Flashcards in Antenatal testing Deck (28)
What percentage of total fetal cardiac output is distributed to the placental circulation?
What percentage of umbilical blood flow passes through the ductus venosus?
What percentage of patients will have category II FHR patterns?
Does the placenta have the ability to "autoregulate" blood flow?
No, the volume of blood of delivered to the intervillous space is dependent on adequate blood flow to the uterus.
How can blood flow to the placenta be increased or decreased?
Flow can be decreased by vasoconstriction due to uterine contractions, hypotension or hypertension, and sympathomimetic drugs. Flow can be increased not through vasodilation, but by providing maximal blood flow to the uterus (lateral decubitus position, tocolytics to decrease contractions).
How is the diffusion of oxygen and CO2 across the placenta facilitated?
By the differential between the higher O2 pressure in the maternal blood and the lower O2 pressure in the fetal capillaries (and vice versa for CO2).
What is the PO2 of blood in the umbilical vein?
Approximately 35 mmHg, the same as the maternal uterine veins.
How does the fetus survive with less PO2 relative to maternal values?
1. Fetal blood has more Hgb than adult blod, allowing it to extract maximal amounts of O2.2. Fetal Hgb has incr O2 affinity - binds to oxgyen more easil than adult Hgb, favoring transfer of O2 from maternal blood to fetal blood3. Fetal blood flow patterns allow for overperfusion of organs with higher O2 requirements (eg, brain)4. Fetus has increased cardiac output and heart rate5. Fetus has more capillaries per unit of tissue than adults do
What happens in the fetus when PO2 falls significantly?
1. Redistribution of blood to vital organs (heart, blood, adrenals)2. Fetal oxygen consumption declines - FHR decreases, myocardium uses less O2-If these 2 mechanisms are not sufficient for supplying O2 for metabolic needs, then anaerobic metabolism will result.
What is the difference between aerobic and anaerobic metabolism?
Both transform glucose into ATP. The aerobic cycle occurs in the presence of O2 and produces 38 ATP, water, and CO2 per one molecule of glucose. The anaerobic cycle produces 2 ATP molecules, water, and lactic acid per one molecule of glucose. Obviously, anaerobic metabolism is inefficient compared to aerobic.
Other than the inefficiency of anaerobic metabolism, what is the consequence?
Lactic acid lowers the pH, creates a metabolic acidosis. Lactic acid diffuses across the placenta more slowly than CO2 diffuses. Over time, ATP depletion and fetal accumulation of lactic acid leads to acidemia, which leads to acidosis and then cell death if O2 isn't restored.
What physiologic factors contribute to the FHR baseline and variability?
Sympathetic, parasympathetic, chemoreceptors, baroreceptors, and higher cortical functions in the brain.
How does the autonomic nervous system control the FHR?
The parasympathetic NS (PNS) influences the heart via the vagus nerve, which conducts impulses from the medulla oblongata to the SA node in the fetal atrium. Stimulation of the PNS slows the FHR by overriding the intrinsic rate generated within the SA node. The sympathetic NS has fibers that terminate throughout the muscle of the heart. Stimulation of these nerves -> increased HR and stroke volume. Some believe that the constant interplay between sympathetic and parasympathetic causes the timing of each successive heartbeat to vary. Others believe that small changes in the rate of firing of the vagus controls variability directly. During gestation, the PNS matures in the 2nd trimester and the vagus nerve gradually becomes dominant over sympathetic, which explains the slow drop in the normal baseline rate.
How do chemoreceptors modulate the FHR?
Chemoreceptors found in the aortic arch and CNS are sensitive to changes in O2 and CO2 in the blood. Increased CO2 -> chemoreceptors signal the medulla oblongata -> vagus nerve stim -> slows FHR gradually (late or prolonged decel)
How do baroreceptors modulate the FHR?
Baroreceptors are found in the aortic and carotid arches, where they detect changes in pressure. When BP rises, a vagal reflex slows the heart rapidly. For example, when the umb cord is compressed, flow within the umb vein slows/stops (more compressible than the umb art), this causes an upstream increase in fetal BP -> rapid drop in FHR (variable).
What are the causes of minimal FHR variability?
Fetal sleepMedicationsBeginning hypoxiaAlmost never caused by hypoxia if decels are absent (intrapartu)
What are the causes of absent FHR variability?
Can be related to hypoxia or not relatedOther causes:CNS depressantsAnencephalyDefective cardiac conduction systemCongenital neuro abnl
What are the causes of fetal tachycardia?
Maternal feverFetal infectionFetal cardiac tachyarrhythmiaCan be seen transiently when the fetus recovers from acute hypoxial stress (due to adrenal stimulation)Tachycardia signifying a fetal acidemia will usu be associated w/ absent variability & decels
What are the causes of fetal bradycardia?
Uncomplicated bradycardias of > 80 bpm with nl variability are not associated with fetal acidemia. Nonhypoxic causes:Complete heart blockBeta-blockersOccasionally, a fetus with an idiopathic baseline below 110 w/o pathologic indications
What is the pathophysiology of late FHR decelerations w/ retained variability?
Nonasphyxial or "reflex lates" w/ retained variability - neurogenic in origin. When a well-oxygenated fetus has an acute reduction in oxygenation (eg, tetanic contraction), the reduced blood flow falls below the capacity to extract sufficient O2 in the intervillous space. Chemoreceptors detect the hypoxemia and initiate the vagal bradycardic response. The bradycardia is "late" because the chemoreceptor has to first detect the hypoxemia. Bc the fetus is centrally well-oxygenated, variability is retained.
What is the pathophysiology of late FHR decelerations with decreased or absent variability?
Asphyxial lates occur when there is insufficient oxygen for myocardial metabolism or normal cerebral function. Likely to occur in chronic placental insufficency.
What is the pathophysiology of variable FHR decelerations?
During the 2nd stage or rapid descent in the 1st stage, variables can be the FHR response to vagal stimulation induced by sudden increases in pressure on the fetal cranium. Cord compression causes an increase in BP -> increased BP -> stimulation of baroreceptors in the aortic arch -> quick bradycardial response. Variable decels are associated with transient hypoxia, and will, if repetitive, lead to acidemia.
What is a sinusoidal FHR pattern?
Regular, smooth sine wave-like baseline, w/ a frequency of approx 3-6 per minute and amplitude range of up to 30 bpm. Waves are extremely regular and smooth, and there is absent beat-to-beat or short-term variability. Noted in anemic and severely asphyxiated infants. Pseudosinusoidal variants of long-term variability are sometimes seen after maternal narcotic administration.
What is the lower limit of nl for umbilical artery blood pH?
7.1, using 2 SDs below average
What is base excess and what is the mean?
Base excess calculates the metabolic contribution to the acidemia by correcting for the elevated bicarb due to the presence of high CO2. Most of the base excess seen in fetal hypoxemia is lactic acid. The mean is -4 milliequivalents/L, the 2.5th percentile is -11 milliequivalents/L.
4 criteria to associate "overshoots" with acidemia
These are ominous, and rareFollows, but does not preceed, the decelAccel takes a long time to return to baselineAssociated with "blunted" variable decels
Fetal pH is normally how much lower than maternal?