A client that I will be training has a special condition called Post-Myocardial Infarction Syndrome. The Post-Myocardial Infarction Syndrome is also known as Dressler’s Syndrome. This condition is an inflammation of the sac surrounding the pericardium (outside fibrous layer of the heart). Dressler's syndrome is an immune system response after damage to heart tissue, due to events such as a heart attack, surgery or traumatic injury.
Symptoms can include prolonged pericardial friction, persistent chest pain (similar to pain during a heart attack), continuing fever, and fluid accumulation in heart and lungs.
Supposedly, these features develop during the first few weeks after the myocardial infarction. Dressler’s Syndrome may pursue a relapsing course for months. The syndrome was first described by Dressler in 1956, and in 1959 he reported its occurrence in 44 patients. He estimated that the syndrome
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This can cause fluids to accumulate, putting pressure on the heart, and forcing it to work harder. Overall this reduces the hearts ability to pump blood efficiently.
• Constrictive pericarditis which is inflammation causing the membrane surrounding the heart to scar or to thicken. This scarring may reduce the heart's ability to pump blood efficiently. A few special considerations to note as the trainer when dealing with a client with Dressler’s syndrome:
• The client may experience shortness of breath and chest pain due to fluid accumulation in membranes surrounding lungs.
• A persistent low grade fever may be present in the client.
• The client may experience Joint Pain due to the syndrome
Most importantly, exercise can make symptoms worse when there is flare up, so I must practice vigilance.
I have formulated a list of do’s and don’ts when dealing with a client who has Dressler’s syndrome:
I will discuss the general symptoms of these two types along with pathology, diagnostic factors, and the different treatments for this disorder (Smith). EDS can vary in severity and are transmitted as autosomal recessive, autosomal dominant, or X-linked recessive traits. The primary characteristics are hyperextensible skin and joints (Dia. 1-2, pg.6), tendency to bruise easily (Dia. 3, pg.6), reduced wound healing capability, pseudotumors, and ocular defects. Differences within the six types may reflect inter/intra familial variability or genetic heterogeneity. Each type of EDS is classified into symptoms and signs that result (Clarke, D., Skrocki-Czerpak, K., Neumann-Potash, L).
is a common heart valve abnormality and is the cause of mitral regurgitation. The flaps of the valve are “floppy” and don’t close tightly allowing the blood to flow backward in your heart. The affect is that blood can’t move through the heart or to the rest of your body as efficiently, making you feel tired and out of breath.
Which theory, model of practice or frame of reference will you use with this client/patient and why?
...ufficiently nourish the organs. This blood flow shortage causes severe damage to organs and tissue. Symptoms of cardiomyopathy include shortness of breath and other breathing difficulties, fatigue, swollen legs and feet, and irregular heartbeat. It can lead to heart failure.
This assignment is a case study that aims to explore the biospychosocial impacts of a myocardial infarction on a service user. It will focus on the interventions used by healthcare professionals throughout the patient’s journey to recovery. To abide by the NMC’s code of conduct (2015) which states that all nurses owe a duty of confidentiality to all those who are receiving care, the service user used in this case study will be referred to as Julie. Julie is a 67 year old lady who was rushed to her local accident and emergency following an episode of acute chest pain and was suspected to have suffered from a myocardial infarction. Julie who lives alone reported she had been experiencing shortness of breath and
...gs causing high pressure in the arteries; leading to an irreversible pulmonary hypertension. Other complications include, “aortic insufficiency, leaking of the valve that separates the left ventricle from the aorta; damage to the electrical conduction system of the heart during surgery causing an irregular heart rhythm; delayed growth and development; heart failure; stroke; infective endocarditis, a bacterial infection of the heart.”
