Pregnancy

Cardiovascular Manifestations [MEDLINE]

  • General Comments
    • Hemodynamic Changes in Pregnancy (Listed Here) Begin During the First Trimester and Peak at 20-24 wks of Gestation
    • During Labor, Cardiac Output Increases Further and Blood Pressure Increases During Uterine Contractions
      • Valsalva Manuever and Pain Increase the Heart Rate and Vascular Resistances
    • In Hours-Days Post-Parturition, Autotransfusion of Blood from Contracting Uterus and Shifting of Peripheral Edema from the Extravascular Compartment Back into the Systemic Vascular Space Occur
    • Pregnancy-Related Hemodynamic Changes Regress by Approximately 6 wks Postpartum
  • Increased Heart Rate (see Sinus Tachycardia, [[Sinus Tachycardia]]): by 10-20 bpm
  • Increased Plasma Volume: increased preload, usually with normal PCWP and CVP
  • Increased Cardiac Output (see Hemodynamics, [[Hemodynamics]])
  • Decreased Pulmonary Vascular Resistance (PVR) (see Hemodynamics, [[Hemodynamics]]): up to 35% by late pregnancy
  • Decreased Systemic Vascular Resistance (SVR) (see Hemodynamics, [[Hemodynamics]])
  • Decreased Blood Pressure

Gastrointestinal Manifestations


Hematologic Manifestations

  • Anemia (Relative) (see Anemia, [[Anemia]])
    • Physiology: due to increased plasma volume
  • Acquired Thrombotic Thrombocytopenic Purpura (Acquired TTP) (see Thrombotic Thrombocytopenic Purpura-Acquired, [[Thrombotic Thrombocytopenic Purpura-Acquired]])
    • Physiology: due to decreased ADAMTS13 activity in last two trimesters of pregnancy (see ADAMTS13 Activity, [[ADAMTS13 Activity]]):
      • Lowest levels of ADAMTS13 occur at 36-40 weeks of gestation and during early puerperium
    • Cases of TTP occurring during the last trimester or at the time of delivery may make it difficult to differentiate from pre-eclampsia/eclampsia (see Pre-Eclampsia, Eclampsia, [[Pre-Eclampsia, Eclampsia]])
    • Cases of relapse with later pregnancies have been reported
  • Hypercoagulable State (see Hypercoagulable States, [[Hypercoagulable States]])
  • Thrombocytopenia (see Thrombocytopenia, [[Thrombocytopenia]])
    • Physiology: xxx

Pulmonary Manifestations

General

  • Dyspnea (see Dyspnea, [[Dyspnea]])
    • Epidemiology: common in all pregnancies
    • Physiology: due to progesterone secreted by placenta)
  • Improvement in Asthma: pregnancy may improve asthma
    • Physiology: due to progesterone-induced bronchodilation and increased circulating histaminase
  • Pleural Effusion (see Pleural Effusion-Exudate, [[Pleural Effusion-Exudate]] and Pleural Effusion-Transudate, [[Pleural Effusion-Transudate]])
    • Epidemiology: small amounts of U/S-detected pleural effusion are a normal finding in pregnancy (unclear whether these are transudates or exudates) [MEDLINE]
  • Altered Ventilation
    • Clinical
      • Increased Minute Ventilation (VE): begins during first trimester, up to 48% increase by term (due to progesterone)
      • Increased Tidal Volume (VT): 30-35% above normal (to around 450-600 ml) with increased chest antero-posterior (A-P) diameter
      • Normal-Mildly Elevated Respiratory Rate

Arterial Blood Gas (ABG) (see Arterial Blood Gas, [[Arterial Blood Gas]])

  • Hypocapnia (see Hypocapnia, [[Hypocapnia]])
    • Clinical: pCO2 is usually <35 mm Hg
  • Slight Metabolic Acidosis (see Metabolic Acidosis-Normal Anion Gap, [[Metabolic Acidosis-Normal Anion Gap]])
    • Clinical: pH ranges from 7.40-7.45
  • Normal pO2

Swan-Ganz Catheter (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]])

  • Increased Cardiac Output
  • Increased Blood Volume with Normal CVP and PCWP
  • Decreased PVR: up to 35% by late pregnancy

