Disorders of the cardiac system

Chapter 9
Disorders of the cardiac system


Sheila Roberts


Aim


The aim of this chapter is for readers to develop their understanding of the anatomy and physiology of the cardiac system in order to appreciate various disorders of this system; to do this effectively the reader has also to understand pathophysiological mechanisms.



Introduction


The cardiovascular system is responsible for providing the body with a continuous supply of oxygen and nutrients while also transporting the waste materials that need to be expelled from the body, such as carbon dioxide. The cardiovascular system includes:



  • the heart, which pumps deoxygenated blood to the lungs, where gaseous exchange takes place, and oxygenated blood to the rest of the body;
  • the veins, which are the blood vessels that transport the blood from the body back towards the heart;
  • the arteries, which are the blood vessels that transport the blood away from the heart;
  • the capillaries, which are very small blood vessels connecting the arteries to the veins.

This chapter will provide a brief overview of the anatomy of the heart. It will then consider a range of anomalies that can affect the heart and the impact that these may have on the infant, child or young person.


Anatomy of the heart


The heart is comprised of four chambers, the left atrium and left ventricle and the right atrium and right ventricle. Deoxygenated blood enters the heart from the superior and inferior vena cava directly into the right atrium. Contraction of the muscle of the right atrium causes an increase in pressure within the right atrium allowing the one‐way valve, the right atrioventricular valve (also known as the tricuspid valve), situated between the right atrium and right ventricle, to open and allow the blood to pass through to the right ventricle.


As the atrium empties of blood and the ventricle fills the atrium relaxes and muscles of the right ventricle begin to contract increasing the pressure within the right ventricle. The atrioventricular valve closes and the blood is then forced through the pulmonary valve into the right and left pulmonary arteries. As the right ventricle empties of blood the pulmonary valve closes to prevent back flow of blood from the pulmonary arteries into the right ventricle.


The deoxygenated blood is transported via the right and left pulmonary arteries to the lungs where gaseous exchange takes place. Carbon dioxide is expelled and replaced with oxygen.


The oxygenated blood returns to the heart via the pulmonary veins directly into the left atrium. The left atrium fills with blood, the muscles of the left atrium contract and the resulting increase in pressure forces the blood through the left atrioventricular valve (also called the mitral or bicuspid valve) into the left ventricle.


Contraction of the left ventricle pumps the oxygenated blood through the aortic valve into the aorta for transportation round the body. Again the aortic valve closes to prevent back flow. Refer to Fig. 9.1 for a diagrammatic representation of the blood flow through the heart. For a more complete understanding of the anatomy and physiology of the heart refer to Roberts (2015).

Diagrammatic representation of the blood flow through the heart indicated by two differently shaded arrows, with parts labeled Aortic valve, Left ventricle, Tricuspid valve, Left atrium, Mitral valve, etc.

Figure 9.1 Diagrammatic representation of the blood flow through the heart.


Source: Peate & Gormley‐Fleming 2015. Reproduced with permission of Wiley.


Congenital disorders of the heart


A congenital heart defect (CHD) is an anatomical malformation of the heart and/or great vessels, which occurs during fetal development (Rao, 2015). A congenital heart defect is the most common of all defects that affects the newborn baby and is apparent in 8–10 of every 1000 live births (Siva et al., 2016). This incidence increases in spontaneous miscarriage, still‐born and premature babies. The reasons a baby may have a CHD are generally unknown, although there are situations where there is a known increased risk (Table 9.1).


Table 9.1 Possible causes for CHD


Source: Adapted from NHS Choices 2015.


































Risk factor Possible congenital heart defect
Mother with type 1 or 2 diabetes Transposition of the great arteries
Alcohol intake during pregnancy Atrial septal defect
Ventricular septal defect
Genetic conditions, e.g., babies with Down syndrome Septal defect
Noonan syndrome Pulmonary valve stenosis
Turner syndrome Coarctation of the aorta
Exposure to rubella virus Patent ductus arteriosus/pulmonary artery stenosis
Medication, e.g., benzodiazepines, (anti‐convulsion medication) and ibuprofen (analgesic medication) Atrial or ventricular septal defects
Mothers with phenylketonuria who do not adhere to a low‐protein diet Coarctation of the aorta and tetralogy of Fallot
Mother’s exposure to organic solvents Various

Cardiac or heart failure


Cardiac failure (CF) occurs when the heart is unable to pump enough blood and therefore oxygen to meet the needs of the metabolising cells. Heart failure is a syndrome characterised by either or both pulmonary and systemic venous congestion generally leading to inadequate peripheral oxygen delivery. It is caused by cardiac dysfunction. Congenital heart defects are the most common reason for cardiac failure in infants; at what age this occurs depends on the severity of the defect. In the older child, cardiac failure may result from a range of problems (Table 9.2).


