Ranzcog FSEP Notes on CTG PDF

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Summary

Notes written based on the RANZCOG FSEP CTG Webinar. Useful notes and tips on reading and understanding CTG....

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RANZCOG FSEP – FETAL SURVEILANCE WEBINAR RANZCOG - 2004 – teaching about FSEP - There were no standardised guidelines - History of CTG – developed in late 50s - No evidenced based - 1967 – first CTG used - 80s – first guidelines - CTG – hasn’t reduced CS rates or cerebral palsy rates -

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Complete online program – certificate o Dopplers o Blood flow Guidelines o What the coroner use for cases o Advocate for women o Changes to the guidelines  Antenatal risk – potential for baby to be monitored during labour o Fetal movements – increased rate of induction The Normal CTG

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Well oxygenated baby – live in time Reduced fetal movements – if they change come back No time limit on when baby’s are well oxygenated Put everything into perspective Antenatal CTG

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Baseline FHR  110-160bpm (28 weeks to 42 weeks) o Never reassuring alone Normal baseline variability 6-25bpm 2 accelerations within a 20 min period (reactivity) No decelerations Intrapartum CTG

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Baseline FHR  110-160bpm Normal baseline variability 6-25bpm Accelerations – not a number or time limit o During labour – episodes during accelerations  When baby moves  Performing VE  Palpation  Mum or dad talks to the baby No decelerations Rare to have a normal CTG during labour Baseline FHR

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Mean resting HR Assessed in the absence of o Fetal movements o Uterine activity

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o Decelerations Assessed – before uterine activity Variability fluctuates around baseline Document everything o Saw, felt, heard, mum said – fetal movements Uterine Activity

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Count activity 60-90 seconds of uterine rest Hypotonus  too much tone o More than 2 mins o Or less than 60 seconds before another contraction o Escalate Coupling o Normalise abnormal uterine activity o Baby isn’t getting oxygenated or getting rid of metabolic waste products o Depends on what the baby is doing – whole clinical picture Hyperstimulation o Due to hypotonus Baseline Variability

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Normal  6 to 25 beats in amplitude, at 3-5 cycles per minute 3-5 fluctuations is considered reduced baseline variability >25 is considered increased variability o Often in second stage labour o Acute hypoxia  Alarm – stop pushing

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Artefact  more than 3-5 cycles o How well the fetal scalp electrode is applied o Babies who have a lot of hair – lots of artefact o Fetal scalp electrode  90 degrees to the scalp o Big heavy show  causes artefact o Membranes  cause artefact o Artefact inhibits the ability to predict baseline variability o Artefact may hide absent variability Accelerations

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Fetal response to stimulation A transient increase in the FHR of at least 15 beats above the baseline, lasting 15 seconds at the baseline Accelerations consistent with every contraction – may be maternal HR

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Reduced or absent variability – abnormal CTG Even if there is accelerations Fetal Physiology

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Control of the fetal heart Utero placental unit Control of the Fetal heart

Cardio regulatory centre (CRC) -

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Situated in the medulla oblongata of the brain stem Integrates input from the various receptors and nervous systems including o Autononic NS o Chemoreceptors o Baroreceptors o Fetal behavioural state (sleep wake cycle)  20-40 minutes – normal limits  Waking baby up  get mum to talk to her baby, position change, palpation, toileting, loud noise, final part – scalp stimulation  Opioids  babies may have extended sleep state  Sleep is the most common reason for reduced variability Function o Functions to maintain optimal oxygen delivery for the fetus via continuous, minute adjustment for the FHR Autonomic NS

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Sympathetic o Accelerator o Stimulates a rise in the HR through the action of catecholamines o Is part of the fright-flight-fight mechanism o Develops earlier than the parasympathetic system o Babies before 28 weeks – sympathetic is in play – higher HR

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Parasympathetic o Vagal stimulation reduces the HR through the action of acetylcholine on the SA node o Drops the HR – to reduce injury to the heart – protect the myocardium from ischemia o Reduced stimulation can result in a rise in the FHR o Is not fully developed until approx. 28 weeks o Matures later than the sympathetic NS Sinoatrial (SA) node

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Primary pacemaker of the heart Situated high in the right atrium Has both sympathetic and parasympathetic innervation Has the highest intrinsic rate The FHR reduced toward term as a result of increasing parasympathetic NS maturation Catecholamines

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Anatomy o Are hormones secreted primarily from the adrenal glands o Include adrenaline and noradrenaline o Prepare the body to meet physiological stressors Function o Increase the FHR o Increase the cardiac output o Cause peripheral vasoconstriction o Redirect limited oxygen to those organs vital for survival

