Acta Obstet Gynecol Scand 57: 23 1-235, 1978
CHANGES IN FETAL SUPRAVENTRICULAR EXTRASYSTOLES DURING UTERINE CONTRACTIONS IN LABOUR Helge Jenssen From the Department of Obstetrics and Gynecology, Aker Hospital (Oslo City Hospitals), Oslo, Norway
Abstract. The electrocardiogram and phonocardiogram were recorded from a fetus exhibiting supraventricular ectopic beats during labour. The ectopic beats showed increased amplitude of the first heart sound (S,) compared to sinus and postectopic beats; the R-S1 interval was prolonged and the mechanical systole, measured as the S , S z interval, shortened. During uterine contractions these parameters were measured every 10 sec. The S , amplitude of the ectopic beats decreased; simultaneously the R S , interval increased and the S , S , interval shortened. The changes were delayed compared to the amniotic pressure curve. The changes found can be explained by a shift of blood between the fetus and placenta, caused by uterine contraction.
Conspicuous changes, related to uterine contractions, were observed in the fetal phonocardiogram (FPCG) in a recording made during labour in which the fetal heart showed supraventricular ectopic beats (Fig. I). An analysis of the FPCG and the simultaneously recorded fetal electrocardiogram (FECG) was undertaken measuring systolic time intervals (5). The arterial pulse was not recorded. CASE STUDY The mother was 28 years old and gravida 11. One and a half years earlier she had delivered a stillborn fetus in the 28th week. She was admitted in the 36th week because of arterial hypertension, RR 140/100. Estriol excretion varied between 12 and 24 mg per 24 hours. Blood pressure fell to normal values within 24 hours, but she was kept in the ward for nearly 2 weeks chiefly due to anxiety caused by the previous stillbirth. Four days after expected term she was readmitted, without signs of preeclampsia, in active labour and had an uneventful spontaneous delivery after 7 hours of contraction. The newborn, a boy, scored Apgar 8/10 at 1/5 min of age and weighed 3 630 g. On the first day of life a pediatrician found some extrasystoles, but no other pathological findings. Three days later no extrasystoles were detected. An ECG of the newborn showed normal P waves and no
extrasystoles. Several routine examinations by another pediatrician up to the age of 1 year showed normal development. The placenta was normal macroscopically and weighed 500 g.
METHOD The FECG and FPCG were recorded during first stage of labour, at a cervical diameter of 4-5 cm. Two hours earlier the mother had received diazepam (Stesolid “Dumex””) i.m. During contractions she was hyperventilating to some degree, breathing N,O/O, Sol50 % through an open mask. Amniotic pressure was registered as earlier described (7). The FECG was registered with a scalp spiral electrode; the signal was passed through a pre-amplifier (EMT 12,). The FPCG was recorded from the maternal abdomen with a heart sound microphone (EMT 25 B’) and passed through a band pass filter with a nominal setting of 50 Hz and a pre-amplifier (EMT 22’). The signals were written on a Mingograph 34, continuously during the contractions, paper speed 100 mmls. Measurements were made every 10 sec (s), starting 40 s before peak contraction pressure (Fig. 2). The parameters measured are given in Table I. As the Q wave varied to some extent, R S , interval was measured
Table I. Characteristics of sinus beats, ectopic beats and postectopic beats. Mean values between uterine contractions R-R, time between the R waves of the actual and preceding beats; S , , first heart sound; S,, second heart sound
R-R interval S,S,interval S4,interval R S ,interval S duration S2duration S, amplitude S2 amplitude
ms ms ms ms ms ms mm mm
Sinus beats
Ectopic beats
Postectopic beats
422 205 220 36
295 167
525 205 37ob 30
90”
75
45 75
63
60
11
23 II
9
84
53 8 6
From S , of the preceding sinus beat to S, of the ectopic beat. * From S, of the ectopic beat to S of the postectopic beat. a
Manufacturer: Elema Schonander, Stockholm
,
Actci Obstrt Gvnecol Sctmd57 (19781
232
H . Jenssen
I
C
Fig. I . Fetal electrocardiogram (FECG) and phonocardiogram (FPCG) recorded simultaneously; A , before uterine contraction; B , 10 seconds after maximal amniotic pressure (peak contraction pressure); and C, 40
seconds after B . SB, sinus beats; EB, ectopic beats; PEB, postectopic beats. The FECG was registered with downward deflection of the R wave.
