Stroke Volume – Cardiac Output (Nursing)

00:01 So taking a closer look at the regulation of stroke volume, we find that our stroke volume is equal to the end diastolic volume minus the end systolic volume.

00:14 Our end diastolic volume is going to be affected by the length of ventricular diastole as well as our venous pressure.

00:24 Our end systolic volume is going to be affected by arterial blood pressure and the force of our ventricular contraction.

00:35 A normal stroke volume is approximately 70 ml per beat.

00:45 There are three main factors that can affect this stroke volume.

00:50 First, we have preload followed by contractility, and then afterload.

00:58 Starting with preload, preload is the degree to which a cardiac muscle cell is stretched just before it contracts and so the preload can cause changes in stroke volume by affecting the end diastolic volume.

01:16 The relationship between preload and stroke volume is referred to as the Frank-Starling law of the heart.

01:25 Our cardiac muscle fibers exhibit a length-tension relationship and at rest, the cardiac muscle cells are going to be shorter than their optimal length.

01:36 Because of this, this is going to cause a dramatic increase in the contractile force of the heart.

01:46 The most important factor in this preload stretching of our cardiac muscle is going to be venous return so blood that is returning to the heart from the veins.

01:59 A slow heartbeat as well as exercise is going to affect or increase this venous return.

02:09 And this increase in venous return or this increase in the amount of blood the coming back to the heart is going to distent or stretch the ventricles and thus is going to increase the force of contraction.

02:26 So next we have contractility.

02:29 And contractility is going to mean the contractile strength at the given muscle length.

02:35 Contractility is going to be independent of stretch and also independent of end diastolic volume.

02:43 So an increased contractility will lower the end-systolic volume.

02:50 Think about it, if I'm more contractile then there's less that is left.

02:55 This is caused by sympathetic epinephrine release that's going to stimulate an increase in that calcium influx and leading to more cross-bridge formations during depolarization.

03:10 Also, positive inotropic agents can increase contractility as well.

03:17 These include things like thyroid hormone thyroxine, glucagon, epinephrine, digitalis as well as high extracellular calcium ions.

03:32 The contractility of the cardiac muscles can also be decreased by negative inotropic agents such as acidosis or increased extracellular potassium or by the blocking of calcium channels with calcium channel blockers.

03:51 The third factor that can regulate stroke volume is afterload.

03:56 Afterload is the pressure the ventricles must overcome in order to eject blood out of the ventricles into circulation.

04:07 Back pressure from the arterial blood is pushing on our semilunar valves and this is a major pressure.

04:17 The aortic pressure is around 80 mmHg and the pulmonary trunk pressure is around 10 mmHg.

04:26 Also, afterload can be affected by things like hypertension.

04:30 So for example, hypertension or high blood pressure will increase the afterload which is gonna result in an increase in the the end systolic volume and that increase in end systolic volume will result in a reduction of the stroke volume.

04:52 So now, let's look at these factors and put them all together.

04:56 So first, the factors that can help determine our cardiac output include things like exercise, ventricular filling time, bloodborne epinephrine or thyroxine or excess calcium or central nervous system output in responds to exercise, fright, anxiety or blood pressure.

05:20 All of these are initial stimuli that will have an effect on our cardiac output.

05:28 With exercise and ventricular filling time, if these are happening so first if you're exercising or if there is a longer ventricular filling time, this is going to increase our venous return of blood into the atria.

05:46 This increase in venous return is gonna increase our end diastolic volume or our preload.

05:56 When it comes to bloodborne epinephrine and other factors, these are going to increase the heart's contractility.

06:05 And an increase in contractility as going to decrease the end-systolic volume Next, the central nervous system outputs in response to exercise can be sympathetic.

06:20 If it is sympathetic, if we are increasing sympathetic activity, then this is going to increase cardiac output and if we're decreasing sympathetic activity, then this can decrease cardiac output.

06:34 Also, sympathetic activity can directly affect contractility as well.

06:42 When it comes to an increase in end diastolic volume or decrease in end-systolic volume, both of these factors will lead to an increase in our stroke volume.

06:55 Sympathetic activity can lead to an increase in the heart rate.

07:02 When we put these together, all of these different factors will affect cardiac output.