S Hunter

Cardiac output during labour.

Serial measurements of cardiac output and mean arterial pressure were performed in 15 women during the first stage of labour and at one and 24 hours after delivery. Cardiac output was measured by Doppler and cross sectional echocardiography at the pulmonary valve. Basal cardiac output (between uterine contractions) increased from a prelabour mean of 6.99 l/min to 7.88 l/min at greater than or equal to 8 cm of cervical dilatation as a result of an increase in stroke volume. Over the same period basal mean arterial pressure also increased. During uterine contractions there was a further increase in cardiac output as a result of increases in both stroke volume and heart rate. The increment in cardiac output during contractions became progressively greater as labour advanced. At greater than or equal to 8 cm of dilatation cardiac output increased from a basal mean of 7.88 l/min to 10.57 l/min during contractions. There were also further increases in mean blood pressure during contractions. One hour after delivery heart rate and cardiac output had returned to prelabour values, though mean arterial pressure and stroke volume remained raised. By 24 hours after delivery all haemodynamic variables had returned to prelabour values. Haemodynamic changes of the magnitude found in this series are of considerable clinical relevance in managing mothers with complicated cardiovascular function.

Prenatal diagnosis of congenital heart disease in the northern region of England: benefits of a training programme for obstetric ultrasonographers

OBJECTIVE To examine the results of fetal cardiac scanning and audit the changes in performance resulting from the introduction of a training programme for obstetric ultrasonographers. METHODS Using the database of the Northern Regional Congenital Abnormality Survey (NORCAS), fetuses with complex or significant congenital heart disease (CCHD) diagnosed prenatally in 1994 were identified. A simple programme of centralised and local training was instituted in 1995 by the department of paediatric cardiology to teach obstetric ultrasonographers in district general hospital maternity departments to identify congenital heart malformations. The results of the training programme were assessed by comparing the 1994 identification rate of CCHD with the rates for 1996 and 1997. RESULTS Birth rate fell during the study from 35 026 in 1994 to 32 874 in 1997. Registration of CCHD also fell, from 115 in 1994 to 87 in 1997. Prenatal recognition of CCHD rose from 17% in 1994 to 30% in 1995 and 36% in 1996. In 1997 it fell slightly to 26.9%. The total number of scans did not change much year on year, but the number of parents choosing termination increased significantly (from 22.7% to 57%). CONCLUSIONS A simple training programme for obstetric ultrasonographers increased their ability to detect serious congenital heart disease at a routine 18–20 week anomaly scan. With a termination rate of more than 50%, the incidence of CCHD in the population fell from 3.3/1000 to 2.6/1000 live births. This audit, conducted within a stable population using ascertainment by a well established fetal malformation registry, suggests that prenatal diagnosis may have a significant effect on the incidence of complex or serious congenital cardiac malformations.

Assessment of total anomalous pulmonary venous connection by two-dimensional echocardiography.

Twenty-three patients with total anomalous pulmonary venous connection were studied by two-dimensional echocardiography. In all cases the diagnosis was made before invasive procedures, with surgical or angiocardiographic confirmation. Eleven patients had supracardiac drainage (three to the coronary sinus, two to the right atrium,) and seven had infracardiac drainage. In the majority of cases the precise pattern of drainage could be identified by combining suprasternal, praecordial, and subcostal views. In 12 cases where the suprasternal cut was used a pulmonary venous confluence could be identified, having a cross-like structure in nine, with three others appearing as a dilated channel behind and separate from the left atrium. Thus, two-dimensional echocardiography reliably makes the diagnosis of total anomalous pulmonary venous connection and in the majority the precise pattern of drainage can be determined.

Non-invasive assessment of pulmonary arterial pressure in healthy neonates.

