Abnormal Cardiotocography – “CTG”

• commonly known as an electronic fetal monitor or external fetal monitor (EFM) or non-stress test (NST)

• measures simultaneously both the fetal heart rate and the uterine contractions,

• two separate disc-shaped transducers laid against the woman's abdomen.

- ultrasound transducer measures the fetal heartbeat.

- pressure-sensitive transducer (tocodynamometer (toco) - measures the strength and frequency of uterine contractions

A Normal Antenatal CTG

Features of a CTG

• Baseline• Short term variability• Accelerations• Decelerations• Response to stimuli

• Contractions• Fetal movements• Other

Baseline Fetal Heart Rate• Mean level of fetal heart rate when stable

excluding acceleration and deceleration• 110 to 150 bpm at term• Faster in early pregnancy• Below 100 = baseline bradycardia• Below 80 = severe bradycardia• Tachycardia common with maternal fever• Tachycardia with reduced STV = early

hypoxia• Look for a rising baseline

Accelerations

• Must be >15 bpm and >15 sec above baseline• Should be >2 per 15 min period• Always reassuring when present• May not occur when fetus is “sleeping”• Should occur in response to fetal movements or fetal

stimulation• Non reactive periods usually do not exceed 45 min

• (>90 min and no accelerations is worrying)

Short Term Variability(or Beat to Beat Variability with a Scalp Clip)

• Should be >5 bpm• The most important feature of any CTG• Is a reflection of competing acceleratory and

decelerating CNS influences on the fetal heart• And therefore represents the best measure of CNS

oxygenation• Will be affected by drugs• Will be reduced in the pre term fetus

Decelerations

• Early: mirrors the contraction• Typically occurs as the head enters the pelvis and is

compressed, i.e. it is a vagal response

• Late: Follows every contraction and exhibits a slow return to baseline

• Is quite rare but is the response of a hypoxic myocardium

• Variable: Show no relationship to contractions• Mild • Moderate• Severe

• In practice many “decels” or “dips” are MIXED

An Abnormal Antenatal CTG

An Abnormal Antenatal CTG cont’d

Abnormal CTG Features

• Reduced STV• No accelerations• Decelerations after

most contractions with a slow return to baseline

In Practice a CTG is best regarded as a screening tool:

• High negative predictive value• >98% of fetuses with a normal CTG will be OK

• Poor positive predictive value• 50% of fetuses with an abnormal CTG will be hypoxic

and acidotic but 50% will be OK

• Therefore the CTG should always be interpreted in its clinical context

• And backed by fetal blood sampling PRN

The RCOG Classification of CTGs

• Normal = all 4 features are reassuring

• Suspicious = One non reassuring feature

• Pathological = Two or more non reassuring features or a abnormal pattern

Accelerations: absent for >40 minutes-first to become apparent, and any of the following

Baseline heart rate bradycardia<110 bpm Tacycardia>150 bpm

Baseline variability:<10 bpm lasting for> 40 min, greater significant if < 5 bpm

Decelerations: variable decelerations without ominous features

Suspicious CTG trace

Accelerations: absent for>40 min and any of the following

Baseline heart rate: abnormal

Baseline variability:less than 5 bpm lasting for >90 min

Deceleration Repetitive late decelerations Variable deceleration with ominous features( duration

>60s; beat loss>60 bpm;late recovery; late deceleration component;poor baseline variability btwn and/or during deceleration

Abnormal CTG tracing

• normal FHR at term 110 – 160 bpm• average fetal heart rate is considered to be

the result of tonic balance between accelerator ( sympathetic ) and decelerator (parasympathetic) influences on pacemaker cells mediated via vagal slowing of heart rate

• Heart rate also is under the control of arterial chemoreceptors such that both hypoxia and hypercapnia can modulate rate.

Baseline fetal heart rate

• Fetal tachycardia – baseline >160 bpm over 10 minutes or more- can be nonpathologic, considered a normal rate in the premature fetus

• Causes : - maternal :

- chorioamnitis- other causes of infection causing fever- use of B-sympathomimetics

- fetal - cardiac arrhythmias- fetal anemia- acute fetal blood loss- abnormal fetal conduction system

Alteration of FHR

FIGURE 4. Fetal tachycardia that is due to fetal tachyarrhythmia associated with congenital anomalies, in this case, ventricular septal defect. Fetal heart rate is 180 bpm. Notice the "spike" pattern of the fetal heart rate.

• Fetal bradycardia – baseline heart rate < 110bpm for greater than 10 minutes.

• Rate : 100 - 119 beats/min, in the absence of other changes, usually is not considered to represent fetal compromise.

• Such low but potentially normal baseline heart rates also have been attributed to vagal response to head compression from occiput posterior or transverse positions, particularly during second-stage labor (Young and Weinstein, 1976).

