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Transcript
The Pressures of the Cardiac Cycle The Peer Teaching Society is not liable for false or misleading information… Frank Starling’s Law of the Heart ‘stroke volume will increase in response to an increase in the volume of blood filling the heart when all other factors remain constant.’ Explanation: cardiac muscle not at optimal stretch for force generation at rest therefore increased filling increases stretch and so increases the force of contraction. The Peer Teaching Society is not liable for false or misleading information… The Length-Tension Relationship • As preload increases there is an increase in the active tension that develops. • This means there is a greater velocity of shortening • So increasing preload allows the muscle to contract harder against a given afterload. • To increase Vmax you need to increase the inotropy (the force of the muscular contractions) The Peer Teaching Society is not liable for false or misleading information… Preload “The amount of filling of the ventricles before contraction, aka the end-diastolic volume. Relates to the amount of stretch on the sarcomeres of the heart muscle before contraction” As a rule preload will be increased by anything that increases the stretch of the cardiac muscle and increases ventricular filling/venous return. e.g. aortic stenosis, ventricular systolic failure It will be decreased by anything that reduces cardiac muscle stretch and reduces venous return/ventricular filling. e.g. mitral or tricuspid valve stenosis, atrial fibrillation The Peer Teaching Society is not liable for false or misleading information… Afterload “the work of the heart while ejecting the blood, depends on the ABP and the thickness of the ventricles” Increase in Afterload DECREASES stroke volume, INCREASES LVEDP Reduces the fibre shortening velocity within the finite time available, thus the contraction is not as strong and more blood remains in the left ventricle. Decrease in Afterload INCREASES stroke volume, DECREASES LVEDP Reduction in ABP leads to a reduction in afterload so ventricles can eject more blood and less remains. The Peer Teaching Society is not liable for false or misleading information… Afterload vs. Preload vs. Frank-Starling Law • As afterload increases it causes an increase in left ventricular end-diastolic pressure (LVEDP) (i.e., increases preload). • This occurs because the increased end-systolic volume combines with the venous return into the ventricle and this increases end-diastolic volume. • This increase in preload activates the Frank-Starling mechanism to partially compensate for the reduction in stroke volume caused by the increase in afterload • Consequently the heart muscle contracts more forcefully, therefore increasing stroke volume again. The Peer Teaching Society is not liable for false or misleading information… Afterload vs. Preload vs. Frank-Starling Law This principle is used in the treatment of heart failure…vasodilators reduce the ABP therefore increases SV as ESV is reduced. EDV is subsequently reduced however SV increases overall as the reduction in EDV is not as great as the reduction in ESV. The Peer Teaching Society is not liable for false or misleading information… Cardiac and Vascular Changes Accompanying Heart Failure Compensatory Mechanisms During Heart Failure Cardiac Decreased stroke volume & cardiac output Increased end-diastolic pressure Ventricular dilation or hypertrophy Impaired filling (diastolic dysfunction) Reduced ejection fraction (systolic dysfunction) Cardiac Frank-Starling mechanism Chronic ventricular dilation or hypertrophy Tachycardia Vascular Increased systemic vascular resistance Decreased arterial pressure Impaired arterial pressure Impaired organ perfusion Decreased venous compliance Increased venous pressure Increased blood volume Hormones Renin-angiotensin-aldosterone system Vasopressin (antidiuretic hormone) Circulating catecholamines Natriuretic peptides Autonomic Nerves Increased sympathetic adrenergic activity Reduced vagal activity to heart The Peer Teaching Society is not liable for false or misleading information… Pressure-Volume Loops Pressure and Volume Changes During Two Cardiac Cycles Image from https://www.emaze.com/@AOLIFFOZ/cvs.pptx 1. As mitral valve closes pressure in LV increases 2. Aortic valve opens and blood moves into the aorta 3. Ventricles ‘wring out’ all the blood into the aorta so pressure increases in both aorta and ventricle 4. Pressure falls and the aortic valve closes. Here you see the ‘dicrotic notch’, a brief increase in pressure as blood flows back towards heart but is blocked by the closed valves causing a transient rise in aortic pressure. 5. Pressure falls until mitral valve opens and ventricles begin to fill again. The Peer Teaching Society is not liable for false or misleading information… The Peer Teaching Society is not liable for false or misleading information… The Normal ECG Image from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ecg.html The Normal ECG The Peer Teaching Society is not liable for false or misleading information… The Heart Sounds Lub= S1, closing of mitral and Tricuspid valves Dub= S2, closing of aortic and pulmonary valves Summary • Be able to define Frank-Starling, Preload, Afterload, SV, CO, EDV and ESV • Integrate them together and understand how changing one affects others (as in heart failure) • Learn the events of the cycle and how the pressure in the heart and arteries changes throughout • Be able to recognise the stages on the pressure volume loops, cardiac cycle graphs and a normal ECG The Peer Teaching Society is not liable for false or misleading information… References CV Physiology Concepts http://www.cvphysiology.com/index.html Vanders Human Physiology, 11th Ed. http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ecg.html The Peer Teaching Society is not liable for false or misleading information…