제일병원 안계형 전임의, 마더세이프라운드 발표자료

1. Asthma in pregnancy
제일병원 주산기 전임의 안계형

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)

8. Pathophysiology of asthma

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.

11. Environmental Stimulants
irritants, viral infections, aspirin, cold air, andexercise etc.
Allergent Irritant

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.

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)

18. Pregnancy Outcome

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)

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.

30. Management of Chronic Asthma

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

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.

46. 감사합니다