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Senior Seminar II
Iae Ferreira, RN
Appendix B
ASTHMA IN PREGNANCY
INTRODUCTION
(Namazy& Schatz, 2011)
 Asthma currently affects
approximately 8% of pregnant
women
 It is one of the most common
potentially serious medical
conditions to complicate
pregnancy.
 Asthma ↑ the risk of adverse
outcomes: perinatal mortality,
preeclampsia, preterm birth
and low-birth weight infants.
 Asthma is a disease of the
airways by reversible airway
obstruction and hyper-
reactivity to a variety of stimuli.
 Although its cause is unknown
there are many triggering
agents that can be identified
such asviral infections,
allergens, exercise, sinusitis,
reflux, weather changes and
stress.
EVALUATION AND DIAGNOSIS
 Physical examination
 Subjective assessment
 Hx of symptoms,
temporal relationships,
triggers
 Pulmonary
impairment/asthma severity
classification
 Response to asthma therapy
 Pulmonary function tests
 Spirometry and forced
expiratory volume in the
first second of expiration
(FEV1)
 Peak expiratory flow rate
(PEFR)
 Fetal assessment during acute
asthma
(National Guideline Clearinghouse, 2012)
ASTHMA DIAGNOSIS DURING PREGNANCY
 Diagnosis of asthma is usually known before pregnancy;
however there are a further proportion of pregnant woman
who possibly have asthma
 Reduced forced expiratory volume in one second (FEV1) or
 Reduced ratio of FEV to forced vital capacity (FVC) and
 12% or greater improvement in FEV1 after inhalation of
rapid acting beta-agonist confirm diagnosis of
asthma(Ivancso, Bohacs, Eszes, Losonczy, &Tamasi, 2013).
 Diagnosis confirmation is made by reversible airway
obstruction after an inhaled short-acting bronchodilator
(Namazy& Schatz, 2011).
SHORTNESS OF BREATH AT REST OR WITH MILD EXERTION IS SO COMMONTHAT
IT IS OFTEN REFERREDTO AS “PHYSIOLOGIC DYSPNEA”
(MCCORMACK &WISE, 2009).
 It is important to be able to
differentiate normal
dyspnea of pregnancy from
disease pathology.
Shortness of breath may
occur in approximately 70%
of pregnant woman and
differs from asthma by its
lack of association with
cough, wheezing and airway
obstruction (Namazy& Schatz,
2011).
 Although dyspnea may be
physiological, tachypnea is
always abnormal and hence
should be sought in any
pregnant patient
complaining of
breathlessness (Bhatia & Bhatia,
2000).
 The ability of a patient to
complete sentences is a
useful bedside indicator of
the severity of the respiratory
insufficiency(Bhatia & Bhatia,
“IT CAN BE CHALLENGING FOR A PHYSICIANTO DIFFERENTIATE
NORMAL DYSPNEA OF PREGNANCY FROM DISEASE PATHOLOGY”.
(MCCORMACK &WISE, 2009).
 Asthma sign and symptoms
 Wheezing, chest tightness, cough and associated
shortness of breath(Namazy& Schatz, 2011).
 Respiratory rate greater than 20 per minute
 Arterial PCO2 less than 30 or greater than 35
 hypoxemia O2Sat <95% room air
 Abnormal measures on forced expiratory
spirometry, or cardiac echocardiography (McCormack
&Wise, 2009).
PHYSIOLOGIC CHANGES OF PREGNANCY
 Structural/Hormonal changes:
 ↑Progesterone (respiratory
stimulant) →Hyperventilation
→ overcompensation ↓ CO2
 ↑Estrogen→hyperemia-rhinitis
 ↑ Hypoxic ventilatory response
2x the normal level due to E&P
 Enlarged uterus ↑ abdominal
pressure ↓ chest wall
compliance 35-40% →
reduction functional residual
capacity (FRC)
 Elevation of diaphragm 4cm
 ↑ Relaxin → ribcage ligaments
relax ↑ circumference 5cm
 ↓ Expiratory muscle strength
 Circulatory changes:
 ↑ Cardiac output
 ↑ Pulmonary blood flow &
capillary blood volume
 ↑ Circulating blood volume
 ↓ Plasma oncotic pressure
→formation of edema in the
lungs.