instead ofQ-S, interval. The start ofS, andS, was defined as the crossing point between the first high frequency vibration and the base line level. Using a magnifying lens and the smallest marks on the Mingograph paper, readings were made to the nearest 2.5 millisec (ms). Each value was the mean of 2-5 individual readings, and the values presented are the means of 2 consecutive contractions.
ure of ventricular filling time. The S z S l interval preceding the ectopic beats is 41 % and that preceding the postectopic beats 168 % of the sinus beats.
RESULTS Between uterine contractions The FECG trace was inverted (Fig. 1). However, between contractions the P waves were well delineated. The P Q time of the sinus beats was 60 ms, of the ectopic beats 80-85 ms and of the postectopic beats 60 ms. The amplitude of SIand Sz was increased in the ectopic beats, the S l S 2interval was shortened and the R S , interval prolonged (Table I). If the time of isovolumetric relaxation of the ventricles is disregarded, the S d ,interval may be taken as a meas-
During uterine contractions Fetal heart rate measured as the R-R interval did not vary during contractions (Fig. 2 ) . The SrSz interval of the ectopic beats shortened at peak contraction pressure, the shortening being maximal ( 15 ms) 20 s later and lasting 3&35 s. The S1 amplitude of the ectopic beats decreased 37 % and of the sinus beats 19% during contractions (Figs. 1 and 3). These changes too were delayed compared to the peak contraction pressure. The S2 amplitude changed as shown in Fig. 4. The duration of the R S ,intervals in the ectopic beats (but not in the sinus or postectopic beats) increased during uterine contractions (Fig. 4), the increase starting at the time of peak contraction pressure, being maximal (27 %) 10 s later and lasting 35-40 s.
Fetal extrasystole changes during labour contraction
233
deflection of S , accompanying decrease of amplitude cannot explain the R S , interval change as the duration of S , did not change. The sum o f R S , and S duration increased during contraction in the same manner as the R-S, interval. The delay of S1 in the ectopic beats is accompanied by delay in central arterial pressure increase in systole (14), and may be partly caused by the increased aortic pressure at the start of the ectopic beats. If the duration of the S z S , interval preceding the ectopic beats is applied to the aortic pressure curve recorded in the newborn (13), aortic pressure at the start of the ectopic beats systole is still about 35% of maximal aortic pressure. In hypertensive adults prolonged Q S ,intervals have been found (15). Among causes of a loud first heart sound Leatham lists reduced ventricular filling from atrioventricular stenosis or tachycardia (9). In dogs Sakamoto et al. (11) showed that among several factors influencing S , amplitude, the only common factor was the rate of left ventricular pressure increase, a rapid pressure increase giving a high S 1 amplitude. Decreased ventricular filling in the ectopic beats therefore explains the high S , amplitude. Shortening of the S,-S2 interval in the ectopic beats may be caused by increased aortic pressure or reduced cardiac filling.
,
100 m m Hg
A m n i o t i c pressure
s0
20
4 0o
60
80
h
Fig. 2. Mean of R-R interval and SrS, interval measured every 10 sec, shown in relation to the amniotic pressure curve. 0-0, sinus beats; V-V, ectopic beats; C B postectopic beats. ms, milliseconds; s, seconds.
