(2024-04-29)Actualización en profilaxis PrEP frente a VIH. (DOC)
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
Notes de l'éditeur
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)