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Summary Table

Feature	Detail
Risk Factors	Placental insufficiency (preeclampsia, IUGR, post-term pregnancy), maternal diabetes, oligohydramnios, cord abnormalities (prolapse, nuchal cord, true knot), chorioamnionitis, uterine tachysystole from oxytocin, maternal hypotension (epidural, supine position)
Etiology	Inadequate fetal oxygenation leading to hypoxemia, hypoxia, and eventually metabolic acidosis; the fetus compensates through redistribution of blood flow to vital organs (brain, heart, adrenals) at the expense of peripheral and splanchnic circulation
Patient Presentation	Abnormal fetal heart rate pattern on cardiotocography; decreased fetal movement reported by the mother; meconium-stained amniotic fluid upon rupture of membranes
Classic Physical Exam	Non-reassuring CTG tracing (recurrent late decelerations, absent variability, prolonged deceleration, bradycardia); thick meconium in amniotic fluid; biophysical profile score of 4 or less
Key Diagnostic Results	Category III CTG tracing; fetal scalp blood pH below 7.20; umbilical artery pH below 7.10 with base deficit greater than 12 mmol/L; lactate above 4.8 mmol/L on scalp sampling
Management	Intrauterine resuscitation first (left lateral positioning, IV fluid bolus, stop oxytocin, tocolysis if tachysystole); if non-reassuring pattern persists, expedited delivery via emergency cesarean section or operative vaginal delivery if fully dilated
Keywords	"Late decelerations," "absent variability," "minimal variability with recurrent decelerations," "sinusoidal pattern," "scalp pH below 7.20," "Category III tracing," "non-reassuring fetal status"

1. Pathophysiology

Fetal distress, more precisely termed non-reassuring fetal status, represents a spectrum of fetal compromise driven by inadequate oxygen delivery. The core mechanism begins with interruption of the oxygen transfer pathway at any point: maternal lungs, maternal circulation, uterine blood flow, placental exchange surface, umbilical cord, or fetal circulation itself.

During a uterine contraction, spiral artery blood flow to the intervillous space is temporarily reduced. A healthy fetus with adequate placental reserve tolerates this intermittent reduction without difficulty. However, when placental reserve is diminished (as in preeclampsia, IUGR, or post-term pregnancy), the fetus cannot maintain adequate oxygenation through repeated contractions. This is why late decelerations reflect uteroplacental insufficiency: the fetal heart rate drop occurs after the contraction peak because the hypoxic insult accumulates over the duration of reduced perfusion and takes additional time to recover.

The fetal response to hypoxemia follows a predictable sequence. The initial compensatory phase involves chemoreceptor-mediated vagal stimulation, which produces decelerations. Simultaneously, catecholamine release causes peripheral vasoconstriction, redistributing blood toward the brain and myocardium. This is the so-called brain-sparing effect and correlates with centralization of Doppler flow. If hypoxia persists, the fetus shifts from aerobic to anaerobic metabolism, generating lactic acid and producing metabolic acidosis. This acidosis depresses myocardial function, reduces heart rate variability, and eventually causes direct myocardial injury.

Fetal heart rate variability is the single most important indicator of fetal neurological integrity. It is generated by the interplay between the sympathetic and parasympathetic nervous systems acting on the sinoatrial node. Moderate variability (6 to 25 bpm amplitude) indicates an intact autonomic nervous system with adequate cerebral oxygenation. When variability becomes absent or minimal, it suggests either fetal acidemia, deep sleep cycle, or drug effect (opioids, magnesium sulfate, betamethasone). The clinical task on the exam is distinguishing benign causes of reduced variability from true fetal compromise.

The sinusoidal pattern deserves special attention. This smooth, undulating, sine-wave-like pattern with an amplitude of 5 to 15 bpm and a frequency of 2 to 5 cycles per minute indicates severe fetal anemia, most often from Rh isoimmunization, fetomaternal hemorrhage, or twin-to-twin transfusion syndrome. It is always pathological when persistent and represents a true emergency.