Alteration n fetal heart rate

• Adverse effect on fetal circulation → severe acute bradycardia- acute hypoxemia→ chemoreceptor reflex→ bradycardia- cord occlusion → fetal hypertension → baroreceptor reflex → vagal response → bradycardia

Causes of fetal bradycardia

• Defined as fluctuations in the FHR baseline of 2 cycles/min or greater with irregular amplitude and inconstant frequency.

• The time interval between 2 heartbeats in a healthy fetus is seldom the same.

• Normal : 5 – 15 bpm• This variability is secondary to the interaction

of the sympathetic and parasympathetic reflexes

Beat to beat variability

• Causes of loss of variability :- fetal sleep - administration of drugs

- narcotics, barbiturates, phenothiazines- MgSO4

- gestational age (28-30wks)- metabolic acidemia

• Upward deflection in the baseline fetal heart rate of at least 15 bpm lasting for at least 15 seconds.

• In pregnancies of fewer than 32 weeks of gestation, accelerations are defined as having a peak 10 beats per minute or more above the baseline and duration of 10 seconds or longer.

Accelerations

• Reductions in fetal heart rate of at least 15bpm lasting for at least 15 seconds

• 4 types :- Type 1 (early)- physiological- Type 2 (late)- pathological - variable- prolonged

Decelerations

• consists of a gradual decrease and return to baseline associated with a contraction.

• Result of a physiologic chain of events that begins with head compression during a uterine contraction

• the degree of deceleration is generally proportional to the contraction strength and rarely falls below 100 to 110 beats/min or 20 to 30 beats/min below baseline.

Early deceleration

• early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores

FIGURE 5. Early deceleration in a patient with an unremarkable course of labor. Notice that the onset and the return of the deceleration coincide with the start and the end of the contraction, giving the characteristic mirror image.

• smooth, gradual, symmetrical decrease in fetal heart rate beginning at or after the peak of the contraction and returning to baseline only after the contraction has ended.

• The magnitude of late decelerations is rarely more than 30 to 40 beats/min below baseline and typically not more than 10 to 20 beats/min.

• Late decelerations usually are not accompanied by accelerations.

Late deceleration (type 2)

• associated with uteroplacental insufficiency• Causes :

- placental dysfunction- placenta abruptio- maternal hypotension- uterine hyperactivity- maternal disease – DM, HPT, Collagen-

vascular diseaseRepetitive late decel increases risk of umbilical

artery acidisis and apgar score less than 7 at 5min

• Inconsistent time of onset when compared to uterine contraction

• The onset of deceleration commonly varies with successive contractions .

• The duration is less than 2 minutes.• represent fetal heart rate reflexes that reflect

either blood pressure changes due to interruption of umbilical flow or changes in oxygenation

Variable deceleration

• significant variable decelerations are those decreasing to less than 70 beats/min and lasting more than 60 seconds.

• Causes : - Umbilical cord entanglement- Eg:

- Umblilical around body or neck- True knot in the umbilical cord - Prolapsed umbilical cord

• isolated deceleration lasting 2 minutes or longer but less than 10 minutes from onset to return to baseline.

• Causes : 1)Total umbilical cord occlusion (cord prolapse)2)Maternal hypotension3)Uterine hypertonia4)VE or artificial ruptured of membrane

Prolonged deceleration

• regular, smooth, undulating form typical of a sine wave that occurs with a frequency of 2-5/minute and an amplitude range of 5-15 bpm

• also characterized by a stable baseline heart rate of 120 to 160 bpm and absent beat-to-beat variability

• Occurs in severe fetal anemia, as occurs in cases of Rh disease or severe hypoxia

Sinusoidal pattern

Sinusoidal Pattern

• Saltatory pattern : - rapidly recurring couplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate- sympathetic stimulation overrides parasympathetic dominance in response to acute but temporary hypoxemia ( umbilical cord compression )- almost exclusively seen during labour

FIGURE 2. Saltatory pattern with wide variability. The oscillations of the fetal heart rate above and below the baseline exceed 25 bpm.

Goal of intrapartum monitoring is to distinguis fetus who is hypoxemic but well compensated from one which is acidotic and at risk for neurological sequelae.1.Determine the likely cause of abnormality, if possible (abruptio, cord prolapse, maternal medication, rapid descent of fetal head)2.Attempt to correct problem or initiate general measures to improve fetaal oxygenation (supplemental oxygen, change in position, increase hydration, treatment of hypotension, discontinue any uterotonic)3.If FHR does not improve, perform ancillary test to determine fetal condition (vibroacustic stimulation, fetal scalp stimulation,fetal blood sampling)4.Determine wheher operative intervention is needed