 Increased metabolic rate with
low oxygen levels at end of
expiration make pregnant
woman particularly susceptible
to develop hypoxemia in the
presence of respiratory
problem
(McCormack &Wise, 2009).
PREGNANCY HAS NO
SIGNIFICANT EFFECT ON FEV1
OR THE FEV1/FVC RATIO.
PEAK EXPIRATORY FLOW
RATES REMAIN CLOSE TO THE
NORMAL RANGE AND DO NOT
CHANGE DURING PREGNANCY.
THE SHAPE OF THE FLOW-
VOLUME CURVE AND
ABSOLUTE FLOW RATES AT
LOW LUNG VOLUMES ARE
NORMAL IN PREGNANT
WOMAN.
THUS IT IS POSSIBLE TO USE NON-PREGNANT
REFERENCES VALUES TO EVALUATE LUNG
FUNCTION IN PREGNANT WOMEN.
“A REDUCTION IN FEV1 OR FVC SHOULD NOT
BE ATTRIBUTED TO PREGNANCY ALONE.THIS IS
IMPORTANT FOR CLINICIANS TO UNDERSTAND,
PARTICULARLY AS THEY ARE FOLLOWING
PATIENTS WITH UNDERLYING LUNG DISEASES,
SUCH AS ASTHMA”.
(McCormack &Wise, 2009).
NORMAL RESPIRATORY PHYSIOLOGIC CHANGES IN PREGNANCY
ChestWall
Compliance
Decreased FEV1 Unchanged
Thoracic Diameter Increased FVC Unchanged
Diaphragm Elevated FEV1/FVC Unchanged
Lung Compliance Unchanged Minute ventilation Increased
Total Lung Capacity Unchanged/slightly
decreased
Tidal volume Increased
Vital Capacity Unchanged/slightly
decreased
Respiratory rate Unchanged
InspiratoryCapacity Slightly increased PH Normal
Functional Residual
Capacity
Decreased PaO2 Slightly elevated
(100-105 mmHg)
ResidualVolume Slightly decreased PaCO2 Slightly decreased
(32-34 mmHg)
Expiratory reserve
volume
Decreased Bicarbonate Slightly decreased
(15-20 meq/L)
(McCormack &Wise, 2009).
PREMATURITY, LOW BIRTH
WEIGHT AND PERINATAL
AND MATERNAL DEATH
WERE MORE LIKELY TO
OCCUR IN PREGNANCIES OF
ASTHMATIC WOMEN.
 Most pregnancies are
unaccompanied by
pulmonary complications,
however pulmonary
edema, pulmonary
thromboembolism,
pulmonary hypertension,
and acute respiratory
failure can occur during
pregnancy.These
conditions can lead to
mortality and hence they
should be sought and
treated appropriately.
(Bhatia & Bhatia, 2000).
ShortAsthma & PregnancyVideo by Asthma Australia
http://www.youtube.com/watch?v=dOiZhdMlT9k
COMORBIDITIES THAT MAY EXACERBATE ASTHMA
 Sinusitis and Reflux are relatively common comorbidities
during pregnancy that may exacerbate asthma.
 Pregnancy may be complicated by new-onset or preexisting
rhinitis, or asthma.
 Rhinitis is a very common problem that may occur during
pregnancy. In the past, rhinitis and asthma may have been
treated as separate disorders.
 The United Airway Disease Hypothesis proposes that upper
and lower airway disease are both manifestations of a single
inflammatory process.
(Namazy& Schatz, 2011) .
ASTHMA… ALMOST ALWAYS ASSOCIATED
WITH NASAL DISEASE.
 Treatment of the upper
airway should improve
asthma for a variety of
reasons
 Mechanisms linking the
development or
exacerbation of asthma in
individuals with upper
airway disease may be
multifactorial
 RELEASE OF SYSTEMIC IMMUNE
MEDIATORS FROMTHE UPPER
AIRWAY, DRAINAGE OF
INFLAMMATORY MEDIATORS FROM
THE UPPER AIRWAY INTOTHE
LOWER AIRWAY
 NEUROGENIC RESPONSES
RESULTING IN MORE GENERALIZED
AIRWAY INFLAMMATION OR
COMMON INHALANT MECHANISMS
WITH ALLERGENS CAUSING
INFLAMMATION INITIALLY INTHE
UPPER AIRWAY FOLLOWED BYTHE
LOWER AIRWAY INVOLVEMENT.