The duration of Sz of the sinus and ectopic beats was 25% shortened simultaneously with the changes in S , amplitude and R S , interval. The duration of Sz of the postectopic beats did not shorten.
t i n . o e r Cent
DISCUSSION The fetal ectopic beats resemble the supraventricular extrasystoles of the human adult in its altered P wave configuration, increased S , amplitude, and prolonged R S , interval (2). The compensatory pause was not complete, and the ventricular complex of the ectopic beats was virtually unchanged. The ectopic beats of the present case is considered to have a supraventricular origin. The duration of R S , and S , S z intervals of the sinus beats are the same as reported by others (3, 12). The pressure increase during uterine contraction is too small to influence the velocity of propagation of the fetal heart sounds to a measurable extent (10).
100 m m
S, amplitude
Hg Amniotic pressure
5a
(
The R S , interval of the ectopic beats increases after peak contraction pressure, simultaneously S amplitude decreases. Disappearance of the initial
,
Fig. 3. Relative changes ofS, amplitude related to uterine contraction. Symbols as in Fig. 2. The values of Table I taken as 100%. Acta Obstet Gvnecol Scand57 (1978)
234
H . Jenssen uterine contractions are mainly caused by changes in return of blood from the placenta. The present case shows that the fetal systolic time intervals has the ability to change, much as in the adult, and that the changes are measurable. The findings add support to the hypothesis that a shift of blood between the fetus and placenta takes place during uterine contraction.
1 0 0 m m Hg
/
A m n i oti c p r e s s u r e
1. Borell,
0
20
40
60
80
Fig. 4. Changes of Sz amplitude and R-S, interval duration related to uterine contraction. Symbols as in Fig. 2.
During uterine contraction the intervillous circulation is partly or totally stopped (1). Peak contraction pressure of the contractions studied was 60 to 70 mmHg, probably occluding intervillous circulation. During amniotic pressure rise there must be a period of intervillous space increase as the veins draining the intervillous space are occluded before the arteries. The intervillous space increase may have an effect on the fetal circulation. A bolus of blood may be squeezed from the placenta to the fetus, temporarily increasing the return of blood to the fetal heart. Resistance in the chorionic tree may increase, causing elevation of the fetal arterial pressure. These circulatory changes may explain the principal variations during uterine contraction found in the present case (change of the S, amplitude and the R S , and S,Sz intervals). A 10% reduction of newborn's predicted total blood volume during exchange transfusion (4) did not alter the R S interval, but significantly shortened the R-S2 interval, and consequently the S , S , interval. However, exact timing of S, was inaccurate due to small amplitude. Khanna et al. (8) reduced stroke index in adults with peripheral cuffs. This procedure prolonged the pre-ejection period and shortened left ventricular ejection time. Presuming that the R S , interval partially reflects pre-ejection period changes (6) and that the S I S Binterval reflects changes of left ventricular ejection time (9, the changes related to
,
Acto Ohstrt Gynecol Sccrtid 57 (1978)
REFERENCES U.,Fernstrom, I., Ohlson, L. & Wiqvist, N.:
An arteriographic study of the blood flow through the uterus and the placenta at midpregnancy. Acta Obstet Gynecol Scand44: 22, 1965. 2. Cossio, P., Dambrosi, R. G. & Warnford-Thomson, H. F.: The first heart sound in auricular and ventricular extrasystoles. Br Heart J 9: 275, 1947. 3. Craige, E. & Harned, H. S.: Phonocardiographic and electrocardiographic studies in normal newborn infants. Am Heart 565: 180, 1963. 4. Gyulai, F. & Walsh, S. Z.: Phonocardiographic studies during experimental hypo- and hypervolemia in the healthy newborn. J Electrocardiol4: 158, 1971. 5 . Hams, L. C., Weissler, A. M., Manske, A. O., Danford, B. H., White, G. D. & Hamill, W. A,: Duration of the phases of mechanical systole in infants and children. Am J CardiolZ4: 448, 1964. 