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Cardiology 2 Ch02.qxd 7/5/04 3:06 PM Page 13 Cardiology 2 FETAL CARDIOVASCULAR PHYSIOLOGY The ‘basic science’ nature of this topic – as well as the potential pathological implications in paediatric cardiology – makes it a likely viva question. Oxygenated blood from the placenta returns to the fetus via the umbilical vein (of which there is only one). Fifty per cent traverses the liver and the remaining 50% bypasses the liver via the ductus venosus into the inferior vena cava. In the right atrium blood arriving from the upper body from the superior vena cava (low oxygen saturation) preferentially crosses the tricus- pid valve into the right ventricle and then via the ductus flows into the descending aorta and back to the placenta via the umbilical arteries (two) to reoxygenate. The relatively oxygenated blood from the inferior vena cava, however, preferentially crosses the foramen ovale into the left atrium and left ventricle to be distributed to the upper body (including the brain and coro- nary circulation). Because of this pattern of flow in the right atrium we have highly oxygenated blood reaching the brain and deoxygenated blood reach- ing the placenta. High pulmonary arteriolar pressure ensures that most blood traverses the pulmonary artery via the ductus. Changes at birth 1. Occlusion of the umbilical cord removes the low-resistance capillary bed from the circulation. 2. Breathing results in a marked decrease in pulmonary vascular resistance. 3. In consequence, there is increased pulmonary blood flow returning to the left atrium causing the foramen ovale to close. 4. Well-oxygenated blood from the lungs and the loss of endogenous prostaglandins from the placenta result in closure of the ductus arteriosus. CONGENITAL HEART DISEASE You should know the approximate incidence of congenital heart disease which is approximately 8/1000 live births. 13 Ch02.qxd 7/5/04 3:06 PM Page 14 Ventricular septal defect – 30% Coarctation of the aorta – 6% PASS Patent ductus arteriosus – 8% Aortic stenosis – 6% Pulmonary stenosis – 8% Transposition of the great vessels – 4% Atrial septal defect – 8% Atrioventricular septal defect – 4% Tetralogy of Fallot – 6% It is important to be familiar with what lesion is likely to present when, since this will be vital when answering a possible clinical scenario in the written or clinical examinations. Cardiovascular lesion chronology — Within the first few hours: pulmonary or aortic atresia/critical stenosis, hypoplastic left heart syndrome. — Within the first few days: transposition of the great arteries, tetralogy of Fallot, hypoplastic left heart syndrome, patent ductus arteriosus (PDA) in Paediatric Exams: A Survival Guide small premature infants. — Within the first few weeks: critical aortic stenosis, coarctation of the aorta. — Within the first few months: any of the left to right (L–R) shunts (caused by falling pulmonary vascular resistance). Presentation of congenital cardiovascular disease A useful way at looking at congenital heart disease (CHD) and its presenta- tion is to divide it up into three categories. These are of course simplifications but nevertheless useful. 1. Those that are ductal dependent for pulmonary blood flow or mixing Main presenting clinical feature is cyanosis. – Decreased pulmonary blood flow: pulmonary stenosis, pulmonary atresia ± ventricular septal defect, Ebstein anomaly, tetralogy of Fallot, single ven- tricle or double outlet right ventricle with pulmonary stenosis. – Increased pulmonary blood flow: transposition without significant mixing. 2. Those that are ductal dependent for systemic blood flow Main presenting clinical features are those of systemic hypoperfusion (decreased peripheral perfusion, reduced urine output, metabolic acido- sis). Remember that the important differential diagnosis of this type will be neonatal sepsis or a metabolic disorder. Examples: coarctation of the aorta, interruption of the aortic arch, critical aortic stenosis, hypoplastic left heart. There are of course non-ductal dependent cardiac causes of systemic hypoperfusion such as cardiomy- opathy, myocarditis and supraventricular tachycardia (SVT). 