The patient with systolic heart failure, or systolic ventricular dysfunction, would present to the clinic with very different symptoms from the patient with diastolic heart failure. In systolic heart failure, the heart is incapable of producing enough cardiac output to supply vital tissues. Because of this insufficiency, the hard must work harder to provide adequate blood supply to its vital organs and tissues. Cardiac output is determined by heart rate, how fast the heart is beating, and stroke volume, how much blood is being pumped through the heart. However, stroke volume is determine by three key factors: contractility, preload, and afterload (McCance 1190). Contractility is capacity at which the heart can contract, how strongly the
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Catecholomines will be activated to stabilize the cardiac output. They increase heart rate and PVR, or afterload. The renin-angiotensin-aldosterone-system will increase preload and after load. However, Angiostensin II also facilitates ventricular remodeling which will further perpetuate the problem; this can decrease cardiac contractility and cause ventricular dilation. Insulin resistance can cause extremely detrimental effects on cardiac contractility by decreasing the body’s ability to supply ATP. Once again, this can lead to cardiac remodeling and heart failure. This heart failure will lead to the activation of RAAS which will perpetuate the cyclical problem. Between the mechanical and the neurohumoral issues seen with systolic ventricular dysfunction, one can see how each system and mechanism feeds the other. Hypertension from an unhealthy life style can cause a small amount of damage to the left ventricle. The repair of that ventricle could cause a small amount of ventricular remodeling, which could be just enough to perpetuate a series of events to send the patient into heart …show more content…
This can occur due to a number of reasons. The most common cause of diastolic dysfunction is myocardial hypertrophy due to hypertension. This is when the heart has enlarged due to work overload. This enlargement has ultimately caused ventricular remodeling; which makes it difficult for many things to happen. This remodeling result in, “a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation” (McCance 1194). There can also be issues involving the effectiveness of the aortic or mitral valves. Inflammation from disease can cause them to become rigid or ineffective at closing so that blood cannot flow freely into the ventricles during diastole. Much of how the heart works is determined by how much blood is able to flow into the ventricle. Contractility is determined, in part, by input. Decreased ventricular compliance and atypical diastolic relaxation are the two major factors in diastolic dysfunction. Compliance of the left ventricle is how much blood is accepted into the ventricle during diastole, during relaxation. This compliance determines the strength of the contraction in systole. If the ventricle is has decreased compliance, the receptors are not stimulated to contract during systole. During abnormal relaxation is
Catecholomines will be activated to stabilize the cardiac output. They increase heart rate and PVR, or afterload. The renin-angiotensin-aldosterone-system will increase preload and after load. However, Angiostensin II also facilitates ventricular remodeling which will further perpetuate the problem; this can decrease cardiac contractility and cause ventricular dilation. Insulin resistance can cause extremely detrimental effects on cardiac contractility by decreasing the body’s ability to supply ATP. Once again, this can lead to cardiac remodeling and heart failure. This heart failure will lead to the activation of RAAS which will perpetuate the cyclical problem. Between the mechanical and the neurohumoral issues seen with systolic ventricular dysfunction, one can see how each system and mechanism feeds the other. Hypertension from an unhealthy life style can cause a small amount of damage to the left ventricle. The repair of that ventricle could cause a small amount of ventricular remodeling, which could be just enough to perpetuate a series of events to send the patient into heart …show more content…
This can occur due to a number of reasons. The most common cause of diastolic dysfunction is myocardial hypertrophy due to hypertension. This is when the heart has enlarged due to work overload. This enlargement has ultimately caused ventricular remodeling; which makes it difficult for many things to happen. This remodeling result in, “a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation” (McCance 1194). There can also be issues involving the effectiveness of the aortic or mitral valves. Inflammation from disease can cause them to become rigid or ineffective at closing so that blood cannot flow freely into the ventricles during diastole. Much of how the heart works is determined by how much blood is able to flow into the ventricle. Contractility is determined, in part, by input. Decreased ventricular compliance and atypical diastolic relaxation are the two major factors in diastolic dysfunction. Compliance of the left ventricle is how much blood is accepted into the ventricle during diastole, during relaxation. This compliance determines the strength of the contraction in systole. If the ventricle is has decreased compliance, the receptors are not stimulated to contract during systole. During abnormal relaxation is