6. Hams, W. S.: Systolic time intervals in the noninvasive assessment of left ventricular performance in man. In Cardiac Mechanics: Physiological, Clinical, and Mathematical Considerations (ed. I. Mirsky, D. N. Ghista & H. Sandler), p. 244. Wiley, New York, 1974. 7. Jenssen, H.: The effect of paracervical block on cervical dilatation and uterine activity. Acta Obstet Gynecol Scand52: 13, 1973. 8. Khanna, P. K., Shah, P. B., Kramer, D. H., Schaefer, R. A. & Tager, I.: Effects of altered preload on left ventricular systolic time intervals in acute myocardial infarction. Br Heart 535: 1102, 1973. 9. Leatham, A.: Auscultation of the Heart and Phonocardiography, p. 26. J. & A. Churchill, London, 1970. 10. Malecki, I. : Physical Foundations of Technical Acoustics. Pergamon Press, Oxford, 1969. 1 1 . Sakamoto, T., Kusukawa, R., MacCanon, D. M, & Luisada, A. A.: Hemodynamic determinants of the amplitude of the first heart sound. Circulat Res 16: 45, 1965. 12. Walsh, S. Z. & Gyulai, F.: Electromechanical intervals in the healthy newborn. J Electrocardiol3: 259, 1970. 13. Walsh, S. Z. & Lind, J.: The dynamics of the fetal heart and circulation and its alteration at birth. I n Physiology of the Perinatal Period, vol. 1 (ed. U. Stave), p. 183. Appleton-Century-Croft, New York, 1970.
Fetal extrasystole changes during labour contraction 14. Weissel, W. & Vetter, H.: Herzkatheteruntersuchungen des Verhaltens der elektro-pressorischen Latenz bei Rhythmusstorungen. Cardiologia 20: 160, 1952. 15. Weissler, A. M., Leonard, J. J . & Warren, J. V.: Observations on the delayed first heart sound in mitral stenosis and hypertension. Circulation 28: 165, 1958.
Submitted for publication March 3 , 1977 Helge Jenssen Department of Obstetrics and Gynecology Aker Hospital Oslo Norge
235
CHANGES IN FETAL SUPRAVENTRICULAR EXTRASYSTOLES DURING UTERINE CONTRACTIONS IN LABOUR Helge Jenssen From the Department of Obstetrics and Gynecology, Aker Hospital (Oslo City Hospitals), Oslo, Norway
Abstract. The electrocardiogram and phonocardiogram were recorded from a fetus exhibiting supraventricular ectopic beats during labour. The ectopic beats showed increased amplitude of the first heart sound (S,) compared to sinus and postectopic beats; the R-S1 interval was prolonged and the mechanical systole, measured as the S , S z interval, shortened. During uterine contractions these parameters were measured every 10 sec. The S , amplitude of the ectopic beats decreased; simultaneously the R S , interval increased and the S , S , interval shortened. The changes were delayed compared to the amniotic pressure curve. The changes found can be explained by a shift of blood between the fetus and placenta, caused by uterine contraction.
Conspicuous changes, related to uterine contractions, were observed in the fetal phonocardiogram (FPCG) in a recording made during labour in which the fetal heart showed supraventricular ectopic beats (Fig. I). An analysis of the FPCG and the simultaneously recorded fetal electrocardiogram (FECG) was undertaken measuring systolic time intervals (5). The arterial pulse was not recorded. CASE STUDY The mother was 28 years old and gravida 11. One and a half years earlier she had delivered a stillborn fetus in the 28th week. She was admitted in the 36th week because of arterial hypertension, RR 140/100. Estriol excretion varied between 12 and 24 mg per 24 hours. Blood pressure fell to normal values within 24 hours, but she was kept in the ward for nearly 2 weeks chiefly due to anxiety caused by the previous stillbirth. Four days after expected term she was readmitted, without signs of preeclampsia, in active labour and had an uneventful spontaneous delivery after 7 hours of contraction. The newborn, a boy, scored Apgar 8/10 at 1/5 min of age and weighed 3 630 g. On the first day of life a pediatrician found some extrasystoles, but no other pathological findings. Three days later no extrasystoles were detected. An ECG of the newborn showed normal P waves and no
extrasystoles. Several routine examinations by another pediatrician up to the age of 1 year showed normal development. The placenta was normal macroscopically and weighed 500 g.
