Intrapartum Surveillance Flashcards
Why do we observe reduced variability in deep fetal sleep?
Withdrawal of parasympathetic input to the SA node, resulting in minor rise in Baseline rate
Diminished feedback required from the cardioregulatory centre, resulting in reduction in baseline variability
Why do we observe reduced variability in extreme prematurity?
Immature parasympathetic system, inherently sympathetic dominant
< 25/40
What causes early decelerations?
Head compression
Normal physiological response to a mild increase in intracranial pressure
What causes variable decelerations?
Caused by cord compression –> increased peripheral vascular resistance and increases fetal systemic BP –> triggers the BAROreceptors to initiate a reflex parasympathetic stimulation (vagal nerve). This results in a release of acetylcholine to the AV node and a rapid fall in the FHR
What are complicated decelerations?
- Variable decelerations complicated by
A) Rising BR
B) Reduced / absent variability
C) Fetal tachycardia - Persistent with large amplitude (>60bpm) and/or long duration (>60 seconds)
- Smooth post-deceleration overshoot
- Slow to return to BR after the contraction
What is shouldering in the context of decelerations?
Pre and post-deceleration is occasionally a feature of variable decelerations.
Normal physiological response to acute hypoxia generated by a sequential CORD compression and release and as such, reflects a well oxygenated fetus.
Occurs because initially, umbilical vein is compressed resulting in decreased fetal venous return (and BP), and a BAROreceptor mediated acceleration. Complete cord occlusion then leads to increase in BP and BAROreceptor triggered activation of vagus nerve and rapid deceleration
Should not be confused with a post-deceleration overshoot which reflects physiological distress
What is a sinusoidal pattern?
Oscillating pattern that is typically smooth and regular (in the timing of the oscillations, not necessarily the amplitude) Stable BR 120-160 Frequency of 2-5 cycles per minute Reduced/absent baseline variability No accelerations
Abnormal - reflective of severe anaemia with Hb < 50
Common feature is RFM
Reflects complete loss of autonomic nervous control
How should intermittent auscultation be performed?
1st stage: 15-30 minute intervals
2nd stage: with each contraction or at least every 5 minutes
Each auscultation should commence toward the end of a contraction and be continued for at least 30-60 seconds after the contraction has finished
When should paired umbilical cord blood gases be taken?
APGAR 1 < 4
APGAR 5 < 7
FBS in labour
Operative delivery for fetal distress
When is FBS contraindicated
- Maternal infection: HIV, Hep B or C, HSV. (GBS NOT a contraindication)
- Maternal / fetal bleeding disorder: thrombocytopenia, haemophilia
- Non vertex presentation
- 34/40 (delay in delivering a vulnerable fetus)
Not appropriate in
- Indication for immediate delivery: placental abruption, uterine rupture, very abnormal CTG
- Chorioamnionitis
- Meconium
Describe the CTG findings of a late deceleration
What causes late decelerations?
Describe the pathophysiology associated.
Uniform, repetitive deceleration with slow onset mid to end of contraction and nadir more than 20 secs after peak of contraction.
Hypoxia (Chronic or Acute). Acidosis develops causing stimulation of chemoreceptors –> PNS stimulation –> which leads to the late deceleration. When contraction ends placental venous sinuses refill with oxygenated blood –> removal of CO2 and elimination of chemoreceptor stimulus –> resolution of deceleration.
At what rate does fetal pH drop during acute hypoxia?
pH drops at rate of 0.01 per minute
Why do growth restricted fetuses have a shorter period of compensation during acute hypoxia?
During acute hypoxia fetal myometrium begins to depend on glycogenolysis and once glycogen stores are depleted, myocardium begins to fail.
Growth restricted fetuses have lower glycogen stores .
What is the ‘3-6-9-12’ rule?
Timing of intervention for reversible causes of abnormal CTG:
- 3 mins: call for help
- 6 mins: interventions to improve oxygenation and treat reversible causes
- 9 mins: move to OT
- 12 mins: prepare for delivery
- 15 mins: accomplish delivery
Outline causes of bradycardia apart from acute hypoxia:
- Some postdates fetuses: needs normal variability, accelerations and consistent with previous CTG BRs.
- Beta-blockers
- Complete fetal heart block
What are the features of a saltatory pattern?
What is the pathophysiology of this pattern?
- FHR baseline amplitude changes greater than 25 beats per minute (hypervariability).
- Oscillatory frequency >6 per mins.
- Minimum duration of 1 min.
Pathophysiology: instability between the SNS and PNS due to rapidly evolving hypoxia to the CNS.
What is the pathophysiology of a sinusoidal pattern?
Derangement or loss of control of FHR:
- Drugs that act on CNS.
- Fetal hypoxia and acidosis: massive feto-maternal haemorrhage or maternal anaemia.
- Chorioamnionitis/maternal pyrexia adversely affects fetal brain function.
Umbilical cord: acute/repeated cord compressions leading to alternating fetal hypovolaemia and hypertension.
What CTG findings are consistent with a preterminal CTG?
- Tachycardia, reduced/absent variability, shallow decels.
- Prolonged and persistent decels.
- Bradycardia esp. if reduced variability.
- Deep amplitude and long-standing decels with short inter-decel interval
What clinical markers of chronic hypoxia should you note?
- RFMs
- Oligohydramnios
- Presence of old meconium staining of liquor.
- Meconium aspiration syndrome and subsequent pulmonary HTN
What CTG findings are consistent with chronic hypoxia?
- Fixed BR with reduced or absent variability, no accelerations (distant insult)
- Tachycardia with reduced or absent variability (more recent insult)
List the fetal scalp lactate categories and levels and what actions you would do in each situation.
Normal: <=4.1 mmol/L
- Action: repeat within 1 hour if same CTG and no accels on scalp stimulation.
Pre-acidotic: 4.2-4.8 mmol/L
- Action: repeat within 30 hour if same CTG and no accels on scalp stimulation.
Acidotic: >=4.9 mmol/L
- Action: expedite delivery
Outline intrauterine resuscitation interventions:
- Oxygen: if reduced maternal oxygen saturations.
- Fluid: even if not hypovolaemic will improve venous return, cardiac output and uterine blood flow
- Maternal repositioning
- Stop oxytocic / give tocolysis
- Vasopressors if maternal hypotension
At what rate does fetal pH drop in subacute hypoxia?
pH drops by 0.01 every 2-3 mins.
Outline the ladder of fetal response to hypoxia:
- Deceleration to reduce cardiac workload
- Loss of accelerations due to RFMs
- Release of catecholamines to:
- increase FHR to pump oxygenated blood from the placenta.
- peripheral vasocontriction / redistribute blood to vital organs
- glycogenolysis to increase energy supply. - Compensated response
- Brain decompensation: loss of baseline varability
- Heart decompensation: progressive reduction in FHR due to myocardial acidosis.