2. Classification and Clinical Manifestation

Three-Tier Classification System

Category	Baseline Rate	Variability	Decelerations	Accelerations	Interpretation
Category I (Normal)	110 to 160 bpm	Moderate (6 to 25 bpm)	No late or variable decelerations; early decelerations may be present	Present (reactive)	Normal acid-base status; routine care
Category II (Indeterminate)	Bradycardia (not accompanied by absent variability); tachycardia	Minimal variability; absent variability without recurrent decelerations; marked variability	Recurrent variable decelerations with minimal or moderate variability; prolonged deceleration (2 to 10 min); recurrent late decelerations with moderate variability	Absence of accelerations after stimulation	Requires evaluation, continued surveillance, and intrauterine resuscitation; most tracings in labor fall here
Category III (Abnormal)	Bradycardia	Absent variability	Recurrent late decelerations with absent variability; recurrent variable decelerations with absent variability	Absent	Abnormal acid-base status; requires immediate intervention and preparation for delivery

Deceleration Types and Their Mechanisms

Deceleration Type	Onset Relative to Contraction	Mechanism	Clinical Significance
Early	Mirrors the contraction (onset, nadir, and recovery coincide)	Head compression causing vagal stimulation	Benign; no intervention needed
Late	Onset after contraction peak; nadir occurs after contraction ends	Uteroplacental insufficiency leading to fetal hypoxemia and chemoreceptor activation	Pathological when recurrent; indicates inadequate placental oxygen transfer
Variable	Variable timing relative to contraction; abrupt onset (onset to nadir under 30 seconds)	Umbilical cord compression causing baroreceptor-mediated vagal response	Common in labor; concerning when recurrent, especially with absent variability or slow return to baseline
Prolonged	Single deceleration lasting 2 to 10 minutes	Cord prolapse, uterine rupture, maternal hypotension, tachysystole, or rapid cervical change	Requires immediate evaluation; if lasting beyond 10 minutes, reclassified as bradycardia

Reassuring vs. Non-Reassuring Features

Feature	Reassuring	Non-Reassuring
Baseline rate	110 to 160 bpm	Below 110 or above 160 bpm
Variability	Moderate (6 to 25 bpm)	Absent (undetectable) or minimal (under 5 bpm)
Decelerations	None or early only	Recurrent late or variable; prolonged
Accelerations	Present and reactive	Absent despite vibroacoustic stimulation
Pattern	Cycling between active and quiet states	Persistent non-reassuring features for over 30 minutes

3. Diagnostic Workup

Test	Role	Key Finding
Cardiotocography (CTG) / Electronic Fetal Monitoring	Best initial test; continuous intrapartum monitoring	Category III tracing (absent variability with recurrent late/variable decelerations or bradycardia or sinusoidal pattern)
Fetal scalp stimulation	Bedside adjunct to CTG during labor	Acceleration in response to stimulation indicates pH above 7.20 (reassuring); absence of acceleration warrants further evaluation
Vibroacoustic stimulation	Alternative to scalp stimulation	Same interpretation as scalp stimulation; elicits acceleration in a non-acidotic fetus
Fetal scalp blood sampling	Confirmatory when available	pH below 7.20 indicates acidosis; lactate above 4.8 mmol/L is abnormal
Umbilical cord blood gas (arterial)	Post-delivery confirmation of fetal acid-base status	pH below 7.10 with base deficit above 12 mmol/L confirms significant metabolic acidosis
Biophysical Profile (BPP)	Antepartum assessment of fetal well-being	Score of 4 or less out of 10 is abnormal; absent breathing, absent tone, absent movement, and oligohydramnios indicate chronic compromise
Doppler velocimetry (umbilical artery)	Antepartum surveillance in IUGR / high-risk pregnancies	Absent or reversed end-diastolic flow indicates severe placental insufficiency

Cardiotocography is the best initial test and the foundation of intrapartum fetal assessment. It continuously records fetal heart rate using an external ultrasound transducer (Doppler) or an internal fetal scalp electrode, alongside uterine contractions via a tocodynamometer or intrauterine pressure catheter. The external approach is non-invasive and used for initial assessment. The fetal scalp electrode provides a more accurate heart rate signal and is indicated when external tracing quality is poor, though it requires ruptured membranes and adequate cervical dilation.

When a CTG tracing is indeterminate (Category II), the next best step is intrauterine resuscitation combined with further assessment. Fetal scalp stimulation is a practical bedside test: during a vaginal exam, the examiner gently stimulates the fetal scalp. If the fetus responds with a heart rate acceleration (rise of 15 bpm lasting 15 seconds), it reliably predicts a scalp pH above 7.20 and rules out significant acidemia at that moment. This test avoids the need for the more invasive scalp blood sampling.