METHOD The FECG and FPCG were recorded during first stage of labour, at a cervical diameter of 4-5 cm. Two hours earlier the mother had received diazepam (Stesolid “Dumex””) i.m. During contractions she was hyperventilating to some degree, breathing N,O/O, Sol50 % through an open mask. Amniotic pressure was registered as earlier described (7). The FECG was registered with a scalp spiral electrode; the signal was passed through a pre-amplifier (EMT 12,). The FPCG was recorded from the maternal abdomen with a heart sound microphone (EMT 25 B’) and passed through a band pass filter with a nominal setting of 50 Hz and a pre-amplifier (EMT 22’). The signals were written on a Mingograph 34, continuously during the contractions, paper speed 100 mmls. Measurements were made every 10 sec (s), starting 40 s before peak contraction pressure (Fig. 2). The parameters measured are given in Table I. As the Q wave varied to some extent, R S , interval was measured
Table I. Characteristics of sinus beats, ectopic beats and postectopic beats. Mean values between uterine contractions R-R, time between the R waves of the actual and preceding beats; S , , first heart sound; S,, second heart sound
R-R interval S,S,interval S4,interval R S ,interval S duration S2duration S, amplitude S2 amplitude
ms ms ms ms ms ms mm mm
Sinus beats
Ectopic beats
Postectopic beats
422 205 220 36
295 167
525 205 37ob 30
90”
75
45 75
63
60
11
23 II
9
84
53 8 6
From S , of the preceding sinus beat to S, of the ectopic beat. * From S, of the ectopic beat to S of the postectopic beat. a
Manufacturer: Elema Schonander, Stockholm
,
Actci Obstrt Gvnecol Sctmd57 (19781
232
H . Jenssen
I
C
Fig. I . Fetal electrocardiogram (FECG) and phonocardiogram (FPCG) recorded simultaneously; A , before uterine contraction; B , 10 seconds after maximal amniotic pressure (peak contraction pressure); and C, 40
seconds after B . SB, sinus beats; EB, ectopic beats; PEB, postectopic beats. The FECG was registered with downward deflection of the R wave.
instead ofQ-S, interval. The start ofS, andS, was defined as the crossing point between the first high frequency vibration and the base line level. Using a magnifying lens and the smallest marks on the Mingograph paper, readings were made to the nearest 2.5 millisec (ms). Each value was the mean of 2-5 individual readings, and the values presented are the means of 2 consecutive contractions.
ure of ventricular filling time. The S z S l interval preceding the ectopic beats is 41 % and that preceding the postectopic beats 168 % of the sinus beats.
RESULTS Between uterine contractions The FECG trace was inverted (Fig. 1). However, between contractions the P waves were well delineated. The P Q time of the sinus beats was 60 ms, of the ectopic beats 80-85 ms and of the postectopic beats 60 ms. The amplitude of SIand Sz was increased in the ectopic beats, the S l S 2interval was shortened and the R S , interval prolonged (Table I). If the time of isovolumetric relaxation of the ventricles is disregarded, the S d ,interval may be taken as a meas-
During uterine contractions Fetal heart rate measured as the R-R interval did not vary during contractions (Fig. 2 ) . The SrSz interval of the ectopic beats shortened at peak contraction pressure, the shortening being maximal ( 15 ms) 20 s later and lasting 3&35 s. The S1 amplitude of the ectopic beats decreased 37 % and of the sinus beats 19% during contractions (Figs. 1 and 3). These changes too were delayed compared to the peak contraction pressure. The S2 amplitude changed as shown in Fig. 4. The duration of the R S ,intervals in the ectopic beats (but not in the sinus or postectopic beats) increased during uterine contractions (Fig. 4), the increase starting at the time of peak contraction pressure, being maximal (27 %) 10 s later and lasting 35-40 s.
