Question

What is the direct effect of a decrease in EDV? (think about the steps in the mechanism)?

1. No effect

2. Increased contractility

3. Decreased contractility

4. Decrease venous return

5. Increase venous return

Explain why your choice is a direct effect in EDV (you can draw or explain)

What would be a plausible cellular mechanism at the level of the cardiomyocyte for this change?

Why is this so? (Draw the cell, indicate type of cardiomyocyte in discussion),   draw the mechanism to defend your answer (include transporters, ions, gradients, organelles, etc)

What cardiovascular law discussed in this unit can be used to defend the physiology taking place in this scenario; explain?

Answer 1

Question-1: Answer:

What is the direct effect of a decrease in EDV? (think about the steps in the mechanism)?

1. No effect

2. Increased contractility

3. Decreased contractility

4. Decrease venous return

5. Increase venous return

Explain why your choice is a direct effect in EDV (you can draw or explain)

Answer:

Decreased contractility:

Decreased contractility ----> Increased after load-------> increase in considerable hydrostatic pressure within the heart --> elevated right atrial pressure = decreased venous return --> decreased End Diastolic Volume --> decreased Systolic Volume --> decreased Cardiac Ouput.

Stroke work in the cardiac cycle is defined as the considerable area under ventricular pressure-volume curve in relation to both preload (measured by EDV, atrial pressure and venous pressure) and afterload. According to the ventricular pressure-volume loop, an increase in afterload produces an increase in end systolic volume. The reason behind this is as the load increase causes ventricle shortening a bit lower. As per end-systolic pressure volume loop, ionotropic effect will be produced with the epinephrine action thereby ventricle shorten further totally due to rise of after load finally result in steeper slope in end-systolic pressure volume loop.

gripping the handlebars tightly result in, rise in systolic blood pressure is observed due to the elevated mean arterial blood preesure with more cardiac output & heart rate compared to the statice level of exercise.

Iscahemic or isometric (static) exercise leading to increased cardiovascular pheripheral resistence associated with systolic blood pressure and diastolic blood pressure finale more mean arterial pressure. In crease of prolonged excersises leading to alterations in cardiovascular drift associated with increased heart rate and decreased stroke volume. Isometric exercises leading to elevated static strength associated with considerable reduced atrophy.

Pressure-Volume loop: Normally, stroke volume (mitral valve opens--àmitral valve closes) is the difference between end systolic pressure and end diastolic blood pressure. It is normal due to ventricular emptying of the blood. Cardiac output id equal to heart rate x stoke volume. For example, in cycling ergometer (or wingate test), when,, sudden gripping the handlebars tightly leading to sudden emptying of the ventricular volume associated increased heart rate there by leading persistent or abnormal blood pressure finally abnormal readings. It is due to change in intra ventricular pressure-volume changes of stroke volume further due to cardiac output.  

Cardiac output = Heart rate x stroke volume (SV)

Cardiac output = Heart rate x (End diastolic volume (EDV) – End systolic volume (ESV))