Table 9.2 Possible causes of CF not associated with congenital heart defects


Source: Adapted from Park (2016).





































Approximate age of child Aetiology leading to heart failure
Toddlers Viral myocarditis
1–4 years Myocarditis associated with Kawasaki disease
School‐age children Acute rheumatic carditis
Older children Rheumatic valvular disease
Any age during childhood/adolescence Cardiomyopathy
Newborns Metabolic abnormalities, e.g., severe hypoxia, hypocalcaemia
Early infancy Supraventricular tachycardia
Any age Hyperthyroidism
Any age Severe anaemia
School‐age children Acute systemic hypertension with glomerulonephritis

Cardiac failure can be categorised simply as caused by abnormal structures within the heart versus a normal heart, or more accurately according to the haemodynamic changes that occur:



  • Preload increase or volume overload – commonly caused by large left‐to‐right shunts, such as ventricular septal defect and patent ductus arteriosus. Very rare before 6–8 weeks of age as pulmonary vascular resistance does not fall low enough to cause the large shunt before this age but then causes congestive cardiac failure (CCF) in the first 6 months of life.
  • Excessive afterload or pressure overload – commonly caused by obstructive abnormalities, such as coarctation of the aorta or valve stenosis. The left ventricle is unable to generate sufficient pressure to overcome the fixed downstream obstruction and it cannot therefore maintain cardiac output (Panesar & Burch, 2016).
  • Impaired contractility – the contractility is the ability of the myocardium (heart muscle) to contract. Impaired contractility is caused by any factor that affects the myocardium and its ability to contract, such as cardiomyopathy or myocarditis.
  • Rhythm disturbances – arrhythmias can induce heart failure as a result of an inadequate heart rate. Tachycardia leads to inadequate filling of the heart chambers and therefore decreased cardiac output. Bradycardia leads to an increase in ventricular filling volume leading to ventricular dilatation.
  • Distensibility disorders – distensibility refers to the ability of the chambers and vessels of the heart to increase in volume without a significant increase in pressure. When the heart is unable to do this cardiac output is affected.
  • Ischaemia – relatively rare in children, it generally appears as a consequence of congenital coronary abnormalities or as a complication following surgical procedures for congenital heart disease. Acquired coronary disease in children is typically from Kawasaki disease (Dedieu & Burch, 2013).

Signs and symptoms


The severity of the symptoms will always depend on the severity of the heart condition. Symptoms also vary according to whether the left or the right side of the heart is primarily affected. Signs and symptoms include:


Infant


  • Poor weight gain although the infant may be of average length – this is because the baby with CF has an increased metabolic rate and therefore needs additional calories; however, they tire easily and are unable to meet this calorific demand.
  • Poor feeding due to fatigue.
  • Diaphoresis (excessive sweating) especially when feeding due to a catecholamine (epinephrine and norepinephrine) surge that occurs when babies are challenged with feeding while in respiratory distress.
  • Tachypnoea – left‐sided heart failure causes congestion of the pulmonary veins and respiratory symptoms, such as breathlessness and grunting.
  • Hepatomegaly (enlargement of the liver) is caused by congestion from right‐sided heart failure.

Child


  • Respiratory distress, tachypnoea and hepatomegaly persist.
  • Increased shortness of breath during activities.
  • Orthopnoea (shortness of breath when lying flat) may be evident in older children caused by increased distribution of blood to the pulmonary circulation.
  • Tire easily.
  • Oedema of the eyelids or feet along with jugular venous distension caused by congestion of the right side of the heart.
  • Weight gain may be present due to oedema.
  • Dizziness due to lack of blood supply and therefore oxygen to the brain.
  • Abdominal pain, nausea and vomiting especially after eating due to mesenteric ischaemia; this is caused by poor blood supply to the mesentery.

General


  • Tachycardia as the body attempts to pump more blood round the body.
  • Gallop rhythm refers to an abnormal rhythm of the heart on auscultation. It includes three or even four sounds, thus resembling the sounds of a gallop. The normal heart rhythm contains two audible heart sounds the ‘lub‐dub’ rhythm caused by the closing of the heart valves.
  • Hypotension due to poor cardiac output.
  • Cool peripheries with a weak, thready pulse due to decreased circulation combined with tachycardia.
  • Decreased urinary output due to low circulatory output.
  • Cardiomegaly seen on chest X‐ray is nearly always present.