Fetal extrasystole changes during labour contraction
233
deflection of S , accompanying decrease of amplitude cannot explain the R S , interval change as the duration of S , did not change. The sum o f R S , and S duration increased during contraction in the same manner as the R-S, interval. The delay of S1 in the ectopic beats is accompanied by delay in central arterial pressure increase in systole (14), and may be partly caused by the increased aortic pressure at the start of the ectopic beats. If the duration of the S z S , interval preceding the ectopic beats is applied to the aortic pressure curve recorded in the newborn (13), aortic pressure at the start of the ectopic beats systole is still about 35% of maximal aortic pressure. In hypertensive adults prolonged Q S ,intervals have been found (15). Among causes of a loud first heart sound Leatham lists reduced ventricular filling from atrioventricular stenosis or tachycardia (9). In dogs Sakamoto et al. (11) showed that among several factors influencing S , amplitude, the only common factor was the rate of left ventricular pressure increase, a rapid pressure increase giving a high S 1 amplitude. Decreased ventricular filling in the ectopic beats therefore explains the high S , amplitude. Shortening of the S,-S2 interval in the ectopic beats may be caused by increased aortic pressure or reduced cardiac filling.
,
100 m m Hg
A m n i o t i c pressure
s0
20
4 0o
60
80
h
Fig. 2. Mean of R-R interval and SrS, interval measured every 10 sec, shown in relation to the amniotic pressure curve. 0-0, sinus beats; V-V, ectopic beats; C B postectopic beats. ms, milliseconds; s, seconds.
The duration of Sz of the sinus and ectopic beats was 25% shortened simultaneously with the changes in S , amplitude and R S , interval. The duration of Sz of the postectopic beats did not shorten.
t i n . o e r Cent
DISCUSSION The fetal ectopic beats resemble the supraventricular extrasystoles of the human adult in its altered P wave configuration, increased S , amplitude, and prolonged R S , interval (2). The compensatory pause was not complete, and the ventricular complex of the ectopic beats was virtually unchanged. The ectopic beats of the present case is considered to have a supraventricular origin. The duration of R S , and S , S z intervals of the sinus beats are the same as reported by others (3, 12). The pressure increase during uterine contraction is too small to influence the velocity of propagation of the fetal heart sounds to a measurable extent (10).
100 m m
S, amplitude
Hg Amniotic pressure
5a
(
The R S , interval of the ectopic beats increases after peak contraction pressure, simultaneously S amplitude decreases. Disappearance of the initial
,
Fig. 3. Relative changes ofS, amplitude related to uterine contraction. Symbols as in Fig. 2. The values of Table I taken as 100%. Acta Obstet Gvnecol Scand57 (1978)
234
H . Jenssen uterine contractions are mainly caused by changes in return of blood from the placenta. The present case shows that the fetal systolic time intervals has the ability to change, much as in the adult, and that the changes are measurable. The findings add support to the hypothesis that a shift of blood between the fetus and placenta takes place during uterine contraction.
1 0 0 m m Hg
/
A m n i oti c p r e s s u r e
1. Borell,
0
20
40
60
80
Fig. 4. Changes of Sz amplitude and R-S, interval duration related to uterine contraction. Symbols as in Fig. 2.
