Describe Aortic Regurgitation, Mitral Regurgitation, Tricuspid Regurgitation, Aortic Stenosis and Mitral Stenosis

Workshop Three Appraisal Guide

5.) Describe aortic regurgitation, mitral regurgitation, tricuspid regurgitation, aortic stenosis and mitral stenosis.

Aortic regurgitation is caused by an acute or chronic lesion of rheumatic fever, bacterial endocarditis, syphilis, hypertension, connective tissue disorders, or atherosclerosis. The heomdynamic repercussions depend on the size of the leak. During systole, blood is ejected from the left ventricle into the aorta. If the aortic semilunar valve is affected, some of the ejected blood flows back into the left ventricle. Volume overload occurs in the ventricle because it receives blood from the left atrium during diastole and blood from the aorta during systole. Over time the end diastolic volume of the left ventricle increases and myocardial fibers stretch to accommodate the extra fluid. Ventricular dilation and hypertrophy eventually cannot compensate for the aortic incompetence and heart failure develops. Clinical manifestations include widened pulse pressure resulting from increased stroke volume and back flow. Turbulence across the aortic valve during diastole produces a characteristic murmur. Large stroke volume and rapid runoff of blood from the aorta cause prominent carotid pulsations and throbbing peripheral pulses. Dysrhythnias and endocarditis are common complications of aortic regurgitation.

Mitral regurgitation permits backflow of blood from the left ventricle into the left atrium during ventricular systole, giving rise to a loud pansystolic (through out systole) murmur that radiates into the back and axilla. It has various causes mitral valve prolapse, rheumatic heart disease, infective endocarditis, CAD, connective tissue disease (Marfan Syndrome) and congestive cardiomyopathty. In mitral regurgitation the left ventricle becomes dilated and hypertrophied to maintain adequate cardiac output, despite increase volume from the left atrium. The volume of backflow reentering the left atrium gradually increases, causing atrial dilation. As the left atrium enlarges, the valve structures stretch and become deformed, left ventricular function may become impaired to the point of failure. Mitral incompetence is usually well tolerated, until ventricular failure occurs.

Tricuspid regurgitation Tricuspid regurgitation is more common than tricuspid stenosis and is usually associated with failure and dilation of the right ventricle secondary to high blood pressure in the pulmonary circulation or right ventricle. Tricuspid valve incompetence leads to volume overload in the right ventricle, increased systemic venous blood pressure, and right heart failure. Aortic stenosis has three common causes 1.) inflammatory damage caused by rheumatic heart disease, 2.) congenital malformation and 3.) degeneration resulting from calcification. The orifice of the aortic semilunar valve narrows, causing diminished blood flow from the left ventricle into the aorta. Outflow obstruction increases pressure within the left ventricle as it tries to eject blood through the narrow opening. Untreated aortic stenosis can lead to dysrhythmias, myocardial infarction and heart failure. Mitral stenosis impairs the flow of blood from the left atrium to the left ventricle. Mitral stenosis is most commonly caused by acute rheumatic fever or bacterial endocarditis, although uncommonly it can be congenital. Narrowing of the orifice occurs as inflammatory lesions in the valvular leaflets heal. Scarring causes the leaflets to become fibrous and fused, and the chordae tendineae cordis become shortened. If left untreated, chronic mitral stenosis develops into pulmonary hypertension, edema and right ventricular failure.

6.) Describe the mechanism that results in decreased oxygen delivery to the tissues in MODS.

In Multiple Organ Dysfunction Syndrome (MODS) oxygen delivery to the tissues decreases despite the supranormal systemic blood flow for several reasons:

* Shunting of blood past selected regional capillary beds, which is caused when inflammatory mediators override the normal vascular tone.

* Interstitial edema, resulting from microvascular changes in permeability that contributes to decreased oxygen delivery by creating a relative hypovolemia and by increasing the distance oxygen must travel to reach the cells.

* Capillary obstruction that occurs because of formation of microvascular thrombi and the aggregation of white blood cells.

Hypermetabolism in MODS with accompanying alterations in carbohydrate, fat, and lipid metabolism is initially a compensatory measure to meet the body's increased demands for energy. The alterations in metabolism affect all aspects of substrate utilization. The net result of hypermetabloism is depletion of oxygen and fuel supplies. Decreased oxygen delivery to the cells caused by maldistribution of blood flow, myocardial depression and the hypermetabolic state combine to create an imbalance in oxygen supply and demand. This imbalance is critical in the pathogenesis of MODS because it results in a pathologic condition known as supply-dependent oxygen consumption.

7.) What mechanisms can cause restriction of the airways in asthma?

In asthma the exposure to allergens or irritants result in a cascade of events that start with mast cell degranulation and the release of multiple inflammatory chemical and vasoactive mediators. The mediators released and the most important during an asthma attack are histamines, interleukins, immunoglobulins, prostaglandins, leukotrienes and nitric oxide. The vasoactive effect of theses cytokines include vasodilation and increased capillary permeability. Chemotaxtic factors are produced that result in bronchial infiltration by neutorphils.eosinophils and lymphocytes.

The resulting inflammatory process produces:

§ bronchial smooth muscle spasm,

§ vascular congestion,

§ edema formation,

§ production of thick tenacious mucus,

§ impaired mucociliary function,

§ thickening of airway walls and increased bronchial hyperresponsiveness

In addition, the autonomic control of bronchial smooth muscle is dyregulated because of the production of toxic neuropepptides and an increase in acetylcholine-mediated bronchospasm. These changes combined with epithelial cell damage caused by eosinophil infiltration, produce airway hyperresponsiveness and obstruction. If left untreated, can lead to long term airway damage that

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