscles.
• Signs of a potentially fatal attack
-> central cyanosis and altered consciousness.
24. Clinical Evaluation
• Arterial blood gas analysis
-> objective assessment of maternal oxygenation,
ventilation, and acid–base status.
• If used, the results must be interpreted in relation
to normal values for pregnancy.
(a pCO2 > 35 mm Hg with a pH < 7.35 is consistent
with hyperventilation and CO2 retention in a pregnant
woman.)
25. Clinical Evaluation
• Pulmonary function testing
-> should be routine in the management of chronic and
acute asthma.
• Sequential measurement of the FEV1 or the peak
expiratory flow rate (PEFR)
-> the best measures of severity.
• An FEV1 less than 1 L, or less than 20 percent of
predicted value -> correlates with severe disease
defined by hypoxia, poor response to therapy, and a
high relapse rate. (Noble and colleagues, 1988)
26.
27. Clinical Evaluation
• PEFR (peak expiratory flow rate)
-> correlates well with the FEV1
-> can be measured reliably with inexpensive portable
meters.
• Each woman determines her own baseline when
asymptomatic—personal best—to compare with values
when symptomatic.
• PEFR did not change during the course of pregnancy
in normal women. ( Brancazio and associates ,1997)
28. Management of Chronic Asthma
Guidelines of the Working Group on Asthma and Pregnancy
• Patient education—general asthma management and its
effect on pregnancy.
• Environmental precipitating factors—avoidance or control.
• Objective assessment of pulmonary function and fetal
well-being—monitor with PEFR or FEV1.
• Pharmacological therapy— appropriate combinations and
doses to provide baseline control and treat exacerbations
(National Heart, Lung and Blood Institute, 2004)
29. Management of Chronic Asthma
• Women with moderate to severe asthma
-> FEV1 or PEFR twice daily.
• The FEV1 ideally is >80 percent of predicted.
• For PEFR, predicted values range from 380 to 550
L/min.
31. Management of Chronic Asthma
• Theophylline
- Methylxanthine
- bronchodilators and anti-inflammatory agents.
- 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
32. Management of Chronic Asthma
• Leukotriene modifiers
- inhibit their synthesis
- include zileuton, zafirinkast, and montelukast.
- orally or by inhalation for prevention,
- not effective for acute disease.
• For maintenance, they are used in conjunction with
inhaled corticosteroids to allow minimal dosing.
• little experience with their use in pregnancy
(Bakhireva and colleagues, 2007)
33. Management of Chronic Asthma
• Cromolyn and nedocromil
- inhibit mast cell degranulation.
- ineffective for acute asthma and are taken
chronically for prevention.
- not as effective as inhaled corticosteroids
- generally been replaced by leukotriene modifiers
(Fanta, 2009)
34. Management of Acute Asthma
• Treatment
- similar to that for the nonpregnant asthmatic.
- An exception
: significantly lowered threshold for hospitalization.
- Intravenous hydration may help clear pulmonary
secretions
- supplemental oxygen is given by mask.
35. Management of Acute Asthma
• The therapeutic aim
- to maintain the pO2 greater than 60 mm Hg
- preferably normal, along with 95-percent oxygen
saturation.
• Baseline pulmonary function
: FEV1 or PEFR
• Continuous pulse oximetry and electronic fetal
monitoring : provide useful information.
36. Management of Acute Asthma
• First-line therapy
- a -adrenergic agonist
- terbutaline, albuterol, isoetharine, epinephrine,
isoproterenol, or metaproterenol.
- given subcutaneously, taken orally, or inhaled.
- modulate bronchial smooth muscle relaxation.
- Long-acting preparations are used for outpatient
therapy.
37. Management of Acute Asthma
• If not previously given for maintenance
- inhaled corticosteroids are commenced along with
intensive -agonist therapy.
• For severe exacerbations
- inhaled ipratropium bromide
• Corticosteroids should be given early to all patients
with severe acute asthma.
38. Management of 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.
39. Management of Acute Asthma
• If initial therapy with -agonists is associated with
improvement of FEV1 or PEFR to above 70 percent of
baseline -> discharge can be considered.
• for the woman with obvious respiratory distress,
or if the FEV1 or PEFR is less than 70 percent of
predicted after three doses of –agonist
-> admission is advisable.
40. Management of Acute Asthma
• Intensive therapy
- agonists
- intravenous corticosteroids
- close observation for worsening respiratory distress
or fatigue in breathing
41.
42. Status Asthmaticus and
Respiratory Failure
• Status asthmaticus.
- Severe asthma of any type not responding after 30
to 60 minutes of intensive therapy
- Early intubation when maternal respiratory status
worsens despite aggressive treatment
- Fatigue, carbon dioxide retention, and hypoxemia
: indications for mechanical ventilation.
43. Labor and Delivery
• Maintenance medications through delivery.
• Stress-dose corticosteroids are administered to any
woman given systemic steroid therapy within the
preceding 4 weeks.
• Usual dose is 100 mg of hydrocortisone given
intravenously every 8 hours during labor and for 24
hours after delivery.
• The PEFR or FEV1 should be determined on admission,
and serial measurements are taken if symptoms
develop.
44. Labor and Delivery
• Oxytocin or prostaglandins E1 or E2 :
for cervical ripening and induction.
• A nonhistamine-releasing narcotic (fentanyl)
- preferable to meperidine for labor
- epidural analgesia is ideal
45. Labor and Delivery
• For surgical delivery
- conduction analgesia is preferred
- tracheal intubation can trigger severe bronchospasm.
• Postpartum hemorrhage
- treated with oxytocin or prostaglandin E2.
- Prostaglandin F2 or ergotamine derivatives
: contraindicated
: cause significant bronchospasm.