During uterine contraction the intervillous circulation is partly or totally stopped (1). Peak contraction pressure of the contractions studied was 60 to 70 mmHg, probably occluding intervillous circulation. During amniotic pressure rise there must be a period of intervillous space increase as the veins draining the intervillous space are occluded before the arteries. The intervillous space increase may have an effect on the fetal circulation. A bolus of blood may be squeezed from the placenta to the fetus, temporarily increasing the return of blood to the fetal heart. Resistance in the chorionic tree may increase, causing elevation of the fetal arterial pressure. These circulatory changes may explain the principal variations during uterine contraction found in the present case (change of the S, amplitude and the R S , and S,Sz intervals). A 10% reduction of newborn's predicted total blood volume during exchange transfusion (4) did not alter the R S interval, but significantly shortened the R-S2 interval, and consequently the S , S , interval. However, exact timing of S, was inaccurate due to small amplitude. Khanna et al. (8) reduced stroke index in adults with peripheral cuffs. This procedure prolonged the pre-ejection period and shortened left ventricular ejection time. Presuming that the R S , interval partially reflects pre-ejection period changes (6) and that the S I S Binterval reflects changes of left ventricular ejection time (9, the changes related to
,
Acto Ohstrt Gynecol Sccrtid 57 (1978)
REFERENCES U.,Fernstrom, I., Ohlson, L. & Wiqvist, N.:
An arteriographic study of the blood flow through the uterus and the placenta at midpregnancy. Acta Obstet Gynecol Scand44: 22, 1965. 2. Cossio, P., Dambrosi, R. G. & Warnford-Thomson, H. F.: The first heart sound in auricular and ventricular extrasystoles. Br Heart J 9: 275, 1947. 3. Craige, E. & Harned, H. S.: Phonocardiographic and electrocardiographic studies in normal newborn infants. Am Heart 565: 180, 1963. 4. Gyulai, F. & Walsh, S. Z.: Phonocardiographic studies during experimental hypo- and hypervolemia in the healthy newborn. J Electrocardiol4: 158, 1971. 5 . Hams, L. C., Weissler, A. M., Manske, A. O., Danford, B. H., White, G. D. & Hamill, W. A,: Duration of the phases of mechanical systole in infants and children. Am J CardiolZ4: 448, 1964. 6. Hams, W. S.: Systolic time intervals in the noninvasive assessment of left ventricular performance in man. In Cardiac Mechanics: Physiological, Clinical, and Mathematical Considerations (ed. I. Mirsky, D. N. Ghista & H. Sandler), p. 244. Wiley, New York, 1974. 7. Jenssen, H.: The effect of paracervical block on cervical dilatation and uterine activity. Acta Obstet Gynecol Scand52: 13, 1973. 8. Khanna, P. K., Shah, P. B., Kramer, D. H., Schaefer, R. A. & Tager, I.: Effects of altered preload on left ventricular systolic time intervals in acute myocardial infarction. Br Heart 535: 1102, 1973. 9. Leatham, A.: Auscultation of the Heart and Phonocardiography, p. 26. J. & A. Churchill, London, 1970. 10. Malecki, I. : Physical Foundations of Technical Acoustics. Pergamon Press, Oxford, 1969. 1 1 . Sakamoto, T., Kusukawa, R., MacCanon, D. M, & Luisada, A. A.: Hemodynamic determinants of the amplitude of the first heart sound. Circulat Res 16: 45, 1965. 12. Walsh, S. Z. & Gyulai, F.: Electromechanical intervals in the healthy newborn. J Electrocardiol3: 259, 1970. 13. Walsh, S. Z. & Lind, J.: The dynamics of the fetal heart and circulation and its alteration at birth. I n Physiology of the Perinatal Period, vol. 1 (ed. U. Stave), p. 183. Appleton-Century-Croft, New York, 1970.
Fetal extrasystole changes during labour contraction 14. Weissel, W. & Vetter, H.: Herzkatheteruntersuchungen des Verhaltens der elektro-pressorischen Latenz bei Rhythmusstorungen. Cardiologia 20: 160, 1952. 15. Weissler, A. M., Leonard, J. J . & Warren, J. V.: Observations on the delayed first heart sound in mitral stenosis and hypertension. Circulation 28: 165, 1958.
Submitted for publication March 3 , 1977 Helge Jenssen Department of Obstetrics and Gynecology Aker Hospital Oslo Norge
235
