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Balancing the Heart and the Lungs in Children with Large Cardiac Shunts Emergencies in Children with Large Cardiac Shunts

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Balancing the Heart and the Lungs in Children with Large Cardiac Shunts Emergencies in Children with Large Cardiac Shunts Balancing the heart and the lungs in children with large cardiac shunts Emergencies in children with large cardiac shunts. B Rossouw, MB ChB, DTM, MMed (Paed), MSc (Sports Med), Certificate Critical Care (Paed) Consultant Paediatric Intensivist, Red Cross War Memorial Children’s Hospital, University of Cape Town Beyra Rossouw is a paediatric intensivist at Red Cross Children’s Hospital, with a special interest in cardiac critical care. Correspondence to: Beyra Rossouw ([email protected]) This article reviews the pathophysiology of low-pressure chamber. Therefore, in the is well preserved until end-stage disease, cardiorespiratory problems in children with normal heart shunt flow will be from the left usually only in late childhood or adulthood. cardiac shunt lesions. The close anatomical to the right heart. The larger the pressure When the LV myocardium contracts a large and physiological relationship of the heart difference between the chambers the more amount of the stroke volume (SV) is ejected and the lungs explains why disease in one blood will be shunted across the defect. through the shunt to the right heart and only system will affect the other. the remainder of the SV is ejected into the In newborns the pulmonary vascular aorta. The implication is that too little SV The pulmonary and cardiac circulations are resistance and the right heart pressures reaches the systemic circulation, giving rise inseparable. The cardiac system is a dual pump are high. Due to the low-pressure gradient to signs of poor perfusion and stimulation system (right and left ventricle) with the lungs between the left and right heart, there is of the neuroendocrine response. in between (Fig. 1). The first pump circulates minimal flow across the defect. A murmur the venous blood to the lungs and the second is often only heard when a pressure gradient Symptoms we describe as ‘cardiac failure’ pump circulates the arterial blood to the body. develops as the neonatal pulmonary vascular are actually signs of cardiac volume loading resistance falls between 4 - 6 weeks of age. and the neuroendocrine response. Classic Cardiac pathophysiology: signs of ‘cardiac failure’ include tachycardia, Large cardiac shunts Murmurs heard in shunt lesions are often cardiomegaly, congested lungs in left heart A cardiac shunt is an abnormal connection generated by turbulent blood flow across a volume loading and congested liver with between the right and the left heart. Common valve. For example, the ASD murmur is not peripheral oedema in right heart volume examples (Figs 2 - 5) are: atrial septum defect the flow across the ASD that you hear but loading. (ASD), ventricle septum defect (VSD), rather the turbulent flow over the pulmonary atrioventricular septum defect (AVSD) and valve caused by a relative pulmonary patent ductus arteriosus (PDA). stenosis (PS). A large VSD will have excess The term ‘cardiac failure’ blood returning to the left atrium (LA) and is a misnomer in cardiac Flow across the cardiac shunt depends on turbulent flow over the mitral valve will two factors: cause a relative mitral stenosis (MS). This is shunts. Myocardial • size of the defect heard as a mid-diastolic rumble. contractility is well • pressure difference between the two preserved until end- chambers of the shunt. The heart chamber directly downstream from the shunt will become volume loaded stage disease, usually Pressure difference is the most important and dilate. only in late childhood or factor determining the amount of flow adulthood. across the shunt. Blood will always flow The term ‘cardiac failure’ is a misnomer in from the high-pressure chamber to the cardiac shunts. Myocardial contractility The neuroendocrine response includes an increased discharge of the sympathetic nervous system and activation of the renal renin angiotensin system. This is a compensatory mechanism. The aim is to increase cardiac output (Q) by increasing the heart rate (HR) and to maintain blood Fig. 1. Two cardiac pumps in series with the lungs in between. RA = right atrium; RV = right pressure (BP) by vasoconstriction (R) and ventricle; LA = left atrium; LV = left ventricle; PA = pulmonary artery; PV = pulmonary veins. fluid retention: Q=HRxSV, BP=SVxHRxR. 