Management


The management of CF in children involves treating the underlying cause, such as correcting anaemia, surgically correcting congenital heart defects where possible or treating infections. Management also involves control of heart failure through the use of medication (Table 9.3), along with general supportive measures, such as rest and help with feeding. This may include high calorific feeds through a nasogastric tube and elimination of salt in the older child’s diet. Too much salt in the body causes water to be retained, which in turn increases fluid retention further increasing oedema and breathing difficulties.


Table 9.3 Drugs that may be used in the treatment of heart failure (Joint Formulary Committee, 2015)
































Drug How it works Possible side effects
Angiotensin‐converting enzyme inhibitors (ACE), e.g., captopril Prevents conversion of angiotensin I to angiotensin II. Dilate the blood vessels, making it easier for the heart to pump blood to the body Hyperkalaemia in children with impaired renal function.
Hypotension
Persistent dry cough
Beta‐blockers, e.g., atenolol Decreases the activity of the heart by blocking the action of hormones such as epinephrine May precipitate asthma
Bradycardia
Sleep disturbance in some instances
Diuretics usually loop diuretics, e.g., furosemide Inhibits the body’s ability to reabsorb sodium at the ascending loop (loop of Henle) in the nephron, which leads to an excretion of water in the urine Hypokalaemia
Dehydration
Aldosterone antagonists, e.g., spironolactone Inhibits sodium resorption in the collecting duct of the nephron in the kidneys. This interferes with sodium/potassium exchange, reducing urinary potassium excretion and weakly increasing water excretion Hyperkalaemia
Hyponatraemia
Dehydration
Positive inotropic drugs, e.g., digoxin Increases the force of contraction of the myocardium Dizziness
Irregular heart beat
Anticoagulation, e.g., heparin Interruption of the process involved in the formation of blood clots Bleeding, which may cause, e.g., haematuria or nose bleeds

Classification of congenital heart defects


Congenital heart defects can be categorised into cyanotic and acyanotic defects. A baby or child with a cyanotic defect will present with a blue discolouring to their lips and extremities whereas the baby or child with an acyanotic heart defect will retain their normal colouring. However, a child with an acyanotic defect may become cyanosed and a child with a cyanotic defect may not show signs of cyanosis and therefore a more accurate classification involves blood flow (Fig. 9.2).



  1. Increased pulmonary blood flow
  2. Decreased pulmonary blood flow
  3. Obstruction to blood flow out of the heart
  4. Mixed blood flow.
Tree diagram for classification of CHD with congenital heart defects branching to acyanotic (left) and cyanotic (right). Both are branching further.

Figure 9.2 Classification of CHD.


Cyanosis occurs when there is an inadequate amount of oxygenated blood circulating in the body. The percentage of oxygen saturation varies through the heart chambers with the left side reaching 100% oxygen saturation as the blood returns from the lungs. Oxygen saturation on the right side of the heart is 75% as the deoxygenated blood returns from the body. The left side of the heart has higher pressure than the right side as the left ventricle is responsible for pumping blood throughout the body whereas the right ventricle is only pumping blood to the lungs. Where there are defects blood will flow from areas of higher pressure to lower pressure (Figs 9.3 and 9.4).

Diagram displaying oxygen saturation levels within the heart with right atrium, right ventricle, and pulmonary artery at 75% and aorta, left atrium, and left ventricle at 100% indicated at the right.

Figure 9.3 Diagram showing oxygen saturation levels within the heart.

Diagram displaying pressure in mmHg within the heart with right atrium (3–7 mmHg), right ventricle (20 mmHg), pulmonary artery (25/10 mmHg), left atrium (5–10 mmHg), aorta (100/70 mmHg), etc. indicated at the right.

Figure 9.4 Diagram showing pressure in mmHg within the heart.


Cardiac investigations


Diagnosing a congenital heart defect involves:



  • History taking

    • gestational and perinatal history
    • postnatal and present history
    • family history

  • Physical examination

    • general appearance, e.g., respiratory state, colour including cyanosis, nutritional state
    • pulse including peripheral pulses and auscultation of the heart
    • blood pressure including four limb measurements

  • Electrocardiogram
  • Chest X‐ray to consider heart size
  • Echocardiogram
  • Magnetic resonance imaging (MRI) and cardiac computed tomography (CT) may occasionally be required
  • Cardiac catheterisation.

