Pernapasan Pada Kehamilan

7/30/2019 Pernapasan Pada Kehamilan

http://slidepdf.com/reader/full/pernapasan-pada-kehamilan 1/3

Pulmonary System

Anatomic Changes

Pregnancy alters the circulation of a number of tissues involved in respiration. For example,

capillary dilatation leads to engorgement of the nasopharynx, larynx, trachea, and bronchi.Prominent pulmonary vascular markings observed on x-ray are consistent with increased

pulmonary blood volume.

As the uterus enlarges, the diaphragm is elevated by as much as 4 cm. The rib cage is displaced

upward, increasing the angle of the ribs with the spine. These changes increase the lower thoracic diameter by about 2 cm and the thoracic circumference by up to 6 cm. Elevation of the

diaphragm does not impair its function. Abdominal muscles have less tone and activity during

pregnancy, causing respiration to be more diaphragm dependent.

Lung Volumes and Capacities

Several lung volumes and capacities are altered by pregnancy (Table 7–1). Dead space volume

increases because of relaxation of the musculature of conducting airways. Tidal volume and

inspiratory capacity increase. Elevation of the diaphragm is associated with reduction in total

lung capacity and functional residual capacity. The latter involves a decrease in both expiratoryreserve and residual volumes.

Table 7–1. Effects of Pregnancy on Lung Volumes and Capacities.

Definition Change

I. Volumes

Tidal Volume inspired and expired with each normal respiratory

cycle 35–

50%

Inspiratory

reserve

Maximum volume that can be inspired over normal end-tidal

inspiration

Expiratoryreserve

Maximum volume that can be expired from resting end-tidalexpiration 20%

Residual Volume remaining in the lungs following maximum expiration20%

II. Capacities

Total lung Total volume at the end of maximum inspiration5%

Vital Maximum volume expired after maximum inspiration

Inspiratory Maximum volume inspired from end-tidal expiration5–10%



Definition Change

Functional Volume at end-tidal expiration that mixes with tidal air upon

inspiration 20%

Respiration

Pregnancy has little affect on respiratory rate. Thus, the increase in minute ventilation

(approximately 50%) results from the rise in tidal volume. This increment in minute ventilationis disproportionately greater than the rise (approximately 20%) in total oxygen consumption in

maternal muscle tissues (cardiac, respiratory, uterine, skeletal) and in the products of the fetal

genome (placenta, fetus), as shown in Figure 7–4. This hyperventilation, which decreases

maternal arterial PcO2 to about 27–32 mm Hg, results in a mild respiratory alkalosis (blood pH of 7.4–7.5). The hyperventilation and hyperdynamic circulation slightly increase arterial PO2.

Increased levels of progesterone appear to have a critical role in the hyperventilation of

pregnancy, which develops early in the first trimester. As in the luteal phase of the menstrualcycle of nonpregnant women, the increased ventilation appears to be caused by the action of progesterone on central neurons involved in respiratory regulation. The overall respiratory effect

appears to be a decrease in the threshold and an increase in the sensitivity of central chemoreflex

responses to CO2. Maternal hyperventilation may be protective in that that it prevents the fetusfrom being exposed to high CO2 tensions, which might adversely affect the development of

respiratory control and other critical regulatory mechanisms.

Functional measurement of ventilation can also change according to posture and duration of

pregnancy. For example, the peak expiratory rate, which declines throughout gestation in thesitting and standing positions, is particularly compromised in the supine position.

Sumber: Current Diagnosis And Treatments in Obstetric and Gynecologic



Documents

Pernapasan Pada Kehamilan