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Brain Heart Adrenal glands

Baroreceptors -

Increased pressure causes a sharp increase in HR Well oxygenated autonomic nervous system that can respond to cord events Chemoreceptors

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Anatomy o Receptors sensitive to changes in blood chemistry o Have high metabolic rates and thus high oxygen requirements o Are sensitive to falling oxygen levels Functions Where there is an abrupt fall in oxygen levels, chemoreceptors are also capable of a reflex stimulation of the parasympathetic/vagal system This abrupt fall in the FHR is through to reduce myocardial work and oxygen requirements to prevent myocardial damage Variable decelerations are likely to be the chemoreceptor (chemoreflex) driven rather than baroreceptor (baroreflex) and so reflex rapid falling oxygen (acute hypoxia) rather than rising pressure o Most likely a cord event Utero Placental Unit

Non-gravid Uterus - Blood flow  90mL per minute Gravid low risk term Uterus - Blood flow  900mL per minute Changes must accommodate the increased blood flow Maternal Uterine Artery  can be found by a doppler at term (right iliac fossa)

Maternal Blood Flow – what impedes blood flow -

Hypotension Position change  lying flat Trauma

Maternal Uterine Artery  Spiral Arteries uncoil (trophoblastic insertion) - Expand with blood pressure - Spiral Arteries become less reactive to blood pressure changes - Contraction of myometrium  ligation and pressure on spiral arteries – no blood flow in or out (no oxygen) -

Spiral arteries come into intervillous space  oxygen tanks for baby o Depends on how big the placenta is o Brings in oxygen rich blood and finds chorionic villi o Chorionic villi  large surface area and thin membrane

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Vein brings in oxygen rich blood

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2 arteries take blood back  metabolic waste products – C02, hydrogen ions

Placenta - Gritty - Infarcted placenta - Determines how much blood flow baby had Factors affecting maternal transport to the placenta -

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Maternal hypotension o Supine hypotension o Regional anaesthesia  Redistribution of blood flow  Monitor baby before epidural o Blood loss  Concealed – baby will tell you  Show  Active bleeding Maternal hypertension o Decreased uterine flow due to mother’s vasoconstriction o Impaired placental development (i.e. pre-eclampsia of maternal cardiovascular or placental origin) Uterine activity o A result of spiral arterial occlusion o Particularly where uterine activity is excessive o Tachysystole or hypotonus  hyperstimulation  Tachysystole  more than 5 contractions in 1 minute with no abnormal CTG  Often see post prostaglandin gel or if there is infection  Trauma, abruption  Hypotonus  no resting tone o Too many contractions or too strong? Can't have both o A lack of rest between contraction – document resting tone as well as contractions Factors affective diffusion across the placenta

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Reduced placental surface area o Small placenta (thickened placental membrane) o Placental abruption or infarction

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Reduced oxygen ability o Maternal hypoxia  Sepsis, seizures, maternal collapse o Maternal hypotension

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Altered fetal oxygen affinity o Fetal metabolic acidosis o Babies have higher cardiac output per kg and HR o Babies have ability to redirect blood to non-essential  Skin, gut, kidneys o Intervillous space  400ml of oxygen rich blood o Fetal haemoglobin  can take up way more oxygen  A great buffer – tries and use bicarb and haemoglobin to reduce acidosis

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Uterine contractions o A lack of rest between contractions  Spiral arteries are squeezed

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Fetal bradycardia  hypoxia VE  excludes full dilation, cord prolapse, scalp stimulation Compensation through sympathetic NS – rising baseline Reduces oxygen requirement  reduced variability Repeated insults  reduced reserves Factors affecting fetal transport to and from the placenta

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Uterine activity o Lack of rest between contractions Cord events – variable decels – may become complicated o Cord occlusion o True knot Fetal Factors o Anaemia – sinusoidal  Placental abruption  Trauma  Twin to twin transfusion  Vaso praevia  Infection  Rh Isoimmunisation o Structural cardiac abnormalities  SVT  VSD o Cardiac arrhythmias o Fetal blood loss Abnormal CTG

Intrapartum CTG -

In terms of hypoxic fetus the CTG is said to be sensitive but not specific Provides continuous information about fetal wellbeing When used in conjunction with fetal blood sampling (FBS) a more accurate picture is obtained Given at least 60% of fetal HR abnormalities do not signify fetal compromise, look for reassuring features Normal trace  well oxygenated fetus Abnormal trace  60-70% + false positive rate for hypoxia Variable decels  cord event o Straight down and straight up o Shouldering  good sign Total clinical picture

