Premature Closure Of The Ductus Arteriosus Case Study

1. The pulmonary circuit is supplied by which ‘side” of the heart? The systemic circuit? The right atrium

2. The defect in Caleb’s heart allows blood to mix between the two ventricular chambers. Due to this defect would you expect the blood to move from left-to-right ventricle or right-to-left ventricle during systole? Explain your answer based on blood pressure and resistance in the heart and great vessels. It goes left to right during systole. The difference is normally, oxygen-poor (blue) blood returns to the right atrium from the body, travels to the right ventricle, and then is pumped into the lungs where it receives oxygen. Oxygen-rich (red) blood returns to the left atrium from the lungs, passes into the left ventricle, and then is pumped out to the body through the aorta. But when an infant has ventricular septal defect it still allows oxygen-rich (red) blood to pass from the left ventricle, through the opening in the septum, and then mix with oxygen-poor (blue) blood in the right ventricle. (ROCHESTER.EDU) but instead when systole occurs the blood gets mixed because of the septum therefore heart needs to pump harder to ensure that enough blood with oxygen reaches the body.

An electrical stimulus was applied to the heart; the following graph shows the refractory period of the frog’s heart when an extra-systole was induced. It can be seen that right after the recording was marked “Refractory 3,” an extra-systole was detected.

R E V I E W S H E E T 30 Anatomy of the Heart

Premature birth has been linked to a vast array of lungs problems, the earlier the birth the greater risk of health complications(Davis R and Mychaliska G, 2013). A majority of the health problems will affect the infant for the rest of their life (Davis R and Mychaliska G, 2013). Infants born between the canalicular and the saccular period (week 25) have lung development that is unsuitable for gas exchange (Davis R and Mychaliska G, 2013). Two major complications that arise with undeveloped lungs is bronchopulmonary dysplasia, and pulmonary arterial hypertension (Mahgoub L. et al. 2017).

Pharmacological therapy would include; prostaglandin E1 or E2 to maintain the patency of the ductus arteriosus, diuretics, dobutamine to increase contractility of the volume loaded right ventricle. (The Lancet)

I was born in 1998 with Patent Ductus Arteriosus (PDA). The ductus arteriosus is only open when a child is in the womb and should close after birth to prevent the oxygenated blood from mixing with the deoxygenated blood in the heart. PDA put a tremendous strain on my heart and lungs and not too long after birth; the doctors put me on a ventilator. A surgery was suggested, called PDA ligation, which involved closing the PDA with a small clip. The doctors had explained to my parents that the surgery may not be successful and if it was, there could be certain lasting effects such as being blind, deaf or mental retardation.

However, in certain cases, the ductus arteriosus does not close and remains patent resulting in a persistent patent ductus arteriosus. A PDA can cause many complications such as bacterial endocarditis, late congestive heart failure, and the development of pulmonary vascular obstructive disease. The hemodynamic effect of PDA is depends on the size of the PDA and the resistance of pulmonary and systemic circulations (Kim, 2016). A continuous murmur is often heard in patients with PDA. A Continuous murmur occurred due to a continuous blood flow shunting from the high-pressure or high resistance circulation to the low-pressure or low resistance circulation, throughout systole and diastole. The continuous murmur in PDA consists of two components, a crescendo systolic one and a decrescendo diastolic one, with a peak of intensity around second sound. The murmur is continuous in PDA because the ductus arteriosus provides a permanent communication between the systemic circulation, with high pressure, and the pulmonary circulation, where pressure level is much lower. About

Tricuspid atresia is treated from birth and involve a combination of operations within the first two years of life. Initially a cardia catheterization procedure is done to evaluate the defects. Then generally 3 operations are done, including a Blalock-Taussig shunt, Glenn Shunt (done at 4-6 months of age) which replaces the initial shunt, and finally a Fontan procedure (done at 2-3 years of age) which forms a second that directs blood from the inferior vena cava to the right pulmonary artery. The Glenn shunt is left in place. Aortic Valve Stenosis is a heart defect that is either congenital or acquired. The disease itself can be described basically as the inability of the valve to open completely. Atrial Septal defect is caused by an opening the atrial septum, there are 2 ways it can be caused, including a congenital cause, or the hole that is present in the heart of every fetus is not properly closed at the postnatal stage. Coarctation of the aorta is the narrowing of the aorta and is a congenital disease. It can occur anywhere in the aorta however most often is found in the segment just after the aortic arch. Patent Ductus Arteriosus is usually found a

Congenital heart defects (CHD) are birth defects that are considered the common in the United States. These defects affect a newborn child’s blood flow to and from the heart and sometimes can leave the heart lacking parts that make it necessary for the heart to do its job. According to the Centers for Disease Control and Prevention (CDC) (2014), 1 in 4 children born with a CHD is considered critical and will result in that child needing heart surgery or other similar procedures within the first years of its life. These CHD’s can range from Atrial Septal Defects, Coarctation of the aorta, Ebstien anomaly, Pulmanary artesia, Tetralogy of Fallot, Trancus Arteriosus, Hypoplastic Left Heart Syndrome, as well as many others (Centers for Disease Control and Prevention, 2014). The specific CHD that will be covered in detail will be the Hypoplastic Left Heart Syndrome (HLHS). HLHS accounts for nearly 960 congenital birth defects per year and

In the valvular disease the regurgitation of blood back to the ventricles occurs when the valves fail to close tightly and this will result in ventricular overload and increased muscle stretching. This increases the heart muscles need for oxygen and energy resulting in the cardiac muscles to contract harder (Karch, 2013). The failure of the left ventricle to pump efficiently will lead to pulmonary vessel congestion and in severe cases, pulmonary edema whereas the inefficient pumping of right ventricle will lead to liver congestion and peripheral edema (edema of the legs and feet). The cardiovascular system works as a closed system and therefore, if one-sided failure left untreated, will eventually lead to failure of both sides (Karch, 2013). The American College of Cardiology (ACC)/ American Heart Association (AHA) has incorporated a classification system of heart failure that include four stages. This staging system (stage A to stage D) recognizes that there are established risk factors and structural abnormalities that are characteristics of the four stages of heart failure.

In the foetal circulation, the primary role of the ductus arteriosus (DA) is to divert the ventricular output away from the lungs towards the placenta in utero by its connection between the pulmonary artery and the descending aorta. The patency of the ductus is mainly regulated by low oxygen tension present in the foetal lung and prostaglandin, which is known for its vasodilating effect in the placental circulation. Prostaglandin levels are usually high as a result of placental production and low clearance ability of the foetal lung (Gardner, Carter, Enzman Hines, Hernandez,2016).

Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further

The S-A node signal is delayed by the atrioventricular node to allow the full contraction of the atria that allows the ventricles to reach their maximum volume. A sweeping right to left wave of ventricular contraction then pumps blood into the pulmonary and systemic circulatory systems. The semilunar valves that separate the right ventricle from the pulmonary artery and the left ventricle from the aorta open shortly after the ventricles begin to contract. The opening of the semilunar valves ends a brief period of isometric (constant volume) ventricular contraction and initiates a period of rapid ventricular ejection.

There is increased blood flow, and blood volume returning to the heart.” - L. Robins 2015