Obstetric Anatomy & Physiology of Labor
Adapted from a lecture by Virginia Jackson CNM
Uterine Physiology & Labor
The uterus is an elegant, complex design, organized to work its specific function in the body. The uterine wall is composed of 3 layers:
internal - myometrium (2 muscle layers) - endometrium - next inner layer
external - epithelial (skin)
The 2 muscle layers of the myometrium are fibers going in different directions and forming a protective web.
The INNER layer is circular and is perpendicular to the long axis. Spirals UP around the body of the uterus.
The OUTER layer runs parallel to the longitudinal axis.
Most of the muscle cells in the (skeletal) body are striated muscle cells.
The uterus and heart are smooth muscle cells. They are arranged in bundles of 10-15 cells in a matrix of connective tissue and collagen - NOT piled upon each other, but rather are in a wash of elastic-type tissue. This matrix transmits the forces of the contractions.
The myometrial cell contains myocin & actin. The myocin heads must attach to the actin, which is spiraled. Once attached, as the actin spirals, it pulls the myocin. Then releases, relaxes, until the next contraction.
Each myometrial cell makes a change (during labor) - EACH CELL contracts & becomes progressively tenser & shorter. The shape of the uterus eventually changes, bunching up on top.
If the uterus stayed a spherical object, the pressures of contractions would be distributed evenly; instead the fundus elongates > ovoid shape > heavier pressure to midpoint; the lower segment actually has very little pressure. The cervix itself is not conducting any contractions, it is reacting to them. The fundus (top segment of the uterus) has the heavier distribution of myometrium & smooth muscle cells, vs. the cervix, which is more connective tissue and collagen.
A normal contraction spreads downward within 15 seconds from the fundus to the cervix - she feels it AFTER the initiation. The actual contraction lasts longer than her subjective experience of it (or palpation or TOCO), and the interval space is shorter (which is why 2 min. apart contractions are hyperstimulation). Contractions exert slow pull, without rebound - they do not return to full resting tonus. The myometrial cells STAY FORESHORTENED in teeny increments. They never go back, they get shorter & shorter.
What causes Labor?
Connective tissue and collagen are easily influenced by hormones
Chemicals ATP & ADP increase at term & are causative to contractions.
The cervix is 85-90% connective tissue covered by a thin layer of smooth muscle. Collagen fibers keep the cervix firm; they decrease at the end of pregnancy, known as softening. Myometrial contractions (labor) have little effect on cervical ripening. Ripening takes place BEFORE contractions occur. Most women will begin labor with a ripe cervix due to hormonal changes - estradial, relaxin, prostaglandins, etc. No one really knows what starts/causes labor. Just theories, measurements.
We don’t know what makes labor start but for labor to occur we need the myocin and actin within the myometrial cells to start up, pull, slide over, shorten the cell, then relax it, never going back to its exact original size. Picture little heads attaching to a spiraling receptor site. Thousands of these produce an increase in bulk- like a bunching-up zipper.
In labor, we also need an increase in “gap junctions” - a nerve-conducted impulse. When the walls of 2 cells touch each other, the result is depolarization. The positive ions (sodium, calcium, potassium) are shoved inside & push the negative out. There must be positive & negative ions in the myometrial tissue at term (pre-term pregnancy has premature gap junctions).
Hormonal influences on initiation of labor must also be in place. The fetus, the membrane and the placenta all participate in producing hormones. Progesterone, which suppresses uterine responses in pregnancy, drops during labor. Even the fetal membranes hold less progesterone during labor. Of 16 prostaglandins (we don’t know all their functions), one of them increases calcium binding. Estrogen, which increases oxytocin receptors, rises at 34-35 weeks to a peak that remains though labor and aids in making gap junctions. The increase in estrogen also increases oxytocin receptors.
All these systems need to interplay for it to work.
Uterine Physiology & Second Stage
Once the uterus is drawn up & the cervix is gone, pressure is directly on the sacrum. Uterus is higher & denser at the fundus, pressure comes straight DOWN, not funneling to sides. A uterus can have enough force to deliver a baby. In second stage, the uterus exerts the primary effort; Mom the secondary effort. At full dilation all the power is concentrated in the fundus. Each muscle cell is shorter, but thick & strong. The pressure of contractions is only going DOWN = expulsive contractions. The fundus has no more cervix to work on.
[ The uterus may have a pacemaker (like the heart), capable of creating rhythmic contractions. We don’t know where yet but speculation is logical because to coordinate the upper pull of the uterus w/the lower, you must have a pacemaker. ]