[Postpartum pulmonary hypertension]. / Hipertensión pulmonar postparto.

Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.

Hipertensión pulmonar postparto / Postpartum pulmonary hypertension

La presencia de hipertensión pulmonar (HP) en el embarazo es poco frecuente y conlleva un alto riesgo para madres e hijos. Existe escasa bibliografía relacionada al diagnóstico de la misma luego del parto. Se describen tres pacientes a quienes se diagnostica HP luego de cursar sus embarazos y partos libres de eventos. A pesar de desconocerse las causas, son varios los mecanismos propuestos, como la hipercoagulabilidad, la hipoxia placentaria o la embolia de líquido amniótico. Resulta difícil definir si la HP diagnosticada en el puerperio, corresponde a una HP en período asintomático que fue desenmascarada por el estrés fisiológico del parto o es una condición de reciente comienzo. A pesar de la falta de datos que avalen la ausencia de HP previa al embarazo en nuestras tres casos, el curso libre de eventos en sus embarazos, sin síntomas y con partos normales, indican que no padecían esta enfermedad hasta el momento del parto, y que la desarrollaron posteriormente. De haberla padecido antes se hubieran presentado síntomas previos al parto o en el puerperio inmediato, ya que las demandas hemodinámicas deterioran gravemente a un ventrículo con poca reserva.

Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.

Hipertensión pulmonar postparto

La presencia de hipertensión pulmonar (HP) en el embarazo es poco frecuente y conlleva un alto riesgo para madres e hijos. Existe escasa bibliografía relacionada al diagnóstico de la misma luego del parto. Se describen tres pacientes a quienes se diagnostica HP luego de cursar sus embarazos y partos libres de eventos. A pesar de desconocerse las causas, son varios los mecanismos propuestos, como la hipercoagulabilidad, la hipoxia placentaria o la embolia de líquido amniótico. Resulta difícil definir si la HP diagnosticada en el puerperio, corresponde a una HP en período asintomático que fue desenmascarada por el estrés fisiológico del parto o es una condición de reciente comienzo. A pesar de la falta de datos que avalen la ausencia de HP previa al embarazo en nuestras tres casos, el curso libre de eventos en sus embarazos, sin síntomas y con partos normales, indican que no padecían esta enfermedad hasta el momento del parto, y que la desarrollaron posteriormente. De haberla padecido antes se hubieran presentado síntomas previos al parto o en el puerperio inmediato, ya que las demandas hemodinámicas deterioran gravemente a un ventrículo con poca reserva.(AU)

Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.(AU)

Hipertensión pulmonar postparto. / [Postpartum pulmonary hypertension].

Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.

Assessment of bronchodilator response through changes in lung volumes in chronic airflow obstruction.

Although FEV1 improvement is routinely used to define bronchodilator (BD) response, it correlates poorly with clinical effects. Changes in lung volumes (LV) have shown better correlation with exercise tolerance and might be more sensitive to detect BD effects. We assessed the additional contribution of measuring LV before and after BD to detect acute improvement in lung function not demonstrated by FEV1, and the influence of the response criteria selected on this contribution. We analyzed 98 spirometries and plethismographies performed pre and post BD in patients with airflow obstruction (FEV1/FVC < 70%). BD response was defined for FEV1 and FVC as per ATS guidelines and for other LV as delta > or = 10% of baseline (delta > or = 5 and > or = 15% were also analyzed). FEV1 identified as responders 32% of patients. Greater proportions were uncovered by slow vital capacity (51%, p < 0.001), inspiratory capacity (43%, p < 0.05) and residual volume (54%, p < 0.001). Slow spirometry identified 11% of responders additional to those detected by FEV1 and FVC. Plethismography added 9% more. The magnitude of volume responses correlated with the degree of baseline hyperinflation. Percentages of responders varied greatly using different thresholds (delta > or = 5 and > or = 15%). Mean change and proportions of responders for each LV varied significantly (p < 0.05) whether change was expressed as percent of baseline or predicted values. A considerable proportion of patients with airflow obstruction shows acute response to bronchodilators identified by changes in lung volumes but not detected by an improvement in FEV1. The selection of LV response criteria has important influence on the magnitude of this additional detection.

