Mitral Valve Dysfunction: A Case Study

The abnormally fast heartbeat caused by SVT, lasts in episodes lasting for several hours. During an episode

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

To determine if the patient’s chest pain is related to cardiac ischemia, you would look for ST-segment depression and/or T wave inversion. If the ST-segment depression is at least 1mm (one small box) below the isoelectric line, it is significant and occurs in response to inadequate supply of blood and oxygen, which leads to an electrical disturbance. Once this is treated, adequate blood flow is restored, the ECG changes will resolve, and the ECG will return back to patient’s baseline.

The use of beta-blockers to slow the heart rate may benefit patients who have episodes of tachycardia, or rapid heartbeats, with the mitral valve prolapse. Unless it has progressed to something severe, the patientwill probably not need treatment. If it has become severe, then the patient can benefit from surgery to repair or replace the leaky valve. Although it sounds scary, it is a condition that can be managed quite easily and the patient can live a normal lifestyle without any impairment or major adjustment to your activities.

With acute aortic insufficiency, pulse pressure widens as the valve deteriorates. Signs and symptoms may include a bounding pulse, atrial and ventricular gallops, chest pain, palpitations, pallor, crackles, dyspnea, and jugular vein distention, may also be present.

Disease, endocarditis or a congenital defect can result in heart valve problems. When the valves don't open or close properly during each heartbeat, the heart muscle has to pump harder to keep blood moving.

Mitral valve prolapse (MVP) was first characterized by Barlow and Bosman in the 1960s.(Barlow and Bosman) It was first called Barlow’s Syndrome before being called mitral valve prolapse by Criley (Barlow and Bosman),(Criley et al.). Barlow’s syndrome was diagnosed by electrocardiogram, phonocardiogram and chest X-ray.3 The mitral valve apparatus includes tow leaflets, chordae tendineae, anulus, left atrium, papillary muscles and left ventricular wall (Devereux et al.). Mitral valve prolapse involves the leaflets, chordae, annulus and left ventricular wall.(Devereux et al.) The anterior leaflet is relatively long and semi-circular, while the posterior leaflet is shorter in normal patients.(Irvine et al.) Most commonly the posterior leaflet is affected.(Devereux et al.) During systole the leaflet balloons in to the left ventricle.(Devereux et al.) Physically, in a patient with mitral valve prolapse, the leaflet is displaced beyond the mitral anulus.(Levine et al.)

Consequences of left ventricular systolic dysfunction include ischemic diseases, atrial fibrillation, increased ventricular response, and myocardial infarctions2. Some of these symptoms were seen in the patient from the case study. Factors leading to left

Mitral Valve Prolapse (MVP) is also knows as Barlow’s Syndrome or Click Murmur Syndrome and it affects about 2-6% of the United States population. While Mitral Valve Prolapse is one of the most common heart valve abnormality that can develop in any person at any age. It is usually not life-threatening and the patient might not even have symptoms. A patient might feel symptoms such as Fatigue, chest pain, or palpitations, which will cause a doctor to run tests such as an echocardiogram; causing a detection and confirmation of the Mitral valve prolapse. The MVP abnormality is caused when one or both of the mitral valve flaps are enlarged or have extra tissue. Causing the valve leaflets to not close correctly and allow leakage of blood back into

Other signs and symptoms include: strokes, atrial fibrillation, some heart diseases, chest pain and dyspnea, which means difficult or labored breathing. Next I will talk about some of the risk factors that play a role in being diagnosed with

Particularly heart beat irregularities (atrial fibrillation), disease of the heart valves, congestive heart failure or recent heart attack.

Mitral stenosis refers to narrowing of the mitral valve resulting in obstruction of blood flow from the left atrium to the left ventricle. The mitral valve is damaged and deformed predisposing it to scarring and narrowing (stenosis) later in life. Rheumatic mitral stenosis is associated with thickening of the mitral valve leaflets and fusion of commissures and chordae tendineae together with fibrosis and calcification. Hypertrophy of the left atrium develops and may be followed by right sided heart failure and pulmonary edema. Symptoms usually develop when the mitral valve area decreases below 2.5cm2 and it is classified as “mild” stenosis .When the mitral valve area decreases below 1.5cm2 it is regarded as “moderate’ stenosis and when

Vasovagal Syncope, also known as fainting, neurocardiogenic syncope, and neurally mediated syncope, is a very common condition, occurring in roughly half of all people at least once within their life; three percent of the population develops it repeatedly. It is not a serious condition.(2) A vasovagal response involves a decrease in the volume of blood that is returned to the heart, which enervates the baroreceptors(2) in the sympathetic nervous system to increase the force of each contraction of the heart. Consequently, the opposing parasympathetic nervous system is alerted to slow the heart rate and dilate the surrounding veins and arteries. These responses of the nervous system cause the blood pressure to drop very low, causing syncope (loss of consciousness).(1) Most patients are young and healthy, although vasovagal syncope can occur in the elderly population that has preexisting cardiac problems. Extremely hot weather and blood-alcohol levels are typical triggers. Some patients suffer from several, often attacks, while others may only experience them sporadically.(3)

Neurocardiogenic syncope is a condition where the heart stops growing, even though the rest of your body continues to grow. Since the heart is not the appropriate size to support the body, people who have Neurocardiogenic syncope syndrome will occasionally have low blood pressure along with an uncomfortable feeling in their chest, confusion, weakness and visual disturbances such as lights seeming too bright or tunnel vision. If these feelings do not pass after a short period of time the person will most likely faint. These feelings will occur after what is called a trigger. A trigger for one person with Neurocardiogenic syncope may not be the same for someone else. For instance, I would get these feelings and faint when I preformed in marching band and get these mild symptoms when I practice, while other people may get these feelings when they exercise

Syncope is defined as a loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom can have life-threatening results for some people. Syncope is related to fainting. Syncope occurs due to global cerebral hypoperfusion. Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, which is the primary metabolic substrate. Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body; therefore, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope. Cerebral perfusion