Right ventricle

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

the stage where fluid surrounds the heart making it incapable of pumping properly. You have four chambers in your heart. Two atria in the upper half of the heart and two ventricles in the lower half of the heart. The ventricles pump blood to the lungs and the rest of the body. Congestive heart failure occurs when your ventricles can not pump enough blood to the body. Eventually causing blood and other fluids to back up inside of your lungs, abdomen and lower body. There are two different types

Atrial septal defects (ASDs) are a deficiency in the wall between the right and left atrium of the heart (5). ASDs account for 10% of all congenital heart defects(19) and 30% of those diagnosed in adulthood (20). Definitive diagnosis is by transthoracic echocardiography, though signs of an ASD can be found on physical examination, electrocardiography and chest radiography (21). There are four types of ASD, classified according to their position in the interatrial septum (Figure 2): • Ostium secundum

What is Heart failure? The heart’s function is to move oxygenated blood from the lungs to the left atrium, then on to the left ventricle, pumps it to the rest of the body. The left ventricle supplies most of the heart 's pumping power; therefore, the left ventricle is larger than the other chambers and essential for normal function. In left-sided or left ventricular (LV) heart failure, the left side of the heart must work harder to pump the same amount of blood (American Heart Association -AHA,

The left side of the heart brings oxygen-rich blood from the lungs through the left atrium to the left ventricle, then out into body. When the left side of the heart is damaged or can’t pump as well, it has to work harder to send blood through the body. This causes fluid to build up in the body, especially the lungs. That’s why shortness of breath is one of the most common symptoms of heart failure. Systolic failure happens when the heart doesn’t pump out blood the way it should. Diastolic means

interventricular septum allows communication between the systemic and pulmonary circulations. As a result, flow moves from a region of high pressure to a region of low pressure. In other words, blood flows from the left ventricle to the right ventricle, hence the name left-to-right shunt. There are various degrees of severity for this disease by having either a small or large shunt. Patients with a small shunt are asymptomatic and their life prognosis is very optimistic compared to those with a large

Heart failure (HF) is the inability of the heart to pump adequately to meet the metabolic needs of the body (Jeffrey et al, 2007). It is caused by structural or functional abnormalities of the heart (NICE, 2003). The reduced contractility leads to a reduced stroke volume, and therefore the heart rate is increased to help maintain cardiac output. HF can either be chronic where it has been occurring over time or acute, where it happens suddenly. Around 900,000 people in the UK have HF, with almost

Tetralogy of Fallot (ToF) and Transposition of the great vessels (TGA) are congenital heart defects affecting the vessels of the heart. In both pathologies, patients present with cyanosis, due to abnormal communication between ventricles. The mechanisms by which cyanosis occurs differs because ToF impacts blood flow due to constriction and TGA impacts the ability of the body to receive re-oxygenated blood.1 Tetralogy of Fallot affects 10% of people with congenital heart defects. Patients present

showed the only a minor increase in amplitude and period. The BPM was the detected as increase up to 30 seconds then a drop back down to 44, then the heart rate shot back up to 48 before recovering. Table 5. The effects of Atropine measured by the ventricle of the frog’s heart by amplitude, period, and BPMs. Treatment Amplitude (V) Period (sec) BPMs Resting 0.008 0.245 42 Atropine 0.009 0.260 42 10 sec after 0.010 0.270 42 20 sec after 0.010 0.285 45 30 sec after 0.010 0.245 48 40 sec after 0.011 0

The definite haemodynamic diagnosis of pulmonary hypertension (PH) requires right heart catheterisation and direct measurements of right ventricular, pulmonary artery and pulmonary capillary wedge pressures and cardiac output. As this is an invasive test with risk and cost implications diagnostic algorithms have been devised that combines clinical assessment, non-imaging cardio-respiratory assessment and non-invasive imaging in patients suspected of having pulmonary hypertension. The initial aim