Essay on Cardiovascular Case Study: Atrial Septal Defect

Atrioventricular Canal Defect is an abnormality that causes the mixing of blood. There is a hole in center of heart where the wall between the upper and lower chambers meet. The tricuspid and mitral valves aren’t formed properly and one large valve crosses the defect. The defect lets oxygen rich blood pass to the heart’s right side and mix with deoxygenated blood, then go back to the lungs. Another abnormality is Atrial Septal Defect (ASD), where the walls of the upper chambers of the heart don’t close completely, causing a left to right movement of blood due to the higher pressure. The mixing of oxygenated and deoxygenated blood may cause the right atrium and ventricle to enlarge due to the higher volume of blood.

You need to explain to him the s/s of blood clotting (since he may have too low an INR d/t treatment and he needs to know this). Explain that his a-fib puts him at risk for blood clots.

A ventricular septal defect or VSD is a heart defect. It’s congenital, this means that a baby is born with it. It is an opening or hole in the dividing wall called the Septum, between the two lower chambers of the heart, right and left ventricles. Ventricular septal defects are the most common type of congenital heart defects. A VSD allows oxygen-rich blood to pass from the left ventricle through the opening in the septum. Then it mixes with oxygen-poor blood in the right ventricle. There are different types of ventricular septal defects, the type your child has depends on which part of the wall between the ventricles is involved. Also the size of the opening or hole varies. A ventricular septal defect may occur more often in some families, this is because of gene defects. But most of the time, the cause is unknown. Similarly to ventricular septal defect, an Atrial septal defect is a birth defect of the heart in which there is also a hole in the wall in the septum, but instead of dividing the lower chambers it divides the upper chambers of the heart (atria), here a hole can vary in size and may close on its own or may require surgery as well. An atrial septal defect is one type of congenital heart defect, in which also the baby is born with it.

A large ventricular septal defect (VSD) is a hole in the wall between your heart’s main pumping chambers.

She was born with Tricuspid Atresia, Vetricula Steptum Defect, along with a Mirtral valve defect and numerous other medical issues. Tricuspid Atresia is a complex heart defect that occurs when the right ventricle in the heart fails to develop correctly during development in the womb. In Smilie’s case, it caused her to have little to no function in the right ventricle of the heart. To save Smilie’s life, doctors at the Prince Charles Hospital preformed a 3-stage surgery over 2 years to redirect blood flow within her body. Smilie had the BT Shunt at a few days old, the Hemi Fontan at 6 months old and the Fenestrated Fontan completed at 2 years of age. Smilie now has Hyploplastic Right Heart Syndrome as a result, which is a generalised term used to encompass the many conditions that can cause a lack of development in the Right Ventricle Side of the heart.

Elderly people like Sharon who is on regular digoxin and frusemide are at high risk of digoxin toxicity (Skidmore-Roth, 2013). Frusemide is a loop diuretic which could effectively help her to get rid of the excessive fluid in her body as well as electrolytes (Skidmore-Roth, 2013). As a result, Sharon might experience hypokalemia, which could induce digoxin toxicity (Skidmore-Roth, 2013).

Information to patient: Indicated for hypertension and angina. Reduce the blood pressure and risk of stroke and heart attack. They are calcium channel blockers which works by widening your blood vessels making it easier for your heart to pump blood around the body and help increase blood and oxygen supply to the heart. Taken once daily with or without food at the same time each day. Swallow the tablet whole with a full glass of water. Taking the tablet at the same time each day will have the best effect. It will also help you remember when to take it. You are currently on 5mg but your doctor might increase this depending on how you respond to the medication. Tell your doctor

Potassium (K+) is a major intracellular cation and is responsible for electrical conduction throughout the body. Additionally, it is necessary for proper heart and muscle function, and digestion. The normal serum potassium range is between 3.5-5.0 mEq/L; hyperkalemia occurs when potassium levels exceed 5.0 mEq/L. Monitoring and treating hyperkalemia is quintessential to primary care as excess potassium can heart blocks and ventricular fibrillation which can result in sudden death (Pannone et al., 2012).

It is very important to determine if medical intervention with medication is needed to control his blood pressure. The blood pressure should be monitored after discontinuing the pseudoephedrine and implementing nonpharmological methods. Some nonpharmological methods involve increasing their exercise, losing weight, and limiting their sodium intake. If the blood pressure is not able to be controlled an antihypertensive medication may need to be implemented. A first line medication should initially be started to help control his blood pressure. There are different types that can be used. Some of these comprise of a thiazide diuretic or an angiotensin converting enzyme (ACE) inhibitor. The patient should first be started on a low dosage of these

When a ventricular septum defect occurs, a mixing of oxygen rich and oxygen poor blood takes place. A ventricular septum defect is a hole in the septum, or the wall between the left and right chambers of the heart. This hole happens to be in between the lower two chambers, or ventricles. The left ventricle receives oxygen rich blood from the lungs, while the right ventricle houses the oxygen poor blood from the body. The purpose of the separation by the septum is to prevent a mixture of the blood. Therefore, as long as there is a defect preventing the separation, the heart will continue to pump a mixture of the blood to the rest of the body. This causes the cells of the body to not receive all of the required oxygen that it would normally obtain with a fully intact septum, thus causing the cyanotic, or blue, appearance of the patient.

