Why is CTG important?

• Alpha and omega of the assessment of fetal condition
• Learn = understand
• Understand: what is happening to the fetus, the mother, why it is happening, if it is okay and what we can do about it

A matter of life and death/health

Cardiotocography


Method of fetal monitoring:

• Fetal heart rate recording (cardiotachogram) 
• Recording of uterine contractions (tocogram)
• Recording of fetal movements

Principle: 

• hypoxic changes affect fetal haemodynamics, and changes in uteroplacental circulation are manifested by a change in the frequency of fetal echoes

Technical aspects of CTG

• The device works on the principle of ultrasound (external probe)
• The internal probe directly senses electrical potentials (like an ECG)
• Pay attention to the speed of paper movement (in the Czech Republic, the standard is 1 cm/min)

Fetal adaptation to hypoxia

• Intrauterine environment = permanent relative hypoxia
  •  -> the fetus is ready

Regulation of FHR

• The heart is a semi-autonomous organ
• Affected by sympathetic (increases FHR) and parasympathetic (decreases FHR)

BF (basal frequency) – gradually decreases with the length of pregnancy (sympathetic matures earlier, parasympathetic later)

Variability – see above, around term balanced action – „struggle for power“ – constant  regulation – BF amplitude

Cardiotocography

• Antepartum (FIGO 1986) – „stricter“
• Intrapartum (FIGO 2015)

Tocography

• Record of uterine contractions (tocogram)
• Measured mostly by an external sensor (rarely internal – rather experimental)
• The absolute pressure values are indicative only.
• The length, intensity and frequency of uterine contractions can be estimated on the tocogram. 
• It is important for the evaluation of medium-term phenomena in the cardiotachogram.

  

Tachysystole

• Excessive uterine activity

>5 contractions per 10 minutes for at least 30 minutes or in two consecutive periods lasting 10 minutes 

Hypertonus

• Uterine contractions lasting more than 2 min (normally 45-120s)
• Increase in the basal tone of the uterus
• Contractions are necessary for the progress of labour, but perfusion in the placenta occurs/can occur during them

Excessive uterine activity can lead to 
 intrauterine fetal distress

Causes:

• Induction (prostaglandins)
• Oxytocin
• CAVE:  placentalabruption, uterinerupture

Therapy: EDA, tocolysis, give birth (in case of  abruption/rupture) -> C-section

Cardiotachogram

• Key component of CTG recording
• Fetal heart rate assessment
• hypoxic changes affect fetal haemodynamics, and changes in the uteroplacental circulation are manifested by a change in the frequency of fetal echoes

Evaluationoftherecordfromthe point ofview:

• Long-term phenomena
• Medium-term phenomena
• Short-term phenomena

Long-term phenomena – basal frequency

• stable heart rate during a period of 10 minutes, from which medium- and short-term phenomena deviate.
• Normal BF (normocardia) - 110–160/min (antepartum 110-150/min)
• Tachycardia -  >160/min  (preterm fetuses +- 160/min)
• Bradycardia -  <110/min (post-term fetuses physiol. 100-110/min)

  

Short-term phenomena – variability

• deviations of the fetal heart action from the basal rate of less than 15 sec
• Normal variability – 5-25/min
• Increased variability - >25/min for more than 30 minutes
• Reduced variability - < 5/min for more than 50 minutes

Reduced variability < 5/min 
 for more than 50 minutes

• Physiologically: low gestational age, drug suppression (EDA, opiates, psychotropic drugs…) 
  • sleep! (cycles are no longer than 50 minutes)
• Pathologically: brain (hypothalamus) perfusion disorder

Medium-term phenomena 

• deviations of the fetal heart action from the basal rate of less than 15 sec
• Acceleration - transient increase of frequency from basal frequency by 15/min lasting more than 15 sec
• Deceleration - transient decrease in frequency from basal frequency by 15/min lasting longer than 15 sec

In termsofevaluation, the most complicatedaspectof CTG!


Accelerations

• transient increase of frequency from basal frequency by 15/min lasting more than 15 sec
• for preterm fetuses at least by 10/min each 10 sec
• Sign of neuro- a cardio-compensated fetus
• Their absence does not have to be pathological (with intrapartum recording)

  

Decelerations

• Transient decrease in frequency from basal frequency by 15/min lasting longer than 15 sec
• Sign of fetal neuro- a cardio-reaction to a particular insult
• Their presence does not have to be pathological (with intrapartum recording)
• There are several types

  

Early decelerations

• Short-term, mostly shallow, mostly with normal variability
• Coinciding with contractions
• Caused by compression of the head (baroreceptors on the dura mater  -> parasympathetic –> slowing of the heart rate)
• They do not indicate fetal acidosis/hypoxia

  

Decelerations variable

• Short-term rapid decline and rapid return, variability preserved, different shape and size
• Caused by compression of the umbilical cord and subsequent response of baroreceptors in the arch of the aorta (parasympathetic)
• THE MOST COMMON TYPE of decelerations!!!
• Variable dependence on contractions
• Typically “shouldering“
• In most cases, they do not lead to fetal acidosis/hypoxia

  

Late decelerations

• gradual decline and return (at least 30 sec),  variability mostly reduced, different shape and size 
• They start more than 20 sec after the start of the contraction
• Caused by a disorder of the uteroplacental circulation -> insufficient oxygenation of the blood occurs -> chemoreceptors in the aorta and carotids -> decrease of frequency -> return only after the receptor is “washed“ with oxygenated blood
• The most serious, but not necessarily pathological! (depends on frequency/variability/depth)

  

Prolonged decelerations 

• Decelerations lasting more than 5 minutes with FHR less than 80/min
• Often associated with acute fetal hypoxia -> require a solution!!!

  

Sinusoid

• Regular smooth wavy signal resembling a sinusoid
• Amplitude 5-15/min
• 3-5 cycles per minute
• Recording lasting more than 30 min (up to 30 min pseudo-sinusoid)

Cause: fetomaternal haemorrhage, anemia…

Pathologicalrecord!!!

Decelerations

• Fetal response (physiological, not pathological) to hypoxic insult
• Cannot increase 02 supply, so has to economize – slowing of FHR
• Cannot remove metabolites, so has to produce less of them – slowing of FHR
• If the decelerations are short (below 60 sec) and with preserved variability (good hypothalamic function), then the fetus is not at risk

Absence of movements/accelerations

• The fetus saves O2, minimizes energy requirements
• So does not move
• Therefore, there are no accelerations
• The physiological reaction of the compensated fetus, does not matter in itself

Loss of variability – CAVE!

• Especially if variability disappears in connection with the above-mentioned phenomena (disappearance of movements/accelerations, decelerations, elevation of FHR)
• -> decompensation!!!
• Brain perfusionmismatch, fetus isat risk
• Interventionneeded

CTG assessment

1. Basal frequency
2. Accelerations
3. Decelerations
4. Variability
5. Physiol. / Susp. / Pathol.

Normal CTG - antepartum

• normal B-FHR (110-150)
• No decelerations
• At least 2 accelerations present (in 20-30 min)
• Normal variability (10-25/min)

⮚neuro- and cardio-compensated fetus without risk of acidosis/hypoxia 

  Normal CTG - intrapartum

• normal B-FHR (110-160) corresponding to grav.hebd. (pregnancy week)
• no severe deceleration (>60 sec), pause between decelerations at least 60 sec
• periods of reduced and increased variability (and accelerations + movements) –> cycling

⮚neuro- and cardio-compensated fetus without risk of acidosis/hypoxia