Doppler echocardiograms were carried out on 51 healthy babies three times during the first 72 hours of life to estimate pulmonary arterial systolic pressure by measuring regurgitant tricuspid jet velocity and applying the Bernoulli equation. Tricuspid regurgitation was detected at some stage in all preterm babies and most of those born at full term. Pulmonary arterial pressure could be measured from peak regurgitant velocity in babies with pansystolic regurgitation. The incidence of pansystolic regurgitation among 34 term babies at 0-12, 13-36, and 32-72 hours of age was 22, 27, and 19%, and in 17 preterm babies (within the same age groups) was 53, 50, and 31%, respectively. Estimates of pulmonary artery pressure in the term babies were in accord with known catheter values. Pressure fell rapidly during the first day in all 51 babies. The ratio of pulmonary:systemic arterial pressure was comparable between the two groups throughout. Ductal flow patterns mirrored the fall in this ratio with age--bidirectional flow was associated with a ratio of between 0.88:1 and 1.22:1 and high velocity left to right flow with a ratio of between 0.49:1 and 0.66:1. Both these techniques are noninvasive ways of assessing neonatal pulmonary arterial pressure.

Reproducibility of cardiac output measurement by cross sectional and Doppler echocardiography.

The variability of Doppler echocardiographic estimation of cardiac output at the aortic orifice was investigated in eight healthy subjects. Cross sectional echocardiograms of the aortic orifice and aortic Doppler velocities were recorded and measured by four echocardiographers. Between subject variability was significantly larger than within subject variability for all variables. Variability owing to different echocardiographers and different measurement times was small compared with total variability. Coefficients of variation for aortic annular diameter, aortic velocity integral, and heart rate were 4.1%, 6.4%, and 5.0% respectively. The coefficient of variation for cardiac output was 8.8% and the 95% confidence interval for measurement of cardiac output by the Doppler method was 4.45 to 6.35 l/min. One echocardiographer reanalysed all the recordings and the results showed that recording the echocardiograms introduces a significantly larger source of error than measuring them. Thus serial measurements of cardiac output by the Doppler method can be performed with acceptable reproducibility; this indicates that the technique can be accurately applied in clinical practice.

Right heart pressure determination by Doppler in infants with tricuspid regurgitation.

Doppler and direct measurements of right ventricle to right atrial pressure drop were made during cardiac catheterisation on 28 occasions in 26 infants with congenital heart disease. Age was 10 days to 12 months (median 4.5 months), and weight was 3.1 to 9.0 kg (median 4.7 kg). We measured peak velocity of tricuspid regurgitation by continuous wave Doppler, and the pressure drop was calculated using the modified Bernoulli equation (delta p = 4v2). There was a high correlation (r = 0.95) between direct and Doppler measurements. Doppler values tended to underestimate the right ventricle to right atrial pressure drop, but this was not of clinical significance (mean 2 mm Hg). The 95% confidence interval for the Doppler velocity was -0.41 to +0.26 m/sec, and was consistent across the range of pressures studied. Variability between observers was tested, by two observers performing sequential paired examinations on 16 newborn babies with tricuspid regurgitation. The coefficient of repeatability was 6.3 mm Hg (95% confidence interval 4.7 to 9.5 mm Hg) or 0.26 m/sec (0.18 to 0.50 m/sec). This method of right ventricular pressure estimation, validated previously only in older children and adults, is a reproducible and accurate technique in infants with tricuspid regurgitation.

Univentricular heart of right ventricular type with double or common inlet.

Seventeen cases are described in which both atria connect directly to a chamber with right ventricular characteristics. The atria connected through separate atrioventricular valves in six hearts and a common valve in 11. All hearts had a posterior rudimentary chamber. The septum which separated it from the main chamber was directed to the crux of the heart. Ten hearts were from patients with atrial situs solitus and seven from patients with atrial situs ambiguus. Arterial connections were concordant in three cases, had a double outlet from the main ventricular chamber in nine and single outlet of the heart in five. The patent artery always arose from the main chamber, with pulmonary atresia in three and aortic atresia in two. This and other studies indicate that double inlet atrioventricular connection does not predict the morphology of the main chamber. Although usually associated with a main chamber of left ventricular type, it may also be associated with a main chamber having right ventricular characteristics. Both types should be considered as univentricular hearts; the posterior chamber in hearts of right ventricular type are analogous to the anterior chamber in univentricular hearts of left ventricular type and are a rudimentary chamber rather than a hypoplastic ventricle. In the right ventricular form of univentricular heart, the trabecular zone of the rudimentary chamber is of left ventricular type

