Focus su : I TRACCIATI CTG NEL TRAVAGLIO DI PARTO: l'importanza della loro
interpretazione nella sofferenza fetale ipossica e nel danno neurologico
The widespread use of fetal heart rate monitoring for Intrapartum fetal well-being controll came in advance on our detailed understanding of the behaviour and specific regulation of the fetal cardiovascular system during " labour-time".
In particular, the fetal heart rate is very sensitive to hypoxaemia and hypoxia, but is quite less specific for fetal acidosis, the last step of fetal distress& intrapartum hypoxic ischaemic brain injury. Hystorical evaluation of fetal heart " decelerations, equated to fetal dystress and therefore a mandatory operative intervention was required, instead of paying attention and
understanding the " WAY HOW THE FETUS COMPENSATES and DEFENDS ITSELF, included those patterns suggesting a progressive LOSS of COMPENSATION . In order to avoid consequently OPERATIVE INTERVENTIONS( Caesarian section ) on " rescue fetuses " that display normal sign of fetal heart adaptation to changes in labour, it should be of value to focus on the FAILURE to recognize ABNORMAL FETAL HEART rate patterns , that suggest failure of the fetal compensatory mechanisms leading to BRAIN INJURY.
DOMANDA: How to define a "normal or near- normal cardiotocograph( CTG ) during labour?
RISPOSTA:
the clinical importance of a CTG is that It establishes that the " fetal neurological and cardiovascular systems" are quite intact and able to react and respond to " DEFEND" the fetus against labour and Intrapartum insults. - Hallmarks of a healthy, wellbeing fetus are : 1) NORMOXIA 2) NORMAL FETAL ACID BASE status 3) absence of ASPHYXIA and low risk of developing Intrapartum fetal asphyxia On the other hand, a " NON-REACTIVE fetal admission CTG is associated with : - adverse fetal outcome/ long-term NEUROLOGICAL INJURY.
DOMANDA: which are the criteria satisfying a " NORMAL Intrapartum CTG?
RISPOSTA:
1) it should have a stable " baseline "fetal heart rate ( FHR ) of between 110-160 bpm WITHOUT DECELERATIONS;
2) it should have normal baseline FHR variability between 5-25 bpm above &below the normal baseline FHR
3) a normal fetal " CYCLING ACTIVITY"( periods of reduced FHR variability, alternating with periods of increased FHR variability, with /without " ACCELERATIONS ). So, fetal cycling activity is " The Fundamental behavioural characteristic of the NEUROLOGICAL NORMAL and NON-HYPOXIC term OR near term fetus. - fetal cycling activity may be ABSENT in Hypoxia, Chorioamnionitis, Intrauterine fetal infection, exposure to drugs( including oxytocin,sedatives,narcotics,atrophine ), complete heart block , fetal brain hemorrhage, malformation (anencephsly ) ( photo of a normal CTG )
Fig. 1: A NORMAL cardiotocograph showing a STABLE BASELINE FETAL HEART RATE of about 130bm without " decelerations", normal baseline " variability", " accelerations", and FETAL CYCLING ACTIVITY
FETAL HEART RATE DECELERATIONS
An FHR deceleration is a reflex chemoreceptor- mediated parasympathetic response to a brief spell of OXIGEN DEPRIVATION ( hypoxic, ischaemic stimulus, or both ). Most of the FHR decelerations ( 85% or more) observed DURING LABOUR, are variabile decelerations , with a sharp fall in FHR from the baseline , reaching the nadir in less than 30s, and vary in depth, shape,duration and temporal relatioship with " contractions ". LATE DECELERATIONS lag behind " uterin contractions "in timing and are caused by. IMPAIRED OXIGEN TRANSFER across the " placenta".
DECELERATIONS that are synchronous with contractions , are are called EARLY, and therefore " benign" The " healthy fetus" with a previous normal CTG will show a predictable set and sequence of FHR changes , in response to HYPOXIC ISCHEMIC insults, dependending on wether these are " slow in onset, mild to moderate and progressive" , or " ACUTE and PROFOUND". The qualify patterns of these response are " PREDICTABLE" and represent " the effective and clinically critical FHR interpretation".
Fig 2. The relationship between hypotension and NEURONAL damage: hypotension induced by " partial uterine artery occlusion.
FIG 3( a -f ) the progression from a NORMAL CTG through a slowly evolving HYPOXIA process
The widespread use of fetal heart rate monitoring for Intrapartum fetal well-being controll came in advance on our detailed understanding of the behaviour and specific regulation of the fetal cardiovascular system during " labour-time".
In particular, the fetal heart rate is very sensitive to hypoxaemia and hypoxia, but is quite less specific for fetal acidosis, the last step of fetal distress& intrapartum hypoxic ischaemic brain injury. Hystorical evaluation of fetal heart " decelerations, equated to fetal dystress and therefore a mandatory operative intervention was required, instead of paying attention and
understanding the " WAY HOW THE FETUS COMPENSATES and DEFENDS ITSELF, included those patterns suggesting a progressive LOSS of COMPENSATION . In order to avoid consequently OPERATIVE INTERVENTIONS( Caesarian section ) on " rescue fetuses " that display normal sign of fetal heart adaptation to changes in labour, it should be of value to focus on the FAILURE to recognize ABNORMAL FETAL HEART rate patterns , that suggest failure of the fetal compensatory mechanisms leading to BRAIN INJURY.
DOMANDA: How to define a "normal or near- normal cardiotocograph( CTG ) during labour?
RISPOSTA:
the clinical importance of a CTG is that It establishes that the " fetal neurological and cardiovascular systems" are quite intact and able to react and respond to " DEFEND" the fetus against labour and Intrapartum insults. - Hallmarks of a healthy, wellbeing fetus are : 1) NORMOXIA 2) NORMAL FETAL ACID BASE status 3) absence of ASPHYXIA and low risk of developing Intrapartum fetal asphyxia On the other hand, a " NON-REACTIVE fetal admission CTG is associated with : - adverse fetal outcome/ long-term NEUROLOGICAL INJURY.
DOMANDA: which are the criteria satisfying a " NORMAL Intrapartum CTG?
RISPOSTA:
1) it should have a stable " baseline "fetal heart rate ( FHR ) of between 110-160 bpm WITHOUT DECELERATIONS;
2) it should have normal baseline FHR variability between 5-25 bpm above &below the normal baseline FHR
3) a normal fetal " CYCLING ACTIVITY"( periods of reduced FHR variability, alternating with periods of increased FHR variability, with /without " ACCELERATIONS ). So, fetal cycling activity is " The Fundamental behavioural characteristic of the NEUROLOGICAL NORMAL and NON-HYPOXIC term OR near term fetus. - fetal cycling activity may be ABSENT in Hypoxia, Chorioamnionitis, Intrauterine fetal infection, exposure to drugs( including oxytocin,sedatives,narcotics,atrophine ), complete heart block , fetal brain hemorrhage, malformation (anencephsly ) ( photo of a normal CTG )
Fig. 1: A NORMAL cardiotocograph showing a STABLE BASELINE FETAL HEART RATE of about 130bm without " decelerations", normal baseline " variability", " accelerations", and FETAL CYCLING ACTIVITY
FETAL HEART RATE DECELERATIONS
An FHR deceleration is a reflex chemoreceptor- mediated parasympathetic response to a brief spell of OXIGEN DEPRIVATION ( hypoxic, ischaemic stimulus, or both ). Most of the FHR decelerations ( 85% or more) observed DURING LABOUR, are variabile decelerations , with a sharp fall in FHR from the baseline , reaching the nadir in less than 30s, and vary in depth, shape,duration and temporal relatioship with " contractions ". LATE DECELERATIONS lag behind " uterin contractions "in timing and are caused by. IMPAIRED OXIGEN TRANSFER across the " placenta".
DECELERATIONS that are synchronous with contractions , are are called EARLY, and therefore " benign" The " healthy fetus" with a previous normal CTG will show a predictable set and sequence of FHR changes , in response to HYPOXIC ISCHEMIC insults, dependending on wether these are " slow in onset, mild to moderate and progressive" , or " ACUTE and PROFOUND". The qualify patterns of these response are " PREDICTABLE" and represent " the effective and clinically critical FHR interpretation".
Fig 2. The relationship between hypotension and NEURONAL damage: hypotension induced by " partial uterine artery occlusion.
FIG 3( a -f ) the progression from a NORMAL CTG through a slowly evolving HYPOXIA process