16 CME January 2013 Vol. 31 No. 1 Large cardiac shunts through the lungs compared with the systemic circulation. Pulmonary hypertension (PHT) develops with chronic pulmonary over-circulation due to a combination of increased blood flow and increased pulmonary pressure. Flow-related endothelial shear stress stimulates pulmonary vasoconstriction. In chronic pulmonary flooding structural changes develop that reduce the cross-sectional area of the pulmonary vasculature, leading to an increase in the Fig. 2. Pathophysiology of a large ASD. Dotted lines indicate the chamber enlargement. Number pulmonary pressure. Structural changes include of arrows demonstrate amount of blood flow. RA = right atrium; RV = right ventricle; LA = left medial hypertophy, intimal proliferation, atrium; LV = left ventricle. fibrosis, luminal occlusion, angiomatoid changes and eventially fibrinoid necrosis. Large cardiac shunts (Qp:Qs >1.5) are at risk to develop PHT. Patients with a large VSD or PDA transmit systemic pressure across the shunt during systoly and develop PHT in childhood. Patients with an ASD usually only develop PHT as adults due to low pressure flow across the ASD only in diastoly. Clinical features of PHT are shortening of the systolic murmur, accentuation of the second heart sound and RV hypertophy. Pulmonary pathophysiology in Fig. 3. Pathophysiology of a large VSD. RA = right atrium; RV = right ventricle; LA = left cardiac shunts (Fig. 6) atrium; LV = left ventricle. Abnormal lung mechanics of an over- circulated pulmonary vascular bed include a decrease in lung compliance, an increase in airway resistance, increase in work of breathing, pulmonary oedema, atelectasis, V/Q mismatch and pulmonary hypertension. The increased lung stiffness (decreased compliance) is attributed to an increase in interstitial oedema and an increase in actual blood volume in the lungs. A negative correlation exsists between lung compliance and the magnitude of pulmonary vascular engorgement as well as the radiological Fig. 4. Pathophysiology of an AVSD. RA = right atrium; RV = right ventricle; LA = left atrium; degree of plethora. LV = left ventricle. Airway obstruction and wheezing are seen in In shunt lesions the systemic circulation systemic circulation (Qs). Normal Qp:Qs cardiac shunt lesions, hence the term ‘cardiac is relatively under-perfused and the is 1:1 with equal flow to the lungs and the asthma’. Over-circulation of the lungs lead pulmonary circulation is flooded. Shunt systemic circulation. A Qp:Qs >1.5:1 is a to mucosal oedema and bronchial lumen size is often expressed as a Qp:Qs ratio.This large haemodynamically significant shunt narrowing. A bronchial lumen narrowing ratio implies how much blood is shunted to that requires surgery. This implies that there of 1 mm will increase airflow resistance 16 the pulmonary circulation (Qp) versus the is one and a half times more blood flowing times (resistance =1/radius4). 17 CME January 2013 Vol. 31 No. 1 Large cardiac shunts contraction becomes less efficient in a flattened position. This is clinically seen as subcostal recession with contraction of the horisontal diaphragm fibres inplanted to the lower ribs. A chronically flattened diaphragm causes permanent deformity of the lower ribs, known as Harrison’s sulci. The infant may compensate by using abdominal and intercostal muscles as an active forced expiration to empty the lungs. However, this extra muscle action tires the infant and breathing may become ineffective, especially at fast breathing rates. Fig. 5. Pathophysiology of a large PDA. RA = right atrium; RV = right ventricle; LA = left The energy cost of breathing is high, with atrium; LV = left ventricle. consequent failure to thrive. Added to the high energy costs, the caloric intake is often Engorged vessels and volume-loaded heart For effective gas exchange the alveolar- low. Infants become too dyspnoeic and chambers can cause external bronchial capillary membrane must remain dry. Once tachypnoeic for coordinated breathing and compression. Common sites of obstruction fluid accumulates, intra-alveolar surfactant feeding. They simply cannot keep up with are the left main bronchus and right will be destroyed, atelectasis develops with the energy demand and start losing weight. middle bronchus. These bronchial sites are V/Q mismatch and hypoxia. Uneven areas compressed between a dilated left atrium of lung atelectasis and airtrapping also Aspiration can be particularly problematic posteriorly and dilated pulmonary artery contribute to V/Q mismatch and hypoxia. in cardiac shunt patients. A dilated left or PDA anteriorly. The peak incidence is atrium compresses the oesophagus, in infancy, when the bronchial cartilage Lung infection and hypoxia-related causing reflux and aspiration. Aerophagia is soft. Chronic compression can lead to inflammation play a role in breakdown of from dyspnoea and difficult feeding can bronchomalacia causing morbidity long the endothelial integrity and capillary leak also contribute to aspiration. Infants with after surgical repair of the cardiac lesion. develops. Inflammation can disrupt the cardiac lesions should be assessed for other activity of pulmonary sodium pumps that congenital abnormalities, for example Complete obstructed airways lead to create an osmotic gradient to clear
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