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Lecture 6

Lecture 6 Notes.pdf

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Department
Biological Sciences
Course
BIOC34H3
Professor
Stephen Reid
Semester
Winter

Description
1    Lecture 6: Stroke Volume Regulation (continued) and Heart Failure 1. Stroke Volume Regulation Continued Factors Affecting End Diastolic Volume: The Skeletal Muscle Pump The third factor to influence end diastolic volume, the skeletal muscle pump, serves to move blood up toward the heart when it is contracting, and to prevent blood backflow when the heart is relaxing. This obviously influences both end diastolic pressure (pre-load) and, therefore, EDV. If we look at the calf muscle, we see a vein flowing through the muscle that has have two valves - one, termed a proximal valve due to it being closer to the heart, and one termed the distal valve for being farther away. When the muscle contracts, the increase in pressure cause the distal valve to close and the proximal valve to open, forcing blood upwards towards the heart through the open proximal valve. Blood does not flow backward because the distal valve is closed. When the heart relaxes, the opposite occurs: the proximal valve closes and the distal valve opens. Blood that has previously been forced upwards towards the heart does not simply fall back into the muscle when the heart relaxes because the proximal valve is closed. Blood in the lower regions of the leg can flow into the vein through the open distal valve. The skeletal muscle pump is sometimes taken advantage of during surgery, to prevent the formation of blood clots. Electrical stimulation of the calf muscle activates the skeletal muscle pump and keeps blood moving toward the heart. This helps prevent the formation of blood clots and the development of deep vein thrombosis. When blood clots do form, it is referred to as thrombosis. A blockage of blood vessels in the lungs, caused by a blood clot, is called a pulmonary embolism. A formation of a blood clot in the legs, for example, can block blood flow, and lead to pain and tissue damage - and they can also break free, and flow through the veins to wedge into the heart or lungs, causing local damage to that particular region. 2    Factors Affecting End Diastolic Volume: The Respiratory Pump The respiratory pump serves to move blood from the abdomen to the chest and from the chest into the heart. During inspiration the diaphragm contracts and moves downward, increasing pressure in the abdomen. If the pressure in the abdomen becomes greater than the pressure in the thoracic cavity (chest), then the pressure difference will drive blood upwards toward the heart. It is, then, just another mechanism of venous return. When we exhale and the diaphragm relaxes, we don't get a backflow of blood into the abdomen – one-way valves similar to those described above prevent this. Expiration still assists in moving blood into the heart though, because the increase in pressure in the chest helps to force blood from the large central veins into the heart. 3    Factors Affecting End Diastolic Volume: Filling Time The final important factor that influences end diastolic volume is the filling time, or the amount of time available for blood to enter (fill) the ventricles before the ventricles contracts. It is essentially equivalent to the time the heart spends in diastole. It can be influenced by altering heart rate, and the speed at which the heart relaxes. If you decrease heart rate, you increase the time the heart spends in diastole, thereby increasing end diastolic volume and stroke volume. However, as heart rate increase stoke volume begins to decrease; due to a reduction in filling time. Initially, the decrease in SV is not great enough to “offset” the increase in heart rate and cardiac output increases. However, there can reach a point where heart rate has increased so much that stroke volume decreases dramatically leading to a reduction in cardiac output. As such, continually increasing heart rate cannot, on its own, lead to infinite increases in cardiac output because filling time becomes so short that not enough blood enters the ventricles and therefore SV becomes very small. However, this can be counteracted by sympathetic stimulation to the heart. This is because sympathetic stimulation can increase the rate at which the heart relaxes by causing an increase in the rate of calcium sequestering in the sarcoplasmic retic2+um. This is accomplished by the sympathetic-stimulation induced phosphorylation of the Ca ATPase on the sarcoplasmic reticulum membrane that moves calcium from the cytosol back into the SR. 4    The examples in the lecture initially show a situation with a SV of 100 ml and a heart rate of 60 beats per minute leading to a CO of 6 litres per min. If heart rate is doubled to 120 beats per minute, the reduction in filling time causes SV to drop to 60 ml. However, the drop in SV isn’t enough to cause a reduction in CO, which increases to 7.2 litres per minute. However, if HR then increases to 180 beats per minute, the greatly reduced filling time causes SV to drop to 35 ml. In this case CO falls to 6.3 litres per minute. So, an increase in HR from 60 to 120 doesn’t cause a decrease in CO but an increase from 120 to 180 does cause a decrease in CO. This can be countered by sympathetic stimulation. 5    In the absence of sympathetic stimulation, when HR is 120 beats per min, SV is 60 ml and CO is 7.2 litres per minute. However, if you add sympathetic stimulation to a HR of 120 beats per minute, SV increases to 160 ml leading to a CO of 19.2 litres per minute. In the extreme tachycardia example, when HR was 180 beats per min in the absence of sympathetic stimulation, SV was 35 ml and CO was 6.3 litres per min. However, when sympathetic stimulation is added to a HR of 180 beats per minute, SV increases from 35 ml to 80 ml leading to a CO of 14.4 litres/min. 6    The Coronary Circulation and Coronary Blood Flow Blood flow to the heart muscle itself (i.e., to the cardiac myocytes), occurs primarily during diastole. The reason for this is that during systole, the heart's contraction compresses some of the coronary arteries, and completely occludes them - it doesn't do it do all of them, but to a large portion. Contraction also causes the closure of the opening of the coronary arteries. In mammals, the heart must be supplied with blood through the coronary arteries. Although blood is constantly flowing through the atria and the ventricles, there is very little diffusion of oxygen to the cardiac muscle from blood within the lumen of the heart. As such, the heart needs its own blood vessels to supply gases to it. These coronary arteries come off from the aorta, and then branch out to the rest of the heart. If we compare the trace of aortic pressure to a trace of coronary blood flow (during the cardiac cycle), we can see some interesting differences. Coronary flow is pulsatile; it moves up and down, although in general the trace is roughly similar to the aortic pressure trace. The main difference is that blood flow reaches its maximum during early diastole, whilst it drops significantly during isovolumetric contraction (down to almost nothing) and remains low during ventricular ejection. In a patient with coronary obstruction, normal blood flow is altered. During the systolic period, blood flow actually becomes negative: it flows slightly backwards, out of the arteries and back into the aorta. Blood still flows properly in diastole, but at a significantly reduced level. Both of these effects remain true during exercise as well, but are enhanced compared to rest. 7    When we look at blood flow distribution, we will see that during exercise, blood flow is maintained to certain organs such as the heart or the brain, whilst it is reduced to other organs such as the gut, liver and kidneys. This is due to the different distributions of adrenergic receptors on the different organs. Coronary arteries have beta adrenergic receptors, which allow them to dilate during exercise, as opposed to alpha receptors which would cause them to constrict. 8    Factors Affecting End Diastolic Volume: Starling’s Law/Effect and Starling Curves Starling's Law can be illustrated by what we call Starling curves - graphs of stroke volume against end diastolic volume. This generates a long, gentle
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