ACYANOTIC CONGENITAL HEART DEFECTS


Increased pulmonary blood flow


Atrial septal defect (ASD)


The interatrial septum is the wall of tissue that separates the right atrium from the left atrium. It develops in stages during the first and second month of fetal development. During development a small section of the wall is left open covered by a small flap; this is the foramen ovale, which is a vital part of fetal circulation as it allows blood to bypass the lungs. During fetal circulation, blood entering the heart bypasses the right ventricle passing directly through the foramen ovale into the left atrium, through the left atrioventricular value to the left ventricle and is then pumped back to the body via the aorta. The fetus receives oxygen from the mother through the placenta. The flap of the foramen ovale closes at birth as the pressures within the heart adjust to normal circulation.


An atrial septal defect occurs when the interatrial septum fails to develop correctly leaving a hole in the atrial wall. Blood is forced back from the higher pressure left atrium to the lower pressure right atrium (Fig. 9.5).

Diagram of ASD with arrows indicating oxygenated blood flow from the left atrium to the right atrium, with parts labeled WC, RA, RV, LV, LA, PA, AO, and PV.

Figure 9.5 Diagram of ASD showing oxygenated blood flowing from the left atrium to the right atrium.


Types of ASD


  • Secundum ASD – this is the most common type of ASD, accounting for 70% of all ASDs. It is in the centre of the atrial wall and is caused because the foramen ovale fails to close after birth, i.e., patent foramen ovale (PFO).
  • Primum ASD – this accounts for about 25% of ASDs and arises from the lower end of the atrial septum.
  • Sinus venosus ASD – this defect accounts for only 5% of ASDs and arises from the upper end of the atrial septum.


Pathophysiology

The slightly higher pressure within the left atrium causes oxygenated blood to flow from the left atrium through the septal defect to the right atrium, a left‐to‐right shunt, causing an increase in oxygenated blood through the right side of the heart. This additional flow is generally well tolerated although it can cause the right side of the heart to stretch and enlarge.


Signs and symptoms

Small defects are mainly asymptomatic, a murmur may be heard on auscultation of the chest and the defect may be detected during a routine health check.


Larger defects may cause symptoms of a left‐to‐right shunt with extra strain on the right‐hand side of the heart. Babies may become breathless especially during feeding and therefore struggle to gain weight. Older children may have poor exercise tolerance. Frequent chest infections may be an additional indication. Left untreated cardiac failure or pulmonary hypertension may develop in later life.


Treatment

Eighty percent of small, secundum defects close spontaneously in the early years and may not require any treatment. A defect larger than 8 mm is unlikely to close spontaneously nor is spontaneous closure likely to occur after the age of 4 years (Park, 2016).


Larger defects may be closed though a cardiac catheterisation procedure using a septal occluder to cover the defect. A small catheter is inserted into a vein in the groin and fed through the vein to the heart. If this is not possible, open‐heart surgery and cardiopulmonary bypass will be required.


Ventricular septal defect (VSD)


A ventricular septal defect is a congenital defect (hole) of the interventricular septum, which is the wall separating the right and left ventricles (Fig. 9.6). At 4–8 weeks’ gestation, the previously single ventricular chamber of the heart is remodelled, and development of the septum occurs to form a four‐chambered heart (Chamley et al., 2005), two ventricles and two atria. An error at this stage will result in a VSD.

Diagram of USD with arrows indicating oxygenated blood flow from the left ventricle to the right ventricle, with parts labeled WC, RA, RV, LV, LA, PA, AO, SVC, and PV.

Figure 9.6 Diagram of VSD showing oxygenated blood flowing from the left ventricle to the right ventricle.


Types of VSD


  • Membranous VSD, which accounts for 80% of all ventricular septal defects.
  • Muscular VSD.


Pathophysiology

Higher pressure in the left ventricle causes a left‐to‐right shunt of blood into the right ventricle and into the pulmonary artery. Increased blood volume in the right ventricle is pumped into the pulmonary artery and to the lungs. The increased blood flow to the lungs will over a period of time increase pulmonary vascular resistance. The increased pressure within the right ventricle and the increased pulmonary vascular resistance will cause the muscle of the right ventricle to hypertrophy. The right atrium may also enlarge as it attempts to overcome the resistance within the right ventricle.