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Clinical reason Indication for monitoring What are the risks Interpret CTG

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Parity o Pre-determined labour based on parity Normalising multis  can be a risk Clinical History o Understands tests Other investigations o AFI o Doppler flow studies Infusions/medications/drugs Previous antenatal traces o Why is there such a change? Trace prior to and following any abnormality o How is the baby reacting to change in environment? Stage of labour o Abnormal trace – variables o Variables in antenatal trace – concerning Rate of progress of labour o Grand multis  VE – cervix can stretch up to 8cm but she’s not in labour Trends in the evolution of the CTG o Go back to first CTG o Where was the baby when it arrived in labour? o Did it have a normal or abnormal CTG? o Can't miss the trend Management of tachysystole or uterine hypertonus

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Tachysystole o More than 5 active labour contractions in 10 mins o Without FHR abnormalities Uterine Hypotonus o Contractions lasting more than 2 min in duration or occurring within 60 sec of each other o Without fetal heart rate abnormalities o Baby is at more risk  Higher pressure in myometrium Management o Continuous CTG o Stay with the women until normal uterine activity is observed o Consideration of reducing or ceasing the oxytocin infusion o Consideration of tocolysis  Tachysystole or uterine hypotonus is not itself a reason for tocolysis Management of uterine Hyperstimulation

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Uterine hyperstimulation o Is defined as tachysystole or uterine hypertonus in the presence of FHR abnormalities Management o Continuous CTG o Reduce or cease the oxytocin infusion o Maternity staff remain with the woman until normal uterine activity is observed o Notify senior staff o Consideration of tocolysis and/or urgent delivery Tocolytic regimens available o Terbutaline, 250mcg SC or IV (IV is good for larger ladies)

 Usually a once off dose  If needed more than once she needs a ECG o Salbutamol, 100mcg IV o GTN spray, 400mcg SL  Relaxes uterus  Good without IV access  Prime the spray before giving  Spray under the tongue -

Late decelerations o Lates have mates – late to contraction o Hypoxia o After the contraction o Chronic hypoxia  shallow decels o Acute hypoxia  reflex late decels  Due to hyperstimulation, hypertonus Maternal heart rate recording

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Clues A change in style A sudden baseline changes Accelerations with contractions likely due to increased preload o 500mL going up to right atrium  increased cardiac preload o To protect the heart – increased heart rate Occurring particularly in second stage Abnormalities in baseline variability and accelerations

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May been seen with anything which results in CNS depression o Deep fetal sleep o Drugs o Hypoxia  Increased oxygen requirements or  Reduced oxygen availability o Extreme prematurity In the intrapartum period, the significance of reduced accelerations in a CTG with otherwise reassuring features is unclear Sleep Trace

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When babies sleep – parasympathetic activity is withdrawn Baseline rises Complicated variables

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Variable decels – cord event Complication – absent variability Risk for hypoxia – may not be hypoxic but risk If hypoxic  rising baseline o Variability would remain absent o Decels will get wider and deeper Bradycardia

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Baseline bradycardia o A baseline rate below 110bpm o May be result of  A mature parasympathetic system  40 plus weeks  Fetal heart conduction defect  Heart block  SA node is in heart block and other pacemakers sit at a lower rate (80pbm) Bradycardia o A fall in the baseline fetal heart rate for more than 5 minutes o Causes:  Maternal hypotension  Prolonged umbilical cord compression  Uterine hyperstimulation  Sustained fetal hypoxia of any cause Tachycardia

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Definition o A baseline FHR of more than 160 o This range is baseline, is not associated with hypoxia in the presence of accelerations or with normal variability and no decelerations Causes of a Tachycardia o Maternal tachycardia o Maternal fever – dehydration is a complicating factor o Drugs - salbutamol o Tachyarrhythmia o Febrile Declarations Early

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May be due to head compression Uniform in shape Start and finish within the contraction Usually drop 60bpm in depth) and/or long duration (>60 sec duration) decelerations A smooth deceleration overshoots A slow return to baseline after a contraction Prolonged decelerations

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Are decelerations of more than 90 seconds duration and up to 5 minutes Generally caused by hypoxia In isolation reflect the fetal environment, rather than the fetal condition May result from o Prolonged contractions o Epidural insertion o Uterine hyperstimulation o Supine hypotension o Ruptured uterus o Abruption o VE Their significance depends on the clinical picture...