In: Nursing
What is the pathophysiology for the following conditions?
1. Pericardial effusion:
2. Myocarditis
3. Infective endocarditis
4. Mitral valve prolapse
1. Pericardial effusion:
Clinical manifestations of pericardial effusion are highly dependent on the rate of accumulation of fluid in the pericardial sac. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 L without symptoms.
The pericardium plays a pivotal role in cardiac changes during inspiration. Normally, as the right atrium and ventricle fill during inspiration, the pericardium limits the ability of the left-sided chambers to dilate. This contributes to the bowing of the atrial and ventricular septums to the left, which reduces left ventricular (LV) filling volumes and leads to a drop in cardiac output. As intrapericardial pressures rise, as occurs in the development of a pericardial effusion, this effect becomes pronounced, which can lead to a clinically significant fall in stroke volume and eventually progress to the development of pericardial tamponade.The pericardium plays a beneficial role during hypervolemic states by limiting acute cardiac cavitary dilatation.
2. Myocarditis
Myocarditis is inflammation of myocardium with necrosis of cardiac myocyte cells. Biopsy-proven myocarditis typically demonstrates inflammatory infiltrate of the myocardium with lymphocytes, neutrophils, eosinophils, giant cells, granulomas, or a mixture.Potential mechanisms that lead to myocardial injuries are
Direct cardiomyocyte injury caused by an infectious or other cardiotoxic agent
Myocardial injury caused by an autoimmune reaction to an infectious or other cardiotoxic agent
Myocardial inflammation can be diffuse or focal. Inflammation can extend into the pericardium causing myopericarditis. The extent of myocardial involvement and extension into adjacent pericardium can determine the type of symptoms. Diffuse involvement can lead to heart failure, arrhythmias and sometimes sudden cardiac death. Focal involvement is less likely to cause heart failure but can lead to arrhythmias and sudden cardiac death. Involvement of the pericardium leads to chest pain and other symptoms typical of pericarditis. Some patients remain asymptomatic whether myocardial involvement is focal or diffuse.
3. Infective endocarditis
Endocarditis is defined as an inflammation of the endocardial surface of the heart. This may include heart valves, mural endocardium or the endocardium that covers implanted material, such as prosthetic valves, pacemaker/defibrillator leads and catheters. Infective and non-infective-related causes must be distinguished. In most cases, the inflammation is related to a bacterial or fungal infection with oral streptococci, group D streptococci, staphylococci and enterococci accounting for 85% of episodes. From various portals of entry (e.g. oral, digestive, cutaneous) and a subsequent bacteraemia, pathogens can adhere and colonize intracardiac foreign material or onto previously damaged endocardium due to numerous complex processes based on a unique host–pathogen interaction. Rarely, endocarditis can be related to non-infective causes, such as immunological or neoplastic
4. Mitral valve prolapse
Mitral valve prolapse (MVP) is characterized primarily by myxomatous degeneration of the mitral valve leaflets. In younger populations, there is gross redundancy of both the anterior and posterior leaflets and chordal apparatus. This is the extreme form of myoxomatous degeneration, known as Barlow’s syndrome. In older populations MVP is characterized by fibroelastic deficiency with superimposed chordal rupture due to a lack of connective tissue support. These anatomic abnormalities result in malcoaptation of mitral valve leaflets during systole, resulting in regurgitation. Mitral annular dilatation may also develop over time, resulting in further progression of mitral regurgitation (MR). Acute severe MR results in congestive heart failure symptoms without left ventricular dilatation. chronic or progressively severe MR can lead to ventricular dilatation and dysfunction, neurohormonal activation, and heart failure. Elevation in left atrial pressures can result in left atrial enlargement, atrial fibrillation, pulmonary congestion, and pulmonary hypertension.Myxomatous proliferation is the most common pathologic basis for MVP, and it can lead to myxomatous degeneration of the loose spongiosa and fragmentation of the collagen fibrils. Disruption of the endothelium may predispose patients to infectious endocarditis and thromboembolic complications.