Signs and symptoms

Infants and children with small VSDs may be asymptomatic. Larger defects will cause problems with growth and development as infants struggle to feed adequately. They may suffer from repeated chest infections, have a decreased exercise tolerance and develop cardiac failure. The degree and position of a murmur will depend on the severity of the defect and a chest X‐ray may show cardiomegaly (enlargement of the heart).


Treatment

Small VSDs may spontaneously close in 30–40% of cases (Park, 2016). Surgical treatment is most likely to be required. Complete repair using sutures or a patch is common; this requires open heart surgery and cardiopulmonary bypass. Depending on size and location, it may be possible to close the VSD through a cardiac catheterisation procedure. Medical treatment for heart failure may be required prior to surgery. Surgery may be delayed in asymptomatic children until the age of 4 or 5 years. Those who respond well to medical treatment may have surgery delayed until approximately 18 months of age, whereas those with large defects and those who do not respond well to medical treatment should be operated on sooner.


Patent ductus arteriosus


Normal fetal circulation involves a small vessel, the ductus arteriosus, which connects the pulmonary artery to the aorta (Fig. 9.7). The fetal circulation bypasses the lungs due to oxygenation taking place at the placenta, blood is therefore diverted from the pulmonary artery directly into the aorta to return to the body. A patent ductus arteriosus is the failure of the vessel to close at or shortly after birth; it accounts for 5–10% of all congenital heart defects, excluding premature infants (Table 9.4).

Diagram of PDA with arrows indicating oxygenated blood returning to the heart from the aorta, with parts labeled WC, RA, RV, LV, LA, PA, AO, SVC, and PV.

Figure 9.7 Diagram of PDA showing oxygenated blood returning to the heart from the aorta.


Table 9.4 Patent ductus arteriosus in the premature infant







  • PDA appears in 45% of infants weighing less than 1.7 kg at birth and in about 80% of infants weighing less than 1.2 kg (Park, 2016).
  • Additional problems are evident in infants with respiratory distress syndrome caused by the lack of surfactant in the lungs of premature infants. The pulmonary vascular resistance of the premature infant is reduced through improved oxygenation but the ductus arteriosus remains open because its response to oxygen remains immature. This results in the shunt of blood from aorta to pulmonary artery and the resulting increased blood volume through the immature lungs and left side of heart. Weaning an infant off ventilation becomes increasingly difficult.
  • Episodes of bradycardia or apnoea may be evident in infants not requiring ventilation. A murmur and bounding peripheral pulses may be present.
  • Pharmacological treatment for closure of a PDA may be achieved with intravenous ibuprofen or indomethacin.

Pathophysiology

Higher pressure within the aorta shunts the blood from the aorta into the pulmonary artery resulting in the blood being returned to the lungs and then back to the left side of the heart. This increases the volume of blood in the left side of the heart thus increasing the workload of the left side of the heart and pulmonary vascular congestion.


Signs and symptoms

If the defect is small, infants may be asymptomatic; larger defects can increase the occurrence of chest infections, lead to heart failure and faltering growth. A murmur may be heard and an echocardiogram may show cardiomegaly.


Treatment

A PDA found incidentally though echocardiogram and causing no symptoms does not require closure. Closure via cardiac catheterisation is recommended when the PDA causes heart failure or concerns about the infant’s growth and development. Surgical closure is indicated in some cases.


Outflow obstruction from ventricles


Outflow obstruction from the ventricles means that the blood leaving the heart from the ventricles, left or right, is met with an anatomical defect, a stenosis or narrowing. This causes an obstruction, which in turn causes an increase in pressure below the stenosis, usually in the ventricles, and a decrease in pressure beyond the stenosis in one of the great arteries. The stenosis is usually found near the valves.


Pulmonary stenosis


Blood leaves the right ventricular through the pulmonary artery, the entrance to which is guarded by the pulmonary valve. The valve consists of three semi‐lunar cusps and their function is to prevent backflow of blood into the right ventricle. Pulmonary stenosis (Fig. 9.8) is narrowing of the pulmonary artery and accounts for 5–8% of all congenital heart defects (Park, 2016). Location of pulmonary stenosis may be:



  • valvular – at the pulmonary valve (most common manifestation)
  • subvalvular – narrowing below the valve
  • supravalvular – narrowing of the pulmonary artery above the valve.
Left: Diagram of pulmonary stenosis with right ventricle hypertrophy. Right: Magnified views of normal pulmonary valve (3 semi-lunar cusps) and stenotic pulmonary valve (thickened cusps with narrowed opening).

