Pocket ObGyn – Respiratory Changes in Pregnancy

Dec 9, 2019 admin PHỤ KHOA, SẢN KHOA 0

Pocket ObGyn – Respiratory Changes in Pregnancy
See Abbreviations

General (Clin Chest Med 2011;32:1)

  • Upper airway: Mucosal hyperemia, edema, glandular May contribute to disordered breathing in sleep from obst. ­ Mallampati score, ­ neck circumference. “Rhinitis of Preg” present during last 6 w of Preg, disappears postpartum in absence of allergy or other pulm pathology.
  • Chest wall: Compliance decreased. Widened subcostal angle, increased anteroposterior dimension mediated hormonally by relaxin. Changes peak at 37 Diaphragmatic excursion increased. Max inspiration/expiration pressures same as prior to Preg.
Lung Function
  • Minute ventilation ­ 20–50% by term (most ­ during 1st trimester). ­ progesterone &

­ CO2 production (VCO2) ­ central stimuli for hyperventilation. Physiologic dyspnea of Preg may be awareness of ­ stimulus to breathe.VT ­.

  • Oxygen consump (VO2) is increased; respiratory exchange rate (VCO2/VO2) unchanged minimally increased
  • FRC ¯ by diaphragm elevation, ¯ chest wall recoil, ¯ abd (Note: Obesity ® ¯ FRC & ­ RV [air trapping]. In Preg, ¯ FRC w/ ¯ RV.) Airway resistance unchanged.
  • (IC; IRV + VT) increases 5–10%. TLC is unchanged or ¯ minimally at
  • FEV1, FEV1/FVC, flow/vol curve not significantly Abn spirometry sugg pathology.
  • DLCO no change. Increased cardiac outpt offset by decreased

Intrapartum/Postpartum Changes
  • Hyperventilation ­ w/ pain/anxiety. Analgesia mitigates Minute ventilation varies widely.
  • Hypocarbia can cause placental vasoconstriction ® hypoperfusion
  • Postpartum, all above changes resolve, except for widened subcostal
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Arterial Blood Gas (ABG) Analysis

Procedure
  • Sterilely prep area overlying radial, femoral, brachial, dorsalis pedis, or axillary artery
  • Consider local anesthesia over puncture Assess for collateral circulation.
  • Obtain 2–3 mL bld in heparinized Remove air bubbles, place on ice for transport.
  • Consider indwelling arterial catheter for serial

Considerations in Pregnancy (Clin Chest Med 2011;32(1))

  • ¯pCO2 from ¯ serum bicarb compens for chronic respiratory alkalosis. ­ pH (7.42–7.46).
  • Chronic alkalosis stimulates ­ 2,3-DPG w/ shift of Hgb dissociation curve; aids in placental O2 ­pO2 facilitates placental O2 exchange. PO2 significantly lower supine vs. sitting. High metabolic rate can cause rapid desaturation if apneic.
Definitions
  • Acidemia: Arterial pH lower than nml (<35)
  • Alkalemia: Arterial pH higher than nml (>45)
  • Metabolic acidosis: Process that decreases serum HCO3 ®¯ pH (bicarb consump)
  • Respiratory acidosis: Process that increases serum pCO2 ®¯ pH (hypoventilation)
  • Metabolic alkalosis: Process that increases serum HCO3 ®­ pH (bicarb excess)
  • Respiratory alkalosis: Process that decreases serum pCO2 ®­ pH (hyperventilation)
Normal Values
  • Nonpregnant: pH, 35–7.45; pCO2, 32–45 mmHg; pO2, 72–104 mmHg; HCO3,22–30 mEq/L

 

Mean ABG values in pregnancy
N = 20 12 w 24 w 32 w 38 w Postpartum
pH 7.46 7.44 7.44 7.43 7.41
pCO2 29.4 (0.4) 29.5 (0.7) 30.3 (0.5) 30.4 (0.6) 35.3 (0.7)
pO2 106.4 (1.1) 103.1 (1.6) 102.4 (1.2) 101.8 (1) 94.7 (1.5)
From Templeton A, Kelman GR. Maternal blood-gases, (PAO2–PaO2), physiological shunt and VD/VT in normal pregnancy. Br J Anaesth. 1976;48(10):1001–1004.

Diagnosis (Harrison’s Principles of Internal Medicine, 18th ed)

  • Obtain ABG & electrolytes Use HCO3 from electrolytes.
  • Determine whether simple or mixed d/o by assessing whether expected compensatory resp is “Compens” cannot change alkalemia to acidemia or vice versa. If apparent insuff or overexuberant compens, mixed d/o likely exists.
  • If acidosis present, calculate AG: (Na -[Cl + HCO3]) w/ adjustment for albumin (nml AG » 5 ´ albumin)

 

Predicted changes for acid–base disorders
D/o Compens
Metabolic acidosis PaCO2 = (1.5 ´ HCO3) + 8 ± 2
Metabolic alkalosis PaCO2 will ­ 6 mmHg per 10 mmol/L ­ in [HCO3]
Respiratory acidosis  
Acute [HCO3] will ¯ 0.2 mmol/L per mmHg ¯ in PaCO2
Chronic (>3–5 d) [HCO3] will ¯ 0.4 mmol/L per mmHg ¯ in PaCO2
Respiratory alkalosis  
Acute [HCO3] will ­ 0.1 mmol/L per mmHg ­ in PaCO2
Chronic (>3–5 d) [HCO3] will ­ 0.4 mmol/L per mmHg ­ in PaCO2

  • Consider ÄAG/ÄHCO3 ratio to determine if simple high AG metabolic acidosis (ratiobtw 1 & 2). If ratio >2, likely additional metabolic If <1, likely additional nongap metabolic acidosis.
  • Ddx guides clinical assessment & final dx:

For high AG metabolic acidosis: Renal failure, lactic acidosis, toxins, ketoacidosis. W/o high AG: Renal tubular acidosis, GI loss.

For metabolic alkalosis: Exogenous alkali, extracellular fluid contraction w/ hypoK, extracellular fluid expansion w/ hypoK/Mineralocort excess

For respiratory acidosis: Hypoventilation (obst, CNS depression, neuromuscular d/o, impaired gas exchange)

For respiratory alkalosis: Hyperventilation (secondary to hypoxia, Preg, pain, sepsis, drugs)

See Abbreviations

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