(Ledford &Lockey, 2013).
“PREGNANT WOMAN MAY OFTEN WORRY ABOUT EFFECTS OFTHEIR ASTHMA
MEDICATIONS, AND MAY DISCONTINUETHEM INAPPROPRIATELY…”
(NELSON,GOSSETT, &GROBMAN, 2010)
 Short-acting beta-agonists for
immediate relief of asthma
symptoms during pregnancy is
generally regarded as being
safe (Ulrik&Gregersen, 2013)
 Inhaled corticosteroids are the
mainstay of controller therapy
during pregnancy. Many
studies have shown no
increased perinatal risks
associated with ICS(Namazy&
Schatz, 2011)
 Most medications used for
asthma for asthma
treatment outside of
pregnancy are also not
contraindicated during
pregnancy(Nelson, Gossett,
&Grobman, 2010).
Budesonide is
considered the
preferred ICS for
asthma during
pregnancy
FDA - MEDICATION CLASSIFICATION FOR USE IN PREGNANCY
Risk category Animal Data Human Data Recommendation
A Negative Negative Use approved
B Negative None available Use approved
B Positive Negative Use approved
C Positive None available Use approved
C None available None available Use approved
D Positive/Negative Positive Use approved
X Positive Positive Contraindicated
(Nelson,Gossett, &Grobman, 2010).
 Ethical considerations have, for obvious reasons, limited the
types of studies that have been possible to conduct. Double-
blind, placebo-controlled studies are, in general unethical in
pregnant women, and this makes it difficult to control variables
and isolate specific therapeutic effects (Ulrik&Gregersen, 2013).
Beta-2 Agonists Binds to beta2 receptors leading to
bronchial relaxation. •short acting
•long acting
Human data scant, lacks
evidence of risk of
congenital malformation
Albuterol (C)
Salmeterol (C)
Inhaled
Corticosteroids
Counteract inflammatory response.
Maintenance therapy.
Not contraindicated in
pregnancy.
Beclomethasone (C)
Budesonide (B)
Fluticasone (C)
Flunisolide (C)
Systemic
corticosteroids*
Reverse inflammatory response of
asthma exacerbation/ short term
therapy for severe/persistent
asthma
Not clear to what extent.
Possible association (0.1-
0.3%) facial cleft lip during
first trimester
Predinisone (C)
Methylprednisone (C)
Dexamethasone (C)
Anticholinergics Bind to acetylcholine, resulting in
inhibition of secretions from
seromucous glands
Add on therapy for beta-
agonist. No association to
increased risk of
congenital
malformation/adverse
outcome
Ipatropium (B)
Methylxanthines Promote smooth muscle relaxation.
Suppress hypersensitivity reaction
of the airways to stimuli
Add on therapy. Not used
in pregnancy due to
multiple drug interactions,
need to monitor levels &
side effects
Not contraindicated during
pregnancy.
Theophylline (C)
Cromoglycates Inhibition of airway inflammatory
cells. Preventive therapy for
persistent asthma
Not associated with
increase risk of congenital
malformation/adverse
maternal outcome
Cromolyn Sodium (B)
Leukotriene
Inhibitors
Act to antagonize leukotriene
activity/inhibit bronchial smooth
Information during
pregnancy is
Zafirlukast (B)
Montelukast (B)
(Nelson,Gossett,&Grobman,2010).