The natural history of ventricular septal defects

AIMS To correlate the size and position of isolated ventricular septal defects with closure rate in a cohort of children with mean follow up of more than six years. DESIGN A birth cohort was identified using the northern region cardiac database. The following were noted from case notes: defect size, position, means of closure, and age at closure. RESULTS 68 children were identified. 49 defects were small, 14 were moderate, and 5 were large. 13 cases required surgical closure, including 12 perimembranous defects. 35 defects closed spontaneously. Nine of the small muscular defects remained open and five of the small perimembranous defects remained open. The spontaneous closure rate for muscular defects was significantly greater than for perimembranous defects. Mean age of follow up for patients who still have defects is 76 months. CONCLUSIONS The position of a ventricular septal defect is extremely relevant to its natural history. Perimembranous defects accounted for most of the moderate and large defects that required surgical intervention. After more than six years almost a third of all perimembranous and just over two thirds of all muscular defects closed spontaneously.

Effect of immunosuppression after cardiac transplantation in early childhood on antibody response to polysaccharide antigen

BACKGROUND Three children who had cardiac transplantation before age 4 years later presented with recurrent sinopulmonary infection caused by organisms including Streptococcus pneumoniae, in which capsular polysaccharide plays an important part, one developed bronchiectasis. We therefore studied responses to polysaccharide antigen after immunosuppression started in early childhood. METHODS Antibodies against pneumococcal and haemophilus polysaccharides, and total IgG, IgG1, IgG2, and IgA concentrations were measured in 33 cardiac-transplant recipients transplanted before the age 4 years (group 1) and after that age (group 2). Patients with low pneumococcal and haemophilus antibody concentrations were immunised with 23 polyvalent pneumococcal and tetanus-haemophilus conjugate vaccines and antibody responses were measured. FINDINGS Five patients from group 1 and seven from group 2 were transplanted for congenital heart disease and ten patients in each group had heart transplants because of cardiomyopathy; none were asplenic. Group 1 (16 patients) were aged 2-10 years when investigated, group 2 (17 patients), were 6-16 years. Four of 16 patients in group 1 responded to pneumococcal polysaccharide vaccine compared with 14 of 17 in group 2 (p=0.0016). This difference remained when those in group 1, aged less than 4 years at investigation, were excluded (p=0.0060). Response to haemophilus-conjugate vaccine was similar in both groups (14 of 16 vs 14 of 17, p=1.0). Significantly more patients who failed to respond to pneumococcal vaccine had low IgG2 concentrations (p=0.0269). INTERPRETATION Children who had a transplantation and immunosuppression in early childhood before they had developed antibody responses to pneumococcal polysaccharide, still failed to show a response when older-ie, when such responses are the norm. Ongoing immunosuppression prevents the maturation of antipolysaccharide responses leaving children susceptible to severe and recurrent damaging infection.

Cardiac abnormalities in end stage renal failure and anaemia.

Thirteen anaemic children on dialysis were assessed to determine the incidence of cardiac changes in end stage renal failure. Nine children had an increased cardiothoracic ratio on radiography. The electrocardiogram was abnormal in every case but no child had left ventricular hypertrophy as assessed by voltage criteria. However, left ventricular hypertrophy, often gross, was found on echocardiography in 12 children and affected the interventricular septum disproportionately. Cardiac index was increased in 10 patients as a result of an increased left ventricular stroke volume rather than heart rate. Left ventricular hypertrophy was significantly greater in those on treatment for hypertension and in those with the highest cardiac index. Abnormal diastolic ventricular function was found in 6/11 children. Children with end stage renal failure have significant cardiac abnormalities that are likely to contribute to the high cardiovascular mortality in this group. Anaemia and hypertension, or its treatment, probably contribute to these changes. Voltage criteria on electrocardiogram are of no value in detecting left ventricular hypertrophy. Echocardiography must be performed, with the results corrected for age and surface area, in order to detect and follow these abnormalities.