Assessment of bronchodilator response through changes in lung volumes in chronic airflow obstruction

Although FEV, improvement is routinely used to define bronchodilator (BD) response, it correlates poorly with clinical effects. Changes in lung volumes (LV) have shown better correlation with exercise tolerance and might be more sensitive to detect BD effects. We assessed the additional contribution of measuring LV before and after BD to detect acute improvement in lung function not demonstrated by FEV, and the influence of the response criteria selected on this contribution. We analyzed 98 spirometries and plethismographies performed pre and post BD in patients with airflow obstruction (FEV,/FVC < 70%). BD response was defined for FEV, and FVC as per ATS guidelines and for other LV as o>_10% of baseline (4>_5 and >_15% were also analyzed). FEV, identified as responders 32% of patients. Greater proportions were uncovered by slow vital capacity (51 %, p<0.001), inspiratory capacity (43%, p<0.05) and residual volume (54%, p<0.001). Slow spirometry identified 11% of responders additional to those detected by FEV, and FVC. Plethismography added 9% more. The magnitude of volume responses correlated with the degree of baseline yperinflation. Percentages of responders varied greatly using different thresholds (A>5 and >_15%). Mean change and proportions of responders for each LV varied significantly (p<0.05) whether change was expressed as percent of baseline or predicted values. A considerable proportion of patients with airflow obstruction shows acute response to bronchodilato rs identified by changes in lung volumes but not detected by an improvement in FEV, The selection of LV response criteria has important influence on the magnitude of this additional detectìon.

Assessment of bronchodilator response through changes in lung volumes in chronic airflow obstruction

Although FEV, improvement is routinely used to define bronchodilator (BD) response, it correlates poorly with clinical effects. Changes in lung volumes (LV) have shown better correlation with exercise tolerance and might be more sensitive to detect BD effects. We assessed the additional contribution of measuring LV before and after BD to detect acute improvement in lung function not demonstrated by FEV, and the influence of the response criteria selected on this contribution. We analyzed 98 spirometries and plethismographies performed pre and post BD in patients with airflow obstruction (FEV,/FVC < 70%). BD response was defined for FEV, and FVC as per ATS guidelines and for other LV as o>_10% of baseline (4>_5 and >_15% were also analyzed). FEV, identified as responders 32% of patients. Greater proportions were uncovered by slow vital capacity (51 %, p<0.001), inspiratory capacity (43%, p<0.05) and residual volume (54%, p<0.001). Slow spirometry identified 11% of responders additional to those detected by FEV, and FVC. Plethismography added 9% more. The magnitude of volume responses correlated with the degree of baseline yperinflation. Percentages of responders varied greatly using different thresholds (A>5 and >_15%). Mean change and proportions of responders for each LV varied significantly (p<0.05) whether change was expressed as percent of baseline or predicted values. A considerable proportion of patients with airflow obstruction shows acute response to bronchodilato rs identified by changes in lung volumes but not detected by an improvement in FEV, The selection of LV response criteria has important influence on the magnitude of this additional detectýon.(AU)

Assessment of bronchodilator response through changes in lung volumes in chronic airflow obstruction.

Although FEV1 improvement is routinely used to define bronchodilator (BD) response, it correlates poorly with clinical effects. Changes in lung volumes (LV) have shown better correlation with exercise tolerance and might be more sensitive to detect BD effects. We assessed the additional contribution of measuring LV before and after BD to detect acute improvement in lung function not demonstrated by FEV1, and the influence of the response criteria selected on this contribution. We analyzed 98 spirometries and plethismographies performed pre and post BD in patients with airflow obstruction (FEV1/FVC < 70

). BD response was defined for FEV1 and FVC as per ATS guidelines and for other LV as delta > or = 10

of baseline (delta > or = 5 and > or = 15

were also analyzed). FEV1 identified as responders 32

of patients. Greater proportions were uncovered by slow vital capacity (51

, p < 0.001), inspiratory capacity (43

, p < 0.05) and residual volume (54

, p < 0.001). Slow spirometry identified 11

of responders additional to those detected by FEV1 and FVC. Plethismography added 9

more. The magnitude of volume responses correlated with the degree of baseline hyperinflation. Percentages of responders varied greatly using different thresholds (delta > or = 5 and > or = 15

). Mean change and proportions of responders for each LV varied significantly (p < 0.05) whether change was expressed as percent of baseline or predicted values. A considerable proportion of patients with airflow obstruction shows acute response to bronchodilators identified by changes in lung volumes but not detected by an improvement in FEV1. The selection of LV response criteria has important influence on the magnitude of this additional detection.