Fetal scalp blood sampling, where available, provides direct measurement of fetal pH or lactate. A pH of 7.25 or above is normal, 7.20 to 7.25 is borderline (repeat in 30 minutes), and below 7.20 is abnormal and warrants expedited delivery. Many institutions have moved away from routine scalp blood sampling due to practical limitations, relying instead on CTG pattern recognition combined with scalp stimulation.

In the antepartum setting, the Non-Stress Test (NST) is the screening tool of choice. A reactive NST shows two or more accelerations of 15 bpm above baseline lasting 15 seconds within a 20-minute window. A non-reactive NST prompts further evaluation with a Biophysical Profile or contraction stress test. The BPP evaluates five parameters (fetal breathing, gross body movement, tone, amniotic fluid volume, and NST reactivity), each scored 0 or 2. A score of 8 to 10 is reassuring; 6 is equivocal; 4 or below is abnormal and typically warrants delivery depending on gestational age.

Umbilical artery Doppler is used in high-risk antepartum surveillance, particularly in IUGR. Progressive worsening follows a pattern: increased systolic-to-diastolic ratio, then absent end-diastolic flow, then reversed end-diastolic flow. Reversed end-diastolic flow carries a high risk of fetal demise and generally prompts delivery after steroid administration if the fetus is at a viable gestational age.

4. Management and Treatment

Clinical Scenario	Intervention	Details
Category I tracing	Continue routine monitoring	Intermittent auscultation acceptable in low-risk labor; continuous CTG for high-risk
Category II tracing	Intrauterine resuscitation and continued surveillance	Left lateral positioning, IV fluid bolus (500 mL to 1 L crystalloid), discontinue oxytocin, oxygen by face mask (debated but still practiced), amnioinfusion if recurrent variable decelerations
Category III tracing	Immediate intrauterine resuscitation and prepare for delivery	All resuscitative measures simultaneously; if no improvement within minutes, emergency cesarean section
Uterine tachysystole with non-reassuring FHR	Stop oxytocin; administer tocolytic	Terbutaline 0.25 mg subcutaneously (single dose) to relax the uterus
Cord prolapse	Elevate presenting part and emergency cesarean	Examiner's hand in the vagina lifting the presenting part off the cord; fill the bladder with 500 to 700 mL saline via Foley catheter; knee-chest or Trendelenburg position
Meconium-stained amniotic fluid	Monitor closely; prepare neonatal team	Amnioinfusion may reduce variable decelerations; no longer routine suctioning of vigorous neonates at delivery
Post-delivery: depressed neonate	Neonatal resuscitation per protocol	Delayed cord clamping only if vigorous; immediate clamping and resuscitation if depressed; intubation and tracheal suctioning only if non-vigorous with airway obstruction

Intrauterine resuscitation is the cornerstone of managing any non-reassuring fetal heart rate pattern and should always be attempted before proceeding to operative delivery. The steps target each potential cause of reduced fetal oxygenation:

Left lateral decubitus positioning relieves aortocaval compression by the gravid uterus, improving venous return and cardiac output, which increases uterine perfusion. If no improvement, try the right lateral or hands-and-knees position.

Intravenous fluid bolus (500 mL to 1000 mL of lactated Ringer's or normal saline) corrects maternal hypovolemia or hypotension, particularly common after epidural placement. This is one of the most effective interventions for late decelerations caused by maternal hypotension.

Discontinuation of oxytocin is mandatory whenever tachysystole (more than 5 contractions in 10 minutes averaged over 30 minutes) accompanies non-reassuring fetal heart rate changes. Oxytocin has a short half-life (3 to 5 minutes), so uterine activity should decrease promptly after cessation. If tachysystole persists despite stopping oxytocin, terbutaline 0.25 mg subcutaneously provides acute uterine relaxation.

Amnioinfusion (transcervical infusion of normal saline into the uterine cavity, typically a 500 mL bolus followed by continuous infusion at 150 to 200 mL per hour) is indicated for recurrent variable decelerations attributed to oligohydramnios or cord compression. It cushions the umbilical cord and has been shown to reduce the rate of cesarean delivery for non-reassuring fetal heart rate in this context. It is not indicated for late decelerations.

Maternal supplemental oxygen via non-rebreather face mask at 10 L/min has been traditionally administered. Current evidence is equivocal regarding its benefit, and prolonged maternal hyperoxia may theoretically produce fetal oxidative stress. Many guidelines still include it as a component of intrauterine resuscitation but with less emphasis than before.

