Respiratory Physiology Lung Volumes change second half of pregnancy. diaphragm ERV & RV 10-25% FRC by term IC, VC, TLC Airway Function Spirometry normal
Respiratory Physiology 2 Ventilation and Pulmonary Gas Exchange Vt, Vd, Ve (50%), Va/Ve, Ve/Vo2 Ve reponse to CO2, hypoxia ABG: respiratory alkalosis (pco2 28-30), pH (7.4-7.47), HCO3 18-21.
Respiratory Physiology 3 »Oxygen Transport MOTHER COincreases by 30-50% maximum by the end of 1/3 supine (3/3): fall (decreased venous return) VO2 increases 20-33% Red cell volume increases by 20-30% Plasma volume increases by 50% Blood volume increases by 25-50% (79 ml/kg) Hemodilution..anemia and decrease in COP maximum during 2/3…hemoglobin to 11-12 g/dL PREDISPOSED TO O2 desaturation PULMONARY EDEMA
Respiratory Physiology 4 »Oxygen Transport BABY placental O2 transport : Qplacenta = 10% Qmother fetal factors: Pao2 (20-30) Hb (155g/L) increased O2 affinity of Hbf (Os diss’n curve shifted to the left) = increased Cao2 (CNS damage with > 75% reduction) increased CO fetus vulnerable to decreases in DO2 startegies to increase CO, Cao2 (maternal Pao2)
16 40 0 1 2 WEEKS FRC Ve CO Blood Vol GFR - 20% + 40% + 50%
MECHANICAL VENTILATION Airway : difficult -Failure to intubate accounts for 47% of all anesthesia-related mortality -8 X incidence in general surgical population -factors : -hyperemic : oral route -low FRC/O2 reservoir -risk of aspiration (GER/LES, increased Pabd) -Gas Exchange Pao2 high Pco2 Nal 30keep <60 -Mechanics Pplateau higher -PEEP for FRC, but keep up preload NIPPV : avoid (see upper airway)
Acute Respiratory Distress in the Obstetric Patient: Differential Diagnosis VTED AFES* PET/HTN* Tocolytics* Aspiration* PP Cardiomyop Air Embolism* Pneumothorax/mediastinum Other : * can lead to ARDS ARDS** Asthma ** sepsis (esp pyelonephritis, PROM, Pneumonia* antepartum infection), hemorrhagic shock, etc. Cardiac disease
ALI/ARDS in the Obstetric Patient: uncommon event, but the most common cause of respiratory failure in the peripartum period. incidence 0.2-.3 % mortality 43% (Smith West J Med 1990), 10.5% (Karetsky Med 1998) risk factors : -cesarian section -placental abruption -fetal distress -dead fetus syndrome
ALI/ARDS in the Obstetric Patient 2 Following Tocolytic Therapy Low incidence 0-.4% Low mortality (<5%) onset of dyspnea associated with tachycardia and tachypnea shortly after tocolytic therapy is terminated Bilateral pulmonary infiltrates and significant hypoxemia are common findings. Resolution within 12-24 hrs of discontinuation. Otherwise, look for other diagnosis The etiology of this syndrome is unknown had at least 1 other coexisting potential pathogenic mechanism accompanying risk factor (maternal or fetal infection,).
ALI/ARDS in the Obstetric Patient 3 Pregnancy-induced hypertension Pulmonary edema rare (2.9%) mortality of 10% usually accompanied by signs of multisystem organ dysfunction pulmonary edema occurred both pre- and postpartum proneness to edema…sensitive to fluids For both…the role of Associated risk factors Cardiogenic factors …remains controversial
Amniotic Fluid Embolism (AFE) classic triad of hypotension, hypoxia, and coagulopathy. recognized since 1926 Rare unique to pregnancy incidence: 1/8,000- 1/80,000 deliveries "it is impossible to state the true incidence of this condition at the present time because the sublethal and even subclinical forms which undoubtedly exist have not been recognized." –undiagnosed nonfatal cases outnumber the fatal cases –acute cardiopulmonary collapse is not an invariable accompanying finding. –Signs and symptoms may be delayed for many hours postpartum, and most patients survive even if undiagnosed
Amniotic Fluid Embolism (AFE) mortality 86% 25-50% of the patients die within the first hour the most common cause of peripartum mortality 5-7% of all maternal deaths Fetal death is common, but this may be a consequence of the cardiovascular collapse occurring in the mother
Amniotic Fluid Embolism (AFE) RISK FACTORS -age -multiparity -uterine stimulants -uterine rupture -tumultuousness of labor -closed abdominal injury -IUD present at full term -Amniocentesis -caesarian section -placenta accreta -retained placenta -meconium-stained amniotic fluid -complication of amnio-infusion for either a therapeutic instillationor to induce abortion
Amniotic Fluid Embolism (AFE) AF in maternal circulation during pregnancy: physiologic or abnormal ? AF: how does it cause for AFES ?
Amniotic Fluid Embolism (AFE) Clinical Presentation May be dramatic, with the abrupt onset of dyspnoea cyanosis, hypotension, coma,and hypotension with rapid progression to cardiopulmonary arrest Pulmonary edema (ALI…ARDS) frequent (24-70% of cases), may predominate. coagulopathy mild in almost every case followed by some degree of consumptive coagulopathy Evidence of CNS hypoxia is present, with alterations in mental status progressing to coma. In 10-20% of cases, the patient my present with seizure activity. Abruptio fetal demise HEMODYNAMIC PROFILE
Amniotic Fluid Embolism (AFE) Diagnosis/Treatment clinical Squames from PAC exclude other causes of respiratory distress and hypotension –septic shock, aspiration pneumonia, uterine rupture, placental abruption, pulmonary thromboembolism, venous air embolism Treatment –Supportive, maintaining DO2, correcting coagulopathy
Why Mothers die The death rate from amniotic fluid embolism could be reduced by avoiding uterine over-stimulation and by prompt diagnosis of obstructed labour Rates of obstetric intervention in the form of amniocentesis and induction and augmentation of labour should be kept as low as possible, and research into the condition is still necessary.
VTED in the OB patient 1 2-5/1000 deliveries 12% of maternal deaths marked increased in the incidence of DVT and PE in the first postpartum month. Pregnancy: acquired thrombophilia alterations in clotting and fibrinolytic factors reduction in venous tone and venous flow from the lower limb Other OB factors that enhance the risks for thromboembolism Other non-OB risk factors
VTED in the OB patient 2 Diagnosis : similar to the nonpregnant state false-positive test result by both IPG and duplex ultrasonography. Treatment Prophylaxis Despite the lack of confirmatory data, the trend has been to treat with subcutaneous heparin all pregnant women at risk for deep venous thrombosis because of a prior history of deep venous thrombosis, antiphospholipid antibody syndrome, or coagulation inhibitor syndrome.