Right Ventricular Analysis

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

Dyspnea and decreased exercise tolerance- which contributes to diastolic dysfunction with an increase in left ventricular filling pressures with exercises.

In systolic ventricular dysfunction or systolic heart failure the heart is not able to produce enough output for adequate tissue perfusion. Heart rate and stroke volume produce cardiac output. Contractility, preload, and afterload influence the heart’s stroke volume. These factors are important in understanding the pathophysiologic consequences of this syndrome and possible treatments. Patients with systolic heart failure usually have dilated, large ventricles and impaired systolic function.

The increased resistance of blood flow through the pulmonary semilunar valve from the right ventricle backs up the pressure of blood

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

With this new invention a systematic way of interpreting an Electrocardiograph soon developed. The layout of the graph is as such: there are 4 columns which correspond to the leads; the first column – I, II, and III; the second column: aVR, AVL, aVF; the third V1-3; and the fourth V4-6. Each column is recorded simulation however they are not always displayed on the strip except for the last rhythm strip which occurs at the bottom of the tracing (lead II and V1).

contractions was replaced by different whole number ratios, e.g. 2:1, 3:1, the heart was in partial heart block.

Additionally, to understand the relationship between the heart disease and the disease associated with diabetes, myocardial performance index was held. According to the strong heart study, the Myocardial performance index is also known as the Tei index, is a Doppler-derived echocardiographic. It is an index that incorporates both systolic and diastolic time intervals in expressing systolic and diastolic ventricular function. Systolic dysfunction prolongs pre-ejection (isovolumic contraction time, IVCT) and a shortening of the ejection time (ET). Both systolic and diastolic dysfunction result in abnormality in myocardial relaxation which prolongs the relaxation period. Various research was done with Indian American people between the age of 59+or-8 in which 66% were women and 44% were men. The data on the correlates and prognostic values of MPI in population without overt cardiovascular (CV). MPI is also abnormal in individuals without the overt cardiac disease who have risk factors such as diabetes mellitus and treated and untreated hypertension. Group of adults who has diabetes, hypertension, and obesity but without overt CV disease, MPI has weak associations with clinical and physiologic determinants of cardiac function. MPI (mean= 0.24+or- 0.17) showed significant negative association with creatinine clearance. C-reactive protein (CRP), LV

Isolated diastolic heart failure is defined as pulmonary congestion despite a normal stroke volume and cardiac output. Two areas of pathophysiologic changes in the ventricle have been identified in diastolic dysfunction: decreased compliance of the left ventricle and abnormal diastolic relaxation

When the ventricles are contracting at a rate greater than one hundred beats per minute, the heart becomes inefficient. Blood cannot properly fill the ventricular chambers before it is forced out. This decreases the amount of oxygenated blood circulating through the body.

Left Ventricular Systolic Dysfunction (LVSD) is an abnormal cardiovascular symptom characterized by a reduction in the left ventricular ejection fraction (LVEF), a measurement of the percentage of blood leaving the heart with each contraction. LVEF is commonly measured using echocardiography and calculated as the ratio between the blood volume exiting the left ventricle over the volume filling the left ventricle. A higher ejection fraction (EF) indicates better strength and contractility of the heart. Recent guidelines from the American and European society of echocardiography have defined an abnormal LVEF as any EF <40-55%.

In a sweeping fashion, the right atrium contracts and forces the final volume of blood into the right ventricle. The left atrium contracts and contributes the final 20% of volume to the left ventricle.

The term that best describes the pressure set upon Roger's heart is increased pre-load. Increased-preload, also called the left ventricular end-diastolic pressure (LVEDP), is the measure of ventricular extend toward the finish of diastole. Consider it the heart stacking up for the following enormous crush of the ventricles amid systole. A few people recollect this by utilizing a similarity of an inflatable – blow air into the

In recent years, advances in the medical field have allowed the body to be studied to a greater extent than ever before. These developments have resulted in better treatment options and prognoses, as well as the opportunity for researchers to find connections between symptoms thought previously to be unrelated. In one such instance, Dr. Michael Salerno and his team at the University of Virginia sought to quantify the amount of scarring of the heart muscle experienced by adult patients with either high blood pressure (HTN) or those with high blood pressure and thickening of the heart muscle (HTN-LVH). A third normal, age-matched group with no history of hypertension was employed as a control in this recent study (Control). One of the ultimate goals of this study is to gain a better understanding of patients that are more prone to particular types of heart failure. The results could have far-reaching implications, as hypertension is a risk factor associated with many adverse cardiovascular outcomes. This project used the data from the Salerno study, and attempted to analyze and explore the variance between the three groups listed above, focusing specifically on the left ventricular end-diastolic volume variable (LVEDV). This variable measures the largest volume that the heart cavity obtains in each cardiac cycle. We expected there to be a significant difference amongst the means of this value within the three populations studied.

reports the amount of force exerted by the blood into the arteries during ventricular contraction.