Figure 9.8 Diagram of pulmonary stenosis with right ventricular hypertrophy.


Pulmonary atresia is the most extreme form of pulmonary stenosis. There is no blood flow through the pulmonary artery and survival is only possible if there is also an interatrial defect, such as an ASD, present.


Pathophysiology

Resistance to blood flow into the pulmonary artery causes increased pressure within and hypertrophy of the right ventricle. As the right ventricle fails, the pressure within the right atrium will increase, which may cause the foramen ovale to re‐open. As the pressure will be higher in the right atrium, deoxygenated blood will be shunted across the foramen ovale and into the left atrium to the left ventricle through the aorta to the body – systemic cyanosis will be present. Severe pulmonary stenosis will lead to heart failure.


Signs and symptoms

Depending on the degree of obstruction, an infant or child may be asymptomatic, have mild cyanosis or have signs and symptoms of heart failure. A heart murmur will be present and an echocardiogram will show a thickened pulmonary valve. The severity of the obstruction does not usually increase in mild cases but may progress with age in moderate to severe cases.


Treatment

Balloon valvuloplasty is the treatment of choice where possible. A catheter, with a small collapsed balloon at the end is inserted into the femoral vein and passed into the heart and the pulmonary artery. The balloon is then positioned in the narrowed valve, is inflated, stretching the valve open, before being deflated and removed. Surgery may be required if this procedure is unsuccessful or not indicated, for example, through position of the stenosis.


Aortic stenosis


The aorta is the body’s largest artery. It begins in the left ventricle of the heart, ascends for a short distance before arching backwards and descending through the thoracic cavity, and on into the abdominal cavity. Blood is pumped from the muscular left ventricle through the aortic valve into the aorta and to the body. The aortic valve, formed of three semi‐lunar cusps, guards the entrance of the aorta and prevents backflow of blood into the left ventricle. Aortic stenosis (Fig. 9.9) causes outflow obstruction from the left ventricle and accounts for 10% of all congenital heart defects (Park, 2016). Aortic stenosis location may be:



  • valvular – at the aortic valve is the most common manifestation and is generally caused by malformation of the cusps resulting in bicuspid rather than tricuspid valve or from fusion of the cusps (Schroeder, Delaney & Baker, 2015). Many cases of bicuspid aortic valve go unnoticed in childhood (Park, 2016);
  • subvalvular – narrowing of the aorta below the valve;
  • supravalvular – narrowing of the aorta above the valve.
Illustrations of normal tricuspid aortic valve (left), stenotic tricuspid aorta valve (middle), and abnormal bicuspid aorta valve (right).

Figure 9.9 Diagram showing (a) normal tricuspid aortic valve; (b) stenotic tricuspid aorta valve; (c) abnormal bicuspid aorta valve.


Aortic atresia is the most extreme form of aortic stenosis. There is no blood flow through the aorta and survival is only possible if the ductus arteriosus remains open. Aortic atresia usually occurs in combination with other heart defects, typically hypoplastic left heart syndrome.


Pathophysiology

Resistance to blood flow into the aorta causes increased pressure within the left ventricle. The extra workload causes hypertrophy (thickening) of the left ventricle. As the left ventricle fails, the pressure within the left atrium will increase, which in turn causes increased pressure within the pulmonary veins, and leads to pulmonary oedema/congestion.


Signs and symptoms

Children with mild to moderate degrees of aortic stenosis may be asymptomatic although they may be exercise intolerant presenting with signs of chest pain and dizziness. Blood pressure is generally normal, as is an electrocardiogram (ECG). Diagnosis is confirmed with echocardiogram. In the case of aortic stenosis, the severity may worsen with time as a result of calcification (Park, 2016).


Neonates with severe aortic stenosis will show signs of reduced cardiac output, weak pulses, hypotension, tachycardia and poor feeding.


Treatment

The critically ill neonate will need medical treatment for heart failure, such as inotropic drugs and diuretics, along with prostaglandin to keep the ductus arteriosus open. Balloon valvuloplasty (see pulmonary atresia) of the aortic valve is the first line of treatment to stretch the aortic valve and increase blood flow. Surgical repair or replacement of the valve may be indicated if valvuloplasty is unsuccessful or as the condition worsens.

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Mar 27, 2019 | Posted by in NURSING | Comments Off on Disorders of the cardiac system

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