During a myocardial infarction, as an immediate treatment, we must try to decrease the workload of the heart so that it will not require the extra oxygen that it would need and cannot get due to the loss of some cardiac mass, right? So during a myocardial infarction, my professor told me that one of the treatments is to increase venous return so that we can compensate for the decrease in cardiac output. But my question is, doesn't the increase in venous return increase the workload of the heart? Or is it that the increase in venous return does not increase the oxygen demand of the heart because the increase in venous return stretches the myocyte, hence the recoil of it is passive, right? This is the Frank-Starling law, right?
Then my professor also said that the sympathetic activation must also be lowered to decrease the blood pressure and the heart rate. Is the Frank-Starling law related to contractility? Or is it that contractility is related to the sympathetic nervous system and that an increase in contractility adds to the oxygen demand of the heart hence why my professor told me that a treatment is to lower the sympathetic activation?
Is this statement true or not: "During a myocardial infarction, increasing the hearts contractility to increase the stroke volume of the left ventricle is a treatment to improve the heart during a myocardial infarction"? Or what is wrong in the statement? I feel like it is not true because first of all, we must lower the sympathetic activation hence we decrease the contractility. Although it would increase the stroke volume, it would increase the oxygen demand too. So I think that we have to increase the stroke volume in ways that would not increase the oxygen demand, for example, by increasing the venous return (if indeed my initial explanation is right that the increase in venous return increases the stroke volume passively due to the recoil of the myocytes).
Narrowed down question: Is one of the reasons for decreasing the sympathetic nervous system activation during a myocardial infarction to decrease the contractility of the heart? If so, is this contractility decreased to decrease the workload of the heart? Does an increase in the end diastolic volume (since we increase the venous return) affect the contractility? Or is it just related to the Frank-Starling law, which passively increases the stroke volume?
Thank you so much for any help!