The efficacy of the treatment can be monitored by observing the blood pressure reading. However, electrolyte disturbance is a common adverse effect of thiazide diuretics as it causes potassium wasting. The frequency of hypokalemia depends on the frequency of administration, dose, diet, and other pharmacologic agents used. During the first two weeks of therapy, electrolytes monitoring is significant. Once a stable state is established, patients are not usually at risk of hypokalemia, unless the dose is increased, extra renal losses of potassium increase, or dietary potassium is reduced. Thiazide diuretics also can cause certain metabolic and endocrine abnormalities such as hypochloremic alkalosis, hypercalcemia and hyponatremia. They can cause photosensitivity and precipitate gout. Hence, it is important to monitor laboratory values periodically in patients on diuretic therapy. The most common drug interactions are pharmacodynamic interactions resulting from potassium depletion caused by the diuretics. Hypokalemia is a risk factor for arrhythmias, and the risk is increased with concomitant therapy with antiarrhythmic agents that prolong the QT interval independently of serum potassium concentration. Therefore, combinations of drugs that can cause hypokalemia such as diuretics, and antiarrhythmic agents require vigilant monitoring of potassium and appropriate replenishment.

It is important to remember the ACEI block the production of angiotensin II altogether, which also block the enzyme kinase. This mechanism allows for vasodilation, decreased blood volume, and the suppression aldosterone: allowing for decreased blood pressure and a slight decrease in edema. While the suppression of kinase can cause an accumulation of bradykinin in the lungs, causing a cough, ACEIs are considered the number one go to drug for hypertension and heart failure. ARBS, working in much the same way as ACEIs, block angiotensin II receptor sites. This allows for kinase to work again bradykinin, and does not produce the adverse cough. Diuretics are a must in most hypertensive patients because they decrease edema, lower blood volume, and decrease the workload of the heart. It is important to watch for adverse side effects such as hypokalemia and hypotension in some patients. By combining all of this knowledge with appropriate lifestyle changes, a clinician can successfully manage a patient’s hypertension and heart

When my mom was 5 months pregnant with me during a routine ultrasound the doctors discovered that I would be born with a heart condition. I have three different disorders, which are Atrioventricular canal defect also known as congenital defect, Heterotaxy, and Pulmonary Atresia. Atrioventricular canal is a condition that occurs when there’s a hole between the heart’s chambers and problems with the valves that regulate blood flow into the heart. Heterotaxy syndrome is a rare birth defect that involves the heart and other organs. Pulmonary Atresia is defined as a birth defect

Those chambers are separated by inter atrial and inter-ventricular septum (IVS) respectively (Kaufman & Bard, 1999; Stadtfeld, Ye, & Graf, 2007). The normal formation of the septa of the embryonic heart depends on the formation of mesenchymal cells in the cardiac cushions. The latter is formed via activating endothelial cells in the atrioventricular (AV) and conus outflow tract (OT) regions to form cushion mesenchyme (Moore, Mjaatvedt, & Gearhart, 1998). Defects in normal development of cardiac cushions or septa results in the well known atrial, atrioventricular canal, conotruncal, and ventricular septal defects (VSD) which all represent major causes of congenital heart disease (LEE, HSIEH, CHEN, & SHIUE, 2009). Ventricular septal defects are one of the most common congenital heart lesions (Stadtfeld et al.,

Several studies have shown that spontaneous closure occurs with small defects that have a diameter of less than 3mm. Patients with muscular and perimembranous defects can expect for spontaneous closure to occur (Zhang et al., 2015). However, when significant shunting produces problems, treatment is unnecessary. Diuretics are often the first in line to relieve symptoms. Afterload reduction may also be used to promote systemic flow from left ventricle, reducing left-to-right shunting as a result. Defects that need surgical correction are often closed by placing a patch directly over it from the right ventricular side. Larger muscular apical defects require banding the pulmonary trunk to correct the pulmonary and systemic resistances and minimize shunting. Closing a defect for patients with Eisenmenger physiology would be detrimental since it would worsen the pulmonary hypertension by causing suprasystemic right ventricular systolic pressure. Cardiac catherization may be needed in these circumstances (Spicer et al., 2014). The prognosis is excellent for isolated ventricular septal defects. Patients who need surgical repair can also anticipate an excellent prognosis with zero mortality and minimal morbidity, without significant changes to the quality of life. Echocardiography plays a significant role in improving the prognosis for patients by