Pathophysiology of Fetal Heart Rate PDF

Summary

This document provides a lecture presenting information on the pathophysiology of fetal heart rate, including fetal circulation, baseline heart rate, variability, decelerations, and abnormal patterns. The lecture covers how the fetus adapts to changes in oxygen levels and discusses factors controlling fetal heart rate. It also provides information about different deceleration shapes, and how these can be used to identify potential problems.

Full Transcript

Physiology and Pathophysiology Heather Helen  Midwifery Text Books  National Women and Infants Health Programme, (NWIHP 2021), on behalf of the Fetal Heart Rate Monitoring Working Group, National Clinical Guideline for Fe...

Physiology and Pathophysiology Heather Helen  Midwifery Text Books  National Women and Infants Health Programme, (NWIHP 2021), on behalf of the Fetal Heart Rate Monitoring Working Group, National Clinical Guideline for Fetal Heart Rate Monitoring: Ireland. Dublin: Health Service Executive. Additional https://www.rcpi.ie/Faculties-Institutes/Institute-of-Obstetr icians-and-Gynaecologists/National-Clinical-Guidelines-in- Reading Obstetrics-and-Gynaecology required  NICE (2022) Fetal Monitoring in Labour, ng229 NICE: UK https://www.nice.org.uk/guidance/ng229  Ayres-de-Campos, D., Spong, C.Y., Chandraharan, E. and (2015), FIGO consensus guidelines on intrapartum fetal monitoring: Cardiotocography. International Journal of Gynecology & Obstetrics, 131: 13-24. https://doi.org/10.1016/j.ijgo.2015.06.020  Recommenced reading list  Fetal heart pumps deoxygenated blood to the placenta via the 2 umbilical arteries  Placenta functions as the lung whilst the baby is in utero Revision of  Free gas exchange depends on normal flow of fetal maternal blood through the placental bed as well Circulation as normal blood flow through the placenta  Blood pumped back to the fetus via the single umbilical vein (Aerobic metabolism)  pH expresses the acidity or alkalinity of a solution  pH It is a measure of the concentration of free (unbuffered) H+ ions  CO2 is carried to the placenta as H+ and HCO3 and then released to the mother pH  The elimination of CO2 means the concentration of free H+ ions in restored to normal  The blood flowing back to the fetus via the umbilical vein has a higher pO2, lower pCO2 and a higher pH  Normal  Cord perfusion of compression uterus and  Fetal placental bed Bradycardia  Hypotension  Severe  Hypoxia bradycardia  Contractions reduces  Chronic  Abruption cardiac output impairment  Abnormal to placenta to extract O2 placental  Fetal circulation arrhythmia (PET)  Fetal anaemia  Two Possible consequences  Accumulation of CO2 Effects on  Reduced supply of O2 Fetus  Very common in labour – normal physiology  Occasionally CO2 may not be able to pass freely to the mother o The pH cannot be restored to normal o Blood in umbilical vein will have higher pCO2 and a Accumulatio lower pH n of CO2  CO2 being produced quicker than it can be eliminated  Situation termed respiratory acidemia - PH falls  Compensation  Fetus has a high concentration of Haemoglobin (Hb)  Fetal Hb has a high affinity for O2 (can extract more O2 at placenta)  Fetal cardiac output is about 4 times greater than an adult Reduced  Normal physiology – fetus is oversupplied and has supply of O2 some even for reserve  Normal labour –  Contractions reduce maternal blood supply to placental bed  Time to recover between contractions Fetus relatively over supplied with O2 – reduction of O2 easily accommodated​ Increased O2 extraction - higher Hb and O2 extraction from the placenta​ Centralisation of blood flow – perfusion to vital organ (brain, heart and adrenal glands) is increased at the expense of organs such as gut, kidneys and skin​ Damage to the heart and brain only occur with profound hypoxia​ Anaerobic metabolism – production of energy- metabolism of glucose or glycogen without O2​ Free H+ ions used up​ Fall in pH  Catecholamines released by the adrenal glands (adrenaline and noradrenaline) act to increase heart rate and constrict peripheral blood vessels ( to ensure that central organs get the priority blood supply  Poor intrauterine nutrition – like cash flow  Spend less (reduce O2 consumption, reduced fetal Fetus adapts movement and reduced fetal growth)  Spend it sensibly – Hb concentration may be increased, O2 supply to vital organs, resulting in oligohydramnios, NEC, asymmetrical growth  Anaerobic metabolism – glycogen stores used up hence leads to hypoglycaemia in the neonatal period Effect on Fetal Heart features The heart ‘s nerve supply- the rate is reduced by the vagus nerve Factors (parasympathetic supply) and increased by the sympathetic supply Circulating catecholamines e.g. adrenaline, released from the that adrenal glands, increases heart rate control Central nervous system activity Changes in fetal blood pressure FHR Changes in fetal blood gas level (O2, CO2, pH) Cord compression Hypoxia Cerebral activity Blood pressure PH Pyrexia pCO2 pO2 Drugs Gestation Deceleration Physiology Decelerations are, broadly speaking, of two types: * Baroreceptor reflex. These decelerations occur secondary to an increase in fetal systemic blood pressure due to an occlusion of umbilical arteries during compression of umbilical cord. They are characterized by a rapid fall in heart rate and a rapid recovery to original baseline. * Chemoreceptors reflex. These decelerations occur secondary to the accumulation of carbon dioxide and metabolic acids during hypoxia. They are caused by utero-placental insufficiency, repeated and sustained uterine contractions or a prolonged umbilical cord compression. They are characterized by a gradual and slow recovery to original baseline. Decelerations Ø Early decelerations Shallow, short lasting, with normal variability Mirror image of the contraction, do not indicate hypoxaemia Ø Variable deceleration (V shaped-baroreceptor response) Rapid drop, good variability within the deceleration, rapid recovery to the baseline Rarely signify important degree of fetal hypoxaemia unless they display a U shape component Ø Late Deceleration (U shaped-likely chemoreceptor response) Gradual onset/gradual return to baseline and/or reduced variability. Indicative of hypoxemia Ø Prolonged (chemoreceptor response) Lasting more than 3 minutes Decelerations last more than 5 minutes, HR

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