When a Category III tracing does not improve with intrauterine resuscitation within a short timeframe (typically a few minutes), the next step is emergent delivery. If the cervix is fully dilated and the station is favorable, operative vaginal delivery (vacuum or forceps) is appropriate. Otherwise, emergency cesarean section is performed. The decision-to-delivery interval should ideally be 30 minutes or less, though this is a benchmark rather than an absolute requirement.

For cord prolapse, the management is distinct and urgent. The examiner must immediately place a hand in the vagina to elevate the presenting part off the compressed cord. The patient is placed in steep Trendelenburg or knee-chest position. Bladder filling with 500 to 700 mL of saline via a Foley catheter can provide additional upward displacement of the presenting part during transfer to the operating room. Delivery is by emergency cesarean section unless vaginal delivery is imminent.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Fetal sleep cycle	Can cause absent accelerations on NST and reduced variability on CTG for up to 40 minutes	Variability typically returns to moderate after 20 to 40 minutes; extend monitoring or use vibroacoustic stimulation to elicit accelerations; no decelerations present
Maternal opioid or magnesium sulfate administration	Causes reduced fetal heart rate variability, mimicking fetal compromise	History of recent drug administration; variability improves as drug effect wears off; no pathological decelerations
Fetal tachycardia from chorioamnionitis	Baseline above 160 bpm may raise concern for fetal distress	Maternal fever, uterine tenderness, foul-smelling amniotic fluid, maternal and fetal tachycardia; variability may still be moderate; treat the infection (antibiotics) rather than immediate cesarean unless other non-reassuring features coexist
Early decelerations (head compression)	Decelerations visible on CTG may alarm test-takers	Mirror the contraction perfectly; uniform shape; associated with active labor and head descent; benign and require no intervention
Physiologic variable decelerations	Abrupt decelerations can appear alarming	Brief (under 60 seconds), with rapid return to baseline, moderate variability between decelerations, and preceded or followed by "shoulders" (small accelerations); no intervention required unless recurrent and progressively deeper
Uterine rupture	Can present with sudden prolonged deceleration and fetal bradycardia	History of prior cesarean scar; sudden onset of constant abdominal pain (distinct from contraction pain); loss of uterine contraction pattern on tocography; regression of the presenting part on vaginal exam; maternal hemodynamic instability
Placental abruption	Non-reassuring fetal heart rate pattern with possible late decelerations	Painful vaginal bleeding (or concealed hemorrhage), uterine hypertonicity and tenderness, tetanic contractions, Couvelaire uterus; maternal coagulopathy in severe cases

6. Traps and High-Yield Pearls

The most common way students lose points on CTG interpretation questions is by fixating on decelerations while ignoring variability. Variability is the single most predictive feature of fetal acid-base status. A tracing with recurrent variable decelerations but moderate variability is Category II and generally managed with observation and intrauterine resuscitation. The same decelerations with absent variability become Category III and demand immediate action. Test-writers exploit this distinction heavily.

Another frequent trap is confusing early and late decelerations. Both are gradual in onset (onset to nadir of 30 seconds or more), but their timing relative to the contraction peak is what distinguishes them. Early decelerations mirror the contraction; late decelerations are offset, with the nadir occurring after the contraction peak. If a question describes "gradual decelerations that persist after the contraction has ended," the answer is late decelerations, not early.

Students also mismanage the non-reactive NST. A non-reactive NST does not automatically mean the fetus is in distress. The next step is to extend monitoring to 40 minutes (to account for fetal sleep) or perform vibroacoustic stimulation. If still non-reactive, proceed to a biophysical profile or contraction stress test. Jumping straight to emergency cesarean from a non-reactive NST is a classic distractor.

The sinusoidal pattern is a pearl that appears occasionally but is always high-yield. It looks superficially like variability but is a smooth, regular, undulating wave without beat-to-beat variability. It indicates severe fetal anemia, and the question stem will usually include clues like Rh-negative mother without prophylaxis, recent trauma (Kleihauer-Betke test positive), or twin pregnancy.

Finally, remember that the presence of moderate variability, even in the setting of other concerning features, is the single most reassuring sign. A fetus with moderate variability is extremely unlikely to be currently acidotic. This principle underlies the entire three-tier classification system and is the core competency being tested: the ability to integrate multiple CTG features into a coherent clinical decision rather than reacting to any single abnormality in isolation.

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