What is after load

When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume. As shown in the figure, an increase in afterload shifts the Frank-Starling curve down and to the right from point A to B , which decreases stroke volume SV and at the same time increases left ventricular end-diastolic pressure LVEDP.

The basis for this is found in the force-velocity relationship for cardiac myocytes. Briefly, an increase in afterload decreases the velocity of fiber shortening. Afterload per se does not alter preload; however, preload changes secondarily to changes in afterload. Increasing afterload not only reduces stroke volume, but it also increases left ventricular end-diastolic pressure LVEDP i.

This occurs because the increase in end-systolic volume residual volume remaining in ventricle after ejection is added to the venous return into the ventricle and this increases end-diastolic volume.

This increase in preload activates the Frank-Starling mechanism to partially compensate for the reduction in stroke volume caused by the increase in afterload. The interaction between afterload and preload is utilized in the treatment of heart failure , in which vasodilator drugs are used to augment stroke volume by decreasing arterial pressure afterload , and at the same time reduce ventricular preload.

This can be illustrated by seeing how ventricular volume changes in response to a decrease in arterial pressure over several heart beats see figure. Arnold Sibanda Quite informative and good for sharpening critical thinking skills! Anita This was very helpful, thank you. I really like it! Paige Thank you! This helped a lot! Krishna gopal Me a nurse in a conmunity as a community nurse.

Evonne Smith Thank you, I like these quizzes to help me remember facts. Norton, James M. Vest, Amanda R. Humana, Cham, Milnor, William R. McDonald's blood flow in arteries: theoretical, experimental and clinical principles.

CRC press, Specifically, Chapter 12 is gold. Moriarty, Thomas F. Its limitations as a relation for diastolic pressure, volume, or wall stress of the left ventricle. Covell, J. Pouleur, and Jr J. Sonnenblick, Edmund H.

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Ritman, and E. Gsell, Matthias AF, et al. Time-varying myocardial stress and systolic pressure-stress relationship: role in myocardial-arterial coupling in hypertension. Determinants of afterload. Previous chapter: Determinants of preload Next chapter: Determinants of contractility. All SAQs related to this topic. All vivas related to this topic. Specifically, afterload seems to be the favourite determinant, as it was the main subject of the majority of past paper questions: Question 18 from the second paper of Question 13 from the first paper of Question 19 from the second paper of Question 17 from the first paper of Question 7 from the first paper of In summary: Afterload can be defined as the resistance to ventricular ejection - the "load" that the heart must eject blood against.

Increased transmural pressure negative intrathoracic pressure increases afterload Decreased transmural pressure eg. References Norton, James M. Specifically, Chapter 12 is gold Moriarty, Thomas F. The left ventricle has a much higher afterload than the right, mainly because of the increased arterial vascular resistance in the systemic circulation. Increased transmural pressure increases afterload in both ventricles. Dilation of either ventricle will increase the wall stress.

LV wall is thicker: this decreases afterload by sharing it among more sarcomeres. Aortic compliance is usually good, as it is an elastic capacitance vessel - this decreases LV afterload. Changes in blood viscosity also affect SVR. SVR is an unreliable indicator of left ventricular afterload [2] since it reflects only peripheral vasomotor tone and not left ventricular systolic wall force.

Discordant changes in left ventricular afterload and SVR can occur during pharmacological interventions as shown by Lang et al. Klabunde, R.