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Lecture

BIOC33/34 Lec 6.docx

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Department
Biological Sciences
Course Code
BIOC33H3
Professor
Stephen Reid

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BIOC34 Lec 6. Jan 22/14  Assignment #1 due Fri  SV regulation o 3 components:  Force of ventricular contraction - affected by sympathetic innervation, leading to enhanced levels of Ca - lead to greater filament binding and sliding  more contraction  Afterload (blood pressure ) - if BP is high, the ventricle is pumping against a higher pressure - harder for ventricle to pump against this • High BP leads to lower SV because pumping against higher pressure downstream  EDV - amount of blood in ventricle at end of relaxation phase • 6 factors affecting: • Preload - pressure in vena system; if this pressure is higher, pushes more blood in atria and ventricle - get higher ventricular filling o Venus pressure pushing blood into ventricles  Ventricular compliance o Compliance =ΔVolume /ΔPressure  measure of how easily ventricle can stretch or fill. Opposite is stiffness  High change in V for any change in P - have a compliant ventricle o Stiffness =ΔPressure /ΔVolume  Small change in V for given change in P - heart will be stiff o Diagram:  Standard way in which seeing compliance curves  Normal curve: For any given change in P (0-10 ml of mercury), EDV goes from 0-125 ml  With a less compliant lung that doesn’t stretch as easily, same change in P leads to an EDV of 50 ml. on increased compliance curve, P=0-10, EDV= 0-250  Increased compliance leads to increases in V  EDV o Easier to take curve and flip axis around; easier to conceptualize o When we flip axis around and plot V as a function of P, see that the increased compliance curve has a higher curve and decreased compliance curve has a smaller curve o Lower compliance = lower change of V for that given change in P  Skeletal muscle pump o This is the action of skeletal muscle contraction on veins and extremities that help force blood up to the heart o E.g. calf muscle  Vein running through  When this muscle is active and contracting, squeezes inward on vein and forces blood upwards  Series of valves preventing blood from falling  When muscle contracts and forces blood goes upwards, there is an increase in P in the vein moving upwards  Causes increase of P in upper region  This causes proximal valve (called proximal because it is closer to the heart) to open. These valves are flaps of tissue. If pressure is closing downward and pressure under valve is high, causes valve to open  In lower regions of leg, do not get blood falling backwards into ankle because there is another valve at the bottom (distal valve) which is closed. This is because we have a high pressure of blood in lower region, which exerts pressure downwards that causes the valve to close downwards  Contraction of muscle forces blood to go upwards, opens valve and moves blood towards the heart  Contraction of muscle puts pressure downwards and keeps distal valve closed o In varicose veins, stretched veins, valves are not able to open and close properly. Blood pools and stretches veins further  Skeletal muscle pump o When the muscle relaxes, there is no longer a build-up of pressure in the vein because the muscle is not squeezing inward on it o Lower pressure causes distal valve to open and it allows blood from the lower regions (ankle, smaller venules) to flow upwards and into larger veins in between the muscles o Lower pressure in the vein when muscle is relaxing, is not sufficient to cause proximal valve to open, so proximal valve closes and blood cannot flow backwards from the upper regions of the thigh back down into leg  During muscle contraction, blood is forced upward and when it relaxes, more blood is able to flow to lower regions of leg and do not get back flow because proximal valve is closed  Waveform o Skeletal muscle pump has been used for home therapeutic treatment to stop deep vein thrombosis (blood clots) - important when on plane flights to walk around every hour or so o Waveform wrap allows blood to move from leg up to the heart o Small blood clot is not a problem; problem is when blood clots form and break loose and travels up the vein towards the heart o Blood clot forming and breaking up = deep vein thrombosis  Goes into atria, ventricle, gets lodged in a blood vessel in the lungs - are very thin and small • Pulmonary embolism o Pulmonary embolism has many negative effects - blood is not flowing to that part of lungs, tissues die. Blood clots lead to build-up of pressure since blood is not flowing to parts of lung. Behind the clot, blood can’t flow and get fluid leaking from blood vessels into lung tissue  Pulmonary edema • Inhibits gas exchange  Respiratory pump o Act of breathing forces blood from abdomen into chest (inspiration) and from vessels in the chest into the heart during expiration o Major respiratory muscle = diaphragm  Forms border between thoracic cavity/chest and abdomen o When we inspire, diaphragm contracts and moves downward - causes chest to expand o When diaphragm contracts and moves downwards, creates a downward pressure causing increase of pressure on the abdomen.Abdominal pressure increases above pressure in the chest (thoracic cavity) o This pressure in the abdomen causes blood to flow upwards to the chest and towards the heart o Expiration - get an increase in pressure in the chest but does not lead to back flow of blood downwards because there are veins preventing this  When diaphragm relaxes and moves upwards, get upward pressure of diaphragm increasing the pressure of chest thoracic cavity. High pressure in chest forces blood from superior vena cava, etc. down into the atria where they flow into ventricle o These help move vena’s blood into heart and enhance EDV  Filling time + starling effect o Blend into each other  Filling time o Filling time:Amount of time available for ventricles to fill with blood; this occurs at early-ish to mid-late diastole phase. In diastole have isovolumetric relaxation where all the valves are closed and move into mid-late diastole phases - increase in volume in ventricles and slow decrease in aortic pressure o Amount of time in these phases =AV valves open and blood flows in o More time in diastole = more time for ventricles to fill o Can increase amount of time in diastole by decreasing heart rate - get more time for ventricles to fill with blood o SV vs. EDV = starling curve o Diagram shows our starling effect o This relationship occurs due to stretching of muscle in cardiac myositis? o Starling effect = EDV increases lead to SV increases o Going to increase HR and see how it decreases SV o Cannot increase HR indefinitely without leading to decreases in CO because increasing HR, filling time decreases; as this decreases, EDV decreases and SV decreases o Large increases in HR can lead to decreases in SV that ultimately become so severe that overall CO decreases as well o Inability to increase CO while continually increasing HR can be dealt with sympathetic stimulation  Can increase HR to high levels without compromising SV  Result of rapid Ca sequestering back into sarcoplasmic reticulum after Ca has been released into cytoplasm of muscle cells, triggering contractile events  Diagrams o Plot left ventricular volume during 2 heart beats; not typical curves  These are more for illustrative purposes o In upper diagram, have a heart rate of 60 beats/min. SV = 100mls. Start at 120ml as EDV and 20 ml over ESV. Difference =100. HR x SV = 6L/min o With tachycardia (bottom diagram)  HR has doubled - 120 beats/min  Since the heart is beating faster, not as much time for heart to fill with each beat. Filling time is decreased to half. SV has decreased from 100 to 60 ml.
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