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

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/samplitude 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

1. mechanical - ↑ pressure, ↓ volume

2. endocrine estrogen - ↑ number of estro receptors,

↓ membrane potential, ↑ ATP in myocytes oxytocine - ↓ membrane potential, ↑ PG prostaglandins – preparing of cervix, contract.

3. 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

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. failure of the abdominal muscle

Pathology

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. 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

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. 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

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. 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

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. 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

1. hypertonus

2. hyperactivity

3. hypoactivity

4. dystokia

5. 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.