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Fisiología del embarazo + circulación fetal
- 1. Fisiología del embarazo Leal Lam Sara Li 406 Ginecología y obstetricia UNIVERSIDAD AUTÓNOMA DE BAJA CALIFORNIA Escuela de Ciencias de la Salud Unidad Valle de las Palmas
- 2. Generalidades ● Se aprecian cambios desde el comienzo del embarazo en todos los sistemas ● Todas las modificaciones físicas y psicológicas son mediadas por hormonas liberadas por la unidad feto- placentaria ○ Estrógeno ○ Progesterona Cambios en la embarazada • Aparato cardiovascular • Aparato respiratorio • Aparato digestivo • Aparato urinario Cambios en el feto • Circulación fetal Fuente: Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. De Gruyter W. Joachim W. Dudenhausen: Practical obstetrics. Gruyter. 2014.
- 3. Cambios cardiovasculares ● Embarazo= estado de gran flujo, baja resistencia ● Cambios aumentan más con múltiples fetos Primer trimestre • Vasodilatación sistémica de la madre • ↓35-40% resist. vasc. sist. (RVS) • ↑Gasto cardíaco (GC) • ↑↑volumen plasmático (10-15%), ↑glóbulos rojos (±20%) Segundo trimestre • ↓RVS llega a una meseta • ↑GC continua de forma no linear • ↑FC • ↓RV • ↑volumen plasmático y ↑GR llega a meseta (máxima hemodilución) • ↓PA 5-10 mmHg por debajo de niveles pre- embarazo Tercer trimestre • ↑GC llega a un pico máximo • ↑FC a su máximo nivel (24%) • ↓PA a niveles pre- embarazo • ↓RV • Volumen plasmático y GR en meseta Efecto patológico del GC aumentado: •Insuficiencia cardíaca Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017.
- 4. Cambios cardiovasculares ● Embarazo= estado de gran flujo, baja resistencia ● Cambios aumentan más con múltiples fetos Intraparto • ↑GC en trabajo de parto •15% en etapas tempranas •25% fase activa •50% segundo estadio • ↑PA Post-parto • ↓FC y PA regresan a niveles normales pre- embarazo y permanecen sin cambios en todo este periodo • ↑RVS a niveles normales • ↑RV • Desaparición de anemia fisiológica (máx. hasta las 8 semanas después del alumbramiento) Ausencia de desaparición de anemia fisiológica •Muerte fetal •Pretérmino •Pequeño para edad gestacional Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017.
- 5. Cambios cardiovasculares Corazón • ↑gasto cardíaco 30-50% • ↓resistencia vascular • Desviación a la izquierda + ligero derrame pericárdico • Fracción de eyección se mantiene sin cambios Circulación y presión arterial • Hipervolemia • PA ↓inicialmente, para luego ↑ Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017.
- 6. Cambios cardiovasculares Corazón • ↑gasto cardíaco 30-50% • ↓resistencia vascular • Desviación a la izquierda + ligero derrame pericárdico • Fracción de eyección se mantiene sin cambios Circulación y presión arterial • Hipervolemia • PA ↓inicialmente, para luego ↑ Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017.
- 7. Cambios cardiovasculares Corazón • ↑gasto cardíaco 30-50% • ↓resistencia vascular • Desviación a la izquierda + ligero derrame pericárdico • Fracción de eyección se mantiene sin cambios Circulación y presión arterial • Hipervolemia • PA ↓inicialmente, para luego ↑ Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017.
- 8. Cambios cardiovasculares Presión venosa • ↑presión venosa femoral por compresión mecánica • presión venosa central se mantiene sin cambios Factores de coagulación • ↓20% TP y TPT • ↑factores I, II, V, VII, VIII, X, XII • ↑inhibidores de la fibrinolisis PAI-1 y PAI-2 Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Foley R. Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes. Ed. Uptodate. 2017. Patologías asociadas: • Trombosis venosa profunda • Arritmias y palpitaciones
- 9. Cambios respiratorios Diafragma, pulmones y costillas • ↑4 cm • ↓resistencia pulmonar total • Cartílagos costales se “relajan” Función pulmonar • ↑30-40% volumen de ventilación pulmonar • ↑40% ventilación/minuto en reposo • ↓20% volumen residual • ↓20% capacidad funcional • ≤FEV1 Gases • ↓25% PaCO2 • ↑20-33% consumo de O2 Equilibrio ácido-base • Alcalosis respiratoria Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Weinberger SE. Maternal adaptations to pregnancy: Physiologic respiratory changes and dyspnea. Uptodate. 2017.