Hypertrophic cardiomyopathy is an inherited disease that affects the cardiac muscle of the heart, causing the walls of the heart to thicken and become stiff. [1] On a cellular level, the sarcomere increase in size. As a result, the cardiac muscles become abnormally thick, making it difficult for the cells to contract and the heart to pump. A genetic mutation causes the myocytes to form chaotic intersecting bundles. A pathognomonic abnormality called myocardial fiber disarray. [2,12] How the hypertrophy is distributed throughout the heart is varied. Though, in most cases, the left ventricle is always affected. [3] The heart muscle can thicken in four different patterns. The most common being asymmetrical septal hypertrophy without obstruction. Here the intraventricular septum becomes thick, but the mitral valve is not affected. Asymmetrical septal hypertrophy with obstruction causes the mitral valve to touch the septal wall during contraction. (Left ventricle outflow tract obstruction.) The obstruction of the mitral valve allows for blood to slowly flow from the left ventricle back into the left atrium (Mitral regurgitation). Symmetrical hypertrophy is the thickening of the entire left ven...
759. Mr. Miller is likely presenting with an acute myocardial infarction. Based on his past medical history of hypertension, hyperlipidemia, obesity, and diabetes, along with his current symptoms of chest pain, shortness of breath, pale skin with beads of sweat on the forehead, as well as elevated lab 's Troponin, CK, and CK-MB, he is most likely presenting with an acute myocardial infarction.
-The patient was having pitting edema and inspiratory rales because the increase of sodium caused an increase of fluid in the vascular system and lungs.
...o those patients with chest pain, in order to maintain oxygen saturations as close to 100%, unknowingly realizing that the patient is being exposed to significant periods of hyperoxia (Moradkham & Sinoway, 2010 ). It has been suggested that this is due to poor monitoring skills by health professionals. (Moradkham & Sinoway, 2010 ). From reading this essay it is clear that there is a high demand and need of further clinical research into the effectiveness of oxygen in the client with chest pain. More research also has to be conducted in order for the health professionals to fully understand what oxygen does to the body. Through completing and implementing more updated and reviewed evidence and research on the effect of oxygen on the client with chest pain, a better practice can be put in place to ensure the patient is receiving the best care to save their life.
These causes will change the heart significantly. The pathophysiology of heart failure is described differently as: (1) an oedematous disorder, by means of which the deviations in renal hemodynamics and excretory ability lead to salt and water holding; (2) a hemodynamic disorder, considered by peripheral vasoconstriction and decreased cardiac output; (3) a neurohormonal disorder, mainly by stimulation of the renin-angiotensin-aldosterone system and adrenergic nervous system; (4) an inflammatory syndrome, related with amplified local and circulation pro-inflammatory cytokines; (5) a myocardial disease, started with an damage to the heart trailed by pathological ventricular transformation. In heart failure, the heart sustains either a sudden or longstanding structural injury. When damage occurs, sequences of firstly compensatory but consequently maladaptive mechanisms follow (Henry & Abraham, ).
Cardiovascular System: He does not experience any chest pain or palpitation. He does not have dyspnea or leg swelling.
In the case study it is the left lung that is in distress, and as the pressure increases within the left lung it can cause an impaired venus return to the right atrium (Daley, 2014). The increased pressure can eventually affect the right lung as the pressure builds in the left side and causes mediastinal shift which increases pressure on the right lung, which decreases the patients ability to breath, and diffuse the bodies tissues appropriately. The increase in pressure on the left side where the original traum... ... middle of paper ... ... 14, January 29).
The patient has high temperature-sign of fever, a very fast pulse rate (tachycardia), and chest wheezing when listened to using a stethoscope (Harries, Maher, & Graham, 2004, p.
Client Profile: Lane Bronson is a 55 year old male with a history of angina, hypertension, Type 2 diabetes, COPD, and sleep apnea. He comes to the physican’s office complaining of worsening shortness of breath. His skin tone is grey, and his angina is worsening. Previously stable, he now does not get relief from rest or nitroglycerin. The physician called 911 and had Mr. Bronson directly admitted to the hospital.