3. Those that are unlikely to be ductal dependent The main presenting clinical feature will be respiratory distress and increased shadowing on the chest X-ray (CXR). Examples: – Mixing lesion: total anomalous pulmonary venous drainage (TAPVD) with no obstruction and adequate foramen ovale, truncus arteriosus, 14 single ventricle without pulmonary stenosis. Ch02.qxd 7/5/04 3:06 PM Page 15 Table 2.1 Cardiac catheter PASS Normal values Cardiology O2 saturation Pressure (mmHg) Vena cava (VC) 75% 0–5 Right atrium (RA) 75% m = 3 Right ventricle (RV) 75% 25/3 Pulmonary artery (PA) 75% 25/8 Left atrium (LA) 98% m = 8 Left ventricle (LV) 98% 110/8 Aorta 98% 110/65 – Left to right lesions: patent ductus arteriosus, ventricular septal defect, atrioventricular canal defect. CARDIAC CATHETER DATA Cardiac catheter data is still a popular topic for the Part 2 examination. In order to attempt any of these questions it is of course vital to know the nor- mal values of pressure and saturation in the various chambers of the heart and the major vessels (see Table 2.1) — The way of attempting these types of question is to follow the pressures and saturations around the heart (through the great vessels and chambers) sys- tematically noting any deviations from the normal values (Table 2.1) and noting any unexpected step-ups or step-downs in saturation or pressure. — In a left to right or right to left shunt the exact point of the step-up or step- down in oxygen saturation (in the right or left sides of the heart respec- tively) indicates the level of the shunt. — A higher than expected pressure in a chamber or vessel can be explained by a stenosis ahead of it, by a shunt such as a left to right shunt (towards the chamber or vessel) or simply by a backlog of pressure. — A drop in pressure between a ventricle and an artery implies a stenosis in the artery. — Equal ventricular pressures may be due to a large ventricular septal defect (VSD), Eisenmenger syndrome, common arterial trunk and tetralogy of Fallot. Let us now go through the lesions that are likely to come up in the examination. 1. O2 saturation Pressure RA 88% 5 RV 87% 35/5 PA 87% 35/12 LA 97% 6 LV 97% 100/8 Aorta 97% 100/58 15 Ch02.qxd 7/5/04 3:06 PM Page 16 This is the result of an atrial septal defect (ASD). There is a rise in saturation PASS going from the vena cava (not given!) to the right atrium. This can also be caused by TAPVD where blood from the pulmonary veins drains directly or indirectly into the right atrium. This is rare and you should remember that this lesion can be cardiac, supracardiac or infracardiac, the last type being associated with obstruction. 2. O2 saturation Pressure SVC 75% — RA 75% 3 RV 75% 35/5 PA 88% 35/14 LA 95% 8 LV 95% 100/8 Aorta 95% 100/55 Paediatric Exams: A Survival Guide There is a step-up in saturation and pressure between the right ventricle and the pulmonary artery. This is an example of a patent ductus arteriosus (PDA). 3. O2 saturation Pressure SVC 68% — IVC 64% — RA 72% 12 RV 84% 85/7 PA 85% 20/8 LA 98% 10/5 LV 91% 90/5 Aorta 88% 90/55 There is a step-up in oxygen saturation between the right atrium and right ventricle implying a left to right shunt at the level of the ventricles. The pres- sures also show a step-up at the same level. This is the pattern one would expect with a VSD. However, in addition to this we notice a step-down in pressure from the right ventricle to the pulmonary artery and this implies a stenosis. We also notice a desaturation as we pass through the left side of the heart and the low saturation in the systemic circulation (aorta). These addi- tional features make the diagnosis tetralogy of Fallot. 4. O2 saturation Pressure LA 98% 10/5 LV 98% 152/60 Aorta 98% 90/50 There is clearly a higher pressure than we would expect in the left ventricle for a paediatric patient and we also see a step-down in pressure between the left ventricle and the aorta implying that this is a coarctation of the aorta. The commonest site is just distal to the left subclavian artery. 16 Ch02.qxd 7/5/04 3:06 PM Page 17 5. O2 saturation Pressure VC 30% — PASS RA 32% — Cardiology RV 32% 90/10 PA 92% 60/7 LA 93% 7 LV 94% 60/7 Aorta 35% 88/60 We can see here that the pressures and saturations in the pulmonary artery and aorta match those of the left ventricle and right ventricle respectively: that is, the reverse to what we would expect in practice. The diagnosis is transposition of the great arteries. 6. O2 saturation Pressure RA 65% — RV 65% 90/10 PA 68% 100/60 LA 95% — LV 82% 100/12 Aorta 83% 100/55 Here we can see high pulmonary pressures which can be caused by large VSD or AV canal defects which if present for long periods result in irreversible pul- monary hypertension and reverse right to left shunting – Eisenmenger syndrome. CYANOSIS AND THE HYPEROXIC TEST (NITROGEN WASHOUT TEST) This is a common topic and you should be familiar with the theory. This is a useful test to help to distinguish between cardiac and respiratory disease causing cyanosis in a baby. An arterial blood gas is taken (preductal) and repeated after breathing 100% oxygen for 10–15 min. A PO2 of less than 20 kPa (usually less than 10 kPa) is suggestive of a fixed right to left shunt (which implies a lesion in which there can be no increase in pulmonary blood flow or mixing of systemic and pulmonary circulations, e.g.
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