Cardiac Quiz Questions And Answers - ProProfs Quiz
Cardiac Quizzes & Trivia The Cardiac quiz questions and answers below are designed to help . Increase preload and no effect on afterload. Tutorials/Quizzes These ventricular changes can be complex because preload, afterload and inotropy are In PV loop diagrams, increased inotropy increases the slope of the end-systolic pressure-volume relationship (ESPVR; upper. Preload and Afterload – What's the Difference? May 26 A recent Quick Quiz on our Facebook page resulted in a mix of responses. Do you.
If preload end-diastolic volume and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume red loop in figure. Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected see force-velocity relationship.
A reduced stroke volume at the same end-diastolic volume results in reduced ejection fraction. If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases green loop in figure.Preload Afterload physiology in 2 minutes
Independent Effects of Inotropy Increasing inotropy increases the velocity of muscle fiber shortening at any given preload and afterload see force-velocity relationship. This enables the ventricle to increase the rate of pressure development and ejection velocity, which leads to an increase in stroke volume and ejection fraction, and a decrease in end-systolic volume red loop in figure.
CV Physiology | Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops
Decreasing inotropy has the opposite effects; namely, increased end-systolic volume and decreased stroke volume and ejection fraction green loop in figure. Interdependent Effects of Preload, Afterload and Inotropy In the intact heart, preload, afterload and inotropy do not remain constant.
To further complicate matters, changing any one of these variables usually changes the other two variables. Therefore, the above PV loops, although they illustrate the independent effects of these three variables, they do not represent what happens when the heart is in the body.
However, if one understands the independent effects of these variables, then it is relatively easy combine the loops to illustrate what occurs when multiple variables change. These materials are for educational purposes only, and are not a source of medical decision-making advice. Therefore, afterload cannot be represented by a single numerical value or described only regarding pressure.
CV - Quiz 3 Cardiac Cycle, Control of Cardiac Output Flashcards Preview
Arterial pressure diastolic, mean, or systolic is frequently used as a surrogate measure, but perhaps the best available techniques involve measuring systemic arterial resistance by various invasive and noninvasive methods.
Several mathematical models have been developed using arterial impedance and pressure-flow relationships to characterize afterload better, but these are complex and less often utilized in practice. The inverse relationship between afterload and cardiac output is important in understanding the pathophysiology and treatment of several diseases including aortic stenosis, systemic hypertension, and congestive heart failure. Mechanism The relationship between afterload and cardiac output is somewhat intuitive as one would expect the flow to increase as the load against which the heart contracts decreases.
Several researchers during the s and s sought to develop this understanding at the cellular level. Experiments by Sonnenblick on isolated cat papillary muscle strips demonstrated that the extent and velocity of muscle shortening decrease as the load on the muscle is increased. A major limitation of this study was its basic design employing the use of isolated muscle strips.
Monroe and French overcame this by using isolated whole-preparation dog hearts to show an inverse relationship between peak aortic flow and arterial impedance.
They reported similar findings to the previous studies giving further support for an inverse relationship between afterload and cardiac output due to alterations in sarcomere shortening.
Figure 1 is a graphic representation of the effect of increases or decreases in afterload on the cardiac output which is illustrated by shifting the baseline Frank-Starling curve downward or upward respectively. Clinical Significance Conditions in which there are chronic elevations in afterload, such as aortic stenosis and systemic hypertension, generate a cascade of adaptive responses which can be both beneficial and ultimately detrimental.
Initially, cardiac output is maintained through various regulatory mediators that increase inotropy. However, the ventricle responds to chronic elevations in afterload by concentric hypertrophy causing increased wall thickness and decreased chamber diameter. This reduces internal wall stress at the expense of ventricular compliance leading to diastolic dysfunction heart failure with preserved ejection fractionwhich can further deteriorate into systolic dysfunction heart failure with reduced ejection fraction.
Afterload reduction agents are an essential component in treating congestive heart failure with reduced ejection fraction as these patients have elevated systemic resistance due to the neurohormonal response to the decreased cardiac output.
They are also frequently used in the management of systemic hypertension. These drugs typically act by dilating the arterial system which reduces the total load on the contracting heart and increases systolic performance. The arterial dilators fall under the broader category of vasodilators which consists of arterial, venous, and mixed acting drugs. Venous dilators reduce preload by pooling blood in the highly compliant venous system and are an important part of treating angina.
The preload reducing properties of venodilators lead to a reduction in cardiac output and arterial pressure. Most drugs have mixed arterial and venous action, and the relative balance between these determines the effect on cardiac output.