SYSTEMIC
CORTICOSTEROIDS
BECAUSE SEVERE,
UNCONTROLLED
ASTHMA IS ASSOCIATED
W/ MATERNAL/FETAL
DEATH,THE USE OF
SYSTEMIC
CORTICOSTEROIDS
ALTHOUGH RISKY, IS
JUSTIFIEDWHEN SEVERE
ASTHMA CANNOT BE
CONTROLLED BY OTHER
MEANS
(Mennick, 2005)
MAJOR GOAL OF CHRONIC ASTHMA MANAGEMENT
ISTHE PREVENTION OF EXACERBATION…
 Pharmacologic approach:
 Inhaled Beta2-agonist (Albuterol)
 InhaledCorticosteroids (Budesonide)
 Alternative add-on medication (long-acting beta2-agonist, cromolyn,
leukotriene inhibitor, theophyline)
 Acute management
 Pharmacologic approach / step therapy
 Fetal monitoring / maternal monitoring.
 SupplementalO2 to maintain PO2 > 70 and O2 sat >95% by pulse
oximetry.
 IV fluids at rate of 100ml/hour with glucose if pt not hyperglycemic.
(Namazy& Schatz, 2011)
(National Guideline Clearinghouse, 2012)
RECOMMENDATIONS
 Management geared towards prevention of chronic
symptoms.
 Pt should be educated how to perform accurate
peakflows
 Action plan (Nelson, Gossett, &Grobman, 2010)
 Monthly assessment in all asthmatic women with
evaluation of arterial sat >95% (Ivancso, Bohacs,
Eszes, Losonczy, &Tamasi, 2013)
PULSE OXIMETER (SPO2)
 Assess oxygenation by
measuring the arterial
oxygen saturation of Hgb
 The proper use of a pulse
oximeter can ensure earlier
detection of hypoxia
 A normal Spo2 range is
95% to 100%
 Spo2 is one patient-
assessment tool and
should be interpreted
along with other patient
data including
 Vital signs
 Cardiac rhythm
 Breath sounds
(Paragas, 2008)
http://www.monaghanmed.com/products/consumer
/truzone-peak-flow-meter-pfm
EDUCATIONAL
PEAK FLOW VIDEO
References
Bhatia, P., & Bhatia, K. (2000). Pregnancy and the lungs. Post Graduate Medical
Journal, 76 (901), 683-689.
Ivancso, I., Bohacs, A., Eszes, N., Losonczy, G., &Tamasi, L. (2013, August 31). Asthma in
Pregnancy - European Medical Journal. Retrieved March 20, 2014, from European Medical
Journal: http://emjreviews.com/wp-content/uploads/Asthma-In-Pregnancy.pdf
Ledford, D. K., &Lockey, R. F. (2013). Asthma and Comorbidities:. Retrieved March 19,
2014, from Medscape: http://www.medscape.com/viewarticle/776917_1?src=emailthis
McCormack, M. C., &Wise, R. A. (2009). Respiratory Physiology in Pregnancy. In G.
Bourjeily, K. Rosene-Montella, & H. Press (Ed.), Pulmonary Problems in Pregnancy (pp. 16-26).
Springer Science and Business Medica, LLC.
Mennick, F. (2005, April).Treating Asthma in Pregnancy. American Journal of Nursing, 105 (4), p.
20.
Namazy, J. A., & Schatz, M. (2011). Asthma and Rhinitis During Pregnancy. Mount Sinai Journal
Of Medicine, 78 (5), 661-670.
National Guideline Clearinghouse. (2012). Asthma in Pregnancy. Retrieved April 1,
2014, fromAgency for Healthcare Research and Quality:
http://www.guideline.gov/content.aspx?id=12630
Nelson, L., Gossett, D. R., &Grobman,W. (2010, December 31). Search Results.
Retrieved March 10, 2014, fromThe Global Library ofWomen's Medicine:
http://www.glowm.com/pdf/section1_chapter4.pdf
Paragas, J. (2008, November). KeepingThe Beat With Pulse Oximetry. Nursing 2008 , pp. 56hn1-
56hn2.
Ulrik, C. S., &Gregersen,T. L. (2013). Safety of bronchodilators and corticosteroids for asthma
during pregnancy: what we know and what we need to do better. Journal of Asthma and Allergy,
6, 117-125.