Pulmonary Function Tests (PFT’s) (see Pulmonary Function Tests, [[Pulmonary Function Tests]])

  • Decreased FRC
  • Decreased RV
  • Preserved FEV1
  • Preserved VC

Exercise Testing (see Exercise Test, [[Exercise Test]])

  • Increased Oxygen Consumption + Increased CO2 Production: these factors may make the pregnant patient more susceptible to hypoxemia/hypercapnia in cases of hypoventilation
    • Oxygen consumption rises to 40-100% above normal
    • CO2 production rises to 30-50% above normal by third trimester

Upper Airway Manifestations

  • Upper Airway Edema/Hyperemia
  • Increased Upper Airway Friability

Interactions of Pregnancy with Other Diseases

Diseases Which May Worsen with Pregnancy

  • Lymphangioleiomyomatosis (LAM) (Lymphangioleiomyomatosis, [[Lymphangioleiomyomatosis]]): estrogen likely plays a role in the pathogenesis of LAM
    • LAM may also abate after menopause
  • Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]])
    • Pulmonary Hypertension Increases the Mortality Rate During Pregnancy
  • Tuberous Sclerosis (see Tuberous Sclerosis, [[Tuberous Sclerosis]]): estrogen likely plays a role in the pathogenesis of tuberous sclerosis

Diseases Which May Improve During Pregnancy

  • Asthma (see Asthma, [[Asthma]])
    • 33% of Cases: pregnancy has no impact on asthma
    • 33% of Cases: pregnancy exacerbates asthma
    • 33% of Cases: pregnancy improves asthma
  • Sarcoidosis (see Sarcoidosis, [[Sarcoidosis]]): sarcoidosis may exacerbate post-partum
  • xxxx
  • xxxx
  • xxxx
  • xxxx

Asthma Treatment During Pregnancy

  • Asthma Drugs: safe in pregnancy (steroids increase cleft palate in animals/ only effect in humans is a decrease birth weight by 300-400 g)
  • Uterine Contractions: common during asthma exacerbation
  • Preterm Labor: treat with magnesium sulfate (it avoids excessive use of ß2-agonists and it produces bronchodilation)
  • xxxx

References

  • Pregnancy, vascular tone, and maternal hemodynamics: a crucial adaptation. Obstet Gynecol Surv. 2000;55(9):574 [MEDLINE]

The adaptation of vascular tone in early pregnancy precedes and probably triggers blood volume and cardiac output increase. Because the endothelium is known to regulate vascular smooth muscle action, the role of nitric oxide (NO) in the setting up of adequate uteroplacental and renal blood flow during normal pregnancy was investigated. The persistence of abnormally high uteroplacental resistance is a strong predisposing factor for intrauterine growth retardation and preeclampsia and can be screened by second trimester Doppler assessment of the uterine arteries. Current hypotheses suggested by experimental and clinical data concerning preeclampsia confirm the crucial role played by the endothelium and vascular tone adaptation. The analysis of these data leads to consider apart early-onset preeclampsia affecting pregnancies with growth retarded fetuses and associated with high vascular resistance. Lastly, NO donors seem to significantly decrease the impedance in the uteroplacental circulation and to improve fetoplacental hemodynamics assessed by Doppler measurements, and their therapeutic use in some forms of preeclampsia might be promising. TARGET AUDIENCE: Obstetricians&Gynecologists, Family Physicians LEARNING OBJECTIVES: After completion of this article, the reader will be able to summarize the events that regulate vascular tone in pregnancy, specifically the role of nitric oxide and other vasoactive prostaglandins in the regulation of vascular tone and to describe the various hypotheses concerning the mechanism and the mediators responsible for initiating endothelial damage in the various disorders of vascular tone in pregnancy.
AD
Department of Obstetrics and Gynecology, Assistance Publique–Hôpitaux de Paris, Hôpital Jean Verdier, Bondy, France. lionel.Carbillon@jvr.ap-hop.paris.fr
PMID
10975484

  • Sonographic detection of physiologic pleural fluid in normal pregnant women. Journal of Clinical Ultrasound; Volume 33, Issue 2, pages 63–66, February 2005 [MEDLINE]