Pulmonary disease in pregnancy

Question 1

What is the effect of progesterone on respiratory adaptions in pregnancy?

Answer 1

• Biochemical changes:
  o Serum progesterone stimulates central respiratory center; increases sensitivity to carbon dioxide
  o Estrogen increases central expression of progesterone receptors
  o Net effect = increased ventilatory drive

Question 2

Changes in respiratory system in pregnancy

Answer 2

• Mechanical changes:
  o Diaphragm raises 4cm
  o Decreased ERV and RV = decreased FRC
  o Chest enlarged 2cm in transverse diameter
  o Vital capacity is preserved
• Decreased FRC:
  o Lung base small airways prone to closure; can increase the Aa gradient by decreasing PaO2
   Term are at greater risk of hypoxemia
  o Sitting better than supine
• Airway function: assessed by spirometry
  o FEV1/FVC
  o PEFR (peak expiratory flow rate) – unchanged from nonpregnancy
• Diffusing capacity: measured by DL (co)
  o Unchanged or increase in early pregnancy; slight decrease in latter half; unchanged
• Ventilation: increased oxygen consumption, carbon dioxide production, and metabolic rate
  o But, increment in minute ventilation (mostly from increased TV) exceeds this
  o RR unchanged
• More susceptible for hypoxemia: increased oxygen consumption, long volume changes

Question 3

What are pregnancy values of ABG

Answer 3

Compensatory respiratory alkalosis

Question 4

What are blood gas values in respiratory distress?

Answer 4

Question 5

Asthma in pregnancy: natural course, diagnosis, workup, risk factors for exacerbations. treatments

Answer 5

• Obstructive lung disease; inflammation
• Hyperreactivity to stimuli; smooth muscle contraction; mucous hypersecretion
• Expiratory limitation of airflow from airway narrowing
• 1/3 rule: 1/3 get better, worse, the same
  o if worse, usually in 3rd trimester
• Depressed FEV1; PEFR
• Hypoxemic, decreased PCO2 (from tachypnea), respiratory alkalosis
• Workup:
  o EKG (r/o cardiac disease)
  o Pulse ox
  o ABG prn
  o CXR
  o Sputum gram stain
• A “normal” PCO2 is an ominous finding
• FEV1 < 20% predicted = severe obstruction  hospitalize
• Pregnancy risks: PNM, PEC, PTB, SGA
• Chronic Treatment: emphasis shifting towards anti-inflammatory agents
  o Patients with occasional mild asthma  inhaled beta agonists are mainstay
  o For everyone else, inhaled steroids are mainstay
  o For patients with more frequent attacks, higher dose inhaled steroids, leukotriene inhibitors, and long acting inhaled beta agonists becomes therapy of choice
  o For patients with severe exacerbations OR not responding to acute bronchodilators: course of oral or IV steroids
• Acute Treatment:
  o Oxygen, sitting position, IVFluids
  o Patients who rsponde to bronchodilators can be outpatient (PEFR > 70%)
  o If no response, admit and steroids
  o initial therapy of acute attack = oxygen and inhaled beta 2
• Theophylline: xanthine bronchodilators
  o No longder considered first line therapy; has a role in nocturnal asthma

Question 6

Indications for intubation for asthma and L&D considerations

Answer 6

• Indications for intubation:
  o Inability to maintain PO2 > 60mmHg
  o Inability to maintain PCO2 < 40mmHg
  o Maternal exhaustion
  o Worsening acidosis pH < 7.25
  o AMS
• L&D Considerations:
  o Give inhaled Beta 2 if PEFR < 80%
  o Stress dose if h/o systemic steroids during pregnancy
  o Non-histamine releasing narcotic (fentanyl) preferred over morphine
  o Avoid PGF2 (use PGE instead)

Question 7

Treatment options for severe asthma

Answer 7

Question 8

Pneumonia: organisms, CXR findings, management

Answer 8

• Diagnosis: new cough, dyspnea, sputum production, fever, CXR infiltrate
• Risk factors: smoking, asthma, flu season, other medication conditions, drug bause
• Etiology: organism not identified in 50-90%
  o Bacterial (common)
   Strep pneumo 5-30% - most common
   Mycoplasma pneumo (5-30%)
   Haemophilus influenza can be common in smokers and HIV+
  o Viral (common)
   Influenze most common
   Varicella
   Bacterial superinfection (influenza)
  o Fungal (uncommon)
   Coccidiomycosis more likely to disseminate or reactivate in pregnancy
• CXR:
  o Typical pneumonia: consolidated, lobular; bacterial
  o Atypical: patchy; bilateral
• Prevention: Pneumococcal vaccine – pulm disease, renal, SCD, DM, HIV
• Work up: CXR, sputum gram stain, blood culture, abg
• Management:
  o Risk of PTL and pulm edema
  o No best regimen in pregnancy; usually azithro

Question 9

Pulmonary Edema in pregnancy
- risks of pregnancy
- pathophysiolog
- diagnosis and management
- diagnosis with hemodynamics

Answer 9

• Pregnancy predisposes to pulm edema (increased volume, fluid and salt retention, decreased colloid osmotic pressure, fluid shifts)
• Increase risk in PEC and beta-mimetic tocolysis
• Starling Forces on the lung:
  o Forces that drive fluid out of pulm capillary:
   Capillary hydrostatic pressure, interstitial fluid COP
  o Forces that drive fluid into pulm capillary:
   Plasma COP, intersitital hydrostatic pressure
• Pathophysiology of pulmonary edema:
  o 1) Increased capillary hydrostatic pressure - #1!!!
   Drives more fluid out of the vascular space (MS, CHF); PCWP will be elevated
  o 2) Decreased COP (colloid osmotic pressure) – less force holding fluid intravascularly; can measure intravascular COP
  o 3) Increased pulmonary capillary permeability – decreased intravascular COP
   ARDS, Heroin OD; COP and PCWP will be normal
• Evaluation: XCR, echo, O2sat, Brain natriuretic peptide
  o Echo: if no response in 12-24 hours; 46% cardiogenic pulm edema
• Management:
• Elevate mothers head; morphine, O2 (CPAP); diuresis, fluid restriction, Afterload reduction, lasix
• Tocolysis: Risk greater with multiples
• PEC: PIH patients have lower COP than normotensive patients at term
  o Altered capillary permeability
  o Vascular damage
  o Renal plasma protein loss
  o Causes: decreased COP, altered capillary permeability, increased pulmonary vascular hydrostatic pressure, increased SVR
• Consider swan ganz if no response to lasix