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Asthma in Pregnancy

  • 1. Senior Seminar II Iae Ferreira, RN Appendix B ASTHMA IN PREGNANCY
  • 2. INTRODUCTION (Namazy& Schatz, 2011)  Asthma currently affects approximately 8% of pregnant women  It is one of the most common potentially serious medical conditions to complicate pregnancy.  Asthma ↑ the risk of adverse outcomes: perinatal mortality, preeclampsia, preterm birth and low-birth weight infants.  Asthma is a disease of the airways by reversible airway obstruction and hyper- reactivity to a variety of stimuli.  Although its cause is unknown there are many triggering agents that can be identified such asviral infections, allergens, exercise, sinusitis, reflux, weather changes and stress.
  • 3. EVALUATION AND DIAGNOSIS  Physical examination  Subjective assessment  Hx of symptoms, temporal relationships, triggers  Pulmonary impairment/asthma severity classification  Response to asthma therapy  Pulmonary function tests  Spirometry and forced expiratory volume in the first second of expiration (FEV1)  Peak expiratory flow rate (PEFR)  Fetal assessment during acute asthma (National Guideline Clearinghouse, 2012)
  • 4. ASTHMA DIAGNOSIS DURING PREGNANCY  Diagnosis of asthma is usually known before pregnancy; however there are a further proportion of pregnant woman who possibly have asthma  Reduced forced expiratory volume in one second (FEV1) or  Reduced ratio of FEV to forced vital capacity (FVC) and  12% or greater improvement in FEV1 after inhalation of rapid acting beta-agonist confirm diagnosis of asthma(Ivancso, Bohacs, Eszes, Losonczy, &Tamasi, 2013).  Diagnosis confirmation is made by reversible airway obstruction after an inhaled short-acting bronchodilator (Namazy& Schatz, 2011).
  • 5. SHORTNESS OF BREATH AT REST OR WITH MILD EXERTION IS SO COMMONTHAT IT IS OFTEN REFERREDTO AS “PHYSIOLOGIC DYSPNEA” (MCCORMACK &WISE, 2009).  It is important to be able to differentiate normal dyspnea of pregnancy from disease pathology. Shortness of breath may occur in approximately 70% of pregnant woman and differs from asthma by its lack of association with cough, wheezing and airway obstruction (Namazy& Schatz, 2011).  Although dyspnea may be physiological, tachypnea is always abnormal and hence should be sought in any pregnant patient complaining of breathlessness (Bhatia & Bhatia, 2000).  The ability of a patient to complete sentences is a useful bedside indicator of the severity of the respiratory insufficiency(Bhatia & Bhatia,
  • 6. “IT CAN BE CHALLENGING FOR A PHYSICIANTO DIFFERENTIATE NORMAL DYSPNEA OF PREGNANCY FROM DISEASE PATHOLOGY”. (MCCORMACK &WISE, 2009).  Asthma sign and symptoms  Wheezing, chest tightness, cough and associated shortness of breath(Namazy& Schatz, 2011).  Respiratory rate greater than 20 per minute  Arterial PCO2 less than 30 or greater than 35  hypoxemia O2Sat <95% room air  Abnormal measures on forced expiratory spirometry, or cardiac echocardiography (McCormack &Wise, 2009).
  • 7. PHYSIOLOGIC CHANGES OF PREGNANCY  Structural/Hormonal changes:  ↑Progesterone (respiratory stimulant) →Hyperventilation → overcompensation ↓ CO2  ↑Estrogen→hyperemia-rhinitis  ↑ Hypoxic ventilatory response 2x the normal level due to E&P  Enlarged uterus ↑ abdominal pressure ↓ chest wall compliance 35-40% → reduction functional residual capacity (FRC)  Elevation of diaphragm 4cm  ↑ Relaxin → ribcage ligaments relax ↑ circumference 5cm  ↓ Expiratory muscle strength  Circulatory changes:  ↑ Cardiac output  ↑ Pulmonary blood flow & capillary blood volume  ↑ Circulating blood volume  ↓ Plasma oncotic pressure →formation of edema in the lungs.  Increased metabolic rate with low oxygen levels at end of expiration make pregnant woman particularly susceptible to develop hypoxemia in the presence of respiratory problem (McCormack &Wise, 2009).