- 10. Cambios respiratorios Diafragma, pulmones y costillas • ↑4 cm • ↓resistencia pulmonar total • Cartílagos costales se “relajan” Función pulmonar • ↑30-40% volumen de ventilación pulmonar • ↑40% ventilación/minuto en reposo • ↓20% volumen residual • ↓20% capacidad funcional • ≤FEV1 Gases • ↓25% PaCO2 • ↑20-33% consumo de O2 Equilibrio ácido-base • Alcalosis respiratoria Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Weinberger SE. Maternal adaptations to pregnancy: Physiologic respiratory changes and dyspnea. Uptodate. 2017.
- 11. Cambios respiratorios Disnea fisiológica • 60-70% de las embarazadas lo padecen • Inicia en 1er-2do trimestre y se estabiliza en el 3er trimestre • Mecanismo no claro Disnea patológica • Inicio súbito • Tos asociada • Ruidos pulmonares anormales • Síntomas asociados • ¿Primeros trimestres o último trimestre? Patología asociada: •Disnea •Embolia pulmonar •Enfermedad cardíaca •Obstrucción de vías respiratorias altas •Neumotórax espontáneo Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Weinberger SE. Maternal adaptations to pregnancy: Physiologic respiratory changes and dyspnea. Uptodate. 2017.
- 12. Cambios digestivos Órganos • gingivitis • ↑presión cámara gástrica • Hígado no palpable Función GI • ↓motilidad gástrica • vaciamiento gástrico no cambia • ↓motilidad de vesícula biliar • ↓motilidad colónica • ↓tiempo de tránsito colónico Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Bianco A. Maternal adaptations to pregnancy: Gastrointestinal tract. Uptodate. 2017. Patologías asociadas: •ERGE •Aspiración de contenido gástrico •Hiperemesis gravidarum •Colelitiasis ± colecistitis •pancreatitis •Constipación •Incontinencia fecal •Hemorroides
- 13. Cambios en el aparato urinario Órganos •↑30% volumen de los riñones; ↑1-1.5 cm de tamaño •↑diámetro ureteral Función renal •↑80% TFG a las 12 SG; ↓ en 3er trimestre •↓25% BUN (8-10 mg/dL), creatinina (0.4 mg/dL en promedio) y ácido úrico •Na+ plasmático sin cambios •↓20% HCO3 plasmático •↑pH sanguíneo •Glucosuria •Proteinuria máx. 200 mg/día Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Thadhani RI. Maternal adaptations to pregnancy: Renal and urinary tract physiology. Uptodate. 2017.
- 14. Cambios en el aparato urinario Órganos •↑30% volumen de los riñones; ↑1-1.5 cm de tamaño •↑diámetro ureteral Función renal •↑80% TFG a las 12 SG; ↓ en 3er trimestre •↓25% BUN (8-10 mg/dL), creatinina (0.4 mg/dL en promedio) y ácido úrico •Na+ plasmático sin cambios •↓20% HCO3 plasmático •↑pH sanguíneo •Glucosuria •Proteinuria máx. 200 mg/día Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Thadhani RI. Maternal adaptations to pregnancy: Renal and urinary tract physiology. Uptodate. 2017. Patologías asociadas: •IVU •Pielonefritis •Insuficiencia renal •Trastornos del equilibrio hidroelectrolítico •Preeclampsia
- 15. Circulación fetal ● Transición exitosa al nacimiento del feto: ○ Aclaramiento del líquido alveolar ○ Expansión pulmonar ○ Cierre de los cortocircuitos derecha-izquierda y cambios circulatorios ● 90% de los recién nacidos no requieren cuidados especiales Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Fernandes CJ. Physiologic transition from intrauterine to extrauterine life. Uptodate. 2017.
