Depicted above is a family of cardiac function curves representing a ventricle under various conditions. Point A represents baseline cardiac function with normal preload; points A1 and A2 show states of decreased and increase preload, respectively. After reviewing this figure, please answer the following questions.
What is Frank-Starling mechanism? Intracellularly, how can it cause a more forceful contraction?
For the Frank-Starling curves depicted in Fig. 75.1, what are other parameters that can be substituted for the cardiac output label on the y-axis?
What parameters can replace preload on the x-axis?
What physiological changes might cause the system to move from:
Point A to A2
Point A to A1
Point A to B
Point A to D
Following a premature ventricular contraction in a normal ventricle, how will the force generated by the next contraction change?
After a single bolus dose of phenylephrine, what effect can be expected on cardiac output?
If starting at point D2 on Fig. 75.1, would a fluid bolus be expected to increase cardiac output? If not, what interventions could increase output?
The Frank-Starling mechanism describes a relationship where increasing ventricular filling increases cardiac output. Increased preload increases sarcomere stretch inside cardiac myocytes which generate more force during contraction and thereby allows the heart to eject more blood. However, there is a limit to which this relationship can be maintained. In failing ventricles, overstretch can limit or decrease cardiac output. In these cases, reducing myocyte stretch to a more optimal length can improve overall cardiac function. Although the cellular basis has not been definitively determined, the most widely accepted mechanism is that as sarcomeres are stretched, there is a length-dependent reduction in the spacing between thick and thin filaments. As the filaments are stretched and get closer together, tropomyosin on the thin filament becomes more sensitive to calcium. When contraction occurs, the sarcoplasmic reticulum releases calcium. The more sensitive tropomyosin now allows more actin-myosin cross-bridges to form yielding greater force generation [1–3].
Multiple measurements have been developed to describe how well or efficiently a cardiac ventricle can pump. Essentially any measure that varies directly to cardiac output can be substituted on the y-axis. Some of the more popular metrics include venous return, stroke volume, cardiac index, and stroke work.
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