  • 8. PREGNANCY HAS NO SIGNIFICANT EFFECT ON FEV1 OR THE FEV1/FVC RATIO. PEAK EXPIRATORY FLOW RATES REMAIN CLOSE TO THE NORMAL RANGE AND DO NOT CHANGE DURING PREGNANCY. THE SHAPE OF THE FLOW- VOLUME CURVE AND ABSOLUTE FLOW RATES AT LOW LUNG VOLUMES ARE NORMAL IN PREGNANT WOMAN. THUS IT IS POSSIBLE TO USE NON-PREGNANT REFERENCES VALUES TO EVALUATE LUNG FUNCTION IN PREGNANT WOMEN. “A REDUCTION IN FEV1 OR FVC SHOULD NOT BE ATTRIBUTED TO PREGNANCY ALONE.THIS IS IMPORTANT FOR CLINICIANS TO UNDERSTAND, PARTICULARLY AS THEY ARE FOLLOWING PATIENTS WITH UNDERLYING LUNG DISEASES, SUCH AS ASTHMA”. (McCormack &Wise, 2009).
  • 9. NORMAL RESPIRATORY PHYSIOLOGIC CHANGES IN PREGNANCY ChestWall Compliance Decreased FEV1 Unchanged Thoracic Diameter Increased FVC Unchanged Diaphragm Elevated FEV1/FVC Unchanged Lung Compliance Unchanged Minute ventilation Increased Total Lung Capacity Unchanged/slightly decreased Tidal volume Increased Vital Capacity Unchanged/slightly decreased Respiratory rate Unchanged InspiratoryCapacity Slightly increased PH Normal Functional Residual Capacity Decreased PaO2 Slightly elevated (100-105 mmHg) ResidualVolume Slightly decreased PaCO2 Slightly decreased (32-34 mmHg) Expiratory reserve volume Decreased Bicarbonate Slightly decreased (15-20 meq/L) (McCormack &Wise, 2009).
  • 10. PREMATURITY, LOW BIRTH WEIGHT AND PERINATAL AND MATERNAL DEATH WERE MORE LIKELY TO OCCUR IN PREGNANCIES OF ASTHMATIC WOMEN.  Most pregnancies are unaccompanied by pulmonary complications, however pulmonary edema, pulmonary thromboembolism, pulmonary hypertension, and acute respiratory failure can occur during pregnancy.These conditions can lead to mortality and hence they should be sought and treated appropriately. (Bhatia & Bhatia, 2000).
  • 11. ShortAsthma & PregnancyVideo by Asthma Australia http://www.youtube.com/watch?v=dOiZhdMlT9k
  • 12. COMORBIDITIES THAT MAY EXACERBATE ASTHMA  Sinusitis and Reflux are relatively common comorbidities during pregnancy that may exacerbate asthma.  Pregnancy may be complicated by new-onset or preexisting rhinitis, or asthma.  Rhinitis is a very common problem that may occur during pregnancy. In the past, rhinitis and asthma may have been treated as separate disorders.  The United Airway Disease Hypothesis proposes that upper and lower airway disease are both manifestations of a single inflammatory process. (Namazy& Schatz, 2011) .
  • 13. ASTHMA… ALMOST ALWAYS ASSOCIATED WITH NASAL DISEASE.  Treatment of the upper airway should improve asthma for a variety of reasons  Mechanisms linking the development or exacerbation of asthma in individuals with upper airway disease may be multifactorial  RELEASE OF SYSTEMIC IMMUNE MEDIATORS FROMTHE UPPER AIRWAY, DRAINAGE OF INFLAMMATORY MEDIATORS FROM THE UPPER AIRWAY INTOTHE LOWER AIRWAY  NEUROGENIC RESPONSES RESULTING IN MORE GENERALIZED AIRWAY INFLAMMATION OR COMMON INHALANT MECHANISMS WITH ALLERGENS CAUSING INFLAMMATION INITIALLY INTHE UPPER AIRWAY FOLLOWED BYTHE LOWER AIRWAY INVOLVEMENT. (Ledford &Lockey, 2013).
  • 14. “PREGNANT WOMAN MAY OFTEN WORRY ABOUT EFFECTS OFTHEIR ASTHMA MEDICATIONS, AND MAY DISCONTINUETHEM INAPPROPRIATELY…” (NELSON,GOSSETT, &GROBMAN, 2010)  Short-acting beta-agonists for immediate relief of asthma symptoms during pregnancy is generally regarded as being safe (Ulrik&Gregersen, 2013)  Inhaled corticosteroids are the mainstay of controller therapy during pregnancy. Many studies have shown no increased perinatal risks associated with ICS(Namazy& Schatz, 2011)  Most medications used for asthma for asthma treatment outside of pregnancy are also not contraindicated during pregnancy(Nelson, Gossett, &Grobman, 2010). Budesonide is considered the preferred ICS for asthma during pregnancy
  • 15. FDA - MEDICATION CLASSIFICATION FOR USE IN PREGNANCY Risk category Animal Data Human Data Recommendation A Negative Negative Use approved B Negative None available Use approved B Positive Negative Use approved C Positive None available Use approved C None available None available Use approved D Positive/Negative Positive Use approved X Positive Positive Contraindicated (Nelson,Gossett, &Grobman, 2010).  Ethical considerations have, for obvious reasons, limited the types of studies that have been possible to conduct. Double- blind, placebo-controlled studies are, in general unethical in pregnant women, and this makes it difficult to control variables and isolate specific therapeutic effects (Ulrik&Gregersen, 2013).
  • 16. Beta-2 Agonists Binds to beta2 receptors leading to bronchial relaxation. •short acting •long acting Human data scant, lacks evidence of risk of congenital malformation Albuterol (C) Salmeterol (C) Inhaled Corticosteroids Counteract inflammatory response. Maintenance therapy. Not contraindicated in pregnancy. Beclomethasone (C) Budesonide (B) Fluticasone (C) Flunisolide (C) Systemic corticosteroids* Reverse inflammatory response of asthma exacerbation/ short term therapy for severe/persistent asthma Not clear to what extent. Possible association (0.1- 0.3%) facial cleft lip during first trimester Predinisone (C) Methylprednisone (C) Dexamethasone (C) Anticholinergics Bind to acetylcholine, resulting in inhibition of secretions from seromucous glands Add on therapy for beta- agonist. No association to increased risk of congenital malformation/adverse outcome Ipatropium (B) Methylxanthines Promote smooth muscle relaxation. Suppress hypersensitivity reaction of the airways to stimuli Add on therapy. Not used in pregnancy due to multiple drug interactions, need to monitor levels & side effects Not contraindicated during pregnancy. Theophylline (C) Cromoglycates Inhibition of airway inflammatory cells. Preventive therapy for persistent asthma Not associated with increase risk of congenital malformation/adverse maternal outcome Cromolyn Sodium (B) Leukotriene Inhibitors Act to antagonize leukotriene activity/inhibit bronchial smooth Information during pregnancy is Zafirlukast (B) Montelukast (B) (Nelson,Gossett,&Grobman,2010).
  • 17. SYSTEMIC CORTICOSTEROIDS BECAUSE SEVERE, UNCONTROLLED ASTHMA IS ASSOCIATED W/ MATERNAL/FETAL DEATH,THE USE OF SYSTEMIC CORTICOSTEROIDS ALTHOUGH RISKY, IS JUSTIFIEDWHEN SEVERE ASTHMA CANNOT BE CONTROLLED BY OTHER MEANS (Mennick, 2005)
  • 18. MAJOR GOAL OF CHRONIC ASTHMA MANAGEMENT ISTHE PREVENTION OF EXACERBATION…  Pharmacologic approach:  Inhaled Beta2-agonist (Albuterol)  InhaledCorticosteroids (Budesonide)  Alternative add-on medication (long-acting beta2-agonist, cromolyn, leukotriene inhibitor, theophyline)  Acute management  Pharmacologic approach / step therapy  Fetal monitoring / maternal monitoring.  SupplementalO2 to maintain PO2 > 70 and O2 sat >95% by pulse oximetry.  IV fluids at rate of 100ml/hour with glucose if pt not hyperglycemic. (Namazy& Schatz, 2011) (National Guideline Clearinghouse, 2012)
  • 19. RECOMMENDATIONS  Management geared towards prevention of chronic symptoms.  Pt should be educated how to perform accurate peakflows  Action plan (Nelson, Gossett, &Grobman, 2010)  Monthly assessment in all asthmatic women with evaluation of arterial sat >95% (Ivancso, Bohacs, Eszes, Losonczy, &Tamasi, 2013)
  • 20. PULSE OXIMETER (SPO2)  Assess oxygenation by measuring the arterial oxygen saturation of Hgb  The proper use of a pulse oximeter can ensure earlier detection of hypoxia  A normal Spo2 range is 95% to 100%  Spo2 is one patient- assessment tool and should be interpreted along with other patient data including  Vital signs  Cardiac rhythm  Breath sounds (Paragas, 2008)
  • 22. References Bhatia, P., & Bhatia, K. (2000). Pregnancy and the lungs. Post Graduate Medical Journal, 76 (901), 683-689. Ivancso, I., Bohacs, A., Eszes, N., Losonczy, G., &Tamasi, L. (2013, August 31). Asthma in Pregnancy - European Medical Journal. Retrieved March 20, 2014, from European Medical Journal: http://emjreviews.com/wp-content/uploads/Asthma-In-Pregnancy.pdf Ledford, D. K., &Lockey, R. F. (2013). Asthma and Comorbidities:. Retrieved March 19, 2014, from Medscape: http://www.medscape.com/viewarticle/776917_1?src=emailthis McCormack, M. C., &Wise, R. A. (2009). Respiratory Physiology in Pregnancy. In G. Bourjeily, K. Rosene-Montella, & H. Press (Ed.), Pulmonary Problems in Pregnancy (pp. 16-26). Springer Science and Business Medica, LLC. Mennick, F. (2005, April).Treating Asthma in Pregnancy. American Journal of Nursing, 105 (4), p. 20. Namazy, J. A., & Schatz, M. (2011). Asthma and Rhinitis During Pregnancy. Mount Sinai Journal Of Medicine, 78 (5), 661-670. National Guideline Clearinghouse. (2012). Asthma in Pregnancy. Retrieved April 1, 2014, fromAgency for Healthcare Research and Quality: http://www.guideline.gov/content.aspx?id=12630 Nelson, L., Gossett, D. R., &Grobman,W. (2010, December 31). Search Results. Retrieved March 10, 2014, fromThe Global Library ofWomen's Medicine: http://www.glowm.com/pdf/section1_chapter4.pdf Paragas, J. (2008, November). KeepingThe Beat With Pulse Oximetry. Nursing 2008 , pp. 56hn1- 56hn2. Ulrik, C. S., &Gregersen,T. L. (2013). Safety of bronchodilators and corticosteroids for asthma during pregnancy: what we know and what we need to do better. Journal of Asthma and Allergy, 6, 117-125.
  • 23. TO ACCESS TO THIS POWER POINT  http://www.slideshare.net/amariaela

Editor's Notes

  1. Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath.Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test.
  2. Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath.Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test.
  3. Functional residual capacity (FRC) refers to the volume of air left in the lungs after a normal, passive exhalation. It is mainly determined by the balance between the forces of the lung and chest wall.Total lung capacity is preserved or minimally decreased as a result of the mild increase in the inspiratory capacityNon-pregnant PACO2 = 40mmhgPregnant PACO2= 32-34mmhgLeading to mild respiratory alkalosis. Kidney excrete excess Bicarbonate to compensate for Respiratory alkalosis – Right shift of oxyhemoglobin dissociation curveIncreased sensitivity to viral/bacterial respiratory infection / GERD – asthma triggers
  4. Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath.Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test.
  5. By term functional residual capacity is reduced by 10-20%
  6. Asthma Triggers – Infections (respiratory) viral + common, Drugs (COX-1 NSAIDS – ex. motrim), Occupational triggers, exercise (cold air reaching bronchial tree), environmental allergies (dust, mites, tobacco, cockroaches, pets), emotional stress :::: COX-2 ex. Celebrex, salycilate. acetaminophe well tolerated
  7. *Systemic corticosteroids– associated preeclampsia, pre-term birth, low birth weight –