- 16. Circulación fetal ● Factores de riesgo: ○ Condiciones de la madre ○ Condiciones del feto ○ Complicaciones del anteparto ○ Complicaciones del alumbramiento Cunningham FG. Williams: Obstetricia 23ª edición. McGraw-Hill. 2011. Fernandes CJ. Physiologic transition from intrauterine to extrauterine life. Uptodate. 2017. Patologías asociadas: •Falta de esfuerzo respiratorio •Bloqueo mecánico de vías aéreas •Función pulmonar alterada •Hipertensión pulmonar persistente •Cardiopatía congénita •Niños pretérmino
Editor's Notes
- Todas las modificaciones físicas y psicológicas son mediadas por hormonas liberadas por la unidad feto-placentaria, que ayudarán a: -Mantener el embarazo -Prepararse para el parto -Prepara a la madre para lo que viene después del embarazo (lactancia materna, etc) Estrógeno: Progesterona: relaja músculo liso
- Gasto cardíaco= volumen sistólico x frecuencia cardíaca Factores que modifican gasto cardíaco: -↑posición decúbito lateral izquierdo -↓posición supina (acostado boca arriba) por compresión de aorta y vena cava Expansion of the plasma volume and an increase in red blood cell mass begin as early as the fourth week of pregnancy, peak at 28 to 34 weeks of gestation, and then plateau until parturition [3-5]. Plasma volume expansion is accompanied by a lesser increase in red cell volume (figure 4) [6]. As a result, there is a modest reduction in hematocrit, with peak hemodilution occurring at 24 to 26 weeks. Compared with the blood volume (65 to 70 mL/kg) in nonpregnant women, the blood volume in pregnant women at term is increased to 100 mL/kg. Plasma volume — Plasma volume increases by 10 to 15 percent at 6 to 12 weeks of gestation [8-10], expands rapidly until 30 to 34 weeks, and then plateaus or falls slightly (figure 4). Total plasma expansion is approximately 40 to 45 percent above the nonpregnant levels by approximately 34 weeks gestation. Red blood cell mass — Red blood cell mass begins to increase at 8 to 10 weeks of gestation and steadily rises, in women taking iron supplements, by 20 to 30 percent (250 to 450 mL) above nonpregnant levels by the end of pregnancy [5,12-15]. Among women not on iron supplements, the red cell mass may only increase by 15 to 20 percent [16]. Increased plasma erythropoietin induces the rise in red cell mass, which partially supports the higher metabolic requirement for oxygen during pregnancy. Physiologic anemia — A greater increase in intravascular volume compared with red cell mass results in the dilutional or physiologic anemia of pregnancy. This becomes most apparent at 30 to 34 weeks of gestation when plasma volume peaks in relation to red cell volume. Assuming normal renal function, blood volume and constituents return to nonpregnant values by eight weeks postpartum, a result of diuresis. Hemoglobin begins to increase from the third postpartum day.
- Gasto cardíaco= volumen sistólico x frecuencia cardíaca Factores que modifican gasto cardíaco: -↑posición decúbito lateral izquierdo -↓posición supina (acostado boca arriba) por compresión de aorta y vena cava Gasto cardíaco: With epidural anesthesia, the baseline increase in cardiac output is attenuated; however, the increases associated with uterine contractions persist. Position changes from supine to lateral decubitus during labor increases cardiac output. This effect is more pronounced during labor, suggesting that cardiac output during labor may be more dependent on preload. Fin de anemia fisiológica: The physiologic effects of hypervolemia and anemia during pregnancy have several benefits: Decreased blood viscosity (from greater increases in plasma volume than red cell volume) results in reduced resistance to flow, facilitating placental perfusion and lowering cardiac work. Total intravascular volume increases to approximately 50 percent above nonpregnant values near term to provide some reserve against the normal blood loss during parturition (about 300 to 500 mL for vaginal delivery, 600 to The absence of physiologic anemia appears to be harmful [19,20]. A population-based, case-control study using data from the Swedish Medical Birth Register reported that women with a hemoglobin concentration of 14.6 g/dL or higher at the first prenatal visit were at increased risk of stillbirth (odds ratio [OR] 1.8), antepartum stillbirth without malformations (OR 2.0), and preterm and small for gestational age nonmalformed stillbirth (OR 2.7 and 4.2, respectively) [19]. The elevated risk persisted despite a subsequent fall in hemoglobin concentration and after excluding women with preeclampsia. It is hypothesized that high blood viscosity increases the risk of thrombosis in the uteroplacental circulation.
- To accomodate the needs of the mother, an enlarging uterus and a growing fetus – as well as having some reserve for the blood loss that happens during delivery - , the cardiovascular system has to expand. ↑GC= ↑FC x ↑volumen sistólico (↓postcarga por ↓resistencia vascular sistémica) ↓PA= ↑GC x ↓resistencia vascular sistémica Patologías asociadas: -Sx de vena cava inferior/ de hipotensión supina -Anemia Presión venosa central: Although changes in blood volume during pregnancy affect right ventricular preload, central venous pressure remains in the normal nonpregnant range throughout pregnancy due to the reduction in cardiac afterload induced by the substantial decrease in both systemic vascular resistance and pulmonary vascular resistance (ie, afterload to the left and right heart, respectively). Regardless of the mechanism, the stress induced by the increase in cardiac output can cause women with underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of pregnancy.
- To accomodate the needs of the mother, an enlarging uterus and a growing fetus – as well as having some reserve for the blood loss that happens during delivery - , the cardiovascular system has to expand. ↑GC= ↑FC x ↑volumen sistólico (↓postcarga por ↓resistencia vascular sistémica) ↓PA= ↑GC x ↓resistencia vascular sistémica Patologías asociadas: -Sx de vena cava inferior/ de hipotensión supina -Anemia Presión venosa central: Although changes in blood volume during pregnancy affect right ventricular preload, central venous pressure remains in the normal nonpregnant range throughout pregnancy due to the reduction in cardiac afterload induced by the substantial decrease in both systemic vascular resistance and pulmonary vascular resistance (ie, afterload to the left and right heart, respectively). Regardless of the mechanism, the stress induced by the increase in cardiac output can cause women with underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of pregnancy.
- To accomodate the needs of the mother, an enlarging uterus and a growing fetus – as well as having some reserve for the blood loss that happens during delivery - , the cardiovascular system has to expand. ↑GC= ↑FC x ↑volumen sistólico (↓postcarga por ↓resistencia vascular sistémica) ↓PA= ↑GC x ↓resistencia vascular sistémica Patologías asociadas: -Sx de vena cava inferior/ de hipotensión supina -Anemia Presión venosa central: Although changes in blood volume during pregnancy affect right ventricular preload, central venous pressure remains in the normal nonpregnant range throughout pregnancy due to the reduction in cardiac afterload induced by the substantial decrease in both systemic vascular resistance and pulmonary vascular resistance (ie, afterload to the left and right heart, respectively). Regardless of the mechanism, the stress induced by the increase in cardiac output can cause women with underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of pregnancy.
- To accomodate the needs of the mother, an enlarging uterus and a growing fetus – as well as having some reserve for the blood loss that happens during delivery - , the cardiovascular system has to expand. ↑GC= ↑FC x ↑volumen sistólico (↓postcarga por ↓resistencia vascular sistémica) ↓PA= ↑GC x ↓resistencia vascular sistémica Patologías asociadas: -Sx de vena cava inferior/ de hipotensión supina -Anemia Presión venosa central: Although changes in blood volume during pregnancy affect right ventricular preload, central venous pressure remains in the normal nonpregnant range throughout pregnancy due to the reduction in cardiac afterload induced by the substantial decrease in both systemic vascular resistance and pulmonary vascular resistance (ie, afterload to the left and right heart, respectively). Regardless of the mechanism, the stress induced by the increase in cardiac output can cause women with underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of pregnancy.
- Aumento importante en el volumen de ventilación pulmonar medio (0.66 a 0.8 L/min) y en la ventilación por minuto (10.7 a 14.1 L/min) con respecto a mujeres no embarazadas La capacidad funcional residual y el volumen residual disminuyen como consecuencia de la elevación del diafragma (fig. 5-12). La velocidad máxima del flujo espiratorio disminuye en forma progresiva a medida que avanza la gestación (Harirah et al., 2005). La distensibilidad pulmonar no cambia por el embarazo, pero la conductancia de las vías respiratorias aumenta y la resistencia pulmonar total disminuye, tal vez por efecto de la progesterona. La capacidad respiratoria máxima y la capacidad vital forzada o cronometrada no tienen cambios apreciables. Está claro que la cantidad de oxígeno que llega a los pulmones con el aumento del volumen de ventilación pulmonar excede las necesidades impuestas por la gestación. ↓PaCO2 hasta 27-32 mmHg Patologías asociadas: -Disnea
- Aumento importante en el volumen de ventilación pulmonar medio (0.66 a 0.8 L/min) y en la ventilación por minuto (10.7 a 14.1 L/min) con respecto a mujeres no embarazadas La capacidad funcional residual y el volumen residual disminuyen como consecuencia de la elevación del diafragma (fig. 5-12). La velocidad máxima del flujo espiratorio disminuye en forma progresiva a medida que avanza la gestación (Harirah et al., 2005). La distensibilidad pulmonar no cambia por el embarazo, pero la conductancia de las vías respiratorias aumenta y la resistencia pulmonar total disminuye, tal vez por efecto de la progesterona. La capacidad respiratoria máxima y la capacidad vital forzada o cronometrada no tienen cambios apreciables. Está claro que la cantidad de oxígeno que llega a los pulmones con el aumento del volumen de ventilación pulmonar excede las necesidades impuestas por la gestación. ↓PaCO2 hasta 27-32 mmHg Patologías asociadas: -Disnea
- Aumento importante en el volumen de ventilación pulmonar medio (0.66 a 0.8 L/min) y en la ventilación por minuto (10.7 a 14.1 L/min) con respecto a mujeres no embarazadas La capacidad funcional residual y el volumen residual disminuyen como consecuencia de la elevación del diafragma (fig. 5-12). La velocidad máxima del flujo espiratorio disminuye en forma progresiva a medida que avanza la gestación (Harirah et al., 2005). La distensibilidad pulmonar no cambia por el embarazo, pero la conductancia de las vías respiratorias aumenta y la resistencia pulmonar total disminuye, tal vez por efecto de la progesterona. La capacidad respiratoria máxima y la capacidad vital forzada o cronometrada no tienen cambios apreciables. Está claro que la cantidad de oxígeno que llega a los pulmones con el aumento del volumen de ventilación pulmonar excede las necesidades impuestas por la gestación. ↓PaCO2 hasta 27-32 mmHg Patologías asociadas: -Disnea When a pregnant woman complains of dyspnea, distinguishing between underlying disease (eg, asthma) (table 1), a new problem (eg, pulmonary embolic disease or peripartum cardiomyopathy), and progesterone-induced hyperventilation (dyspnea of pregnancy) can pose a difficult diagnostic problem [1-4,33]. There are relatively few pregnancy-specific causes of respiratory failure. These include amniotic fluid embolism and pulmonary edema secondary to tocolytics, preeclampsia/eclampsia, or pregnancy-associated cardiomyopathy (peripartum cardiomyopathy).
- Gingivitis: Las encías pueden volverse hiperémicas y blandas durante el embarazo; es posible que sangren con traumatismos leves, como los causados por el cepillo dental. En ocasiones se desarrolla una inflamación focal muy vascularizada de las encías, llamada épulis del embarazo, pero casi siempre remite en forma espontánea después del parto. Casi todos los datos indican que el embarazo no incita la caries dental. Parece que el tiempo de vaciamiento gástrico, estudiado con técnicas de absorción de paracetamol, no cambia entre los trimestres ni en comparación con las mujeres no grávidas (Macfie et al., 1991; Wong et al., 2002, 2007). Sin embargo, durante el trabajo de parto y sobre todo después de la administración de analgésicos, el tiempo del vaciamiento gástrico puede prolongarse de manera considerable. Patologías asociadas: -ERGE -Hemorroides -Hiperemesis gravidarum
- The increase in glomerular filtration rate (GFR) is observed within one month of conception, peaks at approximately 40 to 50 percent above baseline levels by the early second trimester, and then declines slightly toward term [4]. Of note, in late gestation, left lateral positioning increases glomerular filtration rate and sodium excretion [5]. The physiologic increase in GFR during pregnancy results in a decrease in serum creatinine concentration, which falls by an average of 0.4 mg/dL (35 micromol/L) to a normal range of 0.4 to 0.8 mg/dL (35 to 70 micromol/L) [6]. Thus, a serum creatinine of 1.0 mg/dL (88 micromol/L), while normal in a nonpregnant individual, reflects renal impairment in a pregnant woman. Blood urea nitrogen levels fall to approximately 8 to 10 mg/dL (2.9 to 3.9 mmol/L) for the same reason. Glucosuria: Glucosuria by dipstick testing is seen in approximately 50 percent of pregnant women, and hence is not a useful screening tool for diabetes mellitus [34]. Glucosuria is primarily due to decreased proximal tubular glucose reabsorption. Proteinuria: The mechanisms driving the physiologic increase in urinary protein excretion in pregnancy are not well understood, but may include increased GFR, increased glomerular basement membrane pore size [30], increased protein transport across the glomerular filtration barrier via the nondiscriminatory shunt pathway [31], and reduced tubular reabsorption of filtered protein. Patologías asociadas: -IVU -Formación de abscesos
- The increase in glomerular filtration rate (GFR) is observed within one month of conception, peaks at approximately 40 to 50 percent above baseline levels by the early second trimester, and then declines slightly toward term [4]. Of note, in late gestation, left lateral positioning increases glomerular filtration rate and sodium excretion [5]. The physiologic increase in GFR during pregnancy results in a decrease in serum creatinine concentration, which falls by an average of 0.4 mg/dL (35 micromol/L) to a normal range of 0.4 to 0.8 mg/dL (35 to 70 micromol/L) [6]. Thus, a serum creatinine of 1.0 mg/dL (88 micromol/L), while normal in a nonpregnant individual, reflects renal impairment in a pregnant woman. Blood urea nitrogen levels fall to approximately 8 to 10 mg/dL (2.9 to 3.9 mmol/L) for the same reason. Glucosuria: Glucosuria by dipstick testing is seen in approximately 50 percent of pregnant women, and hence is not a useful screening tool for diabetes mellitus [34]. Glucosuria is primarily due to decreased proximal tubular glucose reabsorption. Proteinuria: The mechanisms driving the physiologic increase in urinary protein excretion in pregnancy are not well understood, but may include increased GFR, increased glomerular basement membrane pore size [30], increased protein transport across the glomerular filtration barrier via the nondiscriminatory shunt pathway [31], and reduced tubular reabsorption of filtered protein. Patologías asociadas: -IVU -Formación de abscesos
- TRANSITION AT DELIVERY — To successfully make the transition from intrauterine to extrauterine life when the umbilical cord is clamped at birth, the neonate must rapidly make physiologic changes in cardiopulmonary function. A successful transition is characterized by the following features: ● Alveolar fluid clearance ● Lung expansion Circulatory changes with increases in pulmonary perfusion and systemic pressure, and closure of the right-to-left shunts of the fetal circulation Alveolar fluid clearance — Several mechanisms contribute to the clearance of alveolar fluid, including labor, initial breaths, and thoracic squeeze. Labor − During late gestation, in response to increased concentrations of catecholamines and other hormones, the lung epithelium switches from active secretion of chloride and liquid into the air spaces to active resorption of sodium and liquid [7-9]. Increased oxygen tension at birth enhances the capacity of the epithelium to transport sodium and increases gene expression of the epithelial sodium channel, promoting further resorption of alveolar fluid Initial breaths − The initial effective breaths of the neonate generate high transpulmonary pressures: mean esophageal pressures of -52 cm H O during inspiration and 71 cm H O during expiration have been measured in term infants [10]. The initial negative hydrostatic pressure drives alveolar fluid from the air spaces into the interstitium and subsequently the pulmonary vasculature. Thoracic squeeze − Although once thought to be the primary mechanism for alveolar clearance, the pressure upon the chest wall of the infant during delivery probably is only a minor contributor to alveolar fluid clearance. Lung expansion — With the first effective breath, air movement begins as intrathoracic pressure falls, starting at pressures of less than -5 cm H O. Increasing inspiratory pressure expands the alveolar air spaces and establishes functional residual capacity (FRC). Lung expansion also stimulates surfactant release, which reduces alveolar surface tension, increases compliance, and stabilizes the FRC. Circulatory changes — With the clamping of the umbilical cord, the placenta with its low vascular resistance is removed from the neonatal circulation, resulting in a rise in neonatal systemic blood pressure. At the same time, lung expansion reduces both pulmonary vascular resistance and the pulmonary artery pressure.
- The following risk factors are associated with a greater likelihood of having difficulty making a successful transition and of requiring resuscitation [13]: Maternal conditions − Advanced maternal age, maternal diabetes mellitus or hypertension, maternal substance abuse, or previous history of stillbirth, fetal loss, or early neonatal death Fetal conditions − Prematurity, postmaturity, congenital anomalies, or multiple gestation Antepartum complications − Placental anomalies (eg, placenta previa), or either oligohydramnios or polyhydramnios Delivery complications − Transverse lie or breech presentation, chorioamnionitis, foul-smelling or meconium-stained amniotic fluid, antenatal asphyxia with abnormal fetal heart rate pattern, maternal administration of a narcotic within four hours of birth, or delivery that requires instrumentation (eg, forceps, vacuum, or cesarean delivery)