Physiology and Pathology of Uterine Contractions

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Presentation transcript:

Physiology and Pathology of Uterine Contractions Michael G. Halaška, M.D. Department of Obstetrics and Gynaecology of 2nd Medical Faculty

Physiology myometrium – smooth muscle enlargment of the muscle cells basal tonus first contractions from 20thweek of gravidity Braxton-Hick contractions

Physiology

Montevid Units Montevid Units – addition of amlitudes of contractions in 10 minutes pacemaker – contraction wave – 2cm/s amplitude of an contraction 1st stage – 40-60 mm Hg 2nd stage – 80 mm Hg closure of blood-vessels veins : 20 mm Hg artery: 60 mm Hg

Physiology basal tonus 10 mm Hg 1. stage of labour 30-40 mm Hg - 120 MU 2. stage of labour 50-60 mm Hg - 250 MU resting time >30 s

Physiology Proper shape of the contractions 1. stage 2. stage 3. stage

Physiology – starting factors mechanical - ↑ pressure, ↓ volume endocrine estrogen - ↑ number of estro receptors, ↓ membrane potential, ↑ ATP in myocytes oxytocine - ↓ membrane potential, ↑ PG prostaglandins – preparing of cervix, contract. neurogen Fergusson reflex Parasympaticus reflex

Recording the contractions absolute – intrauterine - intrauterine catheter relative – external - using piesoelectric effect

Indications and contraindications Type of sensor Conditions Indications Contraindications External anytime non-ivasive as CTG none not recommended - obesity Internal cervix dilatated at least 2-3 cm, ruptured membranes, tonus of the uterus mostly scientific use placenta praevia, face presentation, intraovulatory infection

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology - hypertonus etiology: macrosomy, multiple pregnancy, premature separation of placenta pathophysiology: ↑ basal tonus - ↑blood in veins – hypoxy clinics: palpable, changes on CTG treatment: tocolysis

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology - hyperactivity > 390 MU, >7 contrac/min, resting time <30 s etiology: hypersensitivity, overstimulation of the uterus clinics: CTG changes therapy: less oxytocine, tocolysis

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology - hypoactivity < 100 MU, < 30 mm Hg, < 2 contract/min type: primary – from the beginning secondary – during the labour etiology: primary: hypoplasia of U., dystokia secondary: prolonged labour, overstimulation by oxytocine, exhaustion of the mother clinics: CTG, no postup of the labour therapy: oxytocine, tocolysis, rest

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology - dystokia etiology: hypertonus of the cervix, failure of pacemakers, exhaustion of uterus clinics: CTG, no postup of the labour therapy: tocolysis, S.C.

Pathology hypertonus hyperactivity hypoactivity dystokia failure of the abdominal muscle

Pathology - failure of abd. muscle etiology: disease of the muscle or inervation disease which unables higher activity ( heart, eyes .. ) epidural anesthesia exhaustion of the mother obesity not cooperating mother therapy: forceps, VEX, S.C.