Physiology Reinforce Concepts PDF

Vessel Resistance Resistance increases with: Increasing vessel length, Decreasing vessel diameter- largest effect(D^4), Increased viscosity(thickening of blood, ex. polycythemia), Lower shear rate(higher viscosity) As blood crosses an area of high resistance, pressure drops Resistance decreases with...

Vessel Resistance Resistance increases with: Increasing vessel length, Decreasing vessel diameter- largest effect(D^4), Increased viscosity(thickening of blood, ex. polycythemia), Lower shear rate(higher viscosity) As blood crosses an area of high resistance, pressure drops Resistance decreases with: Decreased vessel length, Increased diameter, Thinning of the blood/anemia(reduced viscosity) Stenosis leads to turbulence: An increased chaotic environment in a blood vessel leads to turbulent flow, that chaos includes: ● Increased velocity of flow ● Decreased viscosity ● Decreased area Blood Velocity Velocity(U)=flow(Q)/Area(A) As we go from artery->arteriole->capillary, the summed cross sectional area of the vessels in each category increases. Increased denominator shows why as blood flows from arteries->arterioles->capillaries it loses velocity. Compliance Compliance: How well can a vessel respond when it is filled(transmural pressure increases) The stiffness of a vessel depends on the wall components, and the vessel structure. Wall Components: collagen/elastin ratio ● ● Elastin: flexible material, rubberband-like, more elastin increases compliance Collagen: firm structural material, more collagen increases stiffness Wall Structure: wall thickness/vessel radius ratio ● ● Wall thickness: increased wall thickness increases stiffness Vessel radius: increased vessel radius increases compliance As a compliant vessel expands, its capability to expand more decreases, meaning compliance decreases Non compliant vessels will have higher blood pressures Pulse wave speed is slower in compliant vessels, as the vessel expands in response to the increasing volume(such as a pulse wave) area increases, and remember U=Q/A Compliance can be seen as the slope of a Volume, Pressure graph. Because veins are so compliant, and more dependent on external forces like respiratory motion and muscle contractions to pump blood, they need valves. Without valves, the vertical blood column would cause bowing of the vein distally due to pressure buildup. Pacemaker and Myocyte APs Action potentials are self generated at the SA node, distribute around the atria on their way to the AV node, travel to the bundle of his, down the left and right bundle branches distributing to the interventricular septum, and up the Purkinje fibers distributing to the ventricles Automaticity is made possible because these cells have Funny Channels: activated by hyperpolarization, it is a nonselective cation channel causing sodium and potassium influx bringing cell toward threshold. Sympathetic stimulation increases activity of funny channels and calcium channels, leads to more cation influx during phase 4 allowing pacemaker to reach threshold sooner Parasympathetic stimulation leads to increased potassium efflux by IKACh channels, and low cAMP production lowers activity of funny channels and calcium channels. Pacemaker will have less cation influx and get to threshold later Preload, Afterload, Inotropy Preload is the amount of blood that fills the heart before it contracts ● Increasing preload increases the force of contraction, thereby increasing stroke volume! Afterload is the resistance the ventricle must overcome to eject the blood ● ● ● High afterload slows the contraction velocity of the ventricles Slower contraction velocity causes less blood to be ejected during a ventricular contraction, the stroke volume will reduce Since the stroke volume reduces, more blood remains in the ventricle at the end of systole. High afterload increases the end systolic volume Inotropy is the contractility of the heart ● ● ● Alterations in calcium availability alter inotropy Drugs like digoxin, and sympathetic stimulation increase inotropy Increasing the inotropy will increase the stroke volume if preload is constant Determinants of cardiac function Preload measures: ● ● ● End diastolic volume is best measure of preload, how much did the heart fill? End diastolic pressure, relies on ventricle compliance Central venous pressure, more CVP leads to more venous return, more preload Afterload measures: ● ● ● Wall stress is the best measure of afterload remember the transmural pressure increases the wall tension, in order to contract the cardiomyocyte has to overcome the wall tension Total peripheral resistance Aortic/ventricular pressure-easiest to measure Determinants of Stroke Volume: Frank starling Law of preload, increased preload increases SV, Sympathetic input increases contractility(Inotropy), increased inotropy increases Stroke volume, Increased afterload increases the resistance the heart is contracting against, slows the contraction and reduces the stroke volume Determinants of Heart Rate: Increased sympathetic activity activates funny channels and calcium channels, increases the slope of slow wave action potentials, increases the HR, Vagus nerve is parasympathetic. Increased vagus input will reduce cAMP failing to activate the funny current. Also parasympathetic activates IKACh channels, in total it reduces the slope of phase 4, lowering heart rate Pump failure and valve conditions A systolic failure is an inadequate myocardial contraction, the heart cannot pump blood out.A diastolic failure is a filling defect, the heart does not receive adequate preload. Volume overload is going to be a major symptom of heart failure, there is fluid buildup and backflow in the part of the body behind the failed pump(Right heart: leg swelling, ascites, left heart:pulmonary edema) Aortic Stenosis: systolic murmur, Increased afterload requires larger left ventricular pressure for ejection to occur, this will be seen as a longer isovolumetric contraction on the PV loop, and a increased gradient between LVP and ABP on Wiggers diagrams Aortic Regurgitation: diastolic murmur, The loss of blood volume in the aorta will be seen as a rapid drop in aortic blood pressure on a Wiggers diagram. On the PV loop, volume will increase during the isovolumic contraction and relaxation phases Mitral Stenosis:, diastolic murmur, a large LAP-LVP gradient will be seen on Wiggers Diagram. Since there is more resistance during diastole, a reduced EDV will be seen on PV loop. Contractility remains constant, ESV also reduces Mitral Regurgitation: systolic murmur, Ventricular contraction pushes blood into the atria, this progressively increases LAP throughout the ventricular contraction(seen on Wiggers)this will increase the preload for the next beat and will be seen on the PV loop by increased EDV. On the PV loop there will also be